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Clinical Examination in
z.f
B.N. Vijay Raghawa Rao

CLINICAL EXAMINATION IN
CARDIOLOGY

CLINICAL EXAMINATION IN
CARDIOLOGY

MD, DM (CARDIOLOGY), DHA, FCCP, FICC, MBA (HM)
Formerly Addl. Director, Professor & HOD

Gandhi Medical College/Gandhi Hospital,
Secunderabad, Hyderabad, India
Presently Consultant Interventional Cardiologist
Vijay Marie and Yashoda Superseciality Hospitals,
Hyderabad, India
ELSEVIER
A division of
Reed Elsevier India Private Limited
Clinical Examination in Cardiology
ELSEVIER
A division of
Reed Elsevier India Private Limited
Mosby, Saunders, Churchill Livingstone, Butterworth Heinemann and

Hanley & Belfus are the Health Science imprints of Elsevier.
2007 Elsevier
First Edition 2007
All rights are reserved. No part of this publication may be reproduced,

stored in a retrieval system, or transmitted in any form or by any means,
electronic, mechanical, photocopying, recording or otherwise, without the
prior permission of the publisher.
ISBN-13: 978-81-312-0964-6
Medical knowledge is constantly changing. As new information becomes

available, changes in treatment, procedures, equipment and the use of drugs
become necessary. The authors, editors, contributors and the publisher have,
as far as it is possible, taken care to ensure that the information given in this
text is accurate and up-to-date. However, readers are strongly advised to
confirm that the information, especially with regard to drug dose/usage,
complies with current legislation and standards of practice.
Published by Elsevier, a division of Reed Elsevier India Private Limited

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New Delhi 110 065, India.
Publishing Director: Sanjay K Singh

Commissioning Editor: Sonali Dasgupta
Developmental Editor: Dr Shelley Narula
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Typeset by Olympus Infotech Pvt. Ltd, Chennai, India.
Printed and bound at Nutech Photolithographer, New Delhi.

Dedicated to my parents, Shri B. Narsimha & Smt B. Laxmamma,
my wife Dr Shashikala, my daughters Dr Visha Rao & Vishala Rao
and my teachers, students & patients
who constantly encouraged to write & revise this clinical treatise.
P REFACE TO R EVISED R EPRINT
First Edition of Clinical Examination in Cardiology was published in 2007 by Elsevier India Pvt. Ltd which was
well received and appreciated by PG students of Gen. Medicine, Pediatrics and Cardiology as well as by the prac-
ticing physicians, besides being a great helpful to undergraduate students. However there were some printing
errors which were overlooked inadvertently. These errors have been corrected and even some figures, graphs,
photographs and tables have been revised and updated in this revised reprint which will be an asset to clinical
decision making.
I am thankful to Elsevier India Pvt. for their keen interest shown in revising and reprinting this clinical text
book.
Dr B.N. Vijay Raghawa Rao

P REFACE TO THE E ARLIER E DITION
It is mans mission to learn to understand
Clinical Examination in Cardiology is primarily a clinical treatise. It provides a simple, lucid and comprehensive
description of Basic Anatomy and Physiology of Cardiovascular Medicine, Clinical Cardiology, and Basic Bedside
Investigations (Electrocardiogram and X-ray Chest) in a single book. It is the first of its kind in the present millennium
highlighting the forgotten Clinical Cardiology, in a scenario where cardiovascular disease is now a global problem
with enormous economic consequences.
Besides index, this book consists of six parts with 34 chapters. Part 1 deals with Basic Anatomy and Physiology
of Cardiovascular Medicine with ten chapters comprehensively described for better understanding of clinical car-
diology. Part 2 follows the initial chapters which deal with Cardiac Symptomatology in two chapters. Part 3 with
three chapters consists of General Physical Examination, Arterial Pulse and Blood Pressure described in detail.
Part 4 has two chapters describing Jugular Venous Pulse and Jugular Venous Pressure in detail. Part 5 follows with
five chapters which describe cardiovascular examinationInspection, Palpation, Percussion and Precordium in
Common Heart Diseases, and Auscultation. Finally, basic investigations are described in two portions, which are
essential for comprehensive discussion of diagnosis and management of a cardiovascular disease. This Part 6
includes, Part 6a: Clinical Electrocardiography with nine chapters, which include basic concepts, normal ECG,
common disease conditions, drugs effects, arrhythmias and prediction of coronary artery occlusion in a patient of
acute myocardial infarction. Part 6b: Radiology of the Heart and Great Vessels includes four chapters, describing
introduction, technical facts, routine reporting of an x-ray chest, calcifications and other views. Each chapter has
adequate figures, tables and references, which can be used for rapid review of the material described. In total, there
are 749 figures, 245 tables, and 675 references.
This book is primarily focused for postgraduate students of General Medicine, Cardiology and Paediatrics.
However, it will also be useful for the undergraduate students for better understanding of clinical cardiology, which
is a part of general medicine. It may also prove useful to those who wish to broaden their knowledge of clinical cardi-
ology and will aid in their day-to-day practice of cardiology. Besides my teaching experience of undergraduate and
postgraduate medical students, I have also used standard textbooks and journals of Cardiovascular Medicine as
references in compiling this clinical entity.
I am thankful to my postgraduates, Dr Pramod, Dr Rajkiran and Dr Narender for providing beautiful photo-
graphs. I am indebted to my patients at my clinic, Remedy Superspeciality Hospital and Gandhi Medical College &
Hospital for their immense cooperation.
My special thanks to Mr Sanjay Singh and Dr Shelley Narula of Elsevier India Pvt. Ltd. for their constant encour-
agement and keen interest shown in completing this clinical treatise.
Dr B.N. Vijay Raghawa Rao

C ONTENTS
Preface vii
Abbreviations xi
PART I BASIC ANATOMY AND PHYSIOLOGY 1

Chapter 1 Anatomy of the heart 3
Chapter 2 Lymphatic system of the heart 28
Chapter 3 Venous drainage of the heart 31
Chapter 4 Arterial supply of the heart 34
Chapter 5 Nerve supply of the heart 40
Chapter 6 The conduction system of the heart 47
Chapter 7 Ultrastructure of the myocardium 54
Chapter 8 Basic electrophysiological principles 66
Chapter 9 Molecular basis of muscle contraction 73
Chapter 10 The cardiac cycle 77
PART 2 THE HISTORY AND SYMPTOMATOLOGY 83

Chapter 11 Cardinal symptoms 85
Chapter 12 Other symptoms 144
PART 3 GENERAL PHYSICAL EXAMINATION 159

Chapter 13 General examination 161
Chapter 14 Arterial pulse 225
Chapter 15 Measurement of the blood pressure 249
PART 4 JUGULAR VENOUS PULSE 269

Chapter 16 Introduction and jugular venous pulse waves 271
Chapter 17 Estimation of venous pressure and JVP in diseased conditions 283
PART 5 CARDIOVASCULAR SYSTEM EXAMINATION 297

Chapter 18 Inspection of the precordium 299
Chapter 19 Palpation of the precordium 315
x CONTENTS
Chapter 20 Percussion of the precordium and precordial findings in

common heart diseases 333
Chapter 21 Cardiac auscultation 354
PART 6A BASIC INVESTIGATIONS: CLINICAL

ELECTROCARDIOGRAM 457
Chapter 22 Introduction and basic concepts 459
Chapter 23 The normal electrocardiogram 474
Chapter 24 Abnormal P, T and U waves 490
Chapter 25 Ventricular hypertrophy 500
Chapter 26 Intraventricular conduction defects 516
Chapter 27 Myocardial infarction and ischemia 533
Chapter 28 Pericarditis and myocarditis 560
Chapter 29 Drug effects and electrolyte abnormalities 568
Chapter 30 Arrhythmias 580
PART 6B BASIC INVESTIGATIONS: RADIOLOGY OF

THE HEART AND GREAT VESSELS 659
Chapter 31 Introduction and evaluation of heart 661
Chapter 32 The pulmonary vasculature 684
Chapter 33 Cardiac calcification 693
Chapter 34 Evaluation of extracardiac structures and chest X-ray in other views 701
Index 708
A BBREVIATIONS
PART 1 RFW: rapid filling wave

ADP: adenosine diphosphate RLD: right lymphatic duct
AHA: american heart association RV: right ventricle
AJR: abdominal jugular reflux SA node: Sinoatrial node
AML: anterior mitral leaflet SERCA: sarco endoplasmic reticulum calcium ATPase
ANP: atrial natriuretic peptide SFW: slow filling wave
ATP: adenosine triphosphate SL: semilunar
AV node: atrio ventricular node SVC: superior vena cava
AV: atrioventricular VMC: vasomotor center
AVT: anterior interventricular trunk
CICR: calcium induced calcium release PART 2
CLN: cardiac lymph node Af: atrial fibrillation
CT: chordae tendinae ALCAPA: anomalous left coronary artery from
CVA: cerebrovascular accident pulmonary artery
CVC: cardiac vagal center AMI: acute myocardial infarction
IVC: inferior vena cava AP: angina pectoris
JSR: junctional sarcoplasmic reticulum AR: aortic regurgitation
LA: left atrium ARVD: arrhythmogenic right ventricular dysplasia
LAD: left anterior descending AS: aortic stenosis
LBB: left bundle branch ASD: atrial septal defect
LCx: left circumflex AVRT: atrioventicular reciprocating tachycardia
LCC: left coronary channel BBB: bundle branch block
LMCA: left main coronary artery CAD: coronary artery disease
LV: left ventricle CCS: Canadian cardiovascular society
MHC: myosin heavy chain CHF: congestive heart failure
MLC: myosin light chain CHD: congenital heart disease
MSC: main supracardiac channel CHB: complete heart block
OM: obtuse marginal CM: cardiomyoapthy
OMT: obtuse marginal trunk COA: coarctation of aorta
PDA: patent ductus arteriosus COPD: chronic obstructive pulmonary disease
PFO: patent foreman ovale CRF: chronic renal failure
PML: posterior mitral leaflet CT: cardiac tamponade
PM: papillary muscle CVA: cerebrovascular accident
pCO2: partial pressure of carbon dioxide DCM: dilated cardiomyoapthy
pO2: partial pressure of oxygen DORV: doublet outlet right ventricle
PVT: posterior interventricular trunk HCM: hypertrophic cardiomyopathy
RA: right atrium HOCM: hypertrophic obstructive cardiomyopathy
RBB: right bundle branch LAD: left anterior descending
RCA: right coronary artery LAHB: left anterior hemi block
RCC: right coronary channel LBBB: left bundle branch block
xii ABBREVIATIONS
LCA: left coronary artery CT: cardiac tamponade

LVF: left ventricular failure CT: computed tomography
LVOTO: left ventricular outflow tract obstruction DCM: dilated cardiomyopathy
MI: myocardial infarction DM: diabetes mellitus
MR: mitral regurgitation HCM: hypertrophic cardiomyopathy
MS: mitral stenosis HOCM: hypertrophic obstructive cardiomyopathy
MVP: mitral valve prolapse MI: myocardial infarction
MVV: maximum voluntary ventilation MRI: magnetic resonance imaging
NYHA: New York heart association MS: mitral stenosis
PAPVC: partial anomalous pulmonary venous MVP: mitral valve prolapse
connection PAPVC: partial anomalous pulmonary venous
PAT: paroxysmal atrial tachycardia connection
PDA: patent ductus arteriosus PDA: patent ductus arteriosus
PE: pulmonary embolism PR: peripheral resistance, pulmonary regurgitation
PND: paroxysmal nocturnal dyspnea PS: pulmonary stenosis
PS: pulmonary stenosis PVC: premature ventricular contraction
PVR: pulmonary vascular resistance PVR: pulmonary vascular resistance
PTCA: percutaneous transluminal coronary angioplasty RSOV: rupture of sinus of Valsalva
RBBB: right bundle branch block SLE: systemic lupus erythematosus
RVOTO: right ventricular outflow tract obstruction SVC: superior vena cava
SAC: specific activity scale SV: stroke volume
SLE: systemic lupus erythematosus TAPVC: total anomalous pulmonary venous
SSS: sick sinus syndrome connection
SV: single ventricle TGA: transposition of great arteries
SVR: systemic vascular resistance TOF: tetralogy of Fallot
SVT: supraventricular tachycardia TR: tricuspid regurgitation
TAPVC: total anomalous pulmonary venous TS: tricuspid stenosis
connection VSD: ventricular septal defect
TGA: transposition of great arteries
TOF: tetralogy of Fallot PART 4
TV: tidal volume, tricuspid valve AJR: abdominal jugular reflux
VC: vital capacity ASD: atrial septal defect
VSD: ventricular septal defect CHB: complete heart block
VT: ventricular tachycardia CHF: congestive heart failure
COPD: chronic obstructive pulmonary disease
PART 3 CVP: central venous pressure
ABPM: ambulatory blood pressure monitoring EJV: external jugular vein
AD: autosomal dominant inheritance EMF: endomyocardial fibrosis
AP window: aortopulmonary window IJV: internal jugular vein
AS: aortic stenosis LVF: left ventricular failure
ASD: atrial septal defect MR: mitral regurgitation
AR: aortic regurgitation MS: mitral stenosis
AR: autosomal recessive inheritance PE: pulmonary embolism
BMI: basal metabolic index PS: pulmonary stenosis
CAD: coronary artery disease RVF: right ventricular failure
CHF: congestive heart failure RVEDP: right ventricular end diastolic pressure
CO: cardiac output SVT: supraventricular tachycardia
COA: coarctation of aorta TR: tricuspid regurgitation
ABBREVIATIONS xiii
TS: tricuspid stenosis OS: opening snap

TV: tricuspid valve PADP: pulmonary artery diastolic pressure
VT: ventricular tachycardia PBF: pulmonary blood flow
PDA: patent ductus arteriosus
PART 5 PH: pulmonary hypertension
ACG: apex cardiogram PSM: pan systolic murmur
AFM: Austin Flint murmur PSL: para sternal lift
ALCAPA: anomalous left coronary artery from PVC: premature ventricular contraction
pulmonary artery RSOV: rupture of sinus of Valsalva
AML: anterior mitral leaflet RVF: right ventricular failure
AP window: aortopulmonary window RVEDP: right ventricular end diastolic pressure
AR: aortic regurgitation RVH: right ventricular hypertrophy
AS: aortic stenosis RVOT: right ventricular outflow tract
ASD: atrial septal defect SM: systolic murmur
BVH: biventricular hypertrophy TAPVC: total anomalous pulmonary venous
CAD: coronary artery disease connection
CC: closing click TB: tuberculosis
CHD: congenital heart disease TGA: transposition of great arteries
CHF: congestive heart failure TOF: tetralogy of Fallot
COA: coarctation of aorta TR: tricuspid regurgitation
COPD: chronic obstructive pulmonary disease TS: tricuspid stenosis
DM: diastolic murmur TV: tricuspid valve
DORV: double outlet right ventricle VSD: ventricular septal defect
EDM: early diastolic murmur
ES: ejection sound PART 6A
ESM: ejection systolic murmur Af: atrial fibrillation
HCM: hypertrophic cardiomyopathy Afl: atrial flutter
HOCM: hypertrophic obstructive cardiomyopathy AHA: American Heart Association
ICS: intercostal space AIVR: accelerated idioventricular rhythm
LAP: left atrial pressure AMI: acute myocardial infarction
LVF: left ventricular failure ARVD: arrhythmogenic right ventricular dysplasia
LBBB: left bundle branch block AR: aortic regurgitation
LPSA: left para sternal area AS: aortic stenosis
LVH: left ventricular hypertrophy ASD: atrial septal defect
LVD: left ventricular dysfunction AT: atrial tachycardia
LVED: left ventricular end diastolic AVC: aberrant ventricular conduction
LVEDP: left ventricular end diastolic pressure AVNRT: atrioventricular nodal reciprocating
LVOT: left ventricular outflow tract tachycardia
LVOTO: left ventricular outflow tract AVRT: atrioventricular reentry tachycardia
obstruction BBB: bundle branch block
MDM: mid diastolic murmur CAD: coronary artery disease
MR: mitral regurgitation CABG: coronary artery bypass graft
MRI: magnetic resonance imaging CHF: congestive heart failure
MS: mitral stenosis COA: coarctation of aorta
MSM: mid systolic murmur COPD: chronic obstructive pulmonary disease
MVP: mitral valve prolapse CP: constrictive pericarditis
NES: non ejection sound CT: cardiac tamponade
OC: opening click CTI: cavo tricuspid isthmus
xiv ABBREVIATIONS
DAD: delayed after depolarization SVC: superior vena cava

GUSTO: global utilization of streptokinase and SVT: supraventricular tachycardia
tissue plasminogen activator for occluded TDP: torsades de pointes
coronary arteries TGA: transposition of great arteries
HTN: hypertension TOF: tetralogy of Fallot
ICS: intercostal space TR: tricuspid regurgitation
IVC: inferior vena cava Vf: ventricular fibrillation
LAA: left atrial abnormality Vfl: ventricular flutter
LAE: left atrial enlargement VPC: ventricular premature contraction
LAD: left anterior descending, VT: ventricular tachycardia
left axis deviation WPW: Wolffe Parkinson White
LAFB: left anterior fascicular block
LBBB: left bundle branch block PART 6B
LCx: left circumflex AP view: anteroposterior view
LGL: Lown Ganong Levine ASD: atrial septal defect
LPFB: left posterior fascicular block CAD: coronary artery disease
LVH: left ventricular hypertrophy CHF: congestive heart failure
LVOT: left ventricular outflow tract COPD: chronic obstructive pulmonary disease
MAT: multifocal atrial tachycardia CT: computed tomography
MI: myocardial infarction CT ratio: cardiothoracic ratio
MR: mitral regurgitation IVC: inferior vena cava
MVP: mitral valve prolapse LAE: left atrial enlargement
NCTI: non cavo tricuspid isthmus LAO: left anterior oblique
PAPVC: partial anomalous pulmonary venous LPA: left pulmonary artery
connection LVE: left ventricular enlargement
PAC: premature atrial contraction LVF: left ventricular failure
PAT: paroxysmal atrial tachycardia MRI: magnetic resonance imaging
PDA: patent ductus arteriosus PAPVC: partial anomalous pulmonary venous
PES: preexcitation syndromes connection
PH: pulmonary hypertension PA view: posteroanterior view
PJRT: permanent form of AV junctional reciprocating PBF: pulmonary blood flow
tachycardia PDA: patent ductus arteriosus
POTS: postural orthostatic tachycardia syndrome PNS: paranasal sinuses
PS: pulmonary stenosis RAO: right anterior oblique
PTCA: percutaneous transluminal coronary angioplasty RDPA: right descending pulmonary artery
PVC: premature ventricular contraction RVF: right ventricular failure
RAD: right axis deviation RVOT: right ventricular outflow tract
RAA: right atrial abnormality SVC: superior vena cava
RAE: right atrial enlargement TAPVC: total anomalous pulmonary venous
RBBB: right bundle branch block connection
RCA: right coronary artery TGA: transposition of great arteries
RVH: right ventricular hypertrophy TOF: tetralogy of Fallot
RVOT: right ventricular outflow tract VSD: ventricular septal defect
BASIC ANATOMY AND
PHYSIOLOGY
1. Anatomy of the heart 3

2. Lymphatic system of the heart 28
3. Venous drainage of the heart 31
4. Arterial supply of the heart 34
5. Nerve supply of the heart 40
6. The conduction system of the heart 47
7. Ultrastructure of the myocardium 54
8. Basic electrophysiological principles 66
9. Molecular basis of muscle contraction 73
10. The cardiac cycle 77
CHAPTER 1
A NATOMY OF THE H EART
1. GROSS ANATOMY OF THE HEART 3 4. THE FIBROUS SKELETON OF

2. EXTERNAL FEATURES OF THE HEART 16
THE HEART 4 i. Components and Attachments 16
i. The Sulci of the Heart 4 ii. Extensions 17
ii. The Surfaces of the Heart 5 iii. The Bundle of His 17
iii. The Borders of the Heart 6 5. THE VALVES OF THE HEART 17
3. THE CHAMBERS OF THE HEART 7 General Description 17
i. Right Atrium 7 i. Mitral Valve 18
ii. Right Ventricle 10 ii. Tricuspid Valve 22
iii. Left Atrium 12 iii. Semilunar (SL) Valves 24
iv. Left Ventricle 13 REFERENCES 27
1. GROSS ANATOMY OF THE HEART
The heart is a conical, hollow muscular organ situated in the middle mediastinum
behind the sternum and costal cartilages of the 3rd, 4th & 5th ribs. It lies obliquely so that
2/3 of the heart is to the left of the midline. The heart rests upon the diaphragm and
is tilted forward and to the left so that the apex is anterior to the rest of the heart.
The size and weight of the heart may vary depending upon the age, sex, body
length, epicardial fat, and general nutrition. The average human adult heart measures
about 12 cm 9 cm and weighs about 325 75 g in males and 275 75 g in
females1 (see Table 1.1). It is described as follows:
1. External features
2. Chambers of the heart
Table 1.1 Gross anatomy of the heart
Features Description
1. Shape Conical hollow muscular organ

2. Location Middle mediastinum behind the sternum
and costal cartilages of 3rd5th ribs
3. Average size 12 cm 9 cm
4. Average weight 325 75 g in males
275 75 g in females
4 BASIC ANATOMY AND PHYSIOLOGY
3. The fibrous skeleton of the heart

4. The valves of the heart
2. EXTERNAL FEATURES OF THE HEART
The heart has four chambers, right and left atria, and right and left ventricles, which are
separated from each other by sulci and consist of surfaces and borders. The atria lie
above and behind the ventricles (see Table 1.2).
i. The Sulci of the Heart

The atria are separated from the ventricles externally by the coronary (atrioventricular)
sulci and from each other by an interatrial groove, which is faintly visible posteriorly
and hidden by the aorta and pulmonary trunk anteriorly.
The two ventricles are separated from each other by the interventricular sulci
(grooves), which descend from the coronary sulcus toward the apex:
The anterior interventricular sulcus contains the left anterior descending coronary
artery which courses over the muscular ventricular septum between the right and
left ventricles to the apex (see Figs 1.1 and 1.2).
The posterior interventricular sulcus which is situated on the diaphragmatic surface
of the heart is the pathway for the posterior descending coronary artery, which is
usually the terminal branch of the right coronary artery or less frequently of the left
circumflex artery.
The right coronary artery travels in the right coronary sulcus between the right atrium
and right ventricle until it descends on the posterior surface of the heart while the left cir-
cumflex artery runs in the left coronary sulcus between the left atrium and left ventricle.
The crux of the heart is the area on the posterior basal surface:
Where the coronary sulcus meets the posterior interventricular sulcus.
The coronary artery which crosses the crux (usually the right coronary artery) gives
a small branch to the nearby AV node and
Internally, the atrial septum joins the ventricular septum at this junction.
Table 1.2 External features of the heart
1. Chambers RA, RV, LA and LV

2. Sulci Right and left coronary sulci, interatrial groove and anterior and
posterior interventricular sulci
3. Surfaces Diaphragmatic or inferior, anterior or sternocostal and left surfaces
4. Borders Right border formed by: SVC and RA
Left border formed by: LV and left auricle
Inferior border formed by: RV
RA: right atrium, RV: right ventricle, LA: left atrium, LV: left ventricle, SVC: superior vena cava
ANATOMY OF THE HEART 5
Brachiocephalic artery Left common carotid artery

Left brachiocephalic vein
Right brachiocephalic vein
Left subclavian artery
Superior vena cava Arch of aorta
Left pulmonary artery

Right pulmonary artery
Left auricle
Left ventricle
Right atrium
Anterior interventricular
groove
Coronary sulcus
Posterior interventricular groove
Apex of heart
Inferior vena cava
Right ventricle
Fig. 1.1 | External features of the heartanterior view (diagrammatic).
Aorta
Ligamentum arteriosum
Superior vena cava
Left pulmonary artery
Pulmonary trunk
Left atrial appendage
Right atrial appendage
Right atrium
Right coronary artery in Left anterior descending

atrioventricular groove coronary artery in
(coronary sulcus) interventricular groove
Left ventricle
Right ventricle
Apex
Fig. 1.2 | External features of the heartanterior view.
ii. The Surfaces of the Heart

The area below the crux is known as the diaphragmatic or inferior surface of the
heart. The diaphragmatic surface of the heart is formed in its left 2/3rd by the left
ventricle and its right 1/3rd by the right ventricle.
The anterior or sternocostal surface of the heart is formed mainly by the right
atrium and right ventricle and partly by the left ventricle and left auricle.
Arch of aorta Superior vena cava
Left pulmonary artery Right pulmonary artery
Left pulmonary veins
Left auricle Right pulmonary veins
Coronary sulcus Right atrium
Left atrium
Left ventricle
Posterior interventricular
groove Inferior vena cava
Apex of heart
Right ventricle
Fig. 1.3 | External features of the heartposterior view (diagrammatic).
Aorta Right pulmonary artery
Left pulmonary artery Superior vena cava
Pulmonary veins
Pulmonary veins
Left atrium Right atrium
Coronary sinus and Inferior vena cava

circumflex coronary artery
Crux of the heart

Posterior descending
coronary artery in posterior
Left ventricle interventricular groove
Right ventricle
Fig. 1.4 | External features of the heartposterior view.

The left surface of the heart is mostly formed by the left ventricle and at the upper
end by the left auricle (see Figs 1.3 and 1.4).
iii. The Borders of the Heart

The right border is more or less vertical which is formed by superior vena cava and the
right atrium.
The left border is oblique and curved, mainly formed by the left ventricle and partly
by the left auricle.
The inferior border is nearly horizontal and is formed mainly by the right ventricle.
3. THE CHAMBERS OF THE HEART
i. Right Atrium (RA)

It receives venous blood from whole of the body via the superior vena cava (SVC) at its
upper end and inferior vena cava (IVC) at its lower end and pumps it into the right ven-
tricle through the right atrioventricular (tricuspid) valve during the ventricular diastole.
a) External Features
It is a somewhat quadrilateral chamber situated behind and to the right side of the
right ventricle, externally separated by the right coronary sulcus.
A hollow conical muscular projection, the right auricle (right atrial appendage)
arises from the antero-superior part of the right atrium and extends upwards and to
the left of the ascending aorta.
Along the right border of the right atrium, there is a shallow vertical groove, the sul-
cus terminalis which extends between the orifices of the superior vena cava and infe-
rior vena cava which is produced by an internal muscular ridge called the crista
terminalis. The upper part of the sulcus contains the SA node at the lateral margin
of the junction of the superior vena cava with right atrium and the atrial appendage
(see Table 1.5).
b) Internal Features
The right atrial wall measures about 2 mm in thickness. The interior of the right
atrium is broadly divided into three parts (see Figs 1.5, 1.6 and Table 1.3):
The smooth posterior part or sinus venarum
The rough anterior part or pectinate part (atrium proper) and
The septal wall.
(1) The smooth posterior part or sinus venarum
Developmentally, this portion is derived from the right horn of the sinus venosus.
Superior vena cava opens at the upper end, inferior vena cava opens at the lower end
and the coronary sinus opens between the opening of the inferior vena cava and the
right atrioventricular (AV) orifice.
The orifice of the superior vena cava has no valve while the orifice of the inferior
vena cava is guarded by a rudimentary valve, the Eustachian valve. The Thebesian
valve guards the orifice of the coronary sinus (see Table 1.4).
The caval orifices vary in shape and size depending upon the phase of respiration,
the cardiac cycle and contraction or relaxation of the surrounding muscle bands
which play a role in promoting venous return and preventing atrial reflux.
Superior Aorta
vena cava
Right atrial appendage
Right pulmonary
artery Pulmonary trunk
Pulmonary
veins
Right
ventricle
Fossa ovalis
Tricuspid
valve
Orifice of coronary
sinus
Inferior vena cava
Fig. 1.5 | Interior of right atrium.
Crista terminalis Superior vena cava
Openings of venae
Musculi pectinati cordis minimae
Right auricle
Annulus ovalis
Fossa ovalis
Valve of coronary
Valve of inferior sinus
vena cava
Septal cusp of
Inferior vena cava tricuspid valve
Fig. 1.6 | Interior of the right atrium (diagrammatic).
Table 1.3 Development of the right heart
Fetal structures Portion developed
1. Right horn of sinus venosus Sinus venarum

2. Primitive atrial chamber Atrium proper
3. Septum primum and septum secundum Atrial septal wall
4. Primitive ventricle Inflow tract and body of right ventricle
5. Right part of the bulbus cordis Infundibulum of right ventricle
Table 1.4 Openings into the right atrium
1. Superior vena cava It has no valves

2. Inferior vena cava It has rudimentary Eustachian valve
3. Coronary sinus It has Thebesian valve
Table 1.5 Nodes of the heart
Node Location
1. SA node In sulcus terminalis at the lateral margin of the

junction of SVC with right atrium
2. AV node In the triangle of Koch, anterior and medial to the
coronary sinus just above the septal tricuspid leaflet
(2) The rough anterior part or atrium proper

Developmentally, this portion is derived from the primitive atrial chamber.
Crista terminalis, remnant of the upper part of the right venous valve is a smooth
muscle ridge which extends from the upper part of the atrial septum between the
orifices of SVC and IVC.
A series of transverse muscular ridges called muscular pectinati arise from the crista
terminalis, run forwards and downwards towards the TV orifice, giving the appear-
ance of the teeth of a comb. The muscles are interconnected to form a reticular network
in the auricle.
(3) The septal wall

Developmentally, it is derived from the septum primum and septum secundum.
An oval depression above and to the left of the opening of the inferior vena cava
called fossa ovalis is formed by the septum primum. A sickle shaped sharp margin
that surrounds the upper, anterior, and posterior margins of the fossa ovalis is the
limbus fossa ovalis, developed from the lower free margin of septum secundum.
The anterior limb of the limbus is continuous with the left horn of the valve of infe-
rior vena cava. The remains of the foramen ovale is a small slit like valvular opening
(patent foramen ovale, PFO) between the upper part of the fossa and the limbus
which is normally occluded after birth and is occasionally present (see Table 1.6).
The triangle of Koch, a triangular area bounded in front by the base of the septal
leaflet of tricuspid valve, behind by the antero-medial margin of the opening of
coronary sinus and above by the tendon of Todaro, which is a subendocardial ridge
extending dorsally from the central fibrous body to the left horn of the valve of infe-
rior vena cava. The AV node is located in this triangle anterior and medial to the
coronary sinus, just above the septal leaflet of the tricuspid valve.
The torus aorticus is a slight bulge in the antero-superior part of the septum and
is caused by the bulging of the right posterior aortic (non-coronary) cusp and the
right coronary cusp of the aortic root. The proximity of the aortic root to the
Table 1.6 Description of the inter-atrial septum
1. Fossa ovalis Oval depression above and to the left of the opening of
the superior vena cava
2. Limbus fossa ovalis Sickle shaped sharp margin that surrounds upper, anterior
and posterior margins of the fossa ovalis
3. PFO (normally occluded after birth) Small slit like valvular opening between upper part of
fossa ovalis and limbus
4. Torus aorticus Bulge in antero-superior part of the septum due to bulging
of the right posterior and right coronary cusps of aorta
Table 1.7 Description of right heart
1. Shape of the right atrium (RA) Quadrilateral chamber

2. Verticle groove on the RA Sulcus terminalis: contains SA node
3. Wall thickness of the RA 2 mm
4. Internal portions of RA (i) Smooth sinus venarum
(ii) Rough pectinate (atrium proper)
(iii) Atrial septal wall
5. Shape of the right ventricle (RV) Triangle or crescent
6. RV wall thickness 45 mm
7. Portions of RV (i) Rough inflow tract
(ii) Smooth infundibulum
(iii) Body of the RV
right atrium permits an aneurysm of the sinus of Valsalva to rupture into the right
atrium.
The proximal right coronary artery is in immediate vicinity of the septum as it
enters the coronary sulcus.
ii. Right Ventricle (RV)

It is a triangular or a crescent shaped chamber, which receives the venous blood from
the right atrium during ventricular diastole and pumps it into the pulmonary circula-
tion during ventricular systole (see Table 1.7).
The right ventricle is normally the most anterior cardiac chamber, lying directly
beneath the sternum. It is partially below, in front of, and medial to the right atrium
but anterior and to the right of left ventricle.
It forms 2/3rd of the sterno-costal surface, most of the inferior surface and 1/3rd of
the diaphragmatic surface of the heart.
Aorta
Pulmonary trunk
Superior vena cava
Pulmonary valve
Right atrial appendage Infundibulum
Right atrium
Crista supra-
Parietal band ventricularis
Septal band
Tricuspid valve
Left ventricle
Inferior vena cava
Moderator band
Fig. 1.7 | Interior of the right ventricle
Pulmonary valve
Supraventricular
crest
Anterior cusp of
tricuspid valve
Chordae tandinae
Moderator band
Anterior papillary muscle
Fig. 1.8 | Interior of the right ventricle (diagrammatic)
The right ventricular wall measures 45 mm in thickness,2 thinner than that of left
ventricle in the ratio of 1:3. The interior of the right ventricle consists of three por-
tions (see Figs 1.7 and 1.8):
The rough inflow tract
The smooth outflow tract or infundibulum and
The apical trabecular portion or body of the RV.
(1) The rough inflow tract

Develops from the primitive ventricle of the heart tube, and consists of:
(i) Tricuspid valve and
(ii) The trabecular muscles of the anterior and inferior walls which direct the blood
anteriorly, inferiorly, and to the left at an angle of 60 to the outflow tract.
The trabecular carnae (muscles) are arranged into ridges, bridges and pillars (papil-
lary muscles). The septomarginal trabecula is a muscular ridge extending from the
ventricular septum to the base of the anterior papillary muscle. It contains the right
branch of the AV bundle and is presumed to prevent the over-distension of the right
ventricle, hence also called as the moderator band.
The supraventricular crest, a muscular ridge situated between the tricuspid and
pulmonary orifices separates the inflow and outflow tracts.
(2) The smooth outflow tract or infundibulum
Develops from the right part of the bulbus cordis, forms the superior portion of the
right ventricle and gives rise to the pulmonary trunk.
The apex of the conical shaped infundibulum has pulmonary orifice guarded by three
semilunar cusps.
The blood entering the infundibulum is ejected superiorly and posteriorly into the
pulmonary trunk.
(3) The apical trabecular portion or body of the RV: It is also derived from the primitive
ventricle of the heart tube, and is much coarser than that of the left ventricle.
iii. Left Atrium (LA)

It is a quadrangular chamber situated posteriorly, behind and to the left of the right
atrium, and forms 2/3rd of the base of the heart.
The left atrium receives the oxygenated blood from the pulmonary veins and serves
as a reservoir during left ventricular systole and pumps the blood into the left ventricle
through the left atrio-ventricular (mitral) orifice during the left ventricular diastole.
The posterior part is derived from the incorporation of the single pulmonary vein
while the anterior part including the left auricle is developed from the left half of the
primitive atrium (see Table 1.8).
Table 1.8 Development of the left heart
Fetal structures Portion developed
1. Incorporated pulmonary veins Posterior portion of left atrium (LA)

2. Left half of primitive atrium (i) Anterior portion of LA and
(ii) Left auricle
3. Left part of bulbus cordis Outflow of left ventricle (LV)
4. Left part of primitive ventricle (i) Free wall, apex of LV
(ii) Inflow tract of LV
The anterior wall of the left atrium is formed by the interatrial septum while the
posterior surface of the left atrium forms the anterior wall of the oblique sinus of
the pericardium.
Its appendage, the left auricle projects anteriorly to overlap the infundibulum of the
right ventricle.
The wall of the left atrium is 3 mm thick, slightly thicker than that of the right atrium.
Most of the wall is smooth and only a network of muscular pectinati is present within
the left auricle.
Two pulmonary veins open into the left atrium on each side of the posterior wall.
There are no true valves at the junction of the pulmonary veins and the left atrium,
but the sleeves of the atrial muscle extend from the left atrial wall around the pul-
monary veins for 1 or 2 cm and may exert a partial sphincter-like influence, tending
to lessen the reflux during atrial systole or mitral regurgitation.
The atrial septum is also smooth and shows the fossa lunata corresponding to the
fossa ovalis of the right atrium.
iv. Left Ventricle (LV)

The left ventricle is roughly bullet-shaped with blunt tip directed anteriorly, inferi-
orly and to the left where it forms the apex of the heart with the lower ventricular
septum.
The left ventricle receives blood from the left atrium during ventricular diastole and
ejects blood into the systemic circulation during ventricular systole.
The left ventricle forms:
the apex (with lower ventricular septum)
1/3rd of the sterno-costal surface
most of the left surface and
2/3rd of the inferior surface of the heart.
The left ventricle is posterior and to left of the right ventricle and inferior, anterior and
to the left of the left atrium.
The left ventricular chamber is approximately an ellipsoidal in shape and its walls
measure 815 mm thick. However the tip of the LV apex is often thin, measuring
2 mm or less. The left ventricle consists of (see Fig. 1.9):
The ventricular septum
The free wall of the left ventricle
Ascending aorta
Pulmonary valve Pulmonary trunk
Transverse atrium
Right ventricle
Aortic valve
Left atrium
Interventricular
septum Left ventricle
Diaphragm
Posterior cusp of
mitral valve
Fig. 1.9 | Interior of the left ventricle (diagrammatic).
Table 1.9 Development of ventricular septum
Portion of the
Developed from
ventricular septum
1. Muscular portion Trabeculae and medial walls between the primitive LV

and RV, appose and fuse together to form incomplete
muscular septum at 3 mm stage
2. Membraneous portion Lower edge of conal septum and inferior
endocardial cushion at 6 mm stage
The inflow tract

The outflow tract
The apical portion of the left ventricle.
(1) Ventricular septum

The medial wall of the left ventricle is the ventricular septum.
It is roughly triangular in shape, with the base of the triangle at the level of the aortic
cusps.
It is entirely muscular but a small portion located superiorly just below the right
coronary and posterior coronary cusps, is membranous (see Table 1.9). The upper
1/3rd of the septum is smooth endocardium while the remaining 2/3rd of the
septum and remaining LV walls are ridged by interlacing muscles, the trabeculae
carneae.
(2) The free wall of the left ventricle: The ridged trabeculae carneae excluding the
ventricular septum is the free wall of the left ventricle (see Fig. 1.10).
Pulmonary trunk Aorta

Fossa lunata
Aortic valve
Pulmonary
Left ventricle veins
Left atrium
Trabeculae
carneae cordis Inferior
vena cava
Coronary sinus
Fig. 1.10 | Interior of the left heart with LV free wall and mitral valve removed.
Table 1.10 Description of the left heart
1. Shape of the left atrium (LA) Quadrangular chamber

2. LA wall thickness 3 mm
3. Portions of LA (i) Auricle: has musculi pectinati
(ii) Smooth walled body
(iii) Smooth interatrial septum with fossa lunata
4. Shape of the left ventricle (LV) Bullet shaped with ellipsoidal chamber
5. LV wall thickness 815 mm, while apex is 2 mm thick
6. Portions of LV (i) Triangular ventricular septum
(ii) Free wall is ridged with trabeculae carnae
(iii) Funnel shaped inflow
(iv) Smooth conical shaped out flow
(3) The inflow tract

The anteromedial leaflet of the mitral valve (MV) extending from the top of the
posteromedial septum to the anterolateral ventricular wall separates the LV cavity
into an inflow tract and an outflow tract.
The funnel shaped inflow tract is developed from the left part of the primitive ventricle
and consists of mitral orifice with its mitral valve apparatus, which directs the atrial
blood inferiorly, anteriorly and to the left towards the LV apex.
(4) The outflow tract
The conical smooth walled outflow tract is situated above, in front of and slightly to
the right of the mitral orifice.
It is developed from the left part of the bulbus cordis.
It is surrounded by the inferior surface of the anteromedial mitral leaflet, the ventricular
septum and the left ventricular free wall.
It orients the blood flow from the LV apex to the right and superiorly at an angle of
90 to the inflow tract3 ejecting the blood into the ascending aorta through the
aortic orifice during ventricular systole.
The summit of the aortic vestibule is occupied by the aortic annulus guarded by
three semilunar cusps.
(5) The apical portion of the left ventricle is characterized by fine trabeculations, also
developed from the primitive ventricle (see Table 1.10).
4. THE FIBROUS SKELETON OF THE HEART
i. Components and Attachments

The fibrous skeleton of the heart is made up of four fibrous rings (mitral, tricuspid, pul-
monary and aortic) (see Fig. 1.11 and Table 1.11) at the bases of both ventricles around
the mitral, tricusid, pulmonary and aortic orifices, which provide the attachment to:
(i) Atrial and ventricular musculature
(ii) Valves of the heart and
(iii) Roots of the aorta and pulmonary trunk.
Pulmonary valve
Aortic valve
Tendon of infundibulum Origin of right

coronary artery
Trigonum fibronum
sinistrum
Mitral valve Tricuspid valve
Trigonum fibrosum
dextrum
Fig. 1.11 | Fibrous skeleton of the heart (diagrammatic).
Table 1.11 Fibrous skeleton of the heart
1. Four fibrous rings (i) Pulmonary

(ii) Aortic
(iii) Mitral
(iv) Tricuspid
(iii iv form central fibrous body)
2. Two trigones Right fibrous trigone
Left fibrous trigone
The pulmonary ring lies above, in front of and slightly to the left of the aortic ring.
Both the rings are set at right angles to each other and connected by a fibrous septum
known as tendon of infundibulum.
The medial aspects of mitral and tricuspid rings are fused by the central fibrous
body known as trigonum fibrous dextrum or right fibrous trigone.
The left margin of the trigone connects aortic and mitral rings, which is named as
trigonum fibrosum sinistrum or left fibrous trigone.
The right and left fibrous trigones which partially encircle the mitral and tricuspid ori-
fices are the mitral and tricuspid annuli that give attachment to the mitral and tricuspid
valves, atrial and ventricular muscle.
ii. Extensions
An important extension of the fibrous skeleton is the membranous ventricular septum,
which extends inferiorly and anteriorly from the right fibrous trigone. It is located at
the summit of the muscular septum, and provides support for the right coronary and
noncoronary aortic cusps.
A portion of the membranous septum extends slightly above the tricuspid valve,
forming a small portion of the medial wall of the right atrium.
iii. The Bundle of His

It penetrates the central fibrous body and travels along the inferior margin of the
membranous ventricular septum. At the crest of the muscular septum, above the level
of junction of the right coronary and noncoronary (posterior) aortic cusps, the His
bundle divides into a left bundle branch and a right bundle branch. The right fibrous
trigone is sometimes calcified in old age while this a constant feature in sheeps
heart.
5. THE VALVES OF THE HEART
There are two pairs of valves in the heart (see Fig. 1.12).
A pair of atrioventricular valves: mitral and tricuspid and
A pair of semilunar valves: aorta and pulmonary.
General Description
They maintain unidirectional flow of the blood and prevent its regurgitation in the
opposite direction.
The anatomy of the atrioventricular (AV) valves is more complex than that of the
semilunar (SL) valves.
Each cardiac valve has a central spongiosa (collagenous core) and a peripheral
fibrosa. Both the sides of the fibrosa are covered by a loose fibroelastic tissue usually
containing mucopolysaccharides and the entire valve is covered by endothelium.
Pulmonary orifice
Aortic orifice
Right ventricle
Left ventricle
Septal papillary m.
Tricuspid orifice Anterior papillary m.
Anterior papillary m.
Mitral orifice
Posterior or inferior Posterior

papillary m. papillary m.
Interventricular septum
Fig. 1.12 | Transverse section through the ventricles showing the valves of the heart
(diagrammatic).
Table 1.12 Valve leaflet surfaces
Surface Description
1. Atrialis Atrial surface of atrioventricular valve leaflets

2. Ventricularis Ventricular surface of all leaflets
3. Arterialis Arterial surface of the semilunar valve leaflets
The loose fibroelastic tissue on the atrial aspect of the AV valves is known as atrialis,
ventricular surface of all four valves (AV & SL), the ventricularis, and aortic and pul-
monary surfaces of SL valves are known as arterialis4 (see Table 1.12).
The endothelium and loose connective tissue of the AV valves are continuous with
the atrial and ventricular endothelium and those of the SL valves are continuous
with the aortic and pulmonary intima.
Smooth striated cardiac muscle may extend onto the proximal 1/3rd of the atrialis in
the AV valves and often contain blood vessels. The distal 2/3rd of AV valves and both
SL valves are avascular.48
i. Mitral Valve
Mitral valve develops primarily from (see Table 1.13):
LV muscle wall: predominantly by delamination of the muscular ventricular wall,9
hence valve cusps initially are thick and fleshy.10
Endocardial cushions:
(i) anterior mitral leaflet from superior and inferior endocardial cushions
(ii) posterior mitral leaflet from left lateral endocardial cushion.
The mitral valve consists of six major anatomic components: annulus, leaflets, chordae
tendinae, papillary muscles, posterior left atrial wall and left ventricular free wall (see
Fig. 1.13 and Table 1.14).
Table 1.13 Development of the valves
Part Developed from
1. Mitral
Anterior mitral leaflet Superior and inferior endocardial cushions
Posterior mitral leaflet Left lateral endocardial cushion
2. Tricuspid
Anterior leaflet Right lateral and dextro dorsal endocardial cushions
Posterior leaflet Right lateral endocardial cushion
Septal leaflet Inferior endocardial cushion
3. Semilunar valves Truncus arteriosus
Truncal and intercalated valve cushions
Posterior leaflet
Median Middle Lateral

Anterior leaflet
scallop scallop scallop
Mitral annulus
Basal zone
Clear zone
Cuspal chordae
Ventricular wall
Cuspal chordae Rough zone
Commissural chordae
Cuspal chordae
Papillary muscle
Fig. 1.13 | Mitral valve complex (diagrammatic).
Table 1.14 Structure of the mitral valve
1. Annulus Saddle shaped; 46 cm2 in size; fibrous anteromedial

portion and muscular posterolateral portion
2. Leaflets Sail shaped AML
C shaped scalloped PML
3. Papillary muscles Anterolateral PM at 4o clock position
Posteromedial PM at 7o clock position
4. Chordea tendinae 120 in number
Cuspal: primary, secondary and tertiary
Commissural: anterolateral and posteromedial
a) Mitral Annulus
Shape of the mitral annulus is catenoid or saddle shaped in the embryo as well as in
the adults.
The size of the annulus is 46 cm2 (corresponds to mitral valve areaMVA) and the
circumference of the valve (not really that of the annulus) is 810.5 cm with a mean
of 9.4 cm.1113
Anteromedial portion is formed from the fibrous trigone and collagen fibers which
encircle 1/2 or 2/3rd of the annulus while rest of the annulus (posterolateral portion)
is devoid of fibrous tissue and formed by the myocardium of the LV and left atrium.
The decrease in annular size during ventricular systole is due to contraction of this
posterolateral portion.
b) Leaflets
Mitral valve has two leaflets: anterior mitral leaflet (AML) and posterior mitral leaflet
(PML). However, it can have two small minor commissural cusps which are normally
incomplete.14
(i) AML
AML is sail shaped and is attached in a hinge like to 1/3
rd
of the anteromedial
portion of the annulus.
It is directly continuous with 1/2 of the non-coronary (posterior) cusp and
most of the left coronary cusp of aorta.

It forms the semicircular posterior border of the LV outflow tract.
(ii) PML
PML is C shaped, hinges on the posterolateral 2/3
rd
of the annulus.
It is longer at its base (6 cm of circumference) and shorter in its basal to apical
length (1.2 cm) than AML (3 cm of circumference and 2.3 cm of basal to api-
cal length)15 however both have similar surface area.11,12
The surface area of both leaflets is about 2 times that of the orifice area,
16
while the cross sectional area of both leaflets is 20% more than the mitral orifice.
PML is sub-divided by medial and lateral clefts into three scallops-posteromedial,
middle and anterolateral portions with middle being the largest (1.3 cm width
compared to 1.0 cm for other two).15
(iii) Surface of the leaflets

The atrial surface of the cusps is generally smooth except near the free edge
where chordae tendinea are attached. Slightly away from the free edge on the
atrial surface are fine nodules called the noduli Albini.
The ventricular surface of the cusps is irregular due to insertion of the chordae
tendinae.
(iv) Commissures: The leaflets are connected to each other at junctions called com-
missures (SL valve commissures are spaces), anterolateral and posteromedial
commissures.
c) Papillary Muscles (PM)

There are two papillary muscles: anterolateral and posteromedial, located below the
commissures projecting from the trabeculae carneae. Interpapillary muscle distance is
relatively constant. Each PM has six heads.14
(i) Anterolateral PM: It is situated at 4o clock position and is supplied by a diagonal
branch of left anterior descending) artery and obtuse marginal of left circumflex artery.
(ii) Posteromedial PM: It is situated at 7o clock position and is supplied by posterior
descending artery of right coronary artery in 85%, left circumference artery in 7% and
by both in 8% (co-dominant) of individuals.
d) Chordae Tendinae (CT)

These are complex network of flexible cord like structures primarily made of collagen.
They are of two types: cuspal (leaflet) chords and commissural chords.
There are about 12 chordae attached to each of the six heads of each PM. These
chordae divide about three times before their ultimate attachment. In total, there are
about 120 chordae attached to both mitral leaflets.17
(i) Cuspal (leaflet) chords are classified into three groups: primary, secondary and
tertiary.
Primary group originate near the PM apices, divide into a number of finer
strands that insert at the extreme edge of the cusps. These chordae prevent the
cusp inversion into the left atrium during ventricular systole.
Secondary group of chordae also originate near the PM apices, are thicker in
diameter, but less in number as compared to the first group and tend to insert
on the ventricular surface of the cusps. They serve to anchor the valve.
Tertiary group of chordae originate from the ventricular wall, may actively
contain muscle and are attached to the ventricular aspect of posterior leaflet.
These chords are specific to the PML.14,18
(ii) Commissural chords arise from the anterolateral and posteromedial PM and
branch in a fan-like manner to be inserted on to both commissures.
e) Mitral Valve Closure

The closure of mitral valve involves a complex interplay of active and passive processes.
It consists of three phases: initial leaflet phase, annular phase and ventriculogenic phase.
(i) Initial leaflet phase: At the end of the rapid filling phase, the leaflets gradually
move passively towards the closed position due to vortex currents generated
under their ventricular surfaces.
(ii) Annular phase: With the onset of atrial contraction, annular contraction begins
which continues throughout the ventricular systole. The annular contraction is an
important phase in MV closure and causes 2040% decrease in annular orifice.
Non-homogenous structure of the annulus produces an eccentric narrowing of the
orifice during annular contraction.
(iii) Ventriculogenic phase: With isometric contraction, the contraction of intra-

valvular muscle fibers occurs and leaflets become concave in shape which opposes
leaflet eversion during ventricular systole. The large sail shaped AML swings and
is engulfed by Gusset like C shaped PML causing closure of mitral valve. Leaflets
are further sealed together by the opposing effect of intraluminal pressures.
Papillary muscles and chordae maintain isometric tension and thereby stabilizes
the leaflets during ventricular systole.
ii. Tricuspid Valve

The tricuspid valve develops from: (see Table 1.13)
(i) RV muscle wall by delamination of muscle wall
(ii) endocardial cushion:
Anterior leaflet from right lateral and dextro-dorsal endocardial cushions
Posterior leaflet from right lateral endocardial cushion and
Septal leaflet from inferior endocardial cushion.
The tricuspid valve like mitral valve also consists of six major anatomic components: right
atrial wall, annulus, leaflets, papillary muscles, chordae tendineae and right ventricular
free wall (see Fig. 1.14 and Table 1.15).
Septal leaflet Antero-septal commissure

Postero-septal commissure
Anterior leaflet
Posterior leaflet Basal zone
Tricuspid annulus
Clear zone
Basal chordae Deep chordae
Ventricular wall
Chordae Rough zone

Free chordae Commissural chordae
Papillary muscle Rough zone chordae
Fig. 1.14 | Tricuspid valve complex (diagrammatic).
Table 1.15 Structure of the tricuspid valve
1. Annulus Circumferential in shape, 58 cm2 in size-anterior, posterior and septal portions

2. Leaflets Largest anterior, smallest medial or septal and scalloped posterior
3. Papillary muscles Anterior (largest), posterior (usually multiple) and septal (may be rudimentary)
4. Chordae tendinae Five types: fan shaped, rough, deep, basal and free edged
(deep and free edged are unique to TV)
a) Tricuspid Annulus
It is nearly circumferential, larger than mitral annulus but lies at a lower level than
the mitral annulus.
The size of the tricuspid annulus is 58 cm2 with a mean of 7 cm2 (tricuspid valve
area-TVA) and circumference of 11.4 cm 1.1 in males and 10.8 1.3 in females.
The posterior leaflet makes up the largest portion of the annulus (7.5 cm), followed
by the anterior (3.7 cm), and septal (3.6 cm) leaflets.19
b) Leaflets
Tricuspid valve has three leaflets: anterior, posterior and septal.
Anterior leaflet is the largest with a width of 2.2 cm.19
Septal (medial) leaflet is the smallest with a width of 1.5 cm.19
The posterior leaflet measures 2.0 cm in width19 and may have 13 scallops pro-
duced by small clefts.
There are three commissures:
Anteroposterior with a size of 1.1 cm
Posteroseptal with 0.8 cm size and
Anteroseptal commissure with a size of 0.5 cm.
c) Papillary Muscles (PM)

TV has three papillary muscles: anterior, septal (medial) and posterior.
The anterior PM is the largest, located below the anteroposterior commissure origi-
nating from the moderator band as well as from the anterolateral ventricular wall.
The posterior PM lies beneath the posteroseptal commissure attached to the poste-
rior wall of the RV and receive chordae from posterior and septal leaflets. It is usu-
ally multiple.
The septal PM is small originating from the wall of the infundibulum. It has exten-
sive attachments to the ventricular septum and receives chordae from the anterior
and septal leaflets. At times, septal PM is rudimentary, absent, double or multiple.
d) Chordae Tendineae
It may arise from the papillary muscles or from the muscle of the posterior or septal
walls of the RV.
On an average, there are 25 chordae inserted into the tricuspid valve:
7 chordae are inserted into the anterior leaflet
6 into the posterior leaflet
9 into the septal leaflet and
3 into the commissures.
TV has 5 types of chordae tendinea:19
Fan shaped
Rough
Deep
Basal and
Free-edge.
The deep and free-edge are unique to the tricuspid valve.19 Deep chordae provide a
second arcade for leaflet attachment, while free-edge are single and inserted into the
leaflets free edge.
Fan shaped chordae are inserted into the three commissures while basal chordae are
the shortest and measure an average of 0.6 cm. Rough and deep chordae may be as
long as 2.2 cm.
iii. Semilunar (SL) Valves

Semilunar valves are derived from:
(i) the truncus arteriosus and
(ii) truncal and intercalated valve cushions.
The aortic and pulmonary valves are called semilunar valves because their cusps are
semilunar in shape.
They are situated at the summit of the outflow tract of their corresponding
ventricle, the pulmonary valve is anterior, superior and slightly to the left of the
aortic valve.
Each semilunar valve consists of an annulus, three equal-sized semicircular cusps, three
equal spaced commissures and three sinuses of Valsalva (see Table 1.16).
a) Annulus
Unlike aortic valve the pulmonary valve has no discrete annulus or fibrous ring. The
apex of the infundibulum presents the pulmonary orifice which is circular and
guarded by three semilunar cusps. The pulmonary valve annulus is about 1.5 cm
above the level of the aortic valve annulus, but its circumference is similar: 79 cm.
The average size of the aortic annulus is 2.5 cm2.
Table 1.16 Structure of the semilunar valves
1. Annulus PV: 79 cm in circumference

AV: 2.5 cm2 in area
2. Leaflets AV: 2 anterior: right and left coronary cusps
1 posterior or noncoronary cusp
PV: 2 posterior: right and left cusps
1 anterior cusp
3. Sinuses of Valsalva AV: 2 anterior: right and left
1 posterior
PV: 2 posterior: right and left
1 anterior
PV: pulmonary valve; AV: aortic valve.

b) Leaflets (Cusps)
Each cusp is attached by its semicircular border (lower edge) to the wall of the aorta
or pulmonary trunk while the upper free edges project into the lumen.
The aortic and pulmonary valves are similar in configuration except that the aortic
cusps are slightly thicker.5
The three aortic valve cusps: two anterior-right and left coronary cusps; one posterior or
noncoronary cusp, while the pulmonary valve has two posterior cusps-right and left
and one anterior cusp (see Figs 1.15 and 1.16).
The aortic left and noncoronary cusps are continuous with AML of the mitral valve.
The free margin of each cusp contains a central fibrous nodule on its ventricular sur-
face called noduli Arantii which marks the contact sites of closure. From each side
of the nodule, a thin smooth margin (lunule) extends to the base of the cusp, which
is less prominent in the pulmonary valve (see Fig. 1.17).
There may be variation in the cusps and commissural sizes and positions of
the sinuses of Valsalva which result in asymmetric lines of closure and may acceler-
ate wear and tear (aging) of the valve structure especially of that of the aortic valve.
Normal aortic valve
AORTA Aorta
R N L N
Left cusp
R L
AML Anterior mitral

leaflet Ventricular
diastole
Fig. 1.15 | Structure of the aortic valve (diagrammatic)N: noncoronary cusp, R: right
anterior cusp, L: left anterior cusp, AML: anterior mitral leaflet.
L A R L
R
Pulmonary trunk
A
RV free wall Ventricular diastole

Right ventricular (RV) outflow
Fig. 1.16 | Structure of the pulmonary valve (diagrammatic)R: right posterior cusp,
L: left posterior cusp, A: anterior cusp.
Ascending aorta
Left coronary artery Nodule
Lunule
Anterior aortic sinus
Right coronary
artery
Fig. 1.17 | Structure of the aortic valve (diagrammatic).

Because of less systolic pressure in RV, these acquired senile (aging) changes in pul-
monary valve do not occur.
c) Commissures
Each semilunar valve has equally spaced three commissures i.e. the small space
between the attachments of the adjacent cusps (vs. AV valves).
The circumference connecting these points is termed as the sinotubular junction,
which separates the sinuses of Valsalva from the adjacent tubular portion of the vessel.
In aorta, a distinct hump or line marks this junction which was originally described
by Leonardo da Vinci as the supra-aortic ridge.
The circumference is measured at this sinotubular junction with echocardiography
and at necropsy.
While the lowermost portion of aorta (at the junction of the aortic valve with the
ventricular septum) which is referred as the aortic ring, is measured by the surgeons
to determine the size of the aortic prosthetic valve.
d) Sinuses of Valsalva
A pouch-like dilatation above each cusp is known as sinus of Valsalva. The aortic right
and left sinuses of Valsalva give rise to right and left coronary artery respectively.
The aortic sinuses of Valsalva have close relation with right and left sided chambers.
Hence, rupture of the right and non-coronary sinuses of Valsalva may communicate with
right sided chambers (outflow tract RV and RA) while rupture of left sinus of Valsalva
communicates with left sided chambers (LA or LV outflow tract). With age,
The aortic cusps thicken
Nodules thicken and enlarges
Sinuses of Valsalva calcify and dilate and
Lunules develop fenestrations.
With age, the pulmonary valve cusps also thicken slightly but rest of the changes are
less prominent.
e) SL Valve Closure
During ventricular systole, the cusps are passively thrust upward away from the center
of the lumen. During ventricular diastole, the cusps fall passively into the lumen of the
vessel as they support the column of blood above while the nodules meet in the center
which contributes to the support of the leaflets, thus preventing the regurgitation of
blood.
REFERENCES
1. Edwards WD. Applied anatomy of the heart. In: Brandenburg RO, Fuster V, Giuliani ER, et al. eds.
Cardiology: Fundamentals and Practice. Chicago: Year Book 1987:47109.
2. Prakash R. Determination of right ventricular wall thickness in systole and diastole. Electrocar-
diographic and necroscopy correlation in 32 patients. Br Heart J 1978;40:12571261.
3. Walmsley R, Watson H. Clinical Anatomy of the Heart. New York. Churchill Livingstone 1978:122.
4. Gross L, Kugel MA. Topographical anatomy and history of the valves in the human heart. Am J
Pathol 1931;7:445474.
5. Waller BF. Morphological aspects of valvular heart disease. Part I. Curr Probl Cardiol 1984;9(7):166.
6. Clarke JA. An X-ray microscopic study of the blood supply to the valves of the human heart. Br
Heart J 1965;27:420423.
7. Duran CM, Gunning AJ. The vascularization of the heart valve: A comparative study. Cardiovasc
Res. 1968;2(3):290296.
8. Montiel MM. Muscular apparatus of the mitral valve in man and its involvement in left sided
cardiac hypertrophy. Am J Cardiol 1970;26(4):341344.
9. Dox X, Corone P. Embriologie cardiaque: Malformations (1). In: Embryologie Cardioaque-Editions
Techniques Paris. Encyclopedie Medico-Chirurgicale. 1992:120.
10. Streeter GL. Developmental horizons in human embryos: Description of age groups XI. 1320
somites and age group XII. 2129 somites. Contrib embryol 1942;30:211245.
11. Perloff JK, Roberts WC. The mitral apparatus: Functional anatomy of mitral regurgitation.
Circulation. 1972;46(2):227239.
12. Waller BF, Morrow AG, Maron BJ, Del Negro AA, Kent KM, McGrath FJ, et al. Etiology of clini-
cally isolated, severe, chronic, pure mitral regurgitation: Analysis of 97 patients over 30 years of age
having mitral valve replacement. Am Heart J. 1982;104(2 Pt 1):276288.
13. Roberts WC. Morphologic features of normal and abnormal mitral valve. Am J Cardiol 1983;51(6):
10051028.
14. Netter FH. CIBA collection of medical illustration: Heart vol 5. Summit NJ: CIBA pharmaceutcal.
1987:9112.
15. Ranganathan N, Lam JHC, Wigle ED, Silver MD. Morphology of human mitral valve: II. The
valve leaflets. Circulation 1970;41:459467.
16. Brock RC. The surgical and pathological anatomy of the mitral valve. Br Heart J 1952;14(4):489513.
17. Constant J. Bedside Cardiology. 3rd. Boston, Mass: Little, Brown and Company; 1985. pp. 3839.
18. Carbello BA. Mitral valve disease. Curr Probl Cardiol. 1993;18(7):423478.
19. Silver MD, Lam JHC, Ranganathan N, Wigle ED. Morphology of human tricuspid valve. Circulation
1971;43(3):333348.
CHAPTER 2
LYMPHATIC SYSTEM OF THE H EART
1. FORMATION OF RIGHT CORONARY 4. FORMATION OF RIGHT

CHANNEL 28 LYMPHATIC DUCT 30
2. FORMATION OF LEFT CORONARY REFERENCES 30
CHANNEL 28
3. FORMATION OF MAIN SUPRA-
CARDIAC CHANNEL 29
The lymphatic drainage of the heart flows from subendocardial vessels to an extensive
capillary plexus lying throughout the subepicardium.1,2 These capillaries converge in
collecting lymphatic channels which run alongside the coronary vessels which form
the right lymphatic duct (see Figs 2.1 and 2.2).
There are two main lymphatic channels:
Right coronary channel (RCC) and
Left coronary channel (LCC).
1. FORMATION OF RIGHT CORONARY CHANNEL
The posterior interventricular trunk (PVT) runs along with the posterior descending
artery (PDA) in the posterior interventricular sulcus up to the crus of the heart, and
then encircles around to the right from posterior to anterior in the right coronary
sulcus to become the right coronary channel.
2. FORMATION OF LEFT CORONARY CHANNEL
The two major LV channels are: anterior interventricular trunk and obtuse marginal
trunk.
The anterior interventricular trunk (AVT) ascends from apex to base along with left
anterior descending artery (LAD) in the anterior interventricular sulcus.
The obtuse marginal trunk (OMT) runs alongside the left circumflex artery in left
coronary sulcus.
LYMPHATIC SYSTEM OF THE HEART 29
IJV
RLD
Sci v
CLN
MSC
RCC LCC
OMT
PVT AVT
Fig. 2.1 | Lymphatic drainage of the heart.
Right lymphatic duct
Cardiac
lymph
node
Main
Right coronary Left coronary
supra-cardiac
channel channel
channel
PVT AVT OMT
Fig. 2.2 | Lymphatic drainage of the heart (diagrammatic)PVT: posterior interventricular

trunk, AVT: anterior interventricular trunk, OMT: obtuse marginal trunk.
Near the base of the pulmonary artery; the two LV channels, anterior interventricular
trunk and obtuse marginal trunk join together to form left coronary channel.
3. FORMATION OF MAIN SUPRA-CARDIAC CHANNEL
The right coronary channel unites with the left coronary channel to become main
supra-cardiac channel (MSC), which passes upward beneath the left atrial appendage,
behind the pulmonary artery to enter a pretracheal lymph node (cardiac lymph node;
CLN) between the arch of aorta and the pulmonary artery.
4. FORMATION OF RIGHT LYMPHATIC DUCT
From the CLN, the right lymphatic duct (RLD) arises which runs cephalad in the medi-
astinum to drain into the junction of the internal jugular vein (IJV) and right subclavian
vein (Sci v).
The thoracic duct, the largest lymphatic vessel of the body, extends from the upper
part of the abdomen to the lower part of the neck crossing the posterior and superior
mediastinum and drains into the junction of the left subclavian and left internal jugular
veins or left brachiocephalic vein.
On the right side of the thorax, there are three main lymphatic ducts:
Right jugular lymphatic duct drains into the right jugular vein.
Right subclavian lymphatic duct drains into right subclavian vein and
Right mediastinal lymphatic duct drains into right brachiocephalic vein.
Occasionally, the right jugular and right subclavian lymphatic ducts unite to form right
lymphatic duct.
The lymph vessels like veins contain valves to prevent backward flow.
REFERENCES
1. Feola M, Merklin R, Cho S, Brockman SK. The terminal pathway of the lymphatic system of the
human heart. Ann Thorax Surg 1977;22:531536.
2. Miller AJ. Lymphatics of the Heart. New York: Raven press: 1982.
CHAPTER 3
V ENOUS D RAINAGE OF THE H EART
1. CORONARY SINUS 32 v) Small Cardiac Vein 33

i) Great Cardiac Vein 33 2. ANTERIOR CARDIAC VEINS 33
ii) Oblique Vein of Left Atrium 3. THEBESIAN VEINS (VENAE CORDIS
(or Oblique Vein of Marshall) 33 MINIMI) 33
iii) Posterior Vein of the LV 33 REFERENCE 33
iv) Middle Cardiac Vein (or Posterior
Interventricular Vein) 33
There are three venous drainage systems:1

Coronary sinus
Anterior cardiac veins and
Thebesian veins.
About 60% of the venous blood of the heart drains into the right atrium via the coronary
sinus and remaining 40% drains into the different chambers of the heart via anterior
cardiac veins and Thebesian veins (see Fig. 3.1 and Table 3.1).
Coronary sinus conveys the greater part of the blood from the left coronary artery
territory while the anterior cardiac veins drain most of the blood from the right coro-
nary artery territory (see Fig. 3.2).
Left brachio-cephalic vein

Left superior intercostal vein
Superior vena cava Ligament of left vena cava

Oblique vein of left atrium
Anterior cardiac veins

Right atrium Left marginal vein
Posterior vein of left ventricle

Coronary sinus
Great cardiac vein
Middle cardiac vein
Right marginal vein
Small cardiac vein
Fig. 3.1 | Venous drainage of the heart (diagrammatic).

Table 3.1 Venous drainage of the heart
Coronary sinus Anterior cardiac veins Thebesian veins
1. Drains: LCA territory Drains: RCA territory Drains: Both the territories,
but primarily RCA territory
2. Branches: 5 in number Branches: 14 Branches: Small and
Great cardiac vein numerous
Oblique vein of left atrium
Posterior vein of LV
Middle cardiac vein
Small cardiac vein
Right
Thebesian veins
ventricle
Right
Anterior cardiac veins
atrium
CORONARY SINUS
Great Middle Small

cardiac OV of LV PV of LV cardiac cardiac
vein vein vein
LMV RMV
Fig. 3.2 | Venous drainage of the heart (diagrammatic)OV of LV: obtuse vein of left
ventricle, PV of LV: posterior vein of left ventricle, LMV: left marginal vein, RMV:
right marginal vein.
1. CORONARY SINUS
Coronary sinus is about 23 cm long situated in the posterior part of the atrioven-
tricular groove (coronary sulcus) near the crux of the heart.
It begins in the left part of the AV groove where it receives the great cardiac vein and
oblique vein of left atrium at its left end, then passes downwards and to the right
along the posterior part of the AV groove receiving posterior vein of left ventricle in
its middle part and middle cardiac vein and small cardiac vein at its right end.
Finally, the coronary sinus opens into the inferoposteromedial aspect of the right
atrium between the orifice of the IVC and septal leaflet. The AV node lies just above
its opening.
A crescent shaped rudimentary valve, the Thebesian valve guards the opening of the
coronary sinus. All the tributaries of coronary sinus are provided with valves except
the oblique vein of left atrium.
It is developed from the left horn and body of the sinus venosus. The Thebesian
valve is derived from the lower part or the venous valve.
VENOUS DRAINAGE OF THE HEART 33
i) Great Cardiac Vein

It begins near the apex of the heart as anterior interventricular vein in the anterior
interventricular sulcus, runs upwards along with left anterior descending artery, and
turns leftward near the bifurcation of the left coronary artery to circle posteriorly
under the left atrium in the left AV sulcus to become great cardiac vein.
It receives the left marginal vein near its termination in the coronary sinus.
ii) Oblique Vein of Left Atrium (or Oblique Vein of Marshall)

It drains the posterior surface of the left atrium, runs on the posterior surface of the
left atrium and terminates in the left of the coronary sinus.
It develops from the left common cardinal vein (duct of Cuvier) which may some-
times form a large left superior vena cava.
iii) Posterior Vein of the LV

It drains the inferior surface of the left ventricle, runs on the diaphragmatic surface
of the LV and ends in the middle of the coronary sinus on the left side of the middle
cardiac vein.
iv) Middle Cardiac Vein (or Posterior Interventricular Vein)

It arises near the posterior aspect of the cardiac apex and ascends in the posterior inter-
ventricular sulcus along with the posterior descending artery and terminates into the
right end of the coronary sinus or may sometimes directly drain into the right atrium.
v) Small Cardiac Vein

It lies in the right coronary sulcus accompanying the right coronary artery, receives
the right marginal vein draining the RV and RA and terminates in the right end of
the coronary sinus or sometimes directly into the right atrium.
2. ANTERIOR CARDIAC VEINS
There are 24 anterior cardiac veins which drain the anterior RV wall, run superiorly
on the anterior wall of the RV and cross the right AV sulcus to terminate directly into
the anterior part of the right atrium.
3. THEBESIAN VEINS (VENAE CORDIS MINIMI)
These are small numerous veins draining the myocardium directly into the cardiac
chambers, primarily into the right atrium and right ventricle (see Fig. 3.2).
REFERENCE
1. James TN. Anatomy of the Coronary Arteries. New York: Hoeber Medical Division. Harper & Row.
1961:177.
CHAPTER 4
ARTERIAL SUPPLY OF THE HEART
1. LEFT CORONARY ARTERY 34 2. RIGHT CORONARY ARTERY (RCA) 37

i) Left Anterior Descending Artery 3. DIVERGENT CORONARY ANATOMY 38
(LAD) 35 4. MEASUREMENTS 39
ii) Left Circumflex Artery i) Length 39
(LC or LCx) 35 ii) Luminal Diameter 39
iii) Ramus Intermedius 37 REFERENCES 39
The heart is supplied by two coronary arteries: left coronary artery and right coronary
artery (see Table 4.1).
1. LEFT CORONARY ARTERY
The left main coronary artery (LM or LMCA) arises from left anterior coronary sinus,
passes behind the pulmonary trunk (RVOT), runs forwards and to the left between the
pulmonary trunk and left auricle where it bifurcates into left anterior descending (LAD)
and left circumflex (LC or LCx) branches1 (see Fig. 4.1).
Table 4.1 Coronary artery (CA) distribution
CA branch Distribution
1. Diagonal branches Anterolateral portion of LV

2. Septal branches Anterosuperior 2/3rd of vent. septum
3. LA branch Left atrium
4. OM Lateral free wall of LV
5. Conus branch RVOT
6. SA nodal branch SA node (in 5060%)
7. AV nodal branch AV node (in 85%)
8. PDA Posteroinferior 1/3rd of vent. septum
9. PLV branch Posterolateral LV (85%)
ARTERIAL SUPPLY OF THE HEART 35
Aortic valve
Tubular portion
NC LC Coronary ostia
LM
Sinotubular
L
junction
R R NC L
(P) Sinus portion
LAD
R
Sinotubular junction
AV R
cusp
Pulmonic valve
Fig. 4.1 | Origin of the coronary arteries.

i) Left Anterior Descending Artery (LAD)
It runs in the anterior interventricular groove towards the apex. LAD gives 26
diagonal (D) and 35 septal (S) branches.
In 90%, there are 13 diagonal branches and no diagonal branches are present in
1%. The diagonal arteries course laterally over the free wall of the left ventricle
(LV) in the angle between the LAD and LCx and supply the anterolateral portion of
the LV.
The septal branches originate from the LAD at a right angle and supply anterosuperior
2/3rd portion of the ventricular septum.
LAD terminates:
Beyond the ventricular apex (type-III) along the diaphragmatic aspect in 78%.
At the apex (type II) or before the apex (type-I) in 22%.
Angiographically, LAD is divided into three portions: Proximal, Mid and Distal
(see Figs 4.2, 4.3 and 4.4).
Proximal LAD is the portion from its origin from the LMCA to its first diagonal
(D1) branch.
Mid LAD is the portion between first diagonal (D1) and second diagonal (D2)
branches.
Distal LAD is the portion of the LAD beyond (D2) branch.
ii) Left Circumflex Artery (LC or LCx)

After its origin from the LMCA, LCx travels in the left AV groove (left coronary sulcus)
and in the posterior part of AV groove; it anastomoses with the branches of right coro-
nary artery (RCA).
LCx LAD
OMB
RAO caudal
Fig. 4.2 | Coronary angiogram of LCA-RAO caudal.
LCx
LAO cranial
LAD
Fig. 4.3 | Coronary angiogram of LCA-LAO cranial.

LCx
LMCA D
LAD
AP cranial
Fig. 4.4 | Coronary angiogram of LCA-AP cranial.
In right dominant coronary circulation (85%), LCx gives 12 left atrial branches
which supply the left atrium and 13 obtuse marginal branches (OM) that supply lateral
free wall of the LV.
In left dominant coronary circulation (8%) in addition to left atrial and OM branches,
it gives rise to posterolateral left ventricular (PLV) branch, posterior descending artery
(PDA), AV nodal artery and sinus nodal artery (in 4050%).
Similarly, LCx is angiographically divided into three portions: Proximal, Mid, and
Distal (see Figs 4.2, 4.3 and 4.4).
Proximal LCx is the portion from its origin from the LMCA to the origin of the
first obtuse marginal branch.
Mid LCx is the portion of LCx between the first OM and second OM branches.
Distal LCx is the portion of the LCx beyond second OM branch.
iii) Ramus Intermedius

In some patients, a large intermedius or ramus medianus branch may originate directly
from the LMCA, bisecting the angle between the LAD and LCx, so that there is a tri-
furcation of the LMCA.
2. RIGHT CORONARY ARTERY (RCA)
It arises from the right coronary sinus which is lower is position than that of the left coro-
nary artery, passes forwards and to the right between the pulmonary trunk and right auri-
cle, then runs downwards in the right anterior coronary sulcus, winds round the inferior
border of the heart to reach the diaphragmatic surface of the heart. Here, it passes
upwards and to the left in the right posterior coronary sulcus and reaches the crux of the
heart and terminates by anastomosing with the branches of the LCx.
In general, it gives rise to:
Conus artery
SA nodal branch
Right atrial branches
RV and acute marginal branches which supply the free wall of the right ventricle.
(i) The conus artery: It is usually the first branch of RCA, which supplies the
infundibulum of the RV (RVOT), but in 4050% it may originate from a separate
ostium in the right coronary sinus (third coronary artery).
(ii) SA nodal artery: In 5060%, SA nodal artery originates from the RCA, runs
along the anterior right atrium to the superior vena cava, which it encircles in a clock-
wise or anticlockwise before it penetrates the SA node.
However, when the SA nodal artery arises from the LCx (in 4050%), it crosses
behind the aorta and in front of the left atrium to reach the superior vena cava and pene-
trating the SA node.2
(iii) In right dominant coronary circulation (in 85%), RCA gives rise to AV nodal
artery, PDA which supplies the postero-inferior 1/3rd of the ventricular septum and
one or more posterolateral LV branches (PLV), which supply the posterolateral
portion of LV.
(iv) Co-dominant coronary circulation or balance system occurs in 7% where
PDA and PLV may originate from both RCA and LCx.
LAO straight
RCA PLV
AMB
PDA
Fig. 4.5 | Coronary angiogram of RCA-LAO view.
Conus branch
RCA
PDA
RAO straight
Fig. 4.6 | Coronary angiogram of RCA-RAO view.
(v) In type-I LAD (where it terminates before the apex), the larger and longer
PDA from RCA supplies the ventricular apex also, which is then described as Super
dominant RCA.
(vi) Angiographically, RCA is divided into three parts: Proximal, Mid, and Distal
(see Figs 4.5 and 4.6).
Proximal RCA is the portion of the RCA from its origin from the right anterior
coronary sinus to the origin of its RV branch.
Mid RCA is the portion of RCA between its RV branch and its PDA branch.
Distal RCA includes PDA and PLV branches.
3. DIVERGENT CORONARY ANATOMY
In 12%, there may be divergent coronary anatomic features.3 These include:

Anomalous origin of LCx from RCA
Separate ostia of LAD and LCx or
Separate ostia of RCA and its conus branch
Table 4.2 Coronary artery: Length and luminal diameters
Coronary artery Length (mm) Luminal diameter (mm)
1. LMCA 125 25.5 (4)

2. LAD 100130 25.0 (3.6)
3. LCx 6080 1.55.5 (3)
4. RCA 120140 1.55.5 (3.2)
Occassionally, the right or left coronary ostium arises 1 cm or more (usually 2.5 cm) above
the sinotubular junction. This ostial dislocation is termed as a high-takeoff coronary
artery.4
4. MEASUREMENTS
i) Length
(i) The LMCA usually ranges from 125 mm in length1 and it is termed as short
LMCA if it is 1 cm
(ii) The LAD measures 1013 cm in length
(iii) Non-dominant LCx is 68 cm in length, while
(iv) RCA is 1214 cm in length before it gives rise to PDA (see Table 4.2).
ii) Luminal Diameter

The luminal diameter of LMCA is 2.05.5 mm (mean of 4 mm), LAD: 2.05.0 mm
(mean of 3.6 mm) and LCx: 1.55.5 mm (mean of 3 mm). RCA has a luminal diameter
of 1.55.5 mm (mean of 3.2 mm).1
LAD and LCx generally taper in diameter as they extend from the LMCA, while RCA
maintains a fairly constant diameter till it gives rise to PDA.
REFERENCES
1. Baroldi G. Diseases of the coronary arteries. In: Silver MD, Ed. Cardiovascular Pathology: I. New York,
Churchill Livingstone. 1983:317391.
2. Anderson KR, Ho SY, Anderson RH. Location and vascular supply of sinus node in human heart.
Br Heart J 1979;41:2832.
3. Click RL, et al. Anomalous coronary arteries, location, degree of atherosclerosis and effect on survival
A report from Coronary Artery Surgery study. J Am Coll Cardiol 1989;13:531.
4. Spring DJ, Thomsen JH. Severe atherosclerosis in the single coronary arteryReport of a previously
undescribed pattern. Am J Cardiol 1973;31(5):662665.
CHAPTER 5
N ERVE S UPPLY OF THE H EART
1. CARDIAC PLEXUS 40 2. BARORECEPTORS AND

i) Superficial Cardiac Plexus 40 CHEMORECEPTORS 43
ii) Deep Cardiac Plexus 41 i) Baroreceptors 44
iii) Both Sympathetic and ii) Chemoreceptors 46
Parasympathetic Fibers 43 REFERENCES 46
The nerve supply of the heart is derived from1,2 (see Tables 5.1 and 5.2):
1. The cardiac plexus formed by the sympathetic and parasympathetic (vagal) fibers
(see Figs 5.1 and 5.2) and
2. Baroreceptors and chemoreceptors.
1. CARDIAC PLEXUS
i) Superficial Cardiac Plexus

It is situated below the arch of aorta and in front of the right pulmonary artery.
It is formed by:
(i) The superior cardiac branch of superior cervical ganglion of the left sympathetic
chain and
(ii) The superior cardiac branches (from superior and inferior cervical nerves) of the
left vagus nerve.
Table 5.1 Nerve supply of the heart
Cardiac plexus Branches to
1. Superficial cardiac plexus

RCA (through coronary plexus)
(below the aortic arch)
Left anterior pulmonary plexus

Deep cardiac plexus
2. Deep cardiac plexus
Both atria
(behind the aortic arch)
Both coronary arteries (through coronary plexus)

Right and left anterior pulmonary plexus superficial cardiac plexus
NERVE SUPPLY OF THE HEART 41
The superficial cardiac plexus gives branches to

(i) The deep cardiac plexus
(ii) Right coronary artery (coronary plexus) and
(iii) Left anterior pulmonary plexus.
ii) Deep Cardiac Plexus

It is situated in front of the bifurcation of the trachea and behind the arch of aorta.
It is formed by:
(i) The cardiac branches of superior, middle and inferior cervical ganglia (except the
cardiac branch arising from superior cervical ganglion of left sympathetic chain,
Table 5.2 Peculiarities of nerve supply to the heart
Nerve supply Features
1. Sympathetic innervation More at the base than at the apex of the heart
2. Vagal activity Greater in posterior ventricular myocardium
3. Right sympathetic and vagus nerves Affect SA node AV node
4. Left sympathetic and vagus nerves Affect AV node SA node
Superior cardiac
Right coronary
branch of superior
artery
cervical ganglion
Superficial
cardiac plexus
Superior cardiac Left anterior
branches of left pulmonary plexus
vagus
Cardiac branches
of superior cervical
ganglion Cardiac branches
of upper 45
thoracic ganglia
Cardiac branches
Deep cardiac
of middle cervical
plexus
ganglion Inferior cardiac
branches of vagus/
recurrent laryngeal
Cardiac branches nerve
of inferior cervical
ganglion
Both coronary
Both atria
arteries
Left and right anterior

pulmonary plexus
Fig. 5.1 | Cardiac plexus (diagrammatic).

Thalamus
Cervical
sympathetic
ganglia and
Medulla nerves
Superior
ves
s ner
u
Vag Middle
Inferior
T1 (Stellate ganglion)
(Via superior and
inferior cardiac branches, T1
and thoracic cardiac Thoracic
branches of right and sympathetic
T2 ganglia and
left vagus)
nerves
T3
T4
T5
(Post-ganglionic)
(Pre-ganglionic)
To S-A node, To S-A node,

A-V node, atrial A-V node, atrial
Cardiac plexus
and ventricular and ventricular
muscle muscle
Parasympathetic Sympathetic
Fig. 5.2 | Nerve supply of the heart.
which forms superficial cardiac plexus) and upper 4 or 5 thoracic ganglia of right
and left sympathetic chain.
The inferior cervical ganglion and first thoracic ganglion are fused together to
form a Stellate ganglion.
(ii) Inferior (thoracic) cardiac branches of vagus and/or recurrent laryngeal nerves of
both sides except superior cardiac branches of left vagus (which form superficial
cardiac plexus).
The deep cardiac plexus gives branches to:
superficial cardiac plexus
both atria
both coronary arteries (coronary plexus) and
right and left anterior pulmonary plexus.
iii) Both Sympathetic and Parasympathetic Fibers

These influence the SA node, AV node, both the atrial and ventricular myocardium,
although vagal fibers are sparse to the ventricles.3
(i) Sympathetic stimulation to the heart is largely mediated by the release of norepi-
nephrine and parasympathetic stimulation by acetylcholine.
(ii) The sympathetic innervation is more at the base than at the apex of the
heart, while the vagal activity is greater in the posterior ventricular myo-
cardium which accounts for the vagomimetic effect of the inferior myocardial
infarction.
(iii) The right sympathetic and vagus affect the SA node more than the AV
node while the left sympathetic and vagus affect the AV node more than the SA
node.
(iv) Hence, stimulation of right stellate ganglion causes sinus tachycardia with less affect
on AV nodal conduction. Whereas stimulation of left stellate ganglion shortens
the AV nodal conduction time and refractory period and produces the shift in
sinus pacemaker to an ectopic site.
(v) Also, stimulation of right (cervical) vagus slows sinus node discharge rate (produc-
ing bradycardia) while the stimulation of left vagus prolongs the AV nodal conduc-
tion time and refractoriness.
In general, right sympathetic chain shortens the refractoriness primarily of the anterior
portion of the ventricles while the left sympathetic chain primarily affects the poste-
rior surface of the ventricles.
2. BARORECEPTORS AND CHEMORECEPTORS
The cardiovascular regulatory mechanisms includes4 (see Table 5.3 and Fig. 5.4):
(a) Chemical Regulatory Mechanisms through circulating vasodilators (bradykinin)
and circulatory vasoconstrictors (epinephrine, nor-epinephrine, angiotensin II and
vasopressin) and
(b) Neural Regulatory Mechanisms which consist of:
Sympathetic and parasympathetic systems through superficial and deep cardiac
plexus and
Medullary vasomotor and cardiac vagal centers.
The ventrolateral region of medulla (Pressor area) exerts excitatory effects

(increase) on sympathetic activity while the medial and caudal parts of fourth
ventricle in medulla (Depressor area) cause decrease of sympathetic activity.
Cardiac vagal center consists of inhibitory vagal fibers originating from the
neurons of vagal nuclei located in the medulla (dorso-motor nucleus, nucleus of
tractus solitarius and nucleus ambiguous) to converge on:
The sympathetic pre-ganglionic neurons of spinal cord to decrease the sympa-
thetic activity and
Inferior colliculus
Bronchium pontis
Pressor area
Depressor area
Fig. 5.3 | Vasomotor center (diagrammatic).
Table 5.3 Baroreceptors and chemoreceptors
Receptors Location
Baroreceptors
1. Arterial baroreceptors Carotid sinus
(pressure receptors) Aortic arch
Root of subclavian artery
Pulmonary trunk
2. Cardiac baroreceptors
i. Volume receptors Atriocaval receptors (RA)
Pulmonary venoatrial receptors (LA)
ii. Pressure receptors Atrial: RA, LA, interatrial septum
Ventricular: LV, interventricular septum
(Bezold-Jarisch reflex)
Chemoreceptors
1. Carotid bodies Common carotid artery bifurcation
2. Aortic bodies Around aortic arch
The heart to decrease the heart rate and force of the cardiac contraction. The vaso-
motor and cardiac vagal centers are influenced by the afferent fibers from the
baroreceptor and chemoreceptors (see Fig. 5.3).
i) Baroreceptors
Since they are sensitive to stretch, they are also called as mechanoreceptors. All are
innervated by vagus nerve except the carotid sinus baroreceptors which are supplied by
Cardiovascular and
respiratory medullary
Carotid body IX nerve center
Carotid sinus
Common
Right aortic nerve carotid Left aortic nerve
(branch of vagus) artery (branch of vagus)
Right subclavian
artery
Left subclavian
Aortic bodies artery
Aorta
Fig. 5.4 | Baroreceptors ( ) and chemoreceptors ( ).
carotid sinus nerve, a branch of glossopharyngeal (IX cranial) nerve. Broadly, there are
two types of baroreceptors: arterial and cardiac.
(a) Arterial Baroreceptors

These are located in the walls of the blood vessels mainly in the adventitial layer.
The afferent signals are mainly carried through vagus to the vasomotor center and
the cardio-vagal center in medulla.
The arterial baroreceptors are situated at:
1. Carotid sinus (dilated initial part of internal carotid)
2. Aortic arch
3. Root of subclavian artery
4. Junction of thyroid artery with common carotid artery and
5. Pulmonary trunk near its division.
Increased aortic pressure causes reflex inhibition of vasomotor center (VMC) and
stimulation of cardiac vagal center (CVC), thereby decreasing the heart rate and
systemic vascular resistance, while lowering the aortic pressure results in stimulation
of VMC and inhibition of CVC, thereby increasing the heart rate and systemic
vascular resistance.
The range of operation of these baroreceptors is between 60200 mmHg of mean
blood pressure.
(b) Cardiac Baroreceptors

These are located in the walls of the heart i.e. subendocardial in distribution.
The cardiac baroreceptors are:

1. Atrio-caval receptors located at the junction of right atrium with inferior vena cava
and superior vena cava.
2. Pulmonary veno-atrial receptors located at the junction of pulmonary vein with left
atrium. Both [1] and [2] are volume receptors i.e. increase blood volume causes dis-
tension of the atrial walls producing reflex tachycardia (Bainbridge reflex) and mod-
erate diuresis due to the release of atrial natriuretic peptide (ANP).
3. Atrial receptors scattered throughout the atria and interatrial septum. Increase in
atrial pressure increases their impulse activity (however their discharge is sparse and
irregular) resulting in reflex vasodilatation especially in the renal vessels.
4. Ventricular receptors are scattered throughout the left ventricle and ventricular
septum. They are stimulated (their discharges are also sparse and irregular) by the
injection of veratridine, serotonin or nicotine into coronary artery (especially left)
or pulmonary artery or by partial occlusion of aorta or coronary sinus, resulting
in profound bradycardia and hypotension due to reflex sympathetic inhibition
(Bezold-Jarisch reflex).
ii) Chemoreceptors
Chemoreceptors are sensitive to the changes in the blood chemistry. Their main function
is to keep the alveolar pCO2 at a normal level of 40 mmHg and also to maintain arte-
rial pO2, pCO2 and pH.
The important chemoreceptors are: Carotid bodies and Aortic bodies
(i) Carotid bodies: These are located near common carotid artery bifurcation and are
innervated by carotid sinus nerve, a branch of glossopharyngeal nerve.
(ii) Aortic bodies: These are scattered around aortic arch and are innervated by aortic
nerve, a branch of vagus nerve.
Afferent fibers from these chemoreceptors ascend to relay in the nucleus of tractus
solitarius of medulla. Hypoxia, hypercapnia and acidemia stimulate these receptors
which activates the vasomotor center and respiratory neurons in the medulla producing
pressure effects with an increase in the rate and depth of respiration.
REFERENCES
1. Mitchell GAG. Cardiovascular Innervation. Baltimore: Williams & Wilkins: 1956.

2. Janes RD, Brandys JC, Hopkins DA, Johnstone DE, Murphy DA, Armour JA. Anatomy of human
extrinsic cardiac nerves and ganglia. Am J Cardiol 1986 1;57(4):299309.
3. Randall WC, ed. Nervous Control Cardiovascular Function. New York: Oxford University Press:
1982.
4. Jain AK. Cardiovascular regulatory mechanisms. In: Text book of Physiology: I. New Delhi: Avichal
Publishing Co 2001:324328.
CHAPTER 6
THE CONDUCTION SYSTEM OF
THE HEART
1. SINOATRIAL (SA) NODE (PACEMAKER The Bundle of His (AV Bundle,

NODE OF KEITHFLACK Common Bundle) 51
NODE, 1907) 47 3. THE BUNDLE BRANCHES
P Cells (Pale/nodal cells) 48 AND TERMINAL PURKINJE
Transitional Cells (T cells) 49 FIBERS 51
Internal Atrial Myocardium 49 The Left Bundle Branch (LBB) 51
2. ATRIOVENTRICULAR JUNCTIONAL The Right Bundle Branch (RBB) 51
AREA 50 The Terminal Purkinje Fibers 52
Transitional Cell Zone 50 REFERENCES 52
Atrioventricular (AV) Node
(Tarawa, 1906) 50
The conduction system of the heart consists of three major parts (see Fig. 6.1 and
Table 6.1):
1. Sinoatrial (SA) node
2. AV junctional area and
3. The bundle branches and terminal Purkinje fibers.
1. SINOATRIAL (SA) NODE (PACEMAKER NODE OF

KeithFlack, 1907)
SA node is spindle shaped, 1012 mm long and usually 1 mm thick situated in the
sub-epicardium (less than 1 mm from the epicardial surface) at the lateral junction of
the superior vena cava and right atrium.
Blood supply to the SA node is by the sinus nodal artery, which arises from proximal
RCA in 5560%, LCx in 4045% and from both in 11%.1
Histologically, the sinus node has:
P cells
Transitional cells and
Atrial muscle cells.
Anterior internodal tract
Middle internodal tract

Sinoatrial node
Membranous
Posterior internodal ventricular septum
tract
Muscular
ventricular
Atrioventricular septum
node Atrioventricular Septo-marginal
bundle trabecula
Nodal fibers Transitional fibers Purkinje fibers
Fig. 6.1 | Conduction system of the heart.
Table 6.1 Conduction system of the heart
Structures Location
1. SA node Lateral junction of SVC and RA

2. AV node At the apex of Kochs triangle
3. The bundle of His Chord-like distal continuation of AV node
4. Left bundle branch (LBB) Forms a cascade down the left ventricular
septal surface
5. Right bundle branch (RBB) Beneath the non-coronary aortic cusp
Direct continuation of His bundle along the
right side of the ventricular septum
6. The terminal Purkinje fibers On the endocardial surface of both
ventricles
P Cells (Pale/nodal cells)

P cells are ovoid, small (510 m in greatest diameter) and resemble the primitive
myocardial cells.
The nuclei are of normal size, but double or multiple nuclei in a single cell are not
observed.
There are fewer mitochondria in a P cell compared to the normal contractile
cells.
Myofibrils are few in number and rarely attached to the sarcolemma.
The P cells are the source of normal impulse formation in the SA node. However,
intercellular contact is direct plasma membrane to plasma membrane, a factor
responsible for slow conduction within the sinus node.
THE CONDUCTION SYSTEM OF THE HEART 49
Transitional Cells (T cells)

T cells are intermediate between P cells and atrial myocardial cells (elongated than
P cells but shorter and narrower than atrial myocardial cells).2
They are located at the margins of the sinus node, where nodal cells become contiguous
with atrial myocardium.
T cells provide a functional pathway for the distribution of sinus impulses formed in
the P cells to the rest of the atrial myocardium.
The fibrous tissue and fat increase with advancing age and hence the fibrous tissue is
predominant in adult sinus node as compared to that of an infant.3
Internal Atrial Myocardium

Certain population of atrial myocardial cells have different electrophysiological prop-
erties, and James and Sherf 4 supported the concept of three specific internodal tracts
between SA and AV nodes:
Anterior internodal tract
Middle internodal tract and
Posterior internodal tract.
i) The Anterior Internodal Tract (BachmannJames)

It leaves the antero-superior part of the SA node and curves around in front of the
superior vena cava, divides into two bundles of fibers one entering the left atrium
while the other coursing over the anterior portion of the interatrial septum and de-
scending obliquely behind the root of the aorta to enter the anterosuperior margin of
the AV node.
ii) The Middle Internodal Tract (Wenckebach)

It leaves the postero-inferior margin of the SA node, curves behind the SVC and course
along the posterior margin of the interatrial septum to enter the superior margin of the
AV node.
iii) The Posterior Internodal Tract (Thoral)

It leaves the postero-inferior margin of the SA node and follows the course of crista
terminalis and eustachian ridge to enter the posterior margin of the AV node.
The middle and posterior internodal tracts may also extend the fibers from the
right atrium to the left atrium.5 All the three tracts anastomose with each other above
the AV node and have transitional cells and common atrial myocardial cells. However,
presently the evidence does not support the presence of specialized internodal tracts6
and preferential internodal conduction in some parts of the atrium may be due to atrial
myocardial fiber orientation, size and geometry rather than specialized tracts between
the nodes.2,7,8
2. ATRIOVENTRICULAR JUNCTIONAL AREA
It consists of three distinct areas:

Transitional cell zone
AV node and
His bundle.
Transitional Cell Zone

It is the outer layer of the AV node which connects the right atrial myocardium with
the AV node.9,10 This area is sub-divided into three main groups: Anterior or superior,
Middle and Posterior or inferior.11
Atrioventricular (AV) Node (Tarawa, 1906)

AV node is a small ovoid structure (smaller than SA node) measuring 1 3 5 mm,
lies just beneath the right atrial posterior epicardium, anterior to the ostium of coronary
sinus and directly above the insertion of the septal leaflet of tricuspid valve.
It is located at the apex of the triangle of Koch formed above by the tendon of Todaro,
in front by the base of the septal leaflet of tricuspid valve and base by the ostium of the
coronary sinus.12
The tendon of Todaro originates from the central fibrous body and passes posteriorly
through the atrial septum.
The compact AV node becomes the penetrating bundle of His at the apex of the trian-
gle of Koch and passes through the membranous ventricular septum below the point
of attachment of the tendon of Todaro to the central fibrous body.
The blood supply is through the AV nodal artery, which is a branch of RCA in 8590%
and LCx in 1015%.
Histologically, it has four types of cells: P cells, transistional cells, atrial myocardial
cells and Purkinje cells.
Electrophysiologically, AV node is divided into three regions:
AN region
N region and
NH region.
AN region corresponds to the transitional cell groups in the upper posterior portion of
the AV node.
N region is a small enclosed region where transistional cells merge with mid nodal
cells.
NH region is the anterior portion of the bundle of lower nodal cells.
The dead end pathways consist of groups of cells that form an apparent elec-
trophysiological cul de sac that does not contribute to overall conduction in the
AV node.
The Bundle of His (AV Bundle, Common Bundle)

It is a chord like distal continuation of the AV node measuring 20 mm in length and
up to 2 mm in diameter. It is anatomically subdivided into three portions:
Proximal non-penetrating
Middle penetrating and
Distal branching portion.
Proximal non-penetrating portion is distal to AV node.
Middle penetrating portion is the tunneled segment within the fibrous tissue of the
central body and the membranous septum.
Distal branching portion
i) His bundle bifurcates at the crest of the muscular septum into right and left bundles,
immediately distal to the membranous ventricular septum.
ii) The blood supply is from both LAD and PDA and hence this portion of the con-
duction system is less subject to the ischemic damage.13
iii) Histologically, His bundle primarily consists of Purkinje cells.
3. THE BUNDLE BRANCHES AND TERMINAL PURKINJE FIBERS
The Left Bundle Branch (LBB)

It forms a cascade down the left ventricular septal surface beneath the noncoronary
aortic cusp. The left bundle radiates in a fanlike fashion with two major divisions: thin
anterosuperior and thick posteroinferior fascicles.14 However, Tarawa15 and recent studies
indicated a trifascicular division of the left bundle branch.16,17
The Right Bundle Branch (RBB)

It is the direct continuation of the His bundle positioned along the right side of the
ventricular septum. The right bundle branch becomes a subendocardial structure in
the middle lower thirds of the ventricular septum and remains unbranched to the apex
of the right ventricle (see Fig. 6.2).
Blood Supply
The left bundle branch receives blood supply from both LAD and RCA (see Table 6.2).
The anterosuperior fascicle is supplied by the septal branches of LAD and AV nodal
branch of RCA in 50%; and only by the septal branches of LAD in the other 50%.
The posteroinferior fascicle is supplied by the AV nodal branch of RCA in 50% and
by both the AV nodal branch of RCA and the septal branch of LAD in the other 50%.
The blood supply of right bundle branch is similar to that of the anterosuperior
fascicle of the left bundle branch.
Histologically, the bundle branches (LBB and RBB) mainly consist of Purkinje cells
intermingled with ordinary contractile myocardial cells.
Bundle of His
Left anterior fascicle
Left septal fibers
Left posterior fascicle
Right
bundle branch
Purkinje fibers
Fig. 6.2 | Bundle branches and Purkinje fibers.
Table 6.2 Blood supply of the bundle branches
Structures Arteries
1. LBB Both LAD and RCA

i. Anterosuperior fascicle 50% by septal branch of LAD and AV
nodal branch of RCA
50% only by septal branch of LAD
ii. Posteroinferior fascicle 50% only by the AV nodal branch of RCA
50% by both AV nodal branch of RCA and
septal branch of LAD
2. RBB Similar to that of anterosuperior fascicle of LBB
The Terminal Purkinje Fibers

These fibers connect with the ends of the bundle branches to form interweaving net-
works on the endocardial surface of both ventricles. However, Purkinje fibers tend to be
concentrated at tips of the papillary muscles rather than at the base of the ventricles.
They are more resistance to ischemia than the common myocardial fibres.18
REFERENCES
1. Vieweg MVR, Alpert JS, Hagan DS. Origin of the sinoatrial node and atrioventricular node arteries
in right, mixed and left inferior emphasis systems. Cathet Cardiovasc Diag 1975;1(4):36173.
2. Davies MJ, Anderson RH, Becker AE. The Conduction system of the Heart. Butterworth.
1983:1200.
3. Lev M. Aging changes in the human sinoatrial node. J Gerontol 1952;9(1):19.
4. James TN, Sherf L. Specialized tissues and preferential conduction in the atria of the heart. Am J
Cardiol 1971 Oct; 28(4):414427.
5. James TN. Anatomy of the conduction system of the heart. In: Hurst JW. Logue RB, Rackley CE,
Sonnennblick EH, Wallace AG, et al. The Heart, 5th ed. New York: McGraw-Hill, 1982:2656.
6. Becker AE, Bouman LN, Janse MK, Anderson RH. Functional anatomy of the cardiac conduction
system. In: Harrison DC, ed. Cardiac Arrhythmias: A Decade of Progress, Boston, Hall; 1981:118.
7. Anderson KR, Ho SY, Anderson RH. The location and vascular supply of the sinus node in the
human heart. Br Heart J 1979;41(1):2832.
8. Zipes DP. Genesis of cardiac arrhythmias: Electrophysiological consideration. In: Braunwald E,ed.
Heart Disease: A Text book of Cardiovascular Medicine, 2nd ed. Philadelphia: Saunders, 1982:
581620.
9. Tarawa S. Das Reizeitungs system des Saugetierkerzens. Jena: Gustav Fischer, 1906.
10. Anderson AH, Becker AE, Brechenmacher C, Davies MJ, Rossi L. The human atrioventricular
junctional area: A morphological study of the AV node and bundle. Eur J Cardiol 1975;3(1):1125.
11. James TN. The connecting pathways between the sinus node and AV node and human heart. Am
Heart J 1963;66:498508.
12. Franco PM. Recherches sur les faiseaux de connxion auriculaires dans condition normales et
pathologies. Arch Mal Coer 1951;22:287292.
13. Trautwein W, Uchizono K. Electron microscopic and electrophysiologic study of the rabbit heart.
Z Zellforsch Mikrosk Anat 1963;61:96109.
14. Rosenbaum MB, Elizari JO. The Hemiblocks Tampa FL: Tampa Tracings: 1970.
15. Rossi L. Histopathology of Cardiac Arrhythmias. 2nd ed. Milan: Casa Editrice Ambrosiana: 1970:
175.
16. Massing GK, James TN. Anatomical configuration of the His bundle and bundle branches n the
human heart. Circulation 1976;53:609621.
17. Demoulin JC, Kulbertus HE. Histopathological examination of concept of left hemiblocks. Br Heart J
1972;34:807814.
18. Becker AE, Bowman LN, Janse MJ, Anderson RH. Functional anatomy of the cardiac conduction
system. In: Harrison DC ed. Cardiac Arrhythmias. A Decade of Progress. Boston: Hall: 1981:324.
CHAPTER 7
U LTRASTRUCTURE OF THE
M YOCARDIUM
1. P CELLS 54 a) Sarcolemma 57
2. TRANSITIONAL CELLS 54 b) Intercalated Discs 58
3. PURKINJE CELLS 55 c) Sarcotubular System 59
4. AMOEBOID CELLS 55 d) Diadic Cleft 60
5. CONTRACTILE OR WORKING e) Contractile Proteins 61
MYOCARDIAL CELLS 56 REFERENCES 65
The ultrastructure of the myocardium consists of (see Table 7.1 and Fig. 7.1):
1. P CELLS
See chapter 6.
2. TRANSITIONAL CELLS
See chapter 6.
Table 7.1 Ultra-structure of the myocardium
Cells Location
1. P cells SA node
2. Transistional cells Margins of SA node
3. Purkinje cells Margins of SA node, inter nodal tracts, adjacent to
AV node, in the His bundle, LBB and RBB
4. Amoeboid cells Eustachian ridge
5. Contractile cells Atrial and ventricular myocardium
ULTRASTRUCTURE OF THE MYOCARDIUM 55
Myofibrils
Sarcolemma
Contact of reticulum Transverse tubule

with T-tubules
Z band Sarcoplasmic
I band reticulum
Mitochondrion
A band
Mitochondrion
H zone
M line
T-tubule
T-tubule (sarcolemmal
invagination)
Z band
Contact of reticulum
with T-tubule
Fig. 7.1 | Ultra-structure of the myocardial fibers.
3. PURKINJE CELLS
These cells are broader and shorter than contractile myocardial cells measuring
2050 m in length and 1030 m in cross section. They are found in the margins of
SA node, internodal tracts, adjacent to the AV node, in the His bundle and in its bundle
branches.
4. AMOEBOID CELLS
The conduction system of the heart also consists of elongated, triangular, oval or non-
geometric shaped amoeboid cells in the Eustachian ridge, which have multilobular
nuclei, many mitochondria, myofibrils and granules (which give dark appearance to
these cells) with pseudopodic prolongations that fill the spaces between the neighboring
cells.
They may act as an auxiliary pacemaker or may be a source of atrial natriuretic
peptide (ANP).
5. CONTRACTILE OR WORKING MYOCARDIAL CELLS
They are 1020 m in diameter and 50100 m in length surrounded by a cell

membrane, known as sarcolemma.
The sarcoplasm (cytoplasm) has many mitochondria and centrally located elon-
gated nucleus and many (5060) myofibrils which are inserted in the region of
intercalated disc (see Fig. 7.2 and Table 7.2).
Each myofibril is striated, 12 m in diameter and lie parallel to one another and
composed of a series of sarcomeres, the basic contractile units.
The cell membranes of some adjacent cells form close margins called intercalated
discs or junctions.
The contractile myocardial cells are similar whether they are from the atrial or ven-
tricular myocardium. However, the contractile myocardial cells which contain an
intricate sarcotubular system of tubules, vesicles and cisternae1,2 are absent or rare
in atrial myocardium.
Fig. 7.2 | Branching and anastomosing myocardial fibers with faint striations. The fibers
are made up of cells with centrally placed nucleus. Cells are separated from
one another by intercalated discs (arrows).
Table 7.2 Contractile myocardial cell
1. Size 1020 m in diameter

50100 m in length
2. Sarcolemma Bi-layered phospholipid with channels
3. Intercalated discs Macula adherens, fascia adherens, gap junction
4. Sarcotubular system T system, longitudinal sarcoplasmic reticulum
5. Diadic cleft 10000 diadic clefts/cell; 11 L-type Ca2 channels
and 100 feet/cleft
6. Contractile proteins Myosin, actin, titin, tropomyosin, troponin T, C and I
The myofibrils are made up of the contractile proteins (which give striated appear-
ance) while each intercalated disc consists of three types of specialized junctions.
a) Sarcolemma (Sarco Flesh; Lemma Thin Husk)

The cell membrane consists of a bi-layer boundary of phospholipid molecules (see Fig. 7.3).
The tail end of the phospholipid molecule is non-polar and hydrophobic pointing
toward the center of the cell membrane.
The head end is polar and hydrophilic pointing toward the outer and inner layers
of the cell membrane (see Fig. 7.4).
At rest, the resistance to ions (both cations and anions) is greater across the cell mem-
brane than in the cytoplasm especially in the non polar hydrophobic layer. The cell
membrane has openings called channels that span the cell membrane and serve as conduits
Outer membrane Transmembrane

protein protein
Inner membrane Transmembrane protein

protein forming a channel
Fig. 7.3 | Bi-layered cell membrane showing opening (channel).
Choline
Phosphate
Glycerol forming
the head
Fatty acids
forming the tail
Fig. 7.4 | Tail and head of a phospholipid molecule of the bi-layered cell membrane.
through which ions move. These channels are broadly made up of two types of protein
complexes:
i) Type I Intrinsic Membrane Protein (Voltage Operated Channels)

These protein molecules protrude through the entire cell membrane and have major
part outside the cytoplasm i.e. they are anchored to the inner layer of the cell mem-
brane e.g. Na, K, Ca channels, Na-K pump.
ii) Type II Intrinsic Membrane Protein (Ligand Receptors or

Receptor Operated Channels)
These protein molecules have major part in the cytoplasm with a very small fraction
penetrate:
Only the outer layer of the cell membrane and serve as receptor sites for neurotrans-
mitters and hormones.
The inner layer of the cell membrane and serve as receptors for adenylate cyclase.
b) Intercalated Discs
Three types of specialized junctions make up each intercalated disc:
Macula adherens or desmosome (see Fig. 7.5)
Fascia adherens and
Nexus or gap junctions (see Fig. 7.6).
i) Desmosome and Fascia Adherens

They form the areas of strong adhesions between the cells and may provide a linkage
for the transfer of mechanical energy from one cell to next cell.
Cell membrane
Intermediate
filaments
Gap junction
(gap = 3 nm)
Normal intercellular
Intercellular gap gap (20 nm)
Fig. 7.5 | Intercalated discsDesmosome. Fig. 7.6 | Intercalated discGap junction.

ii) The Gap Junctions

The cells are separated only by about 1020 A and are connected by a series of hexa-
gonally packed subunit bridges but are in functional contact with each other. They
provide:
(i) A low resistance electrical coupling between adjacent cells that permit the move-
ment of ions and other small molecules and
(ii) A biochemical coupling that permit cell to cell movement of ATP and other high
energy phosphates.
The gap junctions permit the conduction velocity faster in the direction of the
long axis of the fiber than transversely. However, the conduction delay or block
occurs more commonly in the longitudinal direction.
The gap junctions permit a multicellular structure like heart to function electri-
cally like an orderly, synchronized and interconnected unit and are also respon-
sible partly for the anisotropic type of conduction in the myocardium.
Acidosis increases and alkalosis decreases gap junctional resistance. An increased
gap junctional resistance slows the rate of action potential propagation which
could lead to conduction delay or block.3
Connexins are the proteins that form the intercellular channels of gap junctions.
c) Sarcotubular System
It is a highly specialized system of internal conduction of depolarization within
the muscle fiber. It is made up of T-system and longitudinal sarcoplasmic reticulum
(see Fig. 7.7).
i) T-system or Transverse Tubular System

The cell membrane invaginates to form the transverse tubular system.
The transverse tubules are arranged perpendicular to the long axis of the cell but
branch longitudinally and can directly connect with other transverse tubules.4
At the area of Z band/line the T tubules give off a cistern-like structure, the inter-
mediary vesicle.5
Thin filaments
Terminal cistern
Longitudinal sarcoplasmic
Triad reticulum
Transverse tubule system

(T tubule)
ECF
Fig. 7.7 | Sarcotubular system; ECF: extracellular fluid.

ii) Longitudinal Sarcoplasmic Reticulum

Longitudinal sarcoplasmic reticulum is a plexiform labyrinth of vesicles and
tubules oriented parallel to the myofibrils.
At Z band, these have local dilatations, lateral sacs or terminal cisternae which are
rich in glycogen and Ca2.
So, a triad of an intermediary vesicle and two lateral sacs is formed at Z line
which is known as sub-sarcolemma cisternae (cisternae baskets, Latin) and their
function is to release calcium from the calcium release channels (ryanodine receptors)
in the longitudinal sarcoplasmic reticulum to initiate the myocardial contraction.
The impulse rapidly spreads down the transverse tubules and intermediary vesicles
to stimulate the lateral sacs (Junctional sarcoplasmic reticulum [JSR]) to release
calcium into the diadic cleft for the initiation of myofibrillar contraction.6
There is one triad per sarcomere (two in skeletal muscle). Hence, the sarcotubular
system plays an important role both in the electrical impulse conduction7 and
electromechanical coupling.5
d) Diadic Cleft
Diadic cleft is a cleft-like space between the lateral sac of sarcoplasmic reticulum
i.e. JSR and T tubular sarcolemmal membrane (It is triadic in skeletal muscle) (see
Fig. 7.8).6
The narrow space or cleft between the sarcolemma and JSR is bridged by struc-
tures called the feet which serve as the sites for calcium release to the diadic cleft
space.
T tubule
Anionic 3Na 3Na

sites Na Ca Na
Channel Channel Channel Sarcolemma
Exchanger
Exchanger
Ca Ca
12 n
m
Foo Cleft
t Foot
Ca
Ca
0.2
m
JSR
Fig. 7.8 | Diadic cleft; JSR: junctional sarcoplasmic reticulum, T tubule: transverse tubule.
The calcium pump in the longitudinal SR plays an important role in the delivery
of calcium to the JSR at the diadic cleft.
There are 11 L-type calcium channels and 100 feet within the cleft, one cleft per
2 half sarcomere and about 10000 diadic clefts in each cell.
There is a preferential localization of Na/Ca exchangers in the sarcolemma at the
cleft through which mainly calcium fluxes out of the cell, while the calcium from
the extracellular space enters the diadic cleft via i) L-type Ca channels in the sar-
colemma and ii) the release of calcium from the JSR via the feet into the cleft (i.e.
calcium induced calcium release [CICR]) by the stimulation from the intermediary
vesicles of T system.
e) Contractile Proteins
The sarcomere, the basic contractile unit between two Z lines is made up of major and
minor proteins organized into thick and thin filaments (A and I bands respectively)
which give a pattern of dark and light bands under light microscope (see Fig. 7.9).
The A band (highly refractile material i.e. Anisotropic) is the wide dark area
between two peripherally located light band, the I band (lower refractile material i.e.
isotropic).
Myofibrils
Contact of reticulum
with T-tubules
Z band
I band
Mitochondrion
A band
H zone
M line
T-tubule
Z band
Fig. 7.9 | Bands in myofibril.

The A band is about 1.5 m in length and consists of both thick myosin and thin
actin filaments arranged in a hexagonal pattern with six actin filaments surrounding
each myosin filament.
The I band is about 1.0 m in length and consists of only thin actin filaments
attached to the Z line (Zwischenscheibe i.e. between disc).
The H zone (after the discoverer Hansen) is a lighter band in the center of the A band
and consists of only myosin filaments.
In the center of the H zone is a thin dark line, the M line to which the thick myosin
filaments are attached. The M line is particularly pronounced during muscle
contraction.
The major contractile proteins are:
Myosin thick filament
Titin
Actin thin filament
Tropomyosin and
Troponin T, C and I.
While the minor contractile proteins are:
Alpha actinin
c-protein and
Nebulin.
i) Myosin
It consists of a short bilobular head and a long tail or shaft (see Fig. 7.10).
(i) The short compact bilobular head is 30 nm in length and 4 nm in diameter. It has
two types of chains (myosin heavy chain and myosin light chain) and two important
sites.
There are three chains around the base of each myosin head:
One myosin heavy chain (MHC) (i.e. 2 MHC/bilobed head), the motor of
contraction and
Actin
ATPa
Tail (LMM): 100 nm

4 nm
Head (HMM)
30 nm
Fig. 7.10 | Myosin bilobed head and tail; Actin: actin binding site, ATPa: ATPase site.
Two myosin light chains (MLC) (i.e. 4 MLC/bilobed head) which perhaps inhibit
the contractile process by interaction with actin.8
The two important sites are:
Actin binding site, where myosin comes in contact with actin and
ATPase site that hydrolysis (breaks) ATP.
(ii) The long tail or shaft is 100 nm in length and 2 nm in diameter. It carries the
load during contraction.
ii) Titin (Connectin)

It is the largest, extraordinarily long, flexible and slender myofibrillar protein.9
It is 0.61.2 m in length extending from Z line to just short of the M line.
It has two distinct segments:
(i) Inextensible segment and
(ii) Extensible segment.
Titin protein has two main functions:10
(i) Inextensible portion tethers the myosin molecule to the Z line.
(ii) Extensible portion stretches as the sarcomere lengthens.
iii) Actin
The thin actin filaments are composed of two actin units, which interwine in a hel-
ical pattern, both being carried on a heavier backbone, the tropomyosin molecule.
(see Fig. 7.11)
The thin actin filament is anchored to the Z line by alpha actinin and stretches from
the Z line to the edge of the H zone.
It is 45 nm in diameter.
iv) TropomysinTroponin Complex

Tropomyosin is a continuous coil of long filaments located in the groove between
the two chains (double helix) of actin (see Fig. 7.12).
It covers the binding site of actin where the myosin head comes in contact with the
actin i.e. it prevents the interaction between actin and myosin filaments.
I C Troponin
T
45 nm
Actin
Tropomyosin
Fig. 7.11 | Actin and Tropomyosintroponin complex.

Tropomysin
T
Troponin C Actin
I
Binding site for
myosin isoforms
T
C
I
Fig. 7.12 | Actin, tropomyosin and troponin.
Located at regular intervals of 38.5 nm along the tropomyosin molecules are three
small globular regulatory proteins, the troponins.
The three regulatory troponins are:
(i) Troponin T: binds other troponins to tropomyosin.
(ii) Troponin I: inhibits the interaction of myosin with actin.
(iii) Troponin C: contains binding sites for Ca2 that initiates the muscle contraction.
v) Myosin isoforms
There are three myosin isoforms depending upon the electrophoretic mobility: V1, V2
and V3.
Each myosin isoform consists of two distinct types of MHC genes.
(i) V1 consists of
MHCs
(ii) V3 consists of MHCs and
(iii) V2 consists of
MHCs.
Each myosin isoform is produced by different gene located on different chromo-
some (V1 on chromosome 3, V3 on chromsome 14).
V1 myosin isoform has high ATPase activity with increased (fast) shortening veloc-
ity but low efficiency of force (tension) production, while V3 myosin isoform
has low ATPase activity with decreased (slow) shortening velocity but high effi-
ciency of force production. The characters of V2 myosin isoform are in between
V1 and V3.
In ventricles: In utero until late fetal life V3 myosin isoform is abundant and V1
myosin isoform predominates only transiently shortly after birth. But thereafter,
MHC becomes and remains as the most abundant with 310% being
MHC.
In atria: V1 myosin isoform is predominant throughout the life.
With increased work load, the ventricles get switched to V2 myosin isoform (

MHC genes) and atria get switched to V3 myosin isoform ( MCH genes).
Re-induction of fetal program is a general adaptative process to the hemodynamic
stress (pressure overload/hypertrophy).
REFERENCES
1. Porter KR, Palade GE. Studies on the endoplasmic reticulum: III. Its form and distribution in striated
muscle cells. J Biophys Biochem Cytol 1957;3(2):269300.
2. Hoffman BF. Physiology of atrioventricular transmission. Circulation 1961;24:506517.
3. Severs NJ. Pathophysiology of gap junctions in heart disease. J Cardiovasc Electrophysiol 1996;5(5):
462475.
4. Fawcett DW, McNutt NS. The ultrastructure of the cat myocardium: I. Ventricular papillary muscle.
J Cell Biol 1969;42:145.
5. Essner E, Novikoff AB, Quintana N. Nucleoside phosphatase activities in rat cardiac muscle. J Cell
Biol 1965;25:201215.
6. Langer GA, Peskoff A. Role of Diadic Cleft in myocardial contractile control. Circulation 1997;96:
37613765.
7. Huxley AF, Taylor RE. Local activation of striated muscle fibers. J Physiol 1958;144(3):426441.
8. Morano I, Ritter O, Bonz A, et al. Myosin light chainactin interaction regulates cardiac contractility.
Cir Res 1995;76(5):720725.
9. Wang K, Ramirez-Mitchell R, Palter D. Titin is an extraordinarily long, flexible and slender myofib-
rillar protein. Proc Natl Acad Sci 1984;81(12):36853689.
10. Trombitas K, Jin JP, Granzier H. The mechanically active domain of titin in cardiac muscle.
Cir Res 1995;77(4):856861.
CHAPTER 8
BASIC E LECTROPHYSIOLOGICAL
P RINCIPLES
SARCOLEMMA, INTERCALATED DISC 66 CARDIAC ACTION POTENTIALS 67

INTRACELLULAR AND EXTRACELLULAR i. Phases of the Cardiac Action
ION CONCENTRATIONS IN Potential 67
CARDIAC MUSCLE 66 ii. Origin and Sequence of Cardiac
PROPERTIES OF TRANSMEMBRANE Activation 71
POTENTIALS 67 REFERENCES 72
SARCOLEMMA, INTERCALATED DISC
See chapter 7.
INTRACELLULAR AND EXTRACELLULAR ION

CONCENTRATIONS IN CARDIAC MUSCLE
The ionic concentrations of sodium (Na) and chloride (Cl) are more in the extra-
cellular fluid while that of potassium (K) and calcium (Ca) are more in the intra-
cellular fluid (see Table 8.1).
Most of the intracellular Ca is bound to or sequestered in intracellular organelles
(mitochondria and sarcoplasmic reticulum).
Table 8.1 Intracellular and extracellular ion concentrations
Extracellular Intracellular Ratio of extracellular to E1 (equilibrium potential

Ion
concentration concentration intracellular concentration for the ion)
Na 145 mM 15 mM 9.7 60 mV

K 4 mM 150 mM 0.027 94 mV
Cl 120 mM 5 mM 24 83 mV
Ca 2 mM 107 M 2 104 120 mV
BASIC ELECTROPHYSIOLOGICAL PRINCIPLES 67
PROPERTIES OF TRANSMEMBRANE POTENTIALS
The resting potential and action potential amplitude and its overshoot are low in SA
and AV nodes than that of atrial and ventricular muscle cells and Purkinje fibers. The
propagation velocity of the stimulus is fastest in the Purkinje fibers due to their large
size (see Table 8.2).
CARDIAC ACTION POTENTIALS
i. Phases of the Cardiac Action Potential

The cardiac transmembrane potential consists of five phases: one phase of depolariza-
tion, three phases of repolarization and one phase of resting membrane potential and
diastolic depolarization (see Fig. 8.1 and Table 8.3):
Phase 0: the upstroke or rapid depolarization
Phase 1: early rapid repolarization
Phase 2: plateau phase
Phase 3: final rapid repolarization
Phase 4: resting membrane potential and diastolic depolarization.
Phase 0: The Upstroke or Rapid Depolarization

The action potential which is conducted throughout the heart and responsible for initi-
ating each heart beat is independent of the size of the depolarizing stimulus. However,
when the stimulus reaches the threshold potential (70 to 65 mV for Purkinje fibers)
upstroke or rapid depolarization occurs which lasts for 12 msec.
Table 8.2 Properties of transmembrane potentials
AV nodal Atrial muscle Ventricular

Properties SA nodal cell Purkinje fiber
cell cell muscle cell
1. Resting
potential (mV) 50 to 60 60 to 70 80 to 90 80 to 90 90 to 95
2. Action potential
Amplitude (mV) 60 to 70 70 to 80 110 to 120 110 to 120 120
Overshoot (mV) 0 to 10 5 to 15 30 30 30
Duration (ms) 100 to 300 100 to 300 100 to 300 200 to 300 300 to 500
Vmax (V/s) 1 to 10 5 to 15 100 to 200 100 to 200 500 to 700
3. Propagation
velocity (m/s) 0.05 0.1 0.3 to 0.4 0.3 to 0.4 2 to 3
4. Fiber
diameter (m) 5 to 10 5 to 10 10 to 15 10 to 16 100
25
1
Transmembrane potential, mV
2
0
25
50 3
75
4
100
Na Ca2 K Na K

Influx Influx Efflux Efflux Efflux
Fig. 8.1 | Phases of action potential.
Table 8.3 Phases of cardiac action potential
Phase Mechanism
1. Phase 0: rapid depolarization INa but ISi in SA and AV nodes

2. Phase 1: early repolarization (i) Inactivation of INa
(ii) Activation of Ito
3. Phase 2: plateau phase (i) Fall of K conductance
(ii) ISi and ICl
4. Phase 3: final (i) Inactivation of ISi and ICl
rapid repolarization (ii) Activation of Ik
5. Phase 4:
(a) resting membrane Iki and Ca
potential
(b) diastolic depolarization (i) Decay of Ik
(ii) ISi and If
INa: inward sodium current, ISi: slow inward current, Ito: transient outward current, ICl: small
inward current through chloride channel, Ik: outward potassium current, Iki: inward potassium
current, If: pacemaker current.
Mechanism for phase 0

(i) The upstroke in atrial and ventricular muscle and Purkinje fibers is due to sud-
den increase in the membrane conductance to Na i.e. increased inward sodium
currents (INa), which is brief (while it is long lasting during plateau phase).
The rate at which depolarization occurs during phase 0 (V
max) is reasonable approx-
imation of the rate and magnitude of Na entry into the cell and when the equilib-
rium potential for Na (ENa 60 mV) is reached, Na no longer enters the cell.
Na
m
Rest h
m
Activated h
m
Inactivated h
30
mV 60
90
Fig. 8.2 | Membrane conductance of Na .
The membrane conductance of Na during phase 0 is hypothetically regulated by

two types of gatesm and h (see Fig. 8.2).
Three m (activation) gates on the extracellular side and
One h (inactivation) gate on the intracellular side of the membrane, which
modulate Na passage through the sodium channels.
When the membrane is in a resting polarized state, the m gates are almost
completely closed and h gate is open and hence, no Na can enter the cell.
However, depolarization of the membrane opens the m gates and closes the h
gate, m gates opening faster than the h gate closing i.e. activation of the Na
channels proceeds faster than inactivation can occur and Na flows through for
about 12 msec when both gates are simultaneously open.1
(ii) The upstroke in SA node and AV node is due to slow inward current (ISi) through
Ca channels.
Phase 1: Early Rapid Repolarization

Following phase 0, the membrane repolarizes rapidly and transiently to near 0 mV.
Mechanism for phase 1: It is partly owing to the inactivation of inward current (INa)
and the activation of a transient outward current (Ito) carried through K channels.
Phase 1 is well defined in Purkinje fibers and some muscle fibers but is indistinct and
not separated in SA and AV nodes.
Phase 2: Plateau Phase

During the plateau phase, the membrane voltage remains zero for more than 100 ms.
Mechanism for phase 2: Plateau phase is due to:
Fall of K conductance
Slow inward current (ISi) through Ca channels and
Small inward Cl (ICl) flux through Cl channel.
Phase 3: Final Rapid Repolarization

During this phase, rapid repolarization occurs.
Mechanism for phase 3: Final phase of rapid repolarization is due to:
Time dependent inactivation of slow inward currents ISi and ICl so that intracellular
movement of positive charges decreases and
Activation of outward K current (Ik).
The net membrane current becomes more outward and the membrane potential shifts in
a negative direction.
Phase 4: (a) The Resting Membrane Potential

It is 50 to 95 mV depending on the cell type i.e. the inside of the cell is negative
in relation to the outside of the cell owing to the distribution of ions: K, Na, Ca2,
and Cl across the cell membrane.
Mechanism for resting membrane potential
The resting negative membrane potential is mainly due to inward K current (IKi ).
During diastole, the cell membrane is quite permeable to K and relatively imperme-
able to Na and the sodium pump (Na, K ATPase) pumps three Na out of the
cell and two K into the cell which results in high intracellular K (150 mM) and low
intracellular Na (15 mM).
The Ca2 contributes little to the resting membrane potential although changes in the
Ca2 concentration can affect the permeability of the cell membrane to other ions, i.e.
an increase in Ca2 increases the K conductance. Besides under normal conditions,
one internal Ca2 is exchanged for three external Na by the Na/Ca2 exchanger.
Phase 4: (b) Diastolic Depolarization

Under normal conditions, the membrane potential of the atrial and ventricular
muscle cells remains steady throughout the diastole.
However in SA node, distal portion of AV node, muscles of mitral and tricuspid
valves and Purkinje fibers; the resting membrane potential does not remain constant
in diastole but gradually depolarizes and when it reaches the threshold potential, it
produces spontaneous action potential.
This property possessed by the spontaneously discharging cells is known as phase 4
diastolic depolarization and automaticity results when it leads to the initiation of
action potential.
Mechanism for automaticity
(i) Normal automaticity by SA node: The discharge rate of SA node normally
exceeds the discharge rates of other potentially automatic pacemaker sites (e.g.
Purkinje fibers) and thus SA node maintains the dominance of the cardiac
rhythm. The automaticity of the SA nodal cells is due:
mainly to the decay of K

current (IK)
long-lasting slow inward current (I ) while
Si
Phase 4 pacemaker current (If ) contributes only 20%, which is an inward K

current produced by the sodium (Na, K ATPase) pump.
(ii) Abnormal automaticity of the Purkinje fibers
It is mainly due to phase 4 pacemaker current (If)2 and
Slow inward current (ISi).
ii. Origin and Sequence of Cardiac Activation

a) Atrial Depolarization
The normal impulse originates in the SA node and traverses the atria in a wave like
front with a velocity of about 1 m/s.
As SA node is situated in right atrium, the impulse initially activates the right
atrium in a right and anterior direction, thereafter activating the interatrial septum,
and lastly, the left atrium in a left and posterior direction.
The region of the left atrium to be activated last is the tip of the left atrial appendage
or the posteroinferior portion of the left atrium underneath the left inferior
pulmonary vein.3
The atrial depolarization is completed in about 0.1 s.
b) Decremental Conduction at the AV Node

The impulse then arrives at the AV node through the preferential internodal pathways
where it is delayed by about 0.1 s due to smaller size of the AV nodal tissue and slower
conduction in the AV node (0.050.1 m/s) as compared to Purkinje fibers and other
muscle fibers.
c) Ventricular Depolarization4
Ventricular depolarization starts with almost simultaneous activation of central left side
of the ventricular septum, the high anterior and apical posterior paraseptal areas of left
ventricle (within 5 msec) proceeding from the endocardial to the epicardial surface.
At 510 ms, left and right ventricles are activated and at 12 ms, remainder of the
septum is activated.
Initial epicardial activation occurs in the anterior right ventricular epicardial surface
near the apex followed by the activation of anterior and inferior left ventricle,
continuing in the lateral and basal areas of the left ventricle. The last portion to be
depolarized is the basal portion of the septum (at 18 msec).
d) The Atrial Repolarization

It follows approximately the same path as atrial depolarization, with the polarity of
repolarization opposite to that of depolarization.
e) The Ventricular Repolarization

It proceeds in a direction opposite to that of depolarization, so its polarity is same as
that of depolarization.
REFERENCES
1. Wit AL, Bigger JT Jr. Possible electrophysiological mechanism for lethal arrhythmias accompanying
myocardial ischemia and infarction. Circulation 1975;52(Suppl. 6):III96115.
2. Irisawa H, Hagiwara N. Ionic current in sinoatrial node cells. J Cardivasc Electrophysiol
1991;2:53140.
3. Bioneau JP, Canavan TE, Schuessler RB, et al. Demonstration of a widely distributed atrial pacemaker
complex in human heart. Circulation 1988;77(6):122137.
4. Durrer D, Van Dam RT, Freud GE, et al. Total excitation of the isolated human heart. Circulation
1970;41(6):899912.
CHAPTER 9
M OLECULAR BASIS OF
M USCLE CONTRACTION
1) MUSCULAR CONTRACTION 73 The Bowditch, Staircase, or

Sliding Filament Theory of Treppe Phenomenon 75
Huxley and Hanson 74 The Frank-Starling Law of
2) MUSCULAR RELAXATION 74 the Heart 75
3) THE VELOCITY AND THE REFERENCES 76
AMOUNT OF TENSION 75
1) MUSCULAR CONTRACTION
Na entry through Na channels (the influx of Na during exit of Ca by Na/Ca
exchanger also generates a small electric current which is insufficient for generation
of normal action potential) generates action potential and depolarizes sarcolemma
which opens up the L-type Ca channels. The Ca spreads down the T tubules, interme-
diate vesicles and the lateral sacs (junctional sarcoplasmic reticulum, JSR) in the sub-
sarcolemma cisternae (Triad at Z line) which in turn is taken up by the calcium pump in
the sarcoplasmic reticulum (i.e. calcium pumping ATPase of sarcoplasmic reticulum, also
called SERCA i.e. sarco-endoplasmic reticulum Ca ATPase) to deliver Ca to the JSR
at the diadic cleft via the feet.
The Ca released in the diadic cleft:
Binds to troponin C which weakens the binding of troponin I to actin. This permits
tropomyosin to move laterally, uncovering the binding sites of actin (7 myosin sites for
each molecule of troponin T that binds a Ca); increases the myosin head ATPase
activity to hydrolyze ATP into ADP and P1 (produces energy) and increases the phos-
phorylation of myosin light chain (which increases the affinity of myosin to actin).
It also stimulates myocardial energy production by activating glycogen phosphorylase
(which results in increased glycogenolysis), phosphofructokinase (which increases gly-
colysis) and pyruvate dehydrogenase (which stimulates the citric acid cycle with produc-
tion of ATPs). The myosin heads interact with actin filaments forming cross-bridges
(cross-linkages between myosin and actin) resulting in contraction through sliding fila-
ment mechanism. As the actin filaments move towards the center of the sarcomere,
drawing the Z line closer, there occurs the shortening of the sarcomere (see Fig. 9.1).
Myosin head attached due to Ca2 release
Myosin head swivels (turns freely on a pivot)
Myosin head detaches ready for next move
Fig. 9.1 | Mechanism of formation of cross bridges.
Sliding Filament Theory of Huxley and Hanson1

The shortening of contractile elements in the muscle is brought about by the sliding of
actin filaments over the thick myosin filaments.
The sliding of the filaments is brought about by formation of the cross-bridges between
the myosin head and actin filament.
Additional Ca2 enters the cytosol through Ca2 channels during the lateral portion
of the plateau phase of the action potential and also a small amount of Ca2 enters by
the Na/Ca2 exchanger. Neither contributes to the CICR (Ca induced Ca release)
in the SR (which is initiated by Ca2 entry via L-type calcium channels) but are stored
in the SR to provide Ca2 for the subsequent contraction.
2) MUSCULAR RELAXATION
The rise in cytosolic (diadic cleft) Ca increases uptake of Ca2 into the SR by the
calcium pump (SERCA) which diffuses back to the lateral sacs (see Fig. 9.2).
This causes Ca2 to dissociate from troponin C which initiates conformational
changes in the toponin-tropomyosin complex that inhibits actin and myosin inter-
action thereby causing relaxation.
The Ca2 in the subsarcolemmal cisternae is effluxed from the myocardial cell
mainly by the Na/Ca2 exchanger in which one Ca2 leaves the cell in exchange for
three Na which are subsequently pumped out of the cell by Na, K-ATPase
(sodium pump) in exchange for two K.
MOLECULAR BASIS OF MUSCLE CONTRACTION 75
Action potential Increased sarcoplasmic reticulum

uptake of Ca2
Depolarization of sarcolemma and
transverse T tubular system Ca2 efflux sarcoplasmic Ca2

Influx of Ca2
Ca2 binding to troponin C
Calcium-induced Ca2 release from
sarcoplasmic reticulum Troponin-tropomyosin complex
inhibition of actinmyosin
Binding of Ca2 to troponin C contraction

Release of inhibition of actin and myosin Actinmyosin relaxation

Actinmyosin contraction
Fig. 9.2 | Myocardial contraction and relaxation.
3) THE VELOCITY AND THE AMOUNT OF TENSION
The velocity and the amount of tension developed by the actin-myosin filaments are
directly related to the amount of Ca2 available to induce contraction.
Hence, an increased iontropic effect is seen in the following conditions where Ca2
availblity for activation is increased:
Drugs such as digitalis, sympathomimetic amines, phosphodiesterase inhibitors
Conditions like increased heart rate, paired pacing, postextrasystolic potentiation.
Similarly, the negative iontropic effect of acidosis is due to decreased amount of
Ca2 availability and decrease in the Ca2 sensitivity of the troponin complex.
So, also at shorter sarcomere lengths, the Ca2 sensitivity of troponin is reduced and
developed force is decreased.
The Bowditch, Staircase, or Treppe Phenomenon

Increased heart rate abruptly increases the contractile force (which is due to increased
availability of Ca2).2
Whereas, a long pause decreases the strength of contraction and is known as the
Woodworth or reverse staircase phenomenon.3
The Frank-Starling Law of the Heart4

The force of contraction of the muscle fiber is directly proportional to its initial length
i.e. the larger the initial length of the cardiac muscle fibers (preload), greater will be
the force of contraction. It is one of the major mechanisms by which the normal right
and left ventricles maintain equal minute outputs but their stroke outputs may vary
considerably during normal respiration.
At sarcomere length of 2 m, the actin filaments bypass one another and developed
tension is less and
At 2.2 m length of sarcomere, actin and myosin filaments are optimally overlapped
to provide greatest tension.
However at than 2.2 m sarcomere length, the developed tension decreases as
myofilaments are partially or completely disengaged.
Theoretically, the normal ventricle may have an ejecton fraction (EF) of 55% with a
shortening of individual sarcomere length of only 13%.5
REFERENCES
1. Huxley HE, Hanson J. Changes in the cross-striations of muscle during contraction and stretch and
their structural interpretation. Nature 1954 May 22;173(4412):9736.
2. Sonnenblick EH, Morrow AG, Williams JF Jr. Effects of heart rate on the dynamics of force devel-
opment in the intact human ventricle. Circulation 2. 1966;33(6):945951.
3. Woodworth RS. Maximal contraction, staircase contraction, refractory period and compensatory
pause of the heart. Am J Physiol 1902;8:213249.
4. Starling EH. The Linacre Lecture on the Law of the Heart. London: Longman. Green: 1918.
5. Wiggers CJ. Determinants of cardiac performance. Circulation 1951;4:485495.
CHAPTER 10
T HE CARDIAC CYCLE
1. VENTRICULAR SYSTOLE 78 iv. Slow Ventricular Filling Phase 80

i. Isovolumic Contraction 79 3. ATRIAL SYSTOLE 81
ii. Rapid Ventricular Ejection Phase 79 4. ATRIAL DIASTOLE 81
iii. Slow or Reduced Ventricular 5. THE DIFFERENCES IN THE
Ejection Phase 79 EVENTS BETWEEN RIGHT AND
2. VENTRICULAR DIASTOLE 79 LEFT SIDES OF THE HEART 81
i. Protodiastole 79 6. ECG CHANGES DURING
ii. Isovolumic Relaxation Phase 80 CARDIAC CYCLE 82
iii. Rapid Ventricular Filling Phase 80 REFERENCES 82
The sequence of changes in the pressure and flow in the cardiac chambers and blood
vessels in between the two subsequent cardiac contractions is known as Cardiac cycle
(see Table 10.1 and Fig. 10.1). The cardiac cycle was first described by Wiggers1 but
was fully assembled by Lewis.2
Normal duration of the cardiac cycle is 0.8 sec at the heart rate of 75/min.
It consists of:
Ventricular systole: 0.3 s
Ventricular diastole: 0.5 s
Table 10.1 The cardiac cycle
Phase of cardiac cycle Duration
1. Ventricular systole 0.3 s

i. Isovolumic contraction 0.05 s
ii. Rapid ventricular ejection phase 0.10 s
iii. Slow ventricular ejection phase 0.15 s
2. Ventricular diastole 0.5 s
i. Protodiastole 0.04 s
ii. Isovolumic ventricular relaxation phase 0.08 s
iii. Rapid ventricular filling phase 0.100.12 s
iv. Slow ventricular filling phase (diastasis) 0.180.20 s
v. Last rapid filling phase 0.060.10 s
3. Atrial systole 0.1 s
4. Atrial diastole 0.7 s
120
100
Pressure (mmHg)
Aorta
80
60
tricle
Left ven
40
t ventricle
Righ
20
Pulmonary artery v
Left atrium y
c Right x atrium
ventricle a
Left atrium
atrium Left
z
Right
0 Right ventricle
PC TO
TC PO
Right AC MO
MC AO
Valve motion
Left
S3
S4 CLICKS S2 OS
Sounds
S1
Volume curve of c
a v
left ventricle
Jugular pulse z x y
E
a
IC
Apex cardiogram
SFW
IR
O RFW
ECG P T
ORS
0 0.1 0.2 0.3 0.4 0.5 0.6
Fig. 10.1 | ponent

The cardiac cycle correlationsMC: mitral component of S , AC: aortic com-
of S , TC: tricuspid component of S , PC: pulmonary component
1
2 1
of S2, MO: mitral valve opening, AO: aortic valve opening, TO: tricuspid valve
opening, PO: pulmonary valve opening.
Atrial systole: 0.1 s

Atrial diastole: 0.7 s.
1. VENTRICULAR SYSTOLE
It is associated with ejection of blood out of the ventricles. It consists of:

Isovolumetric (isovolumic or isochoric) contraction: 0.05 s
Rapid ventricular ejection phase: 0.10 s
Slow ventricular ejection phase: 0.15 s.
THE CARDIAC CYCLE 79
i. Isovolumic Contraction
It is the first phase of ventricular systole. This phase begins with the rise of pressure in the
ventricles after the Z point. Although ventricular contraction occurs during this phase,
there is no ventricular emptying and hence this phase is known as isovolumic contraction.
This phase is associated with:
Initial mitral component (M1) of the first sound as the ventricular pressure exceeds
the atrial pressure causing closure of the atrioventricular (AV) valves and
Beginning of the isovolumic contraction (IC) wave of the apex cardiogram.
ii. Rapid Ventricular Ejection Phase

This phase begins with the opening of the semilunar valves (aortic and pulmonary) when
the LV pressure exceeds the aortic pressure and RV pressure exceeds the pulmonary
artery (PA) pressure.
It is associated with:
Rise in arterial pressure (aorta and PA) as blood enters the great vessels much faster
than it can escape into the peripheral branches
Decrease in ventricular volume
About 2/3rd of the stroke volume is ejected during this phase and
Peak of ejection E wave of the apex cardiogram.
iii. Slow or Reduced Ventricular Ejection Phase

This phase occurs before the closure of the semilunar (SL) valves and:
It is associated with decline in the ventricular pressure as ventricular contraction
begins to subside with slow ejection of blood
During this phase, blood flows out of the aorta and PA more rapidly than it enters
from the ventricles
The blood flow in the aorta is maintained by the aortic distensibility, known as
Windkessel effect.3
2. VENTRICULAR DIASTOLE
It consists of:
Protodiastole : 0.04 s
Isovolumetric (isovolumic) ventricular relaxation phase : 0.08 s
Rapid ventricular filling phase : 0.100.12 s
Slow ventricular filling phase or diastasis : 0.180.20 s
Last rapid ventricular filling phase (due to atrial systole) : 0.060.10 s.
i. Protodiastole
At the end of ventricular systole, the ventricular pressure drops more rapidly but the
pressure in the great arteries is sustained by the elastic recoil of the vessel wall which
exceeds that in the ventricles, resulting in the closure of the SL valves producing second
heart sound and incisura of the arterial pressure tracing.
ii. Isovolumic Relaxation Phase

It begins after the closure of the SL valves and the intraventricular pressure continues
to decline rapidly and ventricular muscle continues to relax without any change in the
ventricular volume. Hence, this phase is known as isovolumic relaxation phase.
It is associated with an inward isovolumic relaxation wave (IRW) of the apex cardio-
gram (see Fig. 10.2).
It lasts until the ventricular pressure falls below the atrial pressure and AV valve opens.
iii. Rapid Ventricular Filling Phase

It accounts for most of the ventricular filling. It begins with the opening of the AV
valves when the intraventricular pressure falls below that of atrial pressure and blood
begins to flow from the atria into the ventricles. It is characterized by:
An increase in the ventricular volume with a fall of intraventricular pressure.
Initiation with O point of apex cardiogram followed by outward rapid filling wave
(RFW) of the apex cardiogram (see Fig. 10.2).
The rapid filling phase may cause the physiological third heart sound (S3) or
ventricular gallop.4
It is associated with a y descent (atrial emptying) both in atrial pressure tracing and
jugular venous pressure (JVP).
iv. Slow Ventricular Filling Phase

During this phase, the intraventricular pressures slowly rises as the ventricles are passively
filled from the atria with decreased rate.
IVC: 0.05 s RVE: 0.10 s

SVE: 0.15 s
S1, IC of ACG E of ACG
Protodiastole: 0.04 s
S2
LRF: 0.06 s SVF: 0.18 s RVF: 0.10 s S3, IVR: 0.08 s

a of ACG SFW of ACG RFW of ACG IRW of ACG
Fig. 10.2 | Cardiac cycle and correlations with heart sounds and apex cardiogram (ACG)
(diagrammatic)IVC: isovolumic contraction, RVE: rapid ventricular ejection,
SVE: slow ventricular ejection, IVR: isovolumic relaxation, RVF: rapid ventricu-
lar filling, SVF: slow ventricular filling, LRF: last rapid filling (atrial systole),
IRW: isovolumic relaxation wave, RFW: rapid filling wave, SFW: slow filling wave.
THE CARDIAC CYCLE 81
There is equalization of atrial and ventricular pressures and ventricular filling partially
stops (diastasis separation). However, renewed ventricular filling (i.e. last rapid
ventricular filling) occurs by atrial systole.
This phase is characterized by slow filling wave (SFW) of apex cardiogram.
3. ATRIAL SYSTOLE
It occurs following the impulse generation in the SA node. With atrial contraction (atrial
kick), the increased atrial pressure results in an increase in the ventricular volume i.e. the
last rapid ventricular filling phase which constitutes about 30% of the ventricular filling.
It produces:
a wave in the atrial pressure tracing and in JVP
Outward a wave of apex cardiogram (see Fig. 10.2)
There may be a fourth heart sound, S4 (atrial gallop) at the peak of the atrial a wave
particularly if there is vigorous atrial contraction and relaxation.
At times, an h wave is present in late diastasis prior to the occurrence of an a wave in
the left atrial pressure tracing.
4. ATRIAL DIASTOLE
During this phase, atrial muscles relax (producing x descent wave in atrial pressure and
JVP) and atrial pressure gradually increases due to the continuous venous return (produc-
ing v wave in atrial pressure and JVP) until the opening of the AV valves.
5. THE DIFFERENCES IN THE EVENTS BETWEEN RIGHT AND

LEFT SIDES OF THE HEART
i) The right atrial systole precedes left atrial systole and opening of the tricuspid
valve occurs slightly before the opening of the mitral valve.
ii) However, the LV systole precedes the RV systole although the RV ejection of
blood into the PA begins before the LV ejection (of the blood into the aorta) since
the PA pressure is lower than the aortic pressure and RV pressure does not have to
increase to such a high level before the ejection commences.
Besides, the RV ejection lasts beyond the LV ejection resulting in a normal gap
between A2 and P2 of the second heart sound.

The shorter duration of LV ejection is related to the greater contractile force of the
LV and to the differences in the aorta and PA impedance and the compression-
chamber (Windkessel) characteristics.
Table 10.2 The cardiac cycle and ECG changes
Waves/intervals Cause
1. P wave Atrial depolarization

2. QRS complex Ventricular depolarization
3. T wave Ventricular repolarization and end of T wave
coincides with SL valves closure
4. PR interval Atrial depolarization and His bundle conduction
5. QT interval Ventricular depolarization and repolarization
6. ST segment Ventricular repolarization
7. TP segment Polarized state of the whole myocardial segment
8. U wave Slow repolarization of the Purkinje fibers/M cells deep
in the subepicardium
6. ECG CHANGES DURING CARDIAC CYCLE
P wave is due to atrial depolarization and precedes atrial systole (see Table 10.2).
QRS complex is due to ventricular depolarization, precedes ventricular systole and
is completed before the opening of the SL valves.
T wave is due to ventricular repolarization and end of the T wave coincides with
the closure of the SL valves.
PR interval represents the atrial depolarization and His bundle conduction.
QT interval represents ventricular depolarization and repolarization.
ST segment represents ventricular repolarization.
TP segment from the end of T wave to the beginning of P wave of next cardiac
cycle is the TP segment. It represents the polarized state of the whole segment.
U wave is sometimes seen as a small positive wave (with 0.08 sec duration and
0.1 mV height) due to slow repolarization of Purkinje fibers,5 but is more recently
found to be due to the repolarization of M cells in subepicardium6 (see Table 10.2).
REFERENCES
1. Wiggere CJ. Modern Aspects of the Circulation in Health and Disease. Philadelphia, Lea and
Febiger, 1915:98.
2. Lewis T. The Mechanism and Graphic Registration of the Heart Beat. London, Shaw and Sons,
1920:24.
3. Belz GG. Elastic properties and Windkessel function of the human aorta. Cardiovasc Drugs Ther
1995;9(1):7383.
4. Glower DD, Murrah RL, Olsen CO, et al. Mechanical correlates of the third heart sound. J Am Coll
Cardiol 1992;19(2):450457.
5. Surawicz B. U wave: Facts, hypothesis, misconceptions, and misnomers. J Cardiovasc Electrophysiol
1998;9(10):11171128.
6. Antzelevitch C, Sicouri S. Clinical relevance of cardiac arrhythmias generated by after depolarizations:
Role of M cells in the generation of U waves, triggered activity and torsades de pointes. J Am Coll
Cardiol 1994;23:259277.
THE HISTORY AND
SYMPTOMATOLOGY
11. Cardinal symptoms 85

12. Other symptoms 144
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CHAPTER 11
CARDINAL SYMPTOMS
IMPORTANCE OF HISTORY TAKING 85 2. SHORTNESS OF BREATH

1. CHEST PAIN 87 (SOB)/DYSPNEA 101
Etiology 87 1. Dyspnea 101
1. The Duration of Chest Pain 89 2. Pathogenesis of Dyspnea 101
2. The Location and Radiation of 3. Etiology 104
Chest Pain 90 4. Evaluation 105
3. Character and Mode of Onset 3. PALPITATION 112
of Chest Pain 93 1. Etiology 112
4. Aggravating and Relieving 2. Evaluation 114
Factors 98 4. FATIGUE 119
5. Patients Gestures During 5. SYNCOPE 119
Chest Discomfort 100 1. Etiopathogenesis 119
6. Associated Symptoms 100 REFERENCES 142
7. Non Cardiac chest pain 101
IMPORTANCE OF HISTORY TAKING
A carefully obtained history and careful clinical examination remains the cornerstone
of the assessment of the patients with known or suspected cardiovascular disease
despite the availability of many specialized investigations.
It is undesirable to subject the patients to unnecessary risks and expenses inherent in
many specialized tests when a diagnosis can be made on the basis of:
An adequate history and clinical examination

Chest roentgenogram
ECG and
Other routine laboratory tests.
Besides, the history and physical examination provide the critical information nec-
essary for the intelligent selection of ever increasing array of these tests.
It provides a glimpse of the patients responsibility, fears, and aspirations which help
to assess patients personality, emotions and stability.
It also establishes a bond with the patient that may be valuable in securing patients
compliance in following a diagnostic workup and treatment plan.
86 THE HISTORY AND SYMPTOMATOLOGY
However, many patients with severe heart disease have no symptoms while others
have many symptoms associated with minor or no heart disease. We also know that
some patients deny the presence of any symptoms as they do not accept the reality
of the situation while others may purposefully withhold the information and some
others overstate their symptoms for personal gains.
Hence, whenever possible the examiner should question the patients relatives
or close friends in order to obtain a clearer understanding of the extent of
patients disability and importance of the disease on both the patient and the
family.
However, the important facts that are not elicited during the initial history taking
are usually not detected later.
The cardinal symptoms of cardiovascular system involvement are (see Table 11.1):
1. Chest pain.
2. SOB/Dyspnea.
3. Palpitation.
4. Fatigue.
5. Syncope.
Table 11.1 Cardiovascular causes of cardinal symptoms
Chest pain Dyspnea Palpitation Syncope Fatigue
1. CAD 1. Cardiomyopathy 1. AR, MR, TR 1. LVOTO: AS, HCM 1. AMI

2. AS, AR, HCM 2. Valvular heart 2. PDA, VSD 2. RVOTO: PS 2. HF
disease
3. Aortic dissection 3. Pericardial disease 3. ARVH 3. CAD 3. Diuretics
4. Pericarditis 4. CHF 4. Ebsteins 4. Aortic dissection 4. Beta
anomaly blockers
5. MVP 5. Pulmonary 5. Cyanotic CHD 5. Tachyarrhytmias
vascular with PBF: bradyarrhythmias
disease TAPVC, TGA pacemaker
without PS related
6. Severe systemic 6. Tachyarrhythmias 6. During and
hypertension bradyarrhythmias, following
pacemaker catheterization
related
7. Pulmonary 7. Nitrate syncope
hypertension
CAD: coronary artery disease, AS: aortic stenosis, AR: aortic regurgitation, HCM: hypertrophic cardiomyopathy,
MVP: mitral valve prolapse, CHF: congenital heart failure; MR: mitral regurgitation, TR: tricuspid regurgitation,
PDA: patent ductus arteriosus, VSD: ventricular septal defect, ARVH: arrhythmogenic right ventricular hyperplasia,
CHD: congenital heart disease, LVOTO: left ventricular outflow tract obstruction, PBF: pulmonary blood flow,
TAPVC: total anomalous pulmonary venous connection, TGA: transposition of great arteries, PS: pulmonary steno-
sis, RVOTO: right outflow tract obstruction, AMI: acute myocardial infarction, HF: heart failure.
CARDINAL SYMPTOMS 87
1. CHEST PAIN
Etiology
The etiology of the chest pain is extensive. The important causes are given below (see
Fig. 11.1):
i. Cardiovascular Causes
1. Coronary artery disease (CAD)
Angina pectoris (AP)
Myocardial infarction (MI).
2. Other cardiovascular causes
a) Likely ischemic in origin:
Aortic stenosis (AS)
Aortic regurgitation (AR)
Hypertrophic cardiomyopathy
Severe systemic hypertension
Severe pulmonary hypertension
Severe anemia/hypoxia.
b) Non ischemic in origin:
Aortic dissection
Pericarditis
Mitral valve prolapse.
ii. Non Cardiovascular Causes

1. Gastrointestinal
Esophageal spasm
Esophageal reflux
Cardiovascular
Ischemic chest pain Non ischemic chest pain
chest pain
CAD: MI, Angina Valvular: 1. HCM 1. Aortic dissection

1. AS 2. Severe systemic 2. Pericarditis
2. AR hypertension 3. MVP
3. Severe pulmonary
hypertension
Fig. 11.1 | Cardiovascular (CV) chest painCAD: coronary artery disease, MI: myocardial
infarction, AS: aortic stenosis, AR: aortic regurgitation, HCM: hypertrophic
cardiomyopathy, MVP: mitral valve prolapse.
Esophageal rupture
Acid peptic disorders
Acute cholecystitis
Acute pancreatitis.
2. Respiratory
a) Pulmonary: pulmonary embolus with or without pulmonary infarction.
b) Pleural:
Pnuemothorax
Pleurisy
Pneumonia with pleural involvement.
3. Neuro-musculoskeletal
Thoracic outlet syndrome
Costochondritis (Tietzes syndrome)
Herpes zoster
Chest wall myalgias, trauma
Cervicodorsal spine:
i. Cervical spondylitis
ii. Osteoarthritis of cervical and upper dorsal spine.
4. Psychogenic
Anxiety
Depression
Cardiac psychosis
Self gain.
The history remains the most important and valuable mode of examination for distin-
guishing among the many causes of chest discomfort (see Table 11.2), and while
obtaining the history the following has to be determined.
Table 11.2 Differential diagnosis of chest pain
Features Cardiac ischemic chest pain Non cardiac chest pain
1. Duration 25 min, 1530 min 20 s, min to hrs

2. Location Precordial or substernal More peripheral, epigastric and
and diffuse localized
3. Radiation Left shoulder, ulnar aspect of Left lower chest or others or no
arm and fore arm, neck radiation
4. Character Squeezing, choking, pressing Sharp, shooting, lancing, catching,
or tightness or dull ache
5. Precipitating or Exertion and/or emotion Not related to exertion, spontaneous
aggravating factors or provoked by food, posture or
respiration
6. Relieving factors Rest, nitrates Food, lying on the same side or
nitrates have some or no response
7. Associated SOB, palpitation or syncope Respiratory, gastrointestinal or
symptoms psychological symptoms
1. Duration, frequency, mode of onset and pattern of recurrences of chest discomfort

if any.
2. Location, radiation and character of chest discomfort.
3. Setting in which it occurs i.e. aggravating and relieving factors.
4. Patients gestures to be observed during chest discomfort.
5. Associated symptoms.
1. The Duration of Chest Pain

It helps in determining its etiology.
a) The Chest Pain Lasting for a Few Seconds

Chest pain lasting for 20 sec: Angina can be excluded and is usually due to
Musculoskeletal causes
Hiatus hernia and
Functional causes.
b) The Chest Pain Lasting for a Few Minutes

Chest pain in angina pectoris usually lasts for 25 min (not 15 min, see Fig. 11.2).
Chest pain in unstable angina lasts for 20 min (see Fig. 11.3).
Hyperventilation: functional chest pain is often preceded by hyperventilation which
causes increased muscle tension which in turn is responsible for diffuse chest tightness
which lasts for 23 min.
c) The Chest Pain Lasting for Minutes to Hours

i) Cardiovascular causes
In acute myocardial infarction, pain usually lasts for 15 min to 30 min. In
30% of the patients, it is painless or atypical especially in diabetic and elderly

patients.
Pericarditis
Stable angina Unstable angina
Fig. 11.2 | Inlastsstable angina, chest pain Fig. 11.3 | Inmayunstable angina, chest pain
for 25 min. lasts for 20 min.
Aortic dissection
Mitral valve prolapse.
ii) Non cardiovascular causes

Neuro-musculoskeletal disorders, including herpes zoster
Gastrointestinal: esophageal causes, acid peptic disorders
Respiratory: pulmonary embolism, pneumothorax and pleurisy
Psychogenic: anxiety.
2. The Location and Radiation of Chest Pain

a) Cardiovascular Causes
i) Cardiac ischemic chest pain: It is usually felt in precordium or substernally.
It is diffuse and eludes precise localization, often radiates or is referred to the
same corresponding segmental dermatomes (C8-T4)1 i.e. left shoulder, ulnar
aspect of left arm and forearm and neck, less often to jaws, epigastrium, right
chest and right arm.
There is some relationship between location of ischemic chest pain and site of
coronary artery occlusion. Substernal or left chest pain with radiation to left
arm usually involves left coronary artery, while epigastric pain radiating to the
neck or jaw usually do not have the disease of left anterior descending artery2
(see Fig. 11.4).
ii) The chest pain in pericarditis: It is more left sided than central and is often
referred to neck, may also radiate to left shoulder, left arm or jaw.
Fig. 11.4 | Usual distribution of chest pain in MI.

iii) The chest pain in aortic dissection: It is acute, excruciating, may migrate from
the anterior chest to the back and may radiate widely including the neck, arms
and legs depending on its location and progression.
Aortic dissection should be considered in the setting of severe hypertension or
Marfan syndrome, chest trauma, direct trauma to aorta or iatrogenic trauma

(intra-arterial catheterization and insertion of intraoartic balloon pump).
The location of pain is helpful in suggesting the location of aortic dissection.
3
When the location of the chest pain is anterior only, involvement of ascending
aorta in 90% of cases (see Fig. 11.5).
When the chest pain is located in the interscapular region only, there is
involvement of descending thoracic aorta in 90% of cases (i.e. De Bakeys
type I or III dissection.) (see Figs 11.6 and 11.7).
Type II Type I Type III
Fig. 11.5 | Anterior location of the chest pain Fig. 11.6 | Type I & III (De Bakeys)
aortic dissection.
usually in type II (De Bakeys)
aortic dissection.
Back
Fig. 11.7 | Interscapular chest pain in aortic dissection (DeBakeys type I or III), but
less commonly in MI.
Fig. 11.8 | Cervical spondylosis. In

this conditions, pain may
Fig. 11.9 | Cervical rib (complete on left side).
In this conditions, pain may radiate
radiate to left shoulder to left shoulder but usually from
but usually from neck. neck.
The presence of any pain (or radiation) in the neck, throat, jaw or face,
strongly predicts the involvement of ascending aorta whereas pain in the back,
abdomen or lower limbs strongly predicts the involvement of descending
aorta.
b) Non Cardiovascular Causes

i) The chest pain localized to left nipple or cardiac apex or that radiates to left lower
chest is usually non cardiac in origin and could be due to:
cervicodorsal osteoarthritis
acid peptic disorder, resulting in gaseous distention of the stomach
functional causes (psychogenic chest pain).
ii) The pain due to disorders of cervical spine: It can also radiates to left shoulder
and left arm (see Figs 11.8 and 11.9).
iii) In Tietzes syndrome: The pain is localized to the costochondral and costosternal
joints (chest wall); while in herpes zoster, persistent pain is localized to a der-
matome along the intercostal space.
iv) In thoracic outlet syndrome: The pain is often associated with paresthesias along
the ulnar nerve distribution and forearm.
v) The pain is substernal or epigastric in location in esophageal disorders, acid peptic
disorders and in acute pancreatitis (see Fig. 11.10).
Epigastrium
Fig. 11.10 | Epigastric pain is usually due to esophageal disorders, acid peptic disease
or acute pancreatitis, but less commonly due to MI.
The esophageal pain radiates more often to the back and less often to the left
shoulder, left arm and forearm Vs the anginal chest pain.
Also, the pain in acute pancreatitis is usually transmitted to the back.
The pain in biliary colic is generally most intense in right upper abdomen but
may be present in the epigastrium or felt in the precordium, often referred to
the scapula, and may radiate to the back or shoulder (in case of diaphragmatic
irritation).
3. Character and Mode of Onset of Chest Pain

a) Cardiovascular Causes
i) Angina: Heberdens4 initial description of chest discomfort is still remarkably
pertinent.
Angina means choking not pain and is often described as: (i) pressing (ii) vice like
(iii) squeezing (iv) heaviness (v) constricting (vi) burning (vii) tightness (viii) burst-
ing (ix) choking (suffocating) (x) or weight in the chest.
However, the quality of chest pain described by the patient is greatly influenced by
the patients intelligence, education and social cultural background. Hence, any
other description should be noted and evaluated appropriately.
Anginal discomfort is crescendo in nature rather than reaching peak intensity instan-
taneously as in aortic dissection. The anginal threshold is lower in the morning and
the activities that cause angina in the morning do not do so later in the day.
Anginal equivalents: Instead of chest pain, some patient may describe other symptoms/
discomfort e.g. a patient may describe:
The mid chest as the site of shortness of breath, whereas true dyspnea is not usually
well localized.
Discomfort in sites of secondary radiation such as shoulders, ulnar aspect of left
arm and forearm, lower jaw or neck.
Dilated aorta
Aortic valve
Dilated left
ventricle
Fig. 11.11 | Nocturnal angina is characteristic of severe chronic AR.

Development of gas and belching, nausea, indigestion, dizziness or diaphoresis.
However, anginal equivalents above the mandible or below the umbilicus are
uncommon.
Nocturnal anginal pain occurs when the diastolic blood pressure decreases to lower
levels in nights and is typically described in severe chronic aortic regurgitation and
in unstable angina (rest angina) (see Fig. 11.11).
ii) In aortic dissection: The pain is sudden in onset, excruciating and persistent with
radiation to the site depending upon its location and progression.
iii) In acute pericarditis: The pain is sharper than angina, more left sided than cen-
tral and often referred to the neck.
iv) The chest pain in MVP: It varies considerably among the patients (see Fig. 11.12). It
may be similar to that of classic angina pectoris or may resemble the chest pain of neu-
rocirculatory asthenia (functional).
b) Non Cardiovascular Causes

i) Shooting or lancing pain of short duration usually suggests musculoskeletal or
neural pain.
The chest pain in Tietze syndrome is associated with swelling and tenderness of
costochondral and costosternal joints while in myositis, pain is associated with
muscular tenderness. In both, pain is aggravated by moving or coughing.
Herpes zoster mimics MI when the left chest is affected, however the persistence
pain, its localization to a dermatome and appearance of characteristic vesicles
allow its recognition (see Fig. 11.13).
LA
LV
Fig. 11.12 | Chest pain in mitral valve prolapse (arrow) is variable-simulating angina to
that of neurocirculatory asthenia.
Fig. 11.13 | Into herpes zoster, pain is persistent with characteristic skin lesions localized
a dermatome.
ii) In GIT etiology

1. In esophageal spasm, substernal or epigastric pain is squeezing, burning or aching
in quality which is brought by eating, during swallowing or by lying down after
meals and may be relieved with antacids and nitroglycerine.
Barium studies may reveal motility problems. Esophageal manometry may show
diffuse esophageal spasm and increased pressure at the lower esophageal sphincter.
Provocative test with methacholine may provoke esophageal pain and manometric
signs of spasm.
UES
LES
Fig. 11.14 | Ingastric

esophageal disorders, the esophageal spasm or reflux, substernal or epi-
pain may mimic anginaUES: upper esophageal sphincter, LES:
lower esophageal sphincter.
2. The chest discomfort due to esophageal reflux less closely mimics angina and is of
heart burn or burning sensation in quality which is most common after meals, occurs
in supine position or on bending and is often relieved by antacids (see Fig. 11.14).
The presence of acid reflux into the mouth (water brash) and/or dysphagia is a
useful diagnostic clue to the esophageal diseases.
Besides, the esophageal disorder frequently coexist with angina pectoris, and
esophageal reflux lowers the threshold for the development of angina.
Bernstein test5 may be helpful to differentiate the esophageal reflux from angina:
alternate infusions of dilute acid and normal saline by a nasogastric tube, placing
the tip at the level of mid esophagus, produces pain in over 90% of patients with
subjective and objective evidence of gastroesophageal acid reflux.
Acid reflux can also be recognized by recording the pH from an electrode placed
at the tip of a catheter inserted into the distal esophagus.
3. In acid peptic disorders, pain is more often burning in character with charac-
teristic relationship to food ingestion and it is relieved by antacids or food (see
Fig. 11.15).
4. Acute pancreatitis may mimic AMI. However, pain is predominantly in the epi-
gastrium, it is position sensitive, usually transmitted to the back and may be partly
relieved by leaning forward, with usual history of alcoholism or biliary tract disease
(see Fig. 11.16).
5. Biliary colic usually caused by a rapid rise in biliary pressure due to obstruction of
the cystic or bile duct. The pain is steady, lasts for 24 hrs and subsides sponta-
neously without any symptoms in between the attacks.
Fig. 11.15 | Iningestion.

acid peptic disorders, the burning pain often has relationship to food
Right hepatic duct Left hepatic duct
Liver
Common hepatic duct

Common bile duct
Cystic duct
Duodenum
Gallbladder
Pancreas
Pancreatic duct
Fig. 11.16 | Acute pancreatitis mimics acute myocardial infarction, but pain is usually
transmitted to the back, while the pain in biliary colic is usually felt in the
right upper abdomen.
iii) Pulmonary/pleural causes of chest pain:

Large pulmonary embolism can cause acute onset of chest pain that mimics AMI
with severe dyspnea, hypotension, and arterial hypoxemia (see Fig. 11.17). However,
a clinical setting of prior immobilization with bed rest, prolonged travel or deep
venous thrombosis should increase the suspicion of pulmonary embolism.
Pneumothorax can cause acute chest pain and is associated with dyspnea, decreased
breath sounds and hyperresonance note on the affected side.
Pleuritic chest pain associated with pleural rub, accentuated by inspiration/move-
ment of the chest wall and relieved to a great extent on lying down on the same side
or holding the breath in deep expiration.
Aorta
PA Pulmonary
embolism
LA
RA
LV
RV
Fig. 11.17 | Inemia

pulmonary embolism chest pain mimics AMI with acute dyspnea, hypox-
and hypotension.
iv) Functional or psychogenic chest pain (Da Costas syndrome or neurocirculatory

asthenia): It is localized, dull, and persistent ache that may last for hours and often
accentuated by or alternates with attacks of sharp lancinating stabs of 12 sec.
4. Aggravating and Relieving Factors

a) Angina Pectoris
It characteristically occurs on exertion, exercise or other forms of stress (emotional
stress, cold weather, heavy meal) except in Prinzmetals angina and unstable angina
where chest pain can occur at rest.
i) Depending on the severity of the anginal pain, patients are functionally classified
from class I to IV by three functional classifications:
NYHA functional classification.
6
Canadian cardiovascular society (CCS) functional classificaion.

7
Specific activity scale (SAC) functional classification.

8
However, CCS functional classification of angina is more popular and appropriate

clinically.
CCS functional classification
Class I: No limitation of ordinary physical activity. Ordinary physical activity such as
walking and climbing stairs does not cause angina. Only strenuous or prolong exertion
causes angina.
Class II: Slight limitation of ordinary physical activity. Ordinary physical activity
causes angina such as:
Walking or climbing stairs rapidly.
Walking uphill.
Walking or climbing stairs after meals.

Walking in cold, in wind.
Walking more than two blocks on the level (one block distance is 100 m).
Climbing more than one flight of ordinary stairs at a normal pace and under normal
conditions or
When under emotional stress.
Class III: Marked limitation of ordinary physical activity. Less than ordinary physical
activity causes angina such as:
Walking one to two blocks on the level or
Climbing one flight of stairs under normal conditions.
Class IV: Inability to do any physical activity without discomfort and anginal syn-
drome may be present at rest.
ii) Linked angina is an episode of angina in patients with established CAD caused by
gastrointestinal factors not related to increase in cardiac work such as stooping or
which occur after meals.9
iii) Anginal chest pain characteristically relieved by stopping the activity and taking
nitroglycerine usually in 15 min. But if it takes more than 10 min for relief of the
discomfort, it could be due to unstable angina, AMI or non ischemic pain.
b) In MVP
Chest pain is atypical, occurs spontaneously and is unrelated to exertion which is due
to tension of the papillary muscles.
c) In Acute Pericarditis
Chest pain is characteristically relieved by sitting and leaning forward (Mohammedans
prayer sign) while in acute pancreatitis, pain is partly relieved by leaning forward. It is
aggravated by breathing, turning in bed and twisting the body.
d) The Esophageal Pain

Usually occurs on eating, during swallowing, or on lying down after meals and may be
relieved with antacids and nitroglycerine.
e) The Pain in Acid Peptic Disorders

Its characteristic relationship to food ingestion and its relief by antacids or food help in
its diagnosis.
f) The Pleuritic Chest Pain

It is associated with a pleural rub, accentuated by inspiration or movement of the chest
wall and is relieved to a greater extent on lying down on the same side or holding the
breath in deep expiration (inhibiting the friction between the pleural layers).
Fig. 11.18 | Clenching of the fist in front of the Fig. 11.19 | Finger pointing to a small circumscribed
area in the left inframammary region
chest while describing the chest
discomfort (Levines sign) is typical while describing the chest discomfort is
of ischemic chest pain. usually of noncardiac originmore of
a psychogenic origin.
g) In Thoracic Outlet Syndrome

Pain is often associated with paresthesias along the ulnar distribution of arm and fore-
arm and is typically precipitated by abduction of the arm, lifting a weight or working
the hands above the shoulder but not by walking as it occurs in angina pectoris.
5. Patients Gestures During Chest Discomfort

Clenching the fist in front of the chest while describing the chest discomfort is a strong
indication of an ischemic origin of the chest pain (Levines sign,10 (see Fig. 11.18) than
when a finger is pointed to a small circumscribed area in the left infra mammary region
which more likely represents the chest pain of psychogenic origin (see Fig. 11.19).
The patient is usually in agony in chest pain due to AMI.
6. Associated Symptoms
Presence of other cardinal symptoms: SOB, palpitation and syncope accompanying
chest pain should be noted which confirms the cardiovascular cause for the chest pain
(see Table 11.3).
In AMI, the chest pain is often accompanied by profuse sweating and palpitation
(due to sympathetic stimulation), syncope, nausea, vomiting or SOB.
However, SOB accompanying chest pain can also occur in pneumothorax and pul-
monary embolism (PE). In PE, the patient in addition has hypotension and arterial
hypoxemia with clinical setting of prior immobilization, prolong travel or deep venous
thrombosis; while in pneumothorax, there are also decreased breath sounds and hyper
resonance note on the affected side.
Table 11.3 Chest pain and associated symptoms
Associated symptoms Cause
1. Sweating and palpitation AMI: acute myocardial infarction, MVP: mitral valve prolapse
2. Shortness of breath (SOB) Myocardial infarction, pulmonary embolism, pneumothorax
3. Syncope Aortic dissection, AMI
4. Hemoptysis Pulmonary embolism, lung tumor
5. Fever Pericarditis, AMI (low grade), pneumonitis, pleurisy
The chest pain accompanied by hemoptysis suggests PE with pulmonary infarction

or lung tumor.
Fever accompanying chest pain occurs in pericarditis, pneumonitis and pleurisy.
In MVP, symptoms of autonomic nervous system dysfunction occur and are associ-
ated with palpitation, fatigue, postural hypotension and other psychiatric symptoms.
Functional chest pain is usually accompanied by numbness and tingling in the
extremities, frequent sighing, dizziness, anxiety or depression.
Definite Typical Anginal Chest Pain (ACC/AHA 2002 Guidelines)10a

It occurs when all the three following characteristics are present:
1. Substernal chest discomfort with a characteristic quality (squeezing, pressing,
choking or tightness) and duration (25 min) that is
2. Provoked by exertion or emotional stress and
3. Relieved by rest or nitroglycerin.
7. Non Cardiac Chest Pain (ACC/AHA 2002 Guidelines)10a

Meets 1 of the typical angina characteristics. The chest pain is described as atypical
angina when 2 of the above characteristics are present.
2. SHORTNESS OF BREATH (SOB)/DYSPNEA
1. Dyspnea
It is defined as [i] difficult or labored breathing or [ii] unpleasant awareness of ones
own breathing.
2. Pathogenesis of Dyspnea
Dyspnea occurs when (see Table 11.4)
Maximum ventilation volume (MVV) is lesser than normal or decreases,
Vital capacity (VC) decreases which in turn decreases MVV or
Pulmonary ventilation (PV) increases by 45 times the normal.
Table 11.4 Pathogenesis of dyspnea: Dyspnea occurs when the dyspnea index becomes
60% which is due to following mechanisms
Mechanism Effects
1. Decreased vital capacity Affects respiratory muscles and

compliance of lungs and thorax
2. Decreased maximum ventilation Affects respiratory muscles and
volume compliance of lungs and thorax
3. Increased pulmonary ventilation Stimulates J receptors, causes
hypoxemia and acidosis
i.e. dyspnea usually occurs when pulmonary reserve percentage (% PR) or Dyspnea index
(DI) is 60% (normally it is about 8090%), i.e. DI or % PR MVV PV
100/MVV.
a) Vital Capacity
It is the maximum volume of air which can be expelled from the lungs by forceful
effort following a maximal inspiration, i.e. VC tidal volume inspiratory reserve
volume expiratory reserve volume (4.8 L in males, 3.2 L in females).
VC provides information about:
The strength of the respiratory muscles and
Elasticity of the lungs.
b) MVV (or Maximum Voluntary Ventilation or Maximum

Breathing Capacity)
It is the largest volume of air that can be moved into and out of the lungs in one minute
by maximum voluntary effort (normally it is 90100 L/min). MVV depends on the
work done during breathing i.e.
Strength of the respiratory muscles
Compliance (distensibility) of the thoracic wall and lungs and
Airway resistance.
Normal total work done during quiet breathing is 0.30.8 kg-m/min. and a healthy
adult spends 5% of O2 consumption on breathing.
i) Respiratory muscles: To move air into the lungs through air passages, the muscles
of respiration have to do work to overcome all forms of resistance (elastic resistance of
lungs and chest wall 65%, viscous resistance 7% and airway resistance 28%).
Dyspnea occurs due to:
Fatigue of respiratory muscles: due to decreased cardiac output.
Weakness of respiratory muscles: deconditioning.
Respiratory muscle diseases: neuromuscular disorder e.g. myasthenia gravis,
poliomyelitis, phrenic nerve dysfunction.
ii) Compliance (distensibility) of lungs and thorax: Normal compliance is 0.13 L/cm
H2O i.e. when there is an increase of airway pressure by 1 cm H2O, then the volume
of lungs inside the thoracic wall increases by 0.13 L. Dyspnea occurs when compliance
decreases. The compliance in turn depends on:
Viscous resistance (7%): Work done in moving the viscous material of the lung tissue.
Airway resistance (28%) which is the work done in moving the air through respira-
tory passages (N 1.52 cm H2O/L/s i.e. when there is a fall of pressure by 2 cm
H2O, there is airflow of 1 L/s). 80% of the total airway resistance is offered by the
trachea and bronchial divisions upto 7th generation.
Alveolar surface tension that is kept low by surfactant secreted by type II pneumocytes
in the alveolar lining thereby it prevents pulmonary edema and keeps the alveoli dry.
c) Pulmonary Ventilation (or Minute Ventilation)

It is the volume of air expired or inspired by the lungs in one minute i.e. PV
(TV) RR/min. (TV tidal volume; RR respiratory rate).
So normal PV is 500 12 6,000 ml or 6 L/min. Dyspnea occurs when PV
increases which may due to:
(i) Stimulation of Juxta-pulmonary capillary (J) receptors (which are non myeli-
nated vagal afferent nerve endings, located in the alveolar wall and sensitive to the
content of interstitial fluid between capillary endothelium and alveolar epithe-
lium) due to pulmonary congestion, pulmonary edema or pulmonary emboli.
(ii) Hypoxemia due to
Decreased V/P ratio (ratio of [V] alveolar ventilation [4 L/min] to [P] pulmonary
blood flow [5 L/min] which is normally 4/5 0.8) (Alveolar ventilation is the
amount of air ventilating the alveoli per minute i.e. V TVDS RR/min.
DS dead space). So, V (500150) 12 4.2 L/min.
Decreased V/P ratio occurs either due to (i) uneven V (as in bronchial asthma,
pneumothorax, emphysema, pulmonary fibrosis, congestive heart failure) or
(ii) due to non uniform pulmonary blood flow (as in shunts e.g. TOF, pulmo-
nary vascular resistance e.g. CHF, pulmonary vascular bed e.g. emphysema).
Hypoxemia due to PO2: Arteriovenous (A-V) O2 difference less than 0.2 ml/
100 mL stimulates the respiratory neurons in medulla (respiratory center) via
the chemoreceptors (in carotid and aortic bodies) to increase PV.
(iii) Acidosis
Respiratory acidosis due to PCO2 (as in emphysema, respiratory depression
due to morphine) causes stimulation of respiratory neurons in medulla via
chemoreceptors to PV that causes CO2 washed out and thereby restoring
H concentration of blood towards normal.
Metabolic acidosis due to diabetic ketoacidosis, renal failure, starvation ketoaci-
dosis and lactic acidosis due to severe muscular exercise stimulates respiratory
medullary center via chemoreceptors to PV which causes wash out of CO2
and restoration of blood H concentration.
3. Etiology
Dyspnea due to cadiovascular causes is usually due to:
(i) Cardiac output (leading to fatigue of respiratory muscles) or
(ii) Pulmonary venous hypertension (which results in compliance, airway resist-
ance and pulmonary congestion stimulating J receptors and thereby affecting
MVV and PV)
(iii) However, neural impulses generated in the underperfuse and metabolically abnor-
mal respiratory muscles could be responsible to ventilatory drive.11
Common Causes of Dyspnea

a) Cardiovascular causes (see Fig. 11.20)
Cardiomyopathy: dilated, hypertrophic, infiltrative, ischemic
Valvular heart disease
Pericardial disease
Pulmonary vascular disease and
Congenital heart disease (CHD).
b) Non cardiovascular causes
i) Pulmonary causes
Airways: upper airway obstruction, asthma, emphysema, cystic fibrosis.
Parenchymal lung: interstitial lung disease, pneumonia, malignancy (primary/
metastatic).
Pleural: effusion, fibrosis, malignancy.
Cardiomyopathy:
Dilated, HCM, restrictive,
ischemic
Pericardial: Effusion, Valvular heart disease:

CT, CP MS, AS, PS
Dyspnea of
CV origin
Heart failure: Pulmonary vascular:

CHF, LVF PH, PE
CHD:
Acyanotic, cyanotic
Fig. 11.20 | Cardiovascular (CV) causes of dyspnea-CT: cardiac tamponade, CP: con-
strictive pericaditis, PH: pulmonary hypertension, PE: pulmonary embolism,
CHF: congestive heart failure, LVF: left ventricular failure, CHD: congenital
heart disease.
Respiratory muscle: neuromuscular disorders e.g. myasthenia gravis, poliomyelitis

phrenic nerve involvement.
Respiratory muscle weakness: deconditioning.
ii) Chest wall involvement
Deformities e.g. kyphoscoliosis
Abdominal loading causes: ascites, pregnancy, obesity.
iii) Metabolic causes: metabolic acidosis due to:
Diabetic ketoacidosis
Renal failure
Starvation ketoacidosis
Severe muscular exercise leading to lactic acidosis.
iv) Anemia (of any cause).
v) Psychogenic: anxiety.
4. Evaluation
The symptom of dyspnea should be evaluated to rule out the non cardiovascular
etiology for:
Duration
Mode of onset
Severity/aggravating factors (functional classification)
Relieving factors
Associated symptoms.
a) Duration
Longer duration of dyspnea usually seen in mitral stenosis (5 yrs) while it is of
shorter duration in most of the diseases e.g. AS, cardiomyopathy, CAD.
b) Mode of Onset
i) In most cardiac disorders, it is usually gradual in onset.
ii) Sudden onset of dyspnea occurs in:
Acute pulmonary edema (see Fig. 11.21),
Pulmonary embolism,
Pneumothorax, pneumonia (see Figs 11.22 and 11.23),
Airway obstruction or
Psychogenic.
Sudden occurrence of dyspnea in a patient of mitral stenosis suggests the develop-
ment of atrial fibrillation, rupture of chordae tendinae, or pulmonary embolism.
iii) Dyspnea is late in onset in the course of mitral regurgitation and aortic regurgita-
tion (palpitation is the initial symptom); while in mitral stenosis, dyspnea occurs
earlier and is the initial symptom.
Fig. 11.21 | Sudden onset of dyspnea occurs in pulmonary edema.
Right
upper lobe
Fig. 11.22 | Pneumonitis. In this conditions

sudden onset dyspnea and chest
pain occurs.
Fig. 11.23 | Pneumothorax. In this conditions sudden
onset dyspnea and chest pain occurs.
(c) Severity/Aggravating Factors

Depending upon the severity of dyspnea (as also chest pain, palpitation and fatigue),
patients are classified from class I to IV by the following functional classifications.
i) New York Heart Association (NYHA) functional classification.6
ii) Canadian Cardiovascular Society (CCS) functional classication.7
iii) Specific Activity Scale (SAC).8
However clinically, NYHA functional classification is usually followed even though this
classification of the severity of symptoms is not applicable and useful for pediatric patients.
NYHA functional classification6
Class I
Patients with cardiac disease but no limitations of physical activity.
Ordinary physical activity does not cause dyspnea, palpitation, fatigue and chest pain.
Class II
Patients with cardiac disease with slight limitation of physical activity.
They are comfortable at rest.
Ordinary physical activity results in dyspnea, palpitation, fatigue and chest pain.
Class III
Patients with cardiac disease with marked limitation of physical activity.
They are comfortable at rest.
Less than ordinary physical activity causes dyspnea, palpitation, fatigue and chest
pain.
Class IV
Patients with cardiac disease with inability to carry out any physical activity without
discomfort.
Symptoms (dyspnea, palpitation, fatigue and chest pain) may be present even
at rest.
If any physical activity is undertaken, discomfort is increased.
Goldman et als SPECIFIC ACTIVITY SCALE8 (modified): This functional classi-
fication is based on the estimated metabolic cost of various activities and is more
reproducible and better predictor of exercise tolerance than either NHYA functional
classification or CCS functional classification.
Class I: Patients can perform to completion any activity that requires 7 metabolic
equivalents (MET) e.g.
Personal activities: can shower and dress, have normal sexual life.
Indoor activities: can do routine household activity: washing clothes, cleaning
windows and floor, cooking, bed making.
Outdoor activities: can do gardening, work in the fields, shovel snow, spade soil,
weight bearing (80 lb).
Sports and recreational activities: dancing, skating, skiing, swimming, cycling (on
flat surface: 15 kmph), running (10 kmph), jog/walk 5 mph (3.10 kmph).
Class II: Patients can perform to completion any activity that requires 5 MET but
7 MET, e.g.
Can do all personal and indoor activities normally as stated above.
Outdoor activity: restricted outdoor activity, can only do gardening.
Sports and recreational activities: restricted, can dance, do skating, cycling (on flat
surface 10 kmph), walk: 4 mph.
Class III: Patients can perform to completion any activity that requires 2 MET but
5 MET, i.e. restriction of all activities. e.g.
Restricted personal and indoor activities: can only shower and dress, make bed,
clean window.
No out door activity.

Restricted sports and recreational activities: can bowl, play golf, drive car, walk:
2.5 mph.
Class IV: Patients cannot perform to completion any activity that requires 2 MET,
i.e. cannot carry out any activity listed above in Class III (1 MET 3.5 mL of O2/kg
consumed). Joseph K Perloff 12 proposed a new functional classification for congenital
heart disease (CHD) patients as NYHA functional classification is inappropriate especially
for dyspnea symptom since dyspnea is in fact, hyperventilation unrelated to heart failure
and these subjects have a substantially greater increase in ventilation during isotonic exercise
than do normal subjects and hence dyspnea may be a prominent subjective complaint.
In cyanotic CHD, shunting of venous blood into systemic circulation lowers arterial O2
tension which stimulates the medullary centers via carotid bodies that results in venti-
lation. Following is the CHD functional classification:
Functional classification for CHD12

Class I: Patients are asymptomatic at all levels of activity.
Class II: Symptoms are present but do not curtail average every day activity.
Class III: Symptoms significantly curtail most but not all average every day activities.
Class IV: Symptoms significantly curtail virtually all average every day activities and
may be present at rest.
American thoracic society scale of dyspnea:13 It quantifies the severity of dyspnea

(see Table 11.5).
Dyspnea at rest:
Pulmonary edema of any cause
Pulmonary embolism
Pneumothorax
Functional.
Table 11.5 Quantifying the severity of dyspnea
Descriptions Grade Degree
1. Not troubled by SOB when hurrying on the level or 0 None

walking on a slight hill
2. Troubled by SOB when hurrying on the level or 1 Mild
walking upon a slight hill
3. Walks more slowly than people of the same age on 2 Moderate
the level because of breathlessness or has to stop for
breath when walking at own pace on the level
4. Stops for breath after walking about 100 yards or 3 Severe
after a few minutes on the level
5. Too breathless to leave the home; breathless on 4 Very severe
dressing or undressing
Drugs aggravating dyspnea:

Beta-blockers (especially nonspecific): increase bronchospasm.
Digoxin: in hypertrophic obstructive cardiomyopathy (HOCM).
Diuretic: in pericardial disease and in patients with isolated diastolic dysfunction.
Steroids: may aggravate heart failure and chronic renal failure.
d) Variants of Dyspnea
i) Episodic dyspnea: It consists of paroxysmal nocturnal dyspnea (PND) and
orthopnea.
(a) Paroxysmal nocturnal dyspnea (PND): This is the occurrence of dyspnea during
sleep, commonly 23 hrs after going to bed. It is often associated with sweating, wheez-
ing, and coughing and is usually relieved by assuming upright position for 515 mins.
PND strongly suggests PVH. It is due to interstitial edema and sometimes due to intra
alveolar edema usually secondary to the left ventricular failure.
MS is the commonest cause for PND. Other valvular heart diseases, DCM and
CAD may also give rise to PND but are often late in occurrence.
Patients with PND are functionally classified into NYHA class III.
Once right ventricular failure develops (CHF), PND disappears (see Table 11.6).
(i) Pathogenesis (mechanism) of PND
Absorption of edema fluid from the interstitial compartments of lower limbs during
supine position increases the venous return to the right heart and subsequently
increases right ventricle (RV) output which cause overfilling of the lungs leading
to pulmonary interstitial edema. Other mechanisms which may play a part in the
pathogenesis are:
Decreased sympathetic drive during sleep which may decrease left ventricular (LV)
contractility.
Nocturnal arrhythmias and dreams may also precipitate PND.
(ii) Other conditions simulating PND
Nocturnal episodes of bronchial asthma (typically occurs in early mornings, 46 AM).
Other COPDs may also wake up the patient in the night. However, cough and
Table 11.6 Variant forms of dyspnea
Variant form Description Cause
1. Paroxysmal nocturnal dyspnea Dyspnea during sleep Mitral stenosis

2. Orthopnea Dyspnea in supine position LVF, COPD, large ascitis
3. Platypnea Dyspnea in upright position LA myxoma, ball valve thrombus
4. Trepopnea Dyspnea in lateral position LA myxoma, ball valve thrombus
5. Tachypnea Rapid breathing Any cause of dyspnea
LVF: left ventricular failure, COPD: chronic obstructive pulmonary disease, LA: left atrium.
Fig. 11.24 | Patient is orthopneic due to left ventricular failure.

expectoration precede dyspnea and SOB is often relieved when the patient rids
himself/herself of secretions.
Nocturnal episodes of recurrent pulmonary emboli.
Post nasal discharge with associated severe cough.
Anxiety with hyperventilation.
Obesity sometimes mimics PND.
(b) Orthopnea: It is dyspnea that occurs in supine position and is promptly relieved
by assuming upright position (sitting or standing).
Orthopneic patients are functionally graded to be in NYHA class IV.
Similarly, it is related to an increased venous return to the right heart in supine posi-
tion and subsequently to increased RV output which further increases the pulmonary
venous congestion.
Etiology of Orthopnea:
Orthopnea is a characteristic of left ventricular failure (see Fig. 11.24) but can also
occur in
COPD
Bilateral weakness or paralysis of diaphragm
Large ascites often due to constrictive pericarditis, chronic renal failure and some-
times associated with congestive heart failure
i) Platypnea is dyspnea that occurs in upright position and may be relieved in
supine position. It may be related to LA myxoma or ball valve thrombus in LA
which obstructs the left inflow (MV) in upright position and results in dyspnea
(see Fig. 11.25)
ii) Trepopnea is dyspnea that occurs only in lateral position and similarly may be due
to LA myxoma or ball valve thrombus in LA which obstructs mitral valve orifice in
lateral position and causes dyspnea
iii) Tachypnea is rapid breathing of any cause
vi) Angina equivalent: See chest pain symptom.
RV
VS
AMVL
LV AO
PMVL
MYXOMA
LA
Fig. 11.25 | Transthoracic echocardiogram showing left atrial myxomaplatypnea or tre-

popnea can occur in a patient with myxomaAMVL: anterior mitral valve
leaflet, PMVL: posterior mitral valve leaflet, LA: left atrium, LV: left ventricle,
RV: right ventricle, AO: aorta, VS: ventricular septum.
e) Relieving Factors
The factors which relieve dyspnea should be evaluated.
Dyspnea (which is often due to cardiac cause) can be relieved by stopping exertion
and taking rest.
By taking drugs:
Nitroglycerine and beta-blockers: in ischemic heart disease presenting as short-
ness of breath (anginal equivalents).
Diuretics and digoxin: in HF.
Bronchodilators and steroids: in bronchospasm.
Assuming upright position: in PND, orthopnea.
Squatting position: in cyanotic congenital heart disease e.g. TOF.
Supine position: in platypnea due to LA myxoma or ball valve thrombus.
By exertion or by sedation: in a psychogenic cause.
Dyspnea present only at rest and absent on exertion: invariably of psychogenic
etiology.
f) Associated Symptoms
Presence of other cardinal symptoms such as chest pain, palpitation and giddiness,
pinpoints to cardiovascular cause of dyspnea (see Table 11.7).
However, SOB and chest pain can also occur in pulmonary embolism and pneu-
mothorax but other characteristic features help in the diagnosis.
Associated productive cough usually indicates respiratory cause for SOB; however in
the presence of secondary infection, productive cough could be present in cardiac
pathology. In COPD, cough and expectoration precede dyspnea.
Presence of fever usually occurs in respiratory causes (COPD, pneumonia, pleuritis/
pleural effusion), but may be associated with pericardial disease and due to infection
Table 11.7 SOB and associated symptoms
Associated symptoms Cardiovascular cause Non cardiovascular cause
1. Chest pain CAD, pericarditis, PE Pneumothorax, COPD

2. Cyanosis Cyanotic CHD (TOF) COPD
3. Cough Secondary infection COPD, pneumonia, pleuritis,
4. Fever Secondary infection, pericarditis, malignancy (low grade)
myocarditis, MI (low grade)
5. Edema HF, CP Large bilateral pleural effusion
SOB: Shortness of breath, CAD: coronary artery disease, PE: pulmonary embolism, CHD: congenital heart disease,
TOF: tetralogy of Fallot, COPD: chronic obstructive pulmonary disease; MI: myocardial infarction, HF: heart failure,
CP: constrictive pericarditis.
in cardiac pathology (bronchitis in MS, bacterial endocarditis in valvular heart disease/

CHD, pulmonary tuberculosis in CHD, low grade fever in malignancy and ischemic
heart disease).
Associated cyanosis usually in cyanotic CHD, but occurs in COPD (chronic
bronchitis).
Associated edema most frequently due to HF. However, dyspnea and edema can also
be observed in patients with large bilateral pleural effusions and angioneurotic edema
with laryngeal involvement.
In functional etiology, claustrophobia or sighing respirations are relieved by exertion,
by taking a few deep breaths or by sedation. Most often, these patients are associated
with emotional instability.
3. PALPITATION
It is an unpleasant awareness of the forceful or rapid beating of the heart. It is the

increased motion of the heart within the chest that is perceived as palpitation rather
than the increase in cardiac contractility which explains the absence of palpitation in
conditions characterized by an increased force of cardiac contraction, such as AS, PS
and severe systemic or pulmonary hypertension.
1. Etiology
The important causes of palpitation are as follows:
Cardiac Causes
i) Valvular heart disease: Due to increased stroke volume: AR, MR, TR (see Fig. 11.26).
ii) Acyanotic congenital heart disease:
With shunts: PDA, VSD, ASD (late onset)
Arrhythmogenic: arrhythmogenic right ventricular dysplasia (ARVD).
Cyanotic CHD: Ebstein

anomaly TAPVC, TGA,
DORV, SV
Acyanotic CHD:
Valvular: AR, MR
PDA, VSD, ARVH
Palpitation
Arrhythmias: VT, SVT, MVP, HCM, CAD

Af, PVC, PAT, CHB, SSS Prolong QT syndrome
Pacemaker related
Fig. 11.26 | Cardiovascular (CV) causes of palpitationAR: aortic regurgitation, MR:

mitral regurgitation, TAPVC: total anomalous pulmonary venous connec-
tion, TGA: transposition of great arteries with PS, DORV: double outlet right
ventricle without PS, SV: single ventricle without PS, ARVH: arrhythmo-
genic right ventricular hyperplasia, VT: ventricular tachycardia, SVT:
supraventricular tachycardia, PVC: premature ventricular contractions,
PAT: premature atrial tachycardia, CHB: complete hart bock, SSS: sick
sinus syndrome, MVP: mitral valve prolapse, HCM: hypertrophic cardiomy-
opathy, CAD: Coronary artery disease, Af: atrial fibrillation.
iii) Cyanotic congenital heart disease

With increased pulmonary blood flow: TAPVC, PAPVC, TGA with VSD without PS
Arrhythmogenic: Ebstein anomaly, after Mustard operation.
iv) Arrhythmias
Tachyarrhythmias: VT, SVT, atrial fibrillation, atrial flutter, paroxysmal atrial tachy-
cardia (PAT), premature atrial contractions (PAC) and premature ventricular con-
tractions (PVC).
Bradyarrhythmias: CHB, Sick sinus syndrome (SSS),
Pacemaker malfunctioning,
MVP, HCM, CAD, Prolong QT syndrome, prosthetic heart valves.
Non Cardiac Causes

i) Hyperkinetic circulatory states
Anemia
Arteriovenous fistula
Fever
Thyrotoxicosis
Pheochromocytoma.
ii) Arrhythmogenic
Thyrotoxicosis
Hypoglycemia
Orthostatic hypotension.
iii) Drugs
Caffeine, alcohol (holiday heart syndrome), nicotine, cocaine and amphetamines
Sympathomimetic drugs
Digitalis
Vasodilators (Calcium blockers, nitrates)
Tricyclic antidepressants.
iv) Psychiatric Anxiety, depression, panic disorders, bereavement and somatization.
Psychiatric causes account for 31%14 to 41%.15
2. Evaluation
The history remains the most important and valuable mode of examination to dis-
tinguish cardiac from non cardiac causes of palpitation. It has to be evaluated in the
following way:
i) Duration and frequency,
ii) Mode of onset,
iii) Nature/character,
iv) Relieving factors,
v) Associated symptoms.
i) Duration and Frequency of Palpitation

i) Acute or chronic
ii) Persistent or non persistent
iii) If it is non persistent, then how frequently it occurs.
Persistent palpitations suggest volume overload conditions such as:
Valvular heart disease: AR, MR, TR (see Figs 11.27 and 11.28)
Acyanotic CHD: PDA, VSD, ASD (see Figs 11.2911.31)
Cyanotic CHD: with PBF: TAPVC, PAPVC, TGA with VSD without PS
Persistent arrhythmia like atrial fibrillation
Non cardiac causes: anemia, arteriovenous fistula, thyrotoxicosis, psychiatric illness.
In these conditions, exertion results in exaggeration, and some patients may not expe-
rience palpitations at rest but may manifest it on exertion. Patients with chronic atrial
fibrillation may not experience palpitations at all.
Non persistent or paroxysmal palpitations are usually of arrhythmogenic origin due to:
Arrhythmias (see Figs 11.3211.35)
Non cardiac causes: thyrotoxicosis, hypoglycemia, addictions and drugs (see Fig.
11.36). Psychiatric illness may also cause paroxysmal palpitations.
Dilated
left atrium
Dilated aorta
Aortic valve
Dilated
left ventricle Dilated left
ventricle
Fig. 11.27 | Mitral regurgitation. Fig. 11.28 | Aortic regurgitation. Persistent palpi-
tation occurs in both the conditions.
Ductus
arteriosus
Aorta
Aorta
PA LA
PA LA (dilated)
(dilated)
(dilated) (dilated)
RA RA
LV
(dilated)
RV LV
(dilated) RV
(dilated)
Fig. 11.29 | Persistent ductus arteriosus. Fig. 11.30 | Ventricular septal defect.
In this acyanotic congeni-
In this acyanotic congenital
heart diseases, persistent pal- tal heart diseases, persist-
pitation occurs. ent palpitation occurs.
Frequency: Palpitations due to arrhythmias and psychiatric etiology may be paroxys-

mal in nature and can occur frequently in a given day. Similarly, recurrent palpitations
with perspiration in a hypertensive patient suggest pheochromocytoma.
ii) Mode of Onset

i) Whether palpitation occurred spontaneously or was precipitated or exaggerated by
exertion?
Aorta
PA
(dilated) LA
RA
LV
RV
(dilated)
Fig. 11.32 | Arrhythmogenic right ventricular

Fig. 11.31 | Atrial septal defect. In this acyanotic
congenital heart diseases, persistent
dysplasiapalpitation is one of
the presenting symptoms.
palpitation occurs.
Aorta
PA
LA
RA
Ventricular tachycardia
LV
RV
Left ventricular damage

Myocardial infarction
Myocarditis
Fig. 11.33 | Ventricular tachycardia (VT). Among arrhythmias VT and SVT are the com-
monest causes of palpitation.
ii) If it begins suddenly and ends abruptly: often due to paroxysmal atrial or junc-
tional tachycardia, atrial flutter or atrial fibrillation.
iii) Gradual onset and cessation of the palpitation suggests: sinus tachycardia or anxiety.
iii) Nature/Character of Palpitation

The patient may describe symptoms of palpitation as pounding, stopping, jumping, racing,
floating or flopping sensation in the chest. Some patients perceive almost every premature
Orthodromic
tachycardia
Fig. 11.34 | Atrioventricular reciprocating tachycardia (AVRT) which is the commonest

cause of supraventricular tachycardia (SVT). Among arrhythmias VT and
SVT are the commonest causes of palpitation.
Fig. 11.36 | Thyrotoxicosis.

Fig. 11.35 | Atrial fibrillation. Both atrial
fibrillation and thyrotoxicosis
can present as persistent or
non persistent palpitation.
beat, while others are totally unaware of frequent or advanced arrhythmias. Patients often
are unaware of palpitation when they first lie down on their sides to sleep, especially on
their left side.16 When the atrial fibrillation becomes permanent, patient perceives the
palpitation only on exertion or excitement i.e. when the ventricular rate increases.
Generally, a thin tense individual is more likely to be aware of the cardiac activity than
others.
i) When palpitation lasts for an instant it is often described as skipped beats or flop-
ping in the chest which is commonly due to premature beats. The premature beats
may be perceived as floating sensation in the chest.
ii) A pounding sensation in the chest occurs due to paroxysmal tachycardia.
iii) The sensation that the heart has stopped beating correlates with the compensatory
pause following a premature beat.
iv) Regular rapid palpitation may be due to sinus tachycardia, SVT or paroxysmal
atrial tachycardia.
v) Irregular rapid palpitation may be due to atrial fibrillation, atrial flutter or atrial
tachycardia with a varying block.
vi) Slow palpitation i.e. with slow heart rate may suggest AV block or sinus node disease.
iv) Relieving Factors/How it Stops?

It stops spontaneously in most of the paroxysmal arrhythmias. However if it is relieved
by vagal maneuvers such as by stooping, breath-holding, or inducing gagging or vomit-
ing, it suggests a diagnosis of paroxysmal SVT.
v) Associated Symptoms
Presence of other cardinal symptoms suggests cardiac etiology (see Table 11.8).
i) Syncope: occurrence of syncope does not indicate a good prognosis. An episode of
syncope following palpitation suggests:
Stokes-Adams attack
Asystole or severe bradycardia following termination of a tachyarrhythmia
Hypoglycemia or
Pheochromocytoma.
ii) Chest pain: palpitation followed by angina suggests myocardial ischemia (precipi-
tated by MVO2 due to rapid heart rate).
iii) Dyspnea: HF/LVF, acute pulmonary embolism, severe bronchial asthma.
iv) Polyuria: paroxysmal atrial tachycardia, paroxysmal atrial fibrillation.
v) Throbbing in the neck: AR.
Table 11.8 Palpitation and associated symptoms
Associated symptoms Causes
1. Syncope Stokes-Adam attack, severe bradycardia, pheochromocytoma, hypoglycemia

2. Chest pain Myocardial ischemia
3. Dyspnea HF, acute pulmonary embolism, bronchial asthma
4. Polyuria Paroxysmal atrial tachycardia, paroxysmal atrial fibrillation
5. Sweating MI, most arrhythmias, pheochromocytoma, hypoglycemia
6. Deafness Prolong QT syndrome
7. Diarrhoea Thyrotoxicosis, hypokalemia induced arrhythmias, irritable bowel syndrome
HF: heart failure, MI: myocardial infarction.

vi) Sweating: MI, hypoglycemia, pheochromocytoma, most of the arrhythmias (with

hypotension) or anxiety.
vii) Anxiety and hyperventilation: psychogenic.
viii) Deafness: prolonged QT syndrome.
ix) Diarrhea: thyrotoxicosis, hypokalemia induced arrhythmias, irritable bowel
syndrome.
4. FATIGUE
It is the most common and non specific symptom (see Fig. 11.37).
However, extreme fatigue sometimes precedes or accompanies AMI.
On exertion, severe fatigue may occur due to global myocardial ischemia. However,
any condition that results in depressed cardiac output is associated with fatigue and
muscular weakness.
It may be due to drug intake such as beta-blockers, diuretics (excess).
Diuretic induced hypokalemia also gives rise to fatigue.
Anemia, thyrotoxicosis, anxiety, depression and other chronic medical diseases are
common conditions associated with fatigue and weakness.
5. SYNCOPE
It is a sudden and transient loss of consciousness associated with a loss of postural tone,
with spontaneous recovery not requiring electrical or chemical cardioversion. It occurs
in all age groups, increases with age and accounts for 3% in men and 3.5% in women.17
In pre-syncope, there is a transient episode of altered consciousness with a loss of
postural tone, i.e. patient feels dizzy and weak without the loss of complete consciousness.
1. Etiopathogenesis
The basic mechanism of syncope and pre-syncope is (see Table 11.9):
i) Reduction in cerebral blood flow due to:
Fall in cerebral perfusion pressure, i.e. 60 mmHg of mean aortic pressure.
Elevation in cerebrovascular resistance or intracranial pressure.
Cardiac output Fatigue Anemia

Thyrotoxicosis
Anxiety
Depression
Chronic medical
Beta blockers AMI diseases
diuretics Hypokalemia
global myocardial
ischemia
Fig. 11.37 | Causes of fatigueAMI: acute myocardial infarction.

Table 11.9 Etiopathogenesis of syncope
Mechanism Causes
1. cerebral blood flow Mean aortic pressure 60 mmHg cerebrovascular

resistance/intracranial tension
2. energy substrates Blood sugar 40 mg% (hypoglycemia) PO2 60 mmHg
(hypoxia)
ii) Reduction of energy substrates:

Hypoglycemia, i.e. blood sugar 40 mg%.
Hypoxia, i.e. PO2 60 mmHg.
Etiologically, syncope and pre-syncope are classified into:
(1) Cardiac
(2) Non cardiac and
(3) Undetermined.
1) Cardiac Syncope
1020% of all causes of syncope.
i) Due to structural abnormalities (311%) leading to decreased cardiac output (CO):
Left ventricular outflow tract obstruction (LVOTO)
Right ventricular outflow tract obstruction (RVOTO)
Coronary artery disease (CAD)
Cardiac tamponade (CT)
Aortic dissection.
ii) Due to arrhythmias (530%):
Tachyarrhythmias
Bradyarrhythmias
Pacemaker related.
iii) Neurally mediated syncope
During and following catheterization
Nitrate syncope.
(2) Non Cardiac Syncope

4050% of all causes of syncope. Broadly, it is subclassified into four groups:
1) Vascular
2) Neurological
3) Metabolic and
4) Psychogenic.
1) Vascular causes: They are the most common causes of syncope and constitute
more than 1/3rd of all the syncopal episodes. They consist of three subgroups: a) reflex
mediated b) orthostatic and c) anatomical.
a) Reflex mediated syncope:
(i) Neurally mediated: Neurocardiogenic/vasovagal syncope (the commonest cause)
(ii)Neurally induced:
Carotid sinus syncope/carotid sinus hypersensitivity:
a. Cardioinhibitory
b. Vasodepressor
c. Mixed.
Situational syncope (18%):
a. Micturition syncope
b. Defecation syncope
c. Cough syncope
d. Swallowing syncope
e. Divers
f. Postprandial syncope
g. Valsalva syncope.
(iii) Neuralgias:
Glossopharyngeal
Trigeminal
b) Orthostatic syncope (orthostatic hypotension) (412%):
Venous pooling or volume depletion
Drug induced
Neurogenic.
c) Anatomical: Subclavian steal syndrome is a rare cause (0.1%) of syncopal
episodes.
2) Neurologic syncope: (neurological disorders causing syncope) (10%):
i) Cerebrovascular syncope (6%): CVA, TIA.
ii) Seizure disorders (2%).
iii) Migraine (1218%).
3) Metabolic syncope: (5%).
4) Psychogenic syncope
(3) Undetermined (Syncope of Unknown Causes)

1341% of all causes of syncope.
1. Cardiac Syncope
Severe obstruction to cardiac output or rhythm disturbance can lead to syncope (see
Fig. 11.38).
Structural Cardiac Arrhythmias

abnormalities syncope
1. LVOTO: AS, HCM 1. Tachyarrhymias: VT, SVT

2. RVOTO: PH, PPH, PS 2. Bradyarrhythmias: SSS, CHB, SB
3. CAD 3. Pacemaker related: malfunctioning,
Neurally
4. CT pacemaker syndrome
mediated
5. Aortic dissection
1. During and following cath

2. Nitrate
Fig. 11.38 | Cardiac syncopeLVOTO: left ventricular outflow tract obstruction, AS:
aortic stenosis, HCM: hypertrophic cardiomyopathy, RVOTO: right ventric-
ular outflow tract obstruction, PPH: primary pulmonary hypertension, PS:
pulmonary stenosis, CAD: coronary artery disease, CT: cardiac tamponade,
SSS: sick sinus syndrome, CHB: complete heart block, SB: sinus bradycardia,
cath: cardiac catheterization.
Post-stenotic dilatation of
aortic arch
Stenosed
aortic valve
Left ventricular
hypertrophy
Fig. 11.39 | Syncope occurs in 42% of severe AS.

a) Due to structural abnormalities leading to obstruction to flow: Exertional syn-
cope is a common manifestation of all types of heart diseases in which cardiac output
is fixed and does not rise or may even fall with exercise.
i) LVOTO: Common conditions are AS, HCM. Other causes include prosthetic
valve malfunction.
Aortic stensis (AS): Syncope occurs in 42% of patients with severe AS, usually
with exertion18 (see Fig. 11.39).
Mechanism of syncope in AS:

Due to fixed CO, CO decreases on exertion due to reflex fall in peripheral vascular
resistance. Exercise/exertion leads to marked increase in LV systolic pressure without
a corresponding increase in aortic pressure, which results in excessive stimulation of
LV mechanoreceptors (Bazold-Jarisch reflex) leading to inhibition of sympathetic
but activation of parasympathetic tone through cardiac vagal afferent fibres.18
Myocardial ischemia contributes to vasodepressor syncope or depressed coronary
artery perfusion due to hypotension and bradycardia.19
Occurrence of arrhythmias: Rarely, ventricular tachyarrhythmias, atrial fibrillation
or paroxysmal AV block cause syncope due to loss of atrial kick.
Stages of syncope in AS: Syncope in AS has two stages.
First stage (2040 sec) (due to vasodepression): There is a sudden fall of blood pres-
sure, light headedness and pallor, followed by transient loss of consciousness. ECG
may be normal and heart sounds are distant during this stage.
Second stage is secondary to decreased coronary blood flow and is characterized by
cyanosis, absent pulse and heart sounds, apnea, twitching of the body or seizures
and abnormal ECG (ST, VT, Atrial fibrillation, AV block, ventricular fibrillation or
asystole).
Prognostic importance: Survival is 3 yrs in AS with syncope unless valve replace-
ment is done.
Hypertrophic cardimyopathy (HCM): Syncope occurs in 30% (see Fig. 11.40).
Mechanism of syncope in HCM
Dynamic LVOTO is worsened by an increase in LV contractility (stimulating the LV
mechanoreceptors), decrease in chamber size, or decrease in after-load. Hence, a Valsalva
maneuver, severe cough or drugs (e.g. digitalis) precipitates hypotension and syncope.
Myocardial ischemia.20
Ventricular arrhythmias especially VT reported in 25% of adult patients.21
Predictors of syncope include.22* age 30 yrs.* LVED volume index 60 mL/m2 and*
unsustained VT.
Prognostic importance: Extensive hypertrophy and VT are associated with poor
prognosis.
ii) LV inflow obstruction: LV inflow obstruction can also cause syncope.
MS: It rarely leads to syncope and the mechanism could be (see Fig. 11.41):
Severe inflow obstruction leads to decreased LV filling which in turn may lead to
decreased cardiac output and syncope
Atrial fibrillation with rapid ventricular rate
PH
Pulmonary embolism (PE)
Cerebral embolic event
Ball valve thrombus
Associated AS or CAD.
Increased
PA pressure
Dilated left
atrium
Stenosed
mitral valve
Normal left
ventricle
Right ventricular
ASH SAM hypertrophy
Fig. 11.40 | Syncope occurs in 30% of hyper-

trophic cardiomyopathy.
Fig. 11.41 | Incommon.
mitral stenosis, syncope is not
RV Aorta
VS
AMVL
LV AO PT
RA LA
PMVL
MYXOMA
LA
LV
RV
Fig. 11.42 | Myxomas can cause syncope when MV

or TV is obstructed especially on change
of posture. Fig. 11.43 | Syncope
complex.
can occur in Eisenmenger
Atrial myxomas: It result in obstruction of MV or TV and may obstruct ventricu-

lar filling leading to decrease cardiac output and syncope especially with change in
body position (see Fig. 11.42).
iii) RVOTO: Causes of syncope due to RVOTO are:
PH: secondary to congenital heart diseases (Eisenmenger complex and syndrome,
TOF), primary pulmonary hypertension (PPH, upto 30%) (see Figs 11.43 and 11.44).
PS
Pulmonary
embolism
Aorta
PA
PT
LA
RA
RA
RV LV
RV
Fig. 11.44 | Syncope is reported upto 30% in

primary pulmonary hypertension.
Fig. 11.45 | Syncope occurs in 1015% in pulmonary
embolism when 50% of pulmonary
vascular bed is obstructed.
PE (syncope occurs in 1015% especially with massive PE i.e. 50% obstruction of

pulmonary vascular bed) (see Fig. 11.45).
Mechanism of syncope
Inability to increase CO in association with a reflex fall of peripheral resistance
results in hypotension and syncope.
Activation of cardiopulmonary mechanoreceptors in the setting of increased force of
ventricular contraction.
In congenital heart disease with right to left shunt as in TOF results in marked arte-
rial hypoxia which may precipitate syncope (see Fig. 11.46).
iv) CAD: Syncope can occur in 512% in AMI especially in elderly patients, while
syncope in unstable angina (USA) and coronary spasm is rare (see Fig. 11.47).
Mechanism of syncope
Sudden pump failure producing hypotension and decreased perfusion of the brain.
Arrhythmias: VT or bradyarrhythmias.
Stimulation of LV baroreceptors during acute inferior wall MI or ischemia involving
right coronary artery.
Other possible mechanisms:
Acute mechanical complications: MR, VSD, ventricular wall rupture.
Drug induced: vasodilators (nitrates, Ca channel blockers, morphine); volume
depletion due to diuretics.
CT: due to postinfarct pericarditis, thrombolysis, and anticoagulant therapy, dur-
ing PTCA, perforation by pacemaker wire.
Acute PE.
Postural hypotension: after prolonged bed rest.
Pulmonary stenosis
(infundibular)
Aorta Pulmonary
stenosis
PA (valvular)
Overriding
LA aorta
RA
Ventricular
RV LV septal defect
Right
ventricular
hypertrophy
Fig. 11.47 | Acute myocardial infarction (AMI)
syncope occurs in 510% in AMI
especially in elderly patients.
Fig. 11.46 | TOFsyncope occurs due to arterial
hypoxia.
Type I
Aorta
PA
LA
RA
LV
RV
Pericardial
tamponade
Fig. 11.48 | Aortic

in 5%.
dissectionSyncope occurs Fig. 11.49 | Syncope can occur in pericardial
tamponade.
v) Aortic dissection: Syncope occurs in 5% (see Fig. 11.48).

Mechanism of syncope: (a) sudden, CT (b) stroke.
vi) Cardiac tamponade (pericardial tamponade): Which affects both right and left
side of the heart, can rarely produce syncope more so if associated with arrhythmias
(see Fig. 11.49).
b) Syncope due to arrhythmias: Arrhythmias account for 530% of causes of syncope,
and about 80% of cardiac causes.
i) Tachyarrhythmias: VT, SVT, atrial fibrillation or atrial flutter with rapid ventricu-
lar response and AV nodal reentrant tachycardia are common causes of syncope.
Ventricular tachycardia: (VT) is commonest arrhythmia producing syncope and
accounts for 39% of cardiac causes of syncope.
VT generally occurs in the setting of known organic heart disease and long QT inter-
val syndrome which could be congenital (with or without deafness) or acquired.
The commonly associated ventricular arrhythmia is Torsades de pointes, and some-
times, polymorphic VT may also be associated.
The most frequent causes of acquired long QT interval syndromes are antiarrhythmic
drugs (quinidine, procainamide, disopyramide, flecainide, encainide, amidarone, and
sotalol) and electrolyte imbalance (hypokalemia, hypomagnesemia).
Supraventricular tachycardia (SVT): It accounts for 8% of cardiac causes of syncope.
In young individuals, paroxysmal SVT usually does not cause syncope. Predisposing
factors for producing syncope in SVT are:
Most often, SVT occurs in the setting of known organic heart disease: AS, HCM,
restrictive CM, PS, and LV dysfunction.
Advanced age.
Rate of SVT: 200/min.
Underlying pre-excitation.
Syncope in WPW syndrome (pre-excitation) is related to rapid rate of reciprocating
SVT or rapid ventricular response over the accessory pathway during atrial fibrillation
and is also related to vasomotor factors as well.23
ii) Bradyarrhythmias and advanced AV block: It accounts for 31% of cardiac causes
of syncope. Profound sinus bradycardia, SA exit block, high AV block and sick sinus
syndrome (SSS) are the common causes. However, SSS and CHB account for majority
of the cases.
Sinus bradycardia (SB): It may be due to excessive vagal tone, decreased sympa-
thetic tone or sinus node disease itself.
In young healthy individuals, sinus bradycardia is due to vagal tone or sympa-
thetic tone and rarely results in syncope.
However, sinus bradycardia due to eye surgery, intracranial or mediastinal tumors,
myxedema and drugs, may cause symptomatic bradycardia that results in syncope.
Sick sinus syndrome (SSS): Syncope is reported in 2570% of SSS patients which
is characterized by the disturbances of SA impulse formation or conduction.
ECG manifestations include: sinus bradycardia, pauses, arrest or exit block. The
appearance of alternating sinus bradycardia with paroxysmal SVT is common and is
known as bradycardiatachycardia syndrome.
There may be associated atrial fibrillation with slow ventricular response, AV and
intraventricular conduction defects. Thus, AV block, impaired junctional escape
rhythm or ventricular arrhythmias may actually be responsible for syncope in the
setting of SSS.
Complete heart block (CHB): Syncope is common in Stokes-Adams syndrome but

rare in patients with congenital CHB as ventricular rate is usually adequate.
Progression to high grade AV block or CHB in patients with conduction defects:
right bundle branch block with left anterior hemiblock (RBBB LAH), RBBB 1
AV block, left bundle branch block (LBBB) 1 AV block, alternating bundle
branch block (BBB), fascicular blocks with Mobitz type II AV block or with prolonged
PR interval can occur, but not usually in patients with bifascicular block and normal
PR interval.
iii) Pacemaker related: Syncope in patients with pacemaker implantation is due to
pacemaker malfunctioning or pacemaker syndrome.
Dual chamber pacemakers can induce pacemaker-mediated tachycardias when there
is retrograde conduction of the ventricular impulse to the atria.
However in the present scenario, this complication is almost eliminated due to
improved technology.
Mechanism of syncope in arrhythmias
(i) In tachyarrhythmias: Mildmoderate tachycardias increase output (CO), whereas
marked tachycardia (140/min) leads to decrease in diastolic filling and CO
(Rauls effect) resulting in hypotension and syncope. Besides tachycardia results in
vigorous ventricular contraction stimulating ventricular mechanoreceptors leading
to hypotension and syncope.
(ii)In bradyarrhythmias: Usually, bradycardia leads to prolonged ventricular filling
resulting in increased stroke volume to maintain CO. However, severe bradycardia
(30/min) may result in inadequate compensatory increase in stroke volume and
leads to syncope.
c) Neurally mediated syncope:
i) During and following cardiac catheterization: Pain associated with femoral punc-
ture and groin compression after sheath removal may produce vasovagal episode and
result in syncope. Most common in anxious and fearful patients and should be sus-
pected when the patient becomes restless, yawns or vomits, since it is potentially dan-
gerous in the left main coronary artery (LMCA) disease, severe three vessel disease
(TVD), severe AS and severe PH.
Prophylactic measures to prevent vasovagal episodes include:
Adequate explanation of the procedure to the patient.
Congenial atmosphere in the cath lab and friendly attitude of the staff.
Intravenous atropine in anxious bradycardia patients prior to removal of the sheath.
Patient should be monitored for rhythm and blood pressure during sheath removal
and immediately afterwards.
ii) Nitrate syncope: Normally, the vasodilator drugs such as nitrates that cause
marked venous dilatation, decreased venous return and decreased CO results in tachy-
cardia and increased cardiac inotrophic state. However, in susceptible individuals and
presence of predisposing factors lead to stimulation of cardiac mechanoreceptors and
syncope.24 When stable angina progresses to USA or evolving MI, nitrate syncope
occurs due to:
Unrelieved ischemia
Additional area of ischemia and
Bradycardia as in inferior wall MI. Hence, a new onset nitrate syncope in a stable
angina patient, prompt hospitalization and further investigation is mandatory.
Predisposing factors include:
Concomitant therapy with:
Beta-blockers (prevent reflex tachycardia)
Diuretics (hypovolemia with veno-dilatation)
Other vasodilators (additional vasodilatation).
Prolonged standing: causes venous pooling.
2) Non Cardiac Syncope

The non cardiac causes of syncope include vascular, neurological, metabolic and
psychogenic (see Fig. 11.50).
(a) Vascular syncope The vascular syncope mainly includes reflex mediated (vasova-
gal,24 situational and carotid sinus syncope) and orthostatic syncope.
(1) Reflex mediated:
i) Neurocardiogenic syncope (vasovagal/vasodepressor syncope/common faint): is one
of the most common causes of syncope. It is characterized by a sudden fall of blood
pressure with or without bradycardia, often preceded by a constellation of prodromal
symptoms such as nausea, headache, sweating, hyperventilation, paraesthesia chest pain
and palpitation. However, these prodromal symptoms may persist for minutes or hours
after the syncopal episode has resolved. It often occurs in young individuals in response
to the facilitating factors and often in the presence of predisposing factors and it classically
resolves spontaneously once the patient assumes supine position (see Fig. 11.51).
Vascular Non cardiac syncope Metabolic
1. Vasovagal Orthostatic 1. Hypoglycemic related

2. Carotid sinus 2. Hypoxia related:
3. Situational Neurological Psychogenic high altitude syncope,
anemia
1. CVA, TIA
2. Subclavian steel
syndrome
3. Neuralgias
4. Migraine related
Fig. 11.50 | Non cardia syncopeCVA: cerebrovascular accident, TIA: transient ischemic
attack.
Facilitating Vasovagal Predisposing

factors syncope factors
1. Emotions 1. Fatigue
2. Pain 2. Surgery
3. Posture 3. Heat
4. Volume status
Fig. 11.51 | Vasovagal syncope.
i) The facilitating factors which precipitate syncope include:

Emotions: grief, anger, humiliation, or death of the loved one
Pain
Prolonged standing
Depleted volume status, venipuncture and blood donation.
ii) The predisposing factors include: fatigue, surgery (eye, dental)25 and heat. But it
may occur without identifiable predisposing factors.
iii) Phases: Vasovagal syncope has three phases:
First phase: During this period, the blood pressure and heart rate increases largely
due to baroreceptor mediated rise in sympathetic tone.
Second phase: There is an abrupt fall of blood pressure and heart rate (occasionally,
there may be asystole of 1020 sec) with prodromal symptoms culminating in
syncope. Atropine may prevent fall in heart rate but not hypotension.
Third phase consists of rapid recovery on assuming supine position.
iv) Pathophysiology
Normal response to upright position (standing): The decrease in venous return, stroke
volume and arterial pressure leads to compensatory responses mediated by barore-
ceptors and medullary centers to increase sympathetic and decrease parasympa-
thetic activity, thereby maintaining blood pressure and heart rate.
In vasovagal syncope: Facilitating factors (such as prolonged standing or grief ) in
susceptible individuals trigger baroreceptors and medullary centers through affer-
ent C fibers, (see Fig. 11.52) activating the parasympathetic tone but inhibiting
the sympathetic tone through vagal efferent fibers resulting in hypotension and
bradycardia, and thereby syncopy.
ii) Situational syncope: accounts for 18%, and occurs in association with various
daily activities, e.g. micturition, defecation, swallowing, coughing, Valsalva maneuver.
(i) Micturition syncope: It is often seen in young men after rising from the bed
in early morning hours and in men who experience sudden loss of consciousness dur-
ing or immediately following voiding. Elderly individuals with multiple medical prob-
lems may also experience micturition syncope often in association with orthostatic
hypotension.26
Central venous volume

(Orthostatic stress, blood volume)
Baroreceptors unloaded
Adrenergic tone
Myocardial contractility and heart rate
Activation of cardiopulmonary mechanoreceptors
Central vasomotor activation
Sympathetic withdrawal and Parasympathetic activation

circulating epinephrine
(from adrenals)
Bradycardia
Vasodilation
Hypotension
Syncope
Fig. 11.52 | Mechanism of neurocardiogenic syncope.

Mechanism: It is similar to vasovagal syncope. The mechanoreceptors in bladder are
triggered in the presence of predisposing and facilitating factors, causing syncope.
Predisposing factors:
Fatigue
Decreased food intake
Alcohol ingestion
Recent urinary tract infection
Bladder pathology, e.g. bladder neck obstruction, pheochromocytoma of bladder.
Facilitating factors:
Physiological changes during sleep i.e. decline of blood pressure and heart rate
mediated by decreased peripheral vascular resistance ( sympathetic activity) dur-
ing sleep.
Changes during micturition, i.e. sudden decompression of bladder, and possible
Valsalva maneuver.
Orthostatic hypotension especially in elderly individuals.
(ii) Defecation syncope most commonly occurs in the elderly individuals, usually
after rising from the bed at night or during manual disimpaction of the rectum.27
Mechanism: There occurs triggering of mechanoreceptors in the gut wall in the pres-
ence of predisposing and facilitating factors.
Fatigue,
Decreased food intake,
Alcohol ingestion,
GIT pathology, e.g. Meckels diverticulum, ruptured appendix, foreign body in
the rectum,
Other underlying medical conditions e.g. CAD, pulmonary embolism, transient
ischemic attack (TIA).
Facilitating factors:
Physiological changes during sleep.
Possible Valsalva maneuver during defecation.
Orthostatic hypotension.
Syncope during rectal and pelvic examination or sigmoidoscopy: Similar mechanism
for syncope.
(iii) Swallowing/deglutition syncope:
Mechanism: During or immediately following swallowing, syncope occurs in patients
associated with structural abnormalities of esophagus or heart due to triggering of
mechanoreceptors in upper GIT, especially esophagus.
Esophagus abnormalities include: diverticula, achalasia, stricture, tumor or diffuse
spasm.
Cardiac: acute myocardial infarction, acute rheumatic carditis treated with digoxin
or calcified mass over the aortic valve or septum. SB, sinus arrest or high degree
AV block have been demonstrated during swallowing syncope.
Similar mechanism is implicated in syncope associated with esophagoscopy.28
(iv) Cough syncope (tussive or post tussive syncope/laryngeal vertigo): Syncope
following a paroxysm of severe cough usually occurs in the middle aged men who drink
alcohol, smoke and have a chronic lung disease. It may occur in children but is rarely
seen in women.
Mechanism
Reflex triggering of pulmonary mechanoreceptors.
Severe coughing increases intrathoracic pressure which decreases venous return and
in turn cardiac output (CO).
Transmission of high intrathoracic pressure to the subarachnoid space during cough-
ing may increase the cerebrovascular resistance and reduce the cerebral blood flow.
Cough syncope is rarely associated with Mobitz II or complete heart block, obstructive
cardiomyopathy, hypersensitive carotid sinus syndrome and severe cerebrovascular dis-
ease. Similar mechanism is implicated for syncope during endotracheal intubation or
bronchoscopy and sneeze syncope associated with Arnold-Chiari malformation.
(v) Valsalva syncope: Valsalva maneuver, usually in the presence of predisposing

factors (such as cerebrovascular disease or sick sinus syndrome) causes syncope due to
progressive fall in venous ruturn, arterial pressure and cardiac output as a result of
prolonged increase in the intrathoracic pressure.27
(vi) Divers syncope: It may occur in underwater diving and may lead to sudden
death. It could be a form of neurocardiogenic syncope and hypoxia and bradycardia of
diving reflex may contribute.27
(vii) Postprandial syncope: Postprandial hypotension (usually 4560 min after
meals)29 due to splanchnic blood pooling and peripheral vasodilatation may lead to
syncope especially in the elderly individuals (up to 36%). Impaired baroreflex func-
tion and thereby inadequate sympathetic activity and release of gastrointestinal pep-
tides could be the contributing factors.30
iii) Carotid sinus hypersensitivity/carotid sinus syncope: Carotid sinus hypersensitivity is
characterized by profound bradycardia and/or hypotension with compression of carotid
sinus in susceptible individuals. It is reported in 525% of asymptomatic population
especially in elderly males, while carotid sinus syncope is characterized by spontaneous
fainting, occurs in 520% of the individuals with abnormal carotid sensitivity.
i) Mechanism: Triggering of carotid sinus baroreceptors (located in the internal
carotid artery just above the bifurcation of common carotid artery) and medullary
centers via afferent fibers (glossopharyngeal and vagus nerves) activates parasympa-
thetic and inhibits sympathetic tone via vagal and sympathetic efferent fibers respec-
tively which further results in profound bradycardia and hypotension.31
ii) Types of carotid sinus hypersensitivity: Three types have been described:32
Cardioinhibitory type is defined as cardiac asystole of 3 sec. It is the most common
type accounting for 3478% and is secondary to marked sinus bradycardia, SA
block, and/or high degree AV block.
Vasodepressor type is defined as a systolic blood pressure decline of 50 mmHg, in
the absence of significant bradycardia. It accounts for 510%. Presyncopal symptoms
and signs, such as nausea, sweating and pallor are not usually observed.
Mixed type is the combination of cardioinhibitory and vasodepressor response, with
bradycardia and hypotension. The vasodepressor component (hypotension) may
not be evident until atropine blockade or during cardiac pacing.
iii) Predisposing factors:
For carotid sinus syncope:
CAD and hypertension in majority.
Neck pathology: Enlarged lymph nodes, tissue scars, carotid body tumors, parotid
tumors, thyroid tumors, head and neck tumors.
Possible associations with digitalis, alpha-methyl dopa and propanol intake have
been reported.
For carotid sinus hypersensitivity: Sinus node dysfunction and AV node conduction
abnormalities are often noted in the patients.

iv) Precipitating factors: Factors which exert pressure on the carotid sinus may
precipitate syncope, e.g. tight collar, shaving, sudden turning of the head.
(2) Orthostatic syncope (hypotension): A decline of 20 mmHg in systolic or

10 mmHg in diastolic blood pressur upon assuming upright posture is often defined
as orthostatic hypotension.
It is a disorder in which assumption of upright posture results in hypotension asso-
ciated with light-headedness, blurring of vision and a sense of profound weakness.27
If the fall in the perfusion pressure to the brain is profound, syncope occurs and if
the individual assumes the recumbent posture, BP rapidly normalizes and conscious-
ness is restored.
These symptoms are often worst on arising in the morning or after meals or exercise.
i) Mechanism
Normally, upright posture results in pooling of 500700 ml of blood in lower limbs
and splanchnic circulation leads to decrease venous return and cardiac output, and
triggering of aortic, carotid and cardiopulmonary baroreceptors. This reflexly increases
sympathetic outflow and inhibit parasympathetic activity, resulting in increase in heart
rate and vascular resistance to maintain systemic blood pressure on standing upright.33
Hence, orthostatic hypotension occurs when a defect exist in the regulation of sys-
temic blood pressure in any element of this system.
ii) Etiology and classification: Etiologically, orthostatic hypotension is classified into
three groups:
Due to venous pooling and/or blood volume depletion:
Prolonged bed rest Pregnancy Blood loss
Prolonged standing Venous varicosities Dehydration
Neurogenic causes
General medical disorders: Diabetes mellitus, renal failure, amyloidosis, and alcoholic
neuropathy.
Autoimmune diseases: Mixed connective tissue disease, SLE, rheumatoid arthritis,
Gullaine Barre syndrome, Eaton-Lambert syndrome.

Central brain lesion: Multiple cerebral infarcts, multiple sclerosis, craniopharyngioma.
Autonomic failure: Shy-Drager syndrome (multiple system atrophy), Parkinsons disease.
Tabes dorsalis, syringomyelia.
Circulating endogenous vasodilators: Hyperbradykinism, carcinoid syndrome, mas-
tocytosis.
Idiopathic orthostatic hypotension.
Drug induced: It accounts for 29%.

Vasodilators: Ca channel blockers, nitrates, hydralazine, ACE inhibitors, and prazosin.
Other antihypertensives: Methyldopa, clonidine, labetalol, and diuretics.
Antidepressants: MAO inhibitors and tricyclic antidepressants.
Tranquilizers: Phenothiazines and barbiturates.
Antiparkinsonian drugs.
iii) Idiopathic orthostatic hypotension is a rare disorder, common in males and is

often associated with other autonomic disturbances such as impotence, impaired erection
and ejaculation, impaired sweating and sphincter malfunction.
b) Neurological syncope: Neurological disorders are infrequent causes of syncope

(10%).
i) Cerebrovascular syncope: 6% of cerebrovascular accidents (CVA) and TIA are
associated with syncope.34
Vertebrobasilar system: In almost all the patients, atherosclerotic occlusive disease of
vertebrobasilar system is involved in this type of syncope,34 with compromised perfu-
sion to the medullary centers, which is usually preceded by symptoms of vertigo,
diplopia, dysarthria and ataxia.
Subclavian artery: Subclavian steal syndrome due to occlusive disease of the subclavian
artery proximal to the origin of the vertebral artery may give rise to syncope.27
Brachiocephalic artery: In the occlusive disease of the origins of the brachiocephalic
vessels e.g. aortic arch syndrome, Takayasus arteritis, syncope is not uncommon.26
Syncope is a rare manifestation: of SLE, giant cell arteritis, sickle cell disease, embolic
complications of rheumatic heart disease and myxoma, dissection of extracranial arterics.
Syncope may occur in the anomalies of cervical spine or cervical spondylosis.
ii) Reflex mediated syncope: It includes neuralgias:
Glossopharyngeal neuralgia: Severe unilateral paroxysmal pain in oropharynx, tonsillar
fossa, base of the tongue, or ear precipitated by swallowing, chewing, or coughing,
occasionally results in syncope and seizure during the attack.
Syncope is mostly caused by asystole or bradycardia and rarely due to vasodepressor
response. It is associated with neoplasms of neck or lymphomas with meningeal
involvement in 1/6th of the patients with syncope.
Trigeminal neuralgia: It may also be associated with syncope due to bradycardia asystole
or vasodepressor response.
iii) Seizure disorders: 2% of seizure patients have syncope.35
Temporal lobe syncope: Temporal lobe epilepsy is rarely associated with bradyarrhyth-
mias and is the most likely form of epilepsy to masquerade as syncope. Hence, the
term temporal lobe syncope is used for partial complex seizures when patients have
drop attacks resembling syncope.36
Non convulsive seizures i.e. atonic seizures or epileptic drop attacks which are com-
mon with secondary generalized seizures or partial epilepsy affecting mesial frontal or
central cortical regions may masquerade as syncope.
iv) Migraine related syncope: 1218% of patients with migraine may have syncope
and orthostatic hypotension due to hyperresponsiveness of dopamine receptors with
the inhibition of vasomotor center and vasovagal reaction secondary to pain.
Syncope usually occurs in less form of migraine due to basilar arterial system
involvement.
This type of migraine usually afflicts young women and has a strong menstrual
association.
c) Metabolic syncope:
i) Hypoglycemia related syncope is associated with weakness, sweating, sensation of
hunger, confusion and altered consciousness, which are not related to posture and
usually promptly respond to food ingestion or intravenous glucose administration.
Most common causes are: due to insulin or oral hypoglycemic drugs, alcohol, prolonged
fasting and rarely, insulinomas.
It is gradual in onset (circulatory cause) and is associated with sinus tachycardia
and rarely, hypotension. However, hypoglycemia may trigger neurocardiogenic
syncope.27
ii) Hypoxia related syncope:
High altitude syncope may occur in young healthy adults exposed to moderate to
very high altitudes37 due to:
Reflex bradycardia, hyperventilation, and subsequent hypocapnia, resulting in
reflex cerebral vasoconstriction which decreases cerebral oxygen delivery.
Mild volume depletion due to diuresis at high altitudes or due to physical activity
may lead to vasovagal syncope.
In the presence of cardiovascular disease, pulmonary insufficiency and anemia; syn-
cope may occur at lesser levels of oxygen deprivation.
It is associated with sinus tachycardia while blood pressure is usually normal.
d) Psychogenic syncope: Syncope may be a manifestation of generalized anxiety dis-
order, major depression or panic disorder, especially in young females by precipitating
vasovagal reactions.38 During hyperventilation seen in psychiatric patients, there is
tachycardia and slight hypotension but no profound fall of blood pressure. Complete
loss of consciousness rarely occurs.
3. Exercise Induced Syncope

Syncope may occur during or immediately after exercise. The most common causes are:
(1) Underlying cardiac diseases: These are the most common causes:
Structural abnormalities:
LVOTO: AS, HCM
RVOTO: PH
Cardiomyopathy: DCM, HCM, RV dysplasia
CAD: atherosclerotic, anomalous origin of coronary arteries (in young).
Arrhythmogenic: VT, SVT, accessory pathways, long QT syndrome. Underlying
cardiac diseases have a potential for sudden cardiac death.
(2) Underlying neurological causes subclavian steal syndrome.
(3) Neurocardiogenic: Exercise syncope without structural heart disease is due to the
increase in catecholamines and force of ventricular contraction results in triggering of
cardiac mechanoreceptors in the setting of mild volume depletion and shifts of blood
flow to dissipate heat.
Evaluation of
Clinical history Clinical history
cardiac syncope
1. Chest X-ray and ECG

Structural heart
2. Echocardiogram
ECG:
Standard Arrhythmogenic
Signal averaged
Holter monitoring
Structural heart Cath study and
disease & ALCAPA angiogram
Electro-physiological
Arrhythmogenic
studies
Fig. 11.53 | Evaluation of cardiac syncopeALCAPA: anomalous left coronary artery from
pulmonary artery.
Evaluation of
noncardiac syncope
BP measurement-
Clinical history Carotid massage
supine and standing
Postural CT scan, EEG, Carotid sinus

HUTT
hypotension carotid doppler syncope
Neurally mediated Neurological cause/

syncope seizure disorder
Fig. 11.54 | Evaluation of noncardiac syncopeHUTT: head up tilt test, CT: computer
tomography, EEG: electroencephalogram.
Evaluation of Syncope
A detailed clinical history from the patient and a witness if present is crucial for diag-
nosis of specific entities and to distinguish syncope from seizure. It is supplemented by
physical examination and baseline investigations (see Figs 11.53 and 11.54).
1) Clinical history: While obtaining the history, the following have to be deter-
mined (see Table 11.10):
Mode of onset
Duration of episode
Precipitating factors (triggers)
How was consciousness regained?
Associated factorsbefore (prodromes, aura), during, and after (postictal)
Predisposing factors
Family history.
Table 11.10 Clinical history in cardiac syncope vs seizure disorder
Features Cardiac syncope Seizure disorder
1. Mode of onset Rapid Rapid

2. Duration 1 min 5 min
3. Posture Unrelated in arrhythmogenic Unrelated
4. Restoration of Promptly Slowly
consciousness
5. Triggering factors Exertion Nil
6. Associations Sweating, nausea before (i) Aura
the event (sometimes)
(ii) Convulsive movements, frothing at
the mouth, tongue bite
(iii) Postictal confusion, sleep, aches
7. Family history In hypertrophic obstructive Usual
cardiomyopathy (HOCM)
i) Mode of onset
Rapid/sudden onset in cardiac and vasovagal syncope and seizure disorder.
Gradual onset in hypoglycemia, drug related syncope and hyperventilation.

Unrelated to posture: Arrhythmogenic and seizure disorder.
Prolong standing: Prolonged standing facilitates vasovagal syncope.

After arising: In orthostatic hypotension.
Syncope on changing position (from sitting to lying, bending, turning over in bed):
In atrial myxomas.
ii) Duration of episode: In syncope, duration of the event is usually 1 min and
duration of episode usually lasts 5 min; while in seizures, the duration of uncon-
sciousness is usually 5 min.
iii) Restoration of consciousness: Regained consciousness promptly in syncope (of
cardiac origin); while in seizure disorder, it occurs slowly.
iv) Triggering factors:
(i) On exertion: On exertion, cardiac syncope occurs due to LVOTO (AS, HOCM),
RVOTO (PH, PE), CAD and sometimes due to arrhythmias.
With arm exercise: Subclavian steal syndrome.
After exercise in well trained athletes: Exercise induced syncope.
(ii) With head rotation/pressure on carotid sinus: Carotid sinus syncope/hypersensitivity.

(iii) Pain, grief, emotional stress, unpleasant sight, sound or smell: Vasovagal syncope.
(iv) During or immediately after micturition, defecation, swallowing, coughing: Situa-
tional syncope.
v) Associations
(i) Associated with aura: In seizure disorders.
(ii) Prodromes of warmth, nausea, sweating, light headedness: They occur in vasovagal
syncope.
Sweating or nausea before the event (sometimes in): Cardiac syncope.

Preceded by vertebrobasilar symptoms such as vertigo, diplopia, dysarthria, ataxia:
CVA (in vertebrobasilar system).
(iii) Episode associated with blue face, frothing at the mouth, tongue biting, urinary
incontinence, convulsive movements in seizure disorders.
(iv) Postictal confusion state, sleepiness, aching muscles in seizure disorders.
vi) Predisposing factors
(i) Fatigue, surgery (eye, dental), exposure to heat: Vasovagal syncope.
(ii) In situational syncope:
Fatigue, alcohol ingestion, UTI, bladder pathology (micturition syncope)
Fatigue, alcohol intake, GIT pathology (defecation syncope)
Esophageal pathology (swallowing syncope)
Smoking, chronic lung diseases, alcohol intake (cough syncope).
(iii) Neck pathology, CAD, hypertension: Carotid sinus syncope.
(iv) Concomitant use of drugs: Postural hypotension, nitrate syncope (diuretics, vasodila-
tors, betablockers).
(v) Head injury: Seizure disorders.
vii) Family history:
(i) Family history of epilepsy may be present in seizure disorders.
(ii) Positive family history in HOCM, long QT syndrome.
2) Blood pressure measurement for detection of orthostatic hypotension: Supine BP and
heart rate are measured after the patient has been lying down for at least for 5 min.
Standing measurements should be obtained immediately and for at least 2 min., and
should be continued for 10 min when there is a high suspicion of orthostatic hypoten-
sion. Sitting blood pressures is not reliable.
3) Carotid massage for the detection of carotid sinus syncope: Even though the tech-
nique is not standardized, carotid massage is done in supine position for 610 sec,39
with continuous ECG and blood pressure monitoring.
Simultaneous bilateral carotid massage should never be done, and at least 15 sec
should be allowed to elapse between the massage from one side to the other.
However, it may be done in sitting or standing positions if vasodepressor variety is
suspected and the test is negative in supine position.
Complications of carotid sinus massage are extremely low and include: prolonged
asystole, transient or permanent neurological deficit, ventricular fibrillation and death.
4) Head up tilt test (HUTT):40 It is a standard diagnostic test for evaluating patients
with syncope.
(i) Indications40
Recurrent syncope or a single syncopal episode in a high risk patient who either has no
evidence of structural heart disease or in whom other causes of syncope have been
excluded.
Evaluation of patients in whom an apparent cause of syncope has been established

(e.g. asystole, AV block) but in whom the presence of neurally mediated syncope
would influence the treatment, and
As a part of the evaluation of patients with exercise-related syncope.
(ii) Potential emerging indications
Recurrent idiopathic vertigo in whom neurally mediated bradycardia and hypoten-
sion may be the cause.
Recurrent TIAs especially if Doppler ultrasound, carotid angiography and trans-
esophageal echocardiogram (TEE) have failed to disclose an etiology for the symptoms.
Chronic fatigue syndrome: In some, neurally mediated bradycardia and hypoten-
sion may contribute to the symptom complex.
Sudden infant death syndrome: Since potentially neurally mediated hypotension
may play a role in this syndrome, HUTT may help in better understanding of this
problem.
(iii) Relative contraindications
Syncope with clinically severe LVOTO.
Syncope in presence of critical mitral stenosis.
Syncope in setting of known critical proximal coronary artery stenosis.
Syncope in conjunction with known critical cerebrovascular stenosis.
(iv) Not warranted
Single syncopal episode which is highly typical of neurally mediated syncope with-
out an injury and also not in a high risk setting.
Syncope in which an alternative specific cause has been established and in which
additional demonstration of a neurally mediated susceptibility would not alter the
treatment plans.
It is not useful in establishing a diagnosis of situational syncope.41
(v) Technique
Preparation
The test is performed in a quiet room/lab, minimizing the surrounding noise
with ample lighting and comfortable temperature in a fasting state (75 mL of nor-
mal saline for each hour of fasting may be infused to decrease the possibility of
false positive result).
All non essential and vasoactive drugs should be withheld for about 5 half-lives.
Tilt table with foot board support is used.
Simultaneous and continues monitoring of minimum 3 ECG leads and BP is
done. Monitoring of BP is usually done non invasively (digital plethysmography) so
as not to provoke the vasovagal reaction.
Procedure: 2045 min supine equilibrium period before the start of the test. HUTT
has two protocols.
Passive tilt testing: Table is tilted to an angle of 6080 (usually 70) for 3045 min.
If there is no positive response i.e. syncope or pre-syncope in association with
hypotension and/or bradycardia, proceed with pharmacological provocation.
Provocative tilt testing: Usually isoproternol, nitroglycerine or edrophonium are

used as pharmacological provocation. 1 g/min of isoproternol infusion is started
while the patient is in supine position and then the patient is tilted for 1015 min
and watched for any positive response. If there is no positive response, the patient
is again brought to supine position and the procedure is continued with increasing
dosage (infusion rate is increased by 1 g/min each time) and patient is tilted for
similar duration till the positive response, or another end point (maximum
dosage of 35 g/min or adverse effects or severe tachycardia) is reached.
Alternatively, increasing bolus dosages (each increment of 12 g) may be given instead
of continuous infusion.
(vi) Positive response: Three types of positive responses have been described:42 mixed,
cardioinhibitory and pure vasodepressor.
Type 1: Mixed response
Heart rate initially rises and then falls, but the ventricular rate does not fall to 40/min
or fall to 40/min for 10 sec with or without asystole for 3 sec.
BP rises initially and then falls before heart rate falls.
Type 2: Cardioinhibitory response: Heart rate rises initially and then falls to a ventric-
ular rate of 40/min for more than 10 sec or asystole occurs for 3 sec.
Type 2A cardioinhibitory: BP rises initially and then falls before heart rate falls.
Type 2B cardioinhibitory: BP rises initially and only falls to 80 mmHg systolic at
or after the onset of rapid and severe fall in heart rate.
Type 3: Pure vasodepressor response
Heart rate rises progressively and does not fall more than 10% from the peak at the
time of syncope.
BP falls to cause syncope.
The estimated sensitivity and specificity for passive tilt test is 65% and 90% respec-
tively while with pharmacologic provocation, sensitivity is 75% and specificity 80%,
with overall reproducibility of 6785%.
5) ECG
(i) Standard ECG: For diagnosis of syncope due to arrhythmias.
(ii) Signal averaged ECG: For the detection of late potentials for prediction of
inducible ventricular tachycardia in patients with syncope.43
(iii) Holter monitoring: It determines the presence or absence of arrhythmias in
patients who develop symptoms during ambulatory monitoring.
6) Electrophysiological (EP) studies: It is indicated in patients with suspected struc-
tural heart disease and unexplained syncope and it should not be performed in
patients with known cause of syncope for whom treatment will not be influenced by
the findings of the test.44 EP studies are helpful in establishing a diagnosis of sick sinus
syndrome, heart block, SVT or VT in patients with syncope.
7) CT scan, EEG, carotid duplex scan: These are helpful in establishing neurologi-
cal causes of syncope and seizure disorders with careful history and neurological
examination.
8) Echocardiography: For detection of occult cardiac disease and impaired ventricu-

lar function to suggest a cardiac cause of syncope.
9) Stress testing
It is reserved for patients in whom syncope or pre-syncope occurred during or
immediately after exertion or in association with chest pain.

It is indicated in young individuals with recurrent syncope during exertion when
other causes of syncope have been excluded and to rule out anomalous coronary
arteries. It is contraindicated in patients suspected of having severe AS or HOCM.
10) Cardiac catheterization: For establishing the diagnosis of structural heart dis-
eases and anomalous coronary arteries with syncope.
11) Routine blood tests: Such as serum electrolytes, glucose and hematocrit levels
may be helpful, but have a low diagnostic value in evaluation of the patient with syncope.
REFERENCES
1. Sampson JJ, Cheitlin MD. Pathophysiology and differential diagnosis of cardiac pain. Prog
Cardiovasc Dis 1971;13(16):507531.
2. Lichstein E, Breitbart S, Shani J, et al. Relationship between location of chest pain and site of coro-
nary artery occlusion. Am Heart J 1988;115(3):564568.
3. Spittell PC, Spittell JA Jr, Joyce JW, et al. Clinical features and differential diagnosis of aortic dissec-
tion: Experience with 236 cases (19801990). Mayo Clin Proc 1993;68:642651.
4. Heberden W. Some accounts of a disorder of the breast. Medical Trans 1772;2:5967.
5. Bernstein LM, Fruin RD, Pacini R. Differentiation of esophagus pain from angina pectoris: Role of
the esophageal acid perfusion test. Medicine 1962;41:143162.
6. The Criteria Committee of the New York Heart Association: Diseases of the Heart and Blood
Vessels Nomenclature and Criteria for Diagnosis. 6th ed Boston, Little Brown and Co., 1964.
7. Campeau L. Grading of angina pectoris. Circulation 1976;54(3):522523.
8. Goldman L, Hashimoto B, Cook EF, and Loscalzo A. Comparative reproducibility and validity of
systems for assessing cardiovascular functional class: Advantages of a new specific activity scale.
Circulation 1981;64(6):12271234.
9. Chauhan A, Mullins PA, Taylor G, Petch MC. Schofield PM. Cardioesophageal reflex: A mecha-
nism for linked angina in patients with angiographically proven coronary artery disease. J Am Coll
Cardiol 1996;27(7):16211628.
10. Levine HJ. Difficult problems in the diagnosis of chest pain. Am Heart J 1980;100(1):108118.
10a. ACC/AHA Guidelines update for the management of patients with chronic stable angina.
Circulation 2003;107:149158.
11. Sullivan M, Higginbotham M, Cobb F. Increased exercise ventilation in patients with chronic heart
failure: intact ventilatory control despite hemodynamic and pulmonary abnormalities. Circulation
1988;77:552559.
12. Joseph K Perloff. Congenital heart disease in adults. In: Braunwald E. ed. Heart Disease: A Textbook
of Cardiovascular Medicine, 5th edn. Bangalore: Prism books Pvt Ltd; 1997:972.
13. American Thoracic Society: Dyspnea: Mechanism, assessment and management. A consensus state-
ment. Am J Respir Crit Care Med 1999;159(1):321340.
14. Weber BE, Kapoor WN. Evaluation and outcomes of patients with palpitations. Am J Med 1996;
100(2):138148.
15. Knudson MP. The natural history of palpitations in a family practice. J Fam Pract 1987;24(4):357360.
16. Vanden Belt RJ. The history. In: Chizner M, ed. Classic Teachings in Clinical Cardiology: A Tribute
to W. Proctor Harvey. Cedar Grove, NJ: Laennac; 1996:4154.
17. Come PC, Pitt B. Nitroglycerine-induced severe hypotension and bradycardia in patients with acute
myocardial infarction. Circulation 1976;54:624628.
18. Grech ED and Ramsdale DR. Exertional syncope in aortic stenosis; evidence to support inappropri-
ate left ventricular baroreceptor response. Am Heart J 1991;121(2 Pt 1):603606.
19. Baltazar RF, Go EH, Benesh S and Mower MM. Case report: Myocardial ischemia: an overlooked
substrate in syncope of aortic stenosis. Am J Med Sci 1992;303(2):105108.
20. Dilsizian V, Bonow RO, Epstein SE and Fananapazir L. Myocardial ischemia detected by thallium
scintigraphy is frequently related in to cardiac arrest and syncope in young patients with hypertrophic
cardiomyopathy. J Am Coll Cardiol 1993;22:796804.
21. Fananapazir L, Tracy CM, Leon MB, et al. Electrophysiologic abnormalities in patients with hyper-
trophic cardiomyopathy. Circulation 1989;80(5):12591268.
22. Nienaber CA, Hiller S, Spielmann RP, et al. Syncope in hypertrophic cardiomyopathy: Multivariate
analysis of prognostic determinants. J Am Coll Cardiol 1990;15(5):948955.
23. Leitch JW, Klein GJ, Yee R, Leather RA, Kim YH. Syncope associated with supraventricular tachy-
cardia. Circulation 1992;85(3):10641071.
24. Raviele AN, Gasparini G, DiPede F, et al. Nitroglycerine infusion during upright tilt: A new test for
the diagnosis of vasovagal syncope. Am Heart J 1994;127(1):103111.
25. Boorin MR. Anxiety. Its manifestation and role in the dental patient. Dent Clin North Am
1995;39(3):523539.
26. Kapoor WN, Peterson J and Karpf M. Micturition syncope. A reappraisal. JAMA 1985;253(6):796798.
27. Schaal SF, Nelson SD, Boudoulas H, Lewis RP. Syncope. Curr Probl Cardiol 1992;17(4):205264.
28. Ferrante L, Artico M, Nardacci B, Frajoli B, Cosentino R, Fortuna A. Glossopharyngeal neuralgia
with cardiac syncope. Neurosurgery 1995;36(1):5863.
29. Vaitkevicius PV, Esserwein DM, Maynard AK, et al. Frequency and importance of postprandial
blood pressure reduction in elderly nursing-home patients. Ann Intern Med 1991;115(11):865870.
30. Jansen RWMM, Lipsitz LA. Postprandial hypotension: Epidemiology, pathophysiology, and clinical
management. Ann Intern Med 1995;122(4):286295.
31. Strasberg B, Sagie A, Erdman S, et al. Carotid sinus hypersensitivity and the carotid sinus syndrome.
Prog Cardiovas Dis 1989;31(5):379391.
32. Weiss S, Baker JP. The carotid sins reflex in health and disease: Its role in the causation of fainting
and convulsions. Medicine 1933;12:297354.
33. Lipsitz L. Orthostatic hypotension in the elderly. N Eng J Med 1989;321(14):952957.
34. Davidson E, Rotenbeg Z, Fuchs J, et al. Transient ischemic attack-related syncope. Clin Cardiol
1991;14(2):141144.
35. Kapoor W. Evaluation and outcome of patients with syncope. Medicine 1990;69(3):160175.
36. Jacome DE. Temporal lobe syncope: Clinical variants. Clin Electroencephal 1989;20:58.
37. Nicholas R, OMeara PD, Calonge N. Is syncope related to moderate altitude exposure? JAMA
1992;268:904.
38. Kapoor WN, Fortunato M, Hanusa BH, and Schulberg. Psychiatric illness in patients with syncope.
Am J Med 1995;99(5):505512.
39. Brignole M, Oddone D, Cogorno S, et al. Long term outcome in symptomatic carotid sinus hyper-
sensivity. Am Heart J 1992;123(3):687692.
40. Benditt DG, Ferguson DW, Grubb BP, et al: Tilt table testing for assessing syncope. ACC Expert
Consensus Document. J Am Coll Cardiol 1996;28:263275.
41. Sumiyoshi M, Nakata Y, et al. Response to head-up tilt testing in patients with situational syncope.
Am J Coll Cardiol 1998;82(9):11171118.
42. Sutton R, Peterson ME. The clinical spectrum of neurocardiogenic syncope. J Cardiovasc Electrophysiol
1995;6(7):569576.
43. Steinberg JS, Prytowsky E, Freedman RA, et al. Use of the signal averaged electrocardiogram for pre-
dicting inducible ventricular tachycardia in patients with unexplained syncope: Relation to clinical
variables in a multivariate analysis. J Am Coll Cardiol 1994;23(1):99106.
44. Bradenburg RO. Syncope and sudden death in hypertrophic cardiomyopathy. J Am Coll Cardiol
1990;15(5):962964.
CHAPTER 12
OTHER SYMPTOMS
1. HEMOPTYSIS 144 i. Definition 147

i. Etiology 144 ii. Types 148
ii. Evaluation 144 iii. Evaluation of Cyanosis 156
2. HOARSENESS 146 REFERENCES 158
3. CYANOSIS 147
1. HEMOPTYSIS
It is defined as coughing of blood or sputum streaked or contaminated with blood.
i. Etiology
The cardiovascular causes of hemoptysis are as follows (see Table 12.1):
Acquired causes: MS, pulmonary edema (due to any cause), pulmonary embolism
(PE) with pulmonary infarction, rupture of aortic aneurysm into bronchopulmonary
tree, rupture of bronchopulmonary collaterals [due to pulmonary venous hyperten-
sion (PVH) as in MS] (see Figs 12.1, 12.2 and 12.3).
Congenital heart diseases: Eisenmenger syndrome (see Fig. 12.4), rupture of pul-
monary arteriovenous fistula, rupture of bronchopulmonary collaterals.
Drug intake: Anticoagulants, immunosuppressive drugs, oral contraceptives (see
Fig. 12.5).
MS pulmonary edema and pulmoanry embolism are the commonest causes.
ii. Evaluation
The history remains the most important and valuable mode of examination to distin-
guish cardiovascular causes of hemoptysis from other causes. While taking history the
following has to be determined:
Duration, frequency and recurrence of hemoptysis.
Quantity of the expectorant.
Associations.
OTHER SYMPTOMS 145
Increased
PA pressure
Dilated left
atrium
Stenosed
mitral valve
Normal left
ventricle
Right ventricular
hypertrophy
Fig. 12.1 | Mitral stenosis.

Fig. 12.2 | Pulmonary edema.
Ao
Aorta
PA Pulmonary
PT
embolism RA LA
LA
RA
LV
LV
RV
RV
Fig. 12.3 | Pulmonary embolism. Fig. 12.4 | Eisenmenger syndromecommonest cause

of hemoptysis in congenital heart disease.
a) Duration, Frequency and Recurrence of Hemoptysis

Recurrent episodes not uncommon in MS, other causes include: tuberculosis, chronic
bronchitis and bronchiectasis.
b) Quantity
Small: MS, pulmonary edema, pulmonary infarction, Eisenmenger syndrome, rupture
of bronchopulmonary collaterals, due to drug ingestion.
Large/massive: Rupture of pulmonary arteriovenous fistula, rupture of aortic
aneurysm into the bronchopulmonary tree.
Other causes: lung carcinoma, pulmonary tuberculosis.
Drug intake
Pulmonary
Mitral stenosis embolism with PI
Acquired causes
Aortic aneurysm
Pulmonary edema rupture into broncho-
pulmonary tree
Hemoptysis
Eisenmenger Congenital Rupture of

syndrome heart diseases pulmonary AV fistula
Rupture of broncho-
pulmonary collaterals
Fig. 12.5 | Cardiovascular causes of hemoptysisPI: pulmonary infarction, AV: arteriove-

nous. Drug intake includes anticoagulants, oral contraceptives and immuno-
suppressants.
c) Associations
Chest pain (pleuritic) in pulmonary embolism and infarction, rupture of aortic
aneurysm.
SOB: In MS, pulmonary edema, PE with infarction, rupture of aortic aneurysm/
pulmonary arteriovenous fistula, Eisenmenger syndrome.
Sputum:
Blood tinged in MS, pulmonary embolism with infarction.
Pink frothy sputum: Pulmonary edema.
Grey sputum: COPD.
Yellowish-green sputum: Pulmonary infections.
Putrid sputum: Lung abscess.
Large quantity: Bronchiectasis.
Weight loss and anorexia: Ca lung, chronic pulmonary infections
Asymptomatic: Bronchial adenoma.
Drug ingestion such as anticoagulants, immunosuppressive drugs, oral contraceptives.
2. HOARSENESS
It is usually not related to cardiovascular diseases. However, hoarseness can occur in

(see Table 12.1):
Aortic aneurysm involving recurrent laryngeal nerve (see Fig. 12.6).
MS: Due to compression of the recurrent laryngeal nerve by the dilated pulmonary
artery, or greatly enlarged left atrium.
OTHER SYMPTOMS 147
Table 12.1 Cardiovascular causes of other symptoms
Hemoptysis Hoarseness
1. Mitral stenosis (MS) 1. Aortic aneurysm

2. Pulmonary edema 2. MS
3. Pulmonary embolism 3. Pericardial effusion (myxedema related)
4. Eisenmengers syndrome 4. Post cardiac surgery (intubation related)
5. Rupture of aortic aneurysm
6. Rupture of pulmonary
arteriovenous (AV) fistula
7. Anticoagulants, immunosuppressive,
drugs, oral contraceptives
Ascending aorta
aneurysm
Fig. 12.6 | Aortic aneurysmhoarseness

occurs if recurrent laryngeal
nerve is also involved.
Fig. 12.7 | Myxedema
voice.
causes hoarseness of
Pericardial effusion may be related to myxedema, which may be associated with

hoarseness of voice (see Fig. 12.7).
Hoarseness and loss of voice following intubation of endotracheal tube during cardiac
surgery.
3. CYANOSIS
Cyanosis, (a Greek word, kyanos blue, osis condition) is both a symptom and a
physical sign.
i. Definition
Cyanosis is a bluish discoloration of skin and mucous membranes resulting from an
increased quantity of reduced hemoglobin (Hb) (4 g/dl) or abnormal hemoglobin
pigments in the blood perfusing these areas1 (0.5 g/dl of methemoglobin).
Raynauds
CHF, septicemia phenomenon
Peripheral
Cold environment Peripheral

vascular disease
Cyanosis
dTGA TOF
Truncus arteriosus Central Single ventricle
DORV TAPVC
Eisenmenger
syndrome
Fig. 12.8 | Causes of cyanosisCHF: congestive heart failure, dTGA: dextro transposition
of great arteries, DORV: double outlet right ventricle, TOF: tetralogy of Fallot,
TAPVC: total anomalous pulmonary venous connection.
ii. Types
Principally, there are three types of cyanosis: peripheral, central and mixed (see Fig. 12.8).
a) Peripheral Cyanosis
It is usually indicates stasis of blood flow in the periphery with normal arterial O2 satu-
ration but widened arteriovenous (AV) O2 difference. The reduced hemoglobin in the
capillaries of the skin exceeds 4 g/dl.
(i) It is most prominent in the cool exposed areas that may not be well perfused, such
as extremities particularly nail beds and nose, and the limbs are cold on palpation.
(ii) Does not worsen on exertion. The resting peripheral cyanosis of CHF may be
slightly accentuated during exertion.
(iii) Immersion of the limbs in warm water for several minutes reverses the cyanosis.
(iv) Etiology: Most commonly secondary to cutaneous vasoconstriction often due to:
Low cardiac output as in: CHF, septicemia
Exposure to cold environment
Raynauds phenomenon (cyanosis localized to hands, see Fig. 12.9)
In a new born, it is mostly acrocyanosis (autonomically controlled alterations
in cutaneous distribution of exposed blood flow)

Peripheral vascular disease (a localized arterial or venous obstruction)
b) Central Cyanosis
It usually becomes apparent at a capillary concentration of 4 g/dl of reduced Hb
(1/3rd of Hb in reduced from) or 0.5 g/dl of methemoglobin.
OTHER SYMPTOMS 149
Fig. 12.9 | Raynauds phenomenon with digital ulcers

and peripheral cyanosis.
Fig. 12.10 | Central cyanosis often associated
with clubbing.
i) O2 saturation: The O2 saturation in normal arterial blood is 95% (i.e. 13.3 g of

14 g/dl is oxyhemoglobin, and 0.7 g/dl is reduced hemoglobin). The O2 saturation in
normal mixed venous blood is 70% (i.e. 9.8 g of 14 g/dl is oxyhemoglobin, and 4.2 g/dl
is reduced hemoglobin). The amount of reduced Hb in capillary blood is assumed to be
the mean of reduced Hb in arterial and mixed venous blood i.e. 0.7 4.2/2 2.45 g/dl.
Hence, the color of the normal skin and mucous membranes is pink, not blue.
Cyanosis is apparent in Caucasians at arterial O2 saturation of 85% while in pig-
mented races, O2 saturation has to further drop to lower levels. Since it is the absolute
quantity of reduced Hb in blood that is responsible for cyanosis, the higher the total
Hb content, the greater is the tendency toward cyanosis. Thus, patients with marked
polycythemia become cyanotic at higher levels of arterial O2 saturation than do
patients with normal hematocrit values, and cyanosis may be absent in patients with
severe anemia (Hb 33%) despite marked arterial O2 desaturation.
ii) Associations: Central cyanosis in severe form is often associated with polycythemia
and clubbing (see Fig. 12.10).
iii) Site: It involves the entire body, including warm well perfused sites, such as con-
junctiva and mucous membrane of the oral cavity, and limbs are warm on palpitation.
iv) Etiology of central cyanosis

At birth: Apparent cyanosis at birth is due to dTGA and Admixture lesions e.g.
TAPVC, single ventricle, DORV (subaortic VSD with PS), truncus arteriosus.
Neonatal period: ASD with transient right to left shunt. However, cyanosis is more
commonly due to pulmonary parenchymal disease or CNS depression.
Infancy: Usually congenital heart disease, hereditary methemoglobinemia
(a) 13 months of age: When spontaneous closure of PDA causes a reduction of pul-
monary blood flow in the presence of right sided obstructive cardiac anomalies,
most commonly Tetralogy of Fallot (TOF). Cyanosis in TOF may be apparent
from days to 46 weeks of birth (see Fig. 12.11).
Pulmonary stenosis
(infundibular)
Ao
Pulmonary
Aorta
stenosis
(valvular)
PA PT
Overriding RA LA
LA aorta
RA
LV
Ventricular
RV septal defect RV
LV
Right
ventricular
hypertrophy
Fig. 12.11 | Tetrology of Fallot (TOF)commonest Fig. 12.12 | Eisenmenger syndromecommonest

cause of cyanosis in children as well as
cause for cyanosis in children.
in adults.
(b) 6 months of age: Due to development or progression of RVOTO in patients

with VSD.
Childhood: Usually, CHD due to progressive increase in pulmonary vascular resistance
and cyanosis secondary to pulmonary arteriovenous fistula.
(a) 25 years of age: TOF, Eisenmenger complex due to VSD (see Fig. 12.12).
(b) After 10 years of age: Eisenmenger complex due to VSD.
(c) After 20 years of age: Eisenmenger syndrome due to ASD.
v) Pathogenesis of central cyanosis: Central cyanosis is due to three causes (see
Fig. 12.13):
Decreased arterial O2 saturation due to inadequate oxygenation owing to impaired
pulmonary function and pulmonary venous blood is not fully saturated. Inhalation of
100% oxygen may diminish or clear the cyanosis. This is known as Anoxemic cyanosis,
e.g. pulmonary disorders.
Decreased arterial O2 saturation due to intracardiac or extracardiac right to left
shunt and pulmonary venous blood is fully saturated. Inhalation of 100% oxygen
does not clear or decrease the cyanosis. This is known as Shunt or admixture cyanosis,
e.g. cyanotic CHD.
Decreased arterial O2 saturation due to replacement of normal by abnormal Hb.
This is Replacement cyanosis, e.g. methemoglobinemia. There is a family history of
cyanosis but absence of heart disease in hereditary methemoglobinemia.
vi) Factors influencing O2 saturation (thereby affecting the intensity of cyanosis):
Temperature and physical activity: Cyanosis appears or intensifies with physical activ-
ity as the oxygen saturation declines concurrently with an increase in right to left
shunt across a defect as peripheral vascular resistance decreases.
OTHER SYMPTOMS 151
Central cyanosis
Inadequate Abnormal Hb-

oxygenation methemoglobinemia
Arterial O2
saturation
Intra or extra Influencing

cardiac shunts factors
Temperature and
Blood PH
physical activity
Large R-to-L shunt

Fetal Hb
> 25% of LV output
Fig. 12.13 | Pathogenesis

ventricular.
of central cyanosisHb: hemoglobin, R: right, L: left, LV: left
Blood pH and 2-3 diphosphoglycerate: Oxygen transport to the tissues is affected by

shifts in oxygen hemoglobin dissociation relation (curve) which may be affected by
blood pH and levels of 2-3 diphosphoglycerate concentration.
Ratio of fetal to adult Hb: Fetal Hb has a higher affinity for oxygen than adult Hb
and would be more highly saturated at any given pO2.
Degree of right to left shunt: Cyanosis occurs when the volume of blood of right to
left shunt exceeds 25% of LV output.
Hence, determination of systemic arterial O2 tension may provide a more accurate
picture of underlying pathophysiology than the measurement of O2 saturation alone.
vii) Types of central cyanosis
Shunt or admixture cyanosis
Anoxemic cyanosis
Replacement cyanosis
Cyanose tardive: Cyanosis in CHD as in Eisenmenger syndrome which first make
its appearance in the second decade of life or later.
Differential cyanosis is applied to the condition where some part of the body
receives more hypoxic blood than others, and virtually always indicates the presence
of CHD which can be brought about by exercise (see Table 12.2).
Differential cyanosis: Cyanosis confined to lower limbs with little or no cyanosis of arm
and face, typically seen in
PH with right to left shunt through PDA (see Fig. 12.14). But if the ductus is prox-
imal to left subclavian artery: then the right hand is less cyanosed than left hand and
both the feet.
Table 12.2 Types of central cyanosis
Type of cyanosis Example
1. Admixture cyanosis Cyanotic CHD

2. Anoxemic cyanosis Pulmonary disorders
3. Replacement cyanosis Methemoglobinemia
4. Cyanosis tardive Eisenmenger syndrome
5. Differential cyanosis PDA PH with right to left shunt
6. Reversed differential cyanosis TGA and COA with retrograde flow through PDA
CHD: congenital heart disease, PDA: patent ductus arteriosus, PH: pulmonary hypertension, TGA:
transposition of great arteries, COA: coarctation of aorta.
RCC
Aorta LCC LSA

Ductus
RSA
arteriosus
PDA
PA LA
COARC
Ao
RA
RV LV
PT
Fig. 12.15 | Differential cyanosis also occurs in

Fig. 12.14 | Differential cyanosis occurs in patent
ductus arteriosus (PDA) with PH and
coarctation of aorta (COARC) with PDA
and right-to-left shuntRSA: right sub-
right to left shunt. clavian, RCC: right common carotid, LCC:
left common carotid, LSA: left subclavian.
Coarctation of aorta or interrupted aortic arch: oxygenated blood to upper part of

the body and desaturated blood to lower part of the body by way of right to left
shunt through PDA (see Fig. 12.15).
Cyanosis of the fingers exceeds that of the toes is known as Reversed differential cyanosis,
seen in:
TGA with preductal narrowing of aorta (either coarctation or interrupted aortic
arch) PH and reverse flow (i.e. from pulmonary artery to aorta) through PDA2
(see Fig. 12.16).
DORV with subpulmonary VSD (Taussig-Bing anomaly), PH (pulmonary vascular
disease) and reverse flow (i.e. from pulmonary artery to aorta) through PDA.3
TGA with intact ventricular septum, PH and reverse flow through PDA4 (see
Fig. 12.17).
OTHER SYMPTOMS 153
Interrupted PDA
arch ASD
LCA Ao
Innom. a. LSA
Asc. ao. PDA
PT
Desc. ao.
PT RA LA
RA
LA
RV LV
RV LV
Fig. 12.16 | Differential cyanosis in inter- Fig. 12.17 | Reverse differential cyanosis occurs in transpo-
sition of great arteries (TGA) with intact ventric-
rupted aortic arch with PDA
and right-to-left shunt. ular septum, PH and reverse flow through PDA.
viii) Differentiation of cyanosis of cardiac origin from that of pulmonary causes

1. Respiratory patterns
Tachypnea:
In CHD: Cyanosis, tachypnea but no other signs of respiratory distress. In upper or
lower air obstruction: There may be cyanosis, tachypnea with flaring of alae nasi,
chest wall retraction and grunting.
Apnea: Intermittent apneic episodes are rare in cardiac diseases but common in:
Premature infants with CNS immaturity or disease and
Intracranial diseases.
Cheyne stokes breathing can occur both in heart failure and respiratory failure.
2. Arterial blood gas analysis in patients with cyanosis (blood sample from radial or
temporal artery) also helps in differentiating cyanosis of cardiac origin from that of
respiratory cause (see Table 12.3).
c) Mixed Cyanosis
It is the presence of both peripheral and central cyanosis which occurs in conditions like
chronic cor pulmonale due to chronic emphysema or fibrosis of lung. The lung lesion
tends to produce central cyanosis while associated right heart failure tends to cause
peripheral cyanosis.
d) Methemoglobinemia
i) Normal physiology
The major function of Hb is the transport of oxygen from the lungs to body tissues,
which is mediated by reversible binding of molecular O2 to heme iron. The heme
Table 12.3 Arterial blood gas analysis in infants with cyanosis
Response
PH PO2 PCO2
Pattern to O2 Suggested condition
(7) (80100 mmHg) (3545 mmHg)
inhalation
1. Due to PO2 Hyaline membrane

respiratory disease or other
cause pulmonary parenchymal
disease often
associated with PVR
and shunting across
PFO or PDA
2. Due to PO2 Hypoventilation
respiratory (CO2 retention)
cause
3. Cardiac _ _ PO2 Obligatory venous
cause admixture e.g. TAPVC
4. Cardiac _ _ pulmonary blood flow
cause e.g. TOF
5. Peripheral _ _ PO2 Systemic hypoperfusion
cyanosis
_: no effect, : decrease, : increase, PO2: partial pressure of oxygen, PCO2: partial pressure of carbon dioxide,
PFO: patent foramen ovale, PDA: patent ductus arteriosus, TAPVC: total anomalous pulmonary venous connection,
TOF: tetralogy of Fallot.
iron of deoxy Hb must be in the ferrous (Fe2) state to allow reversible binding with
O2. This ferrous iron is continually subjected to oxidant stresses resulting in the for-
mation of a stable ferric (Fe3) hemoglobin i.e. methemoglobin, which is incapable
of reversible O2 binding. Hence, if the significant portion of total Hb exists in the
ferric state, then fatal tissue hypoxia may develop.
However; under normal circumstances, the rate of endogenous methemoglobin
production is relatively constant at 3% per day, and RBCs are able to decrease
methemoglobin 250 times of the rate at which it is normally formed by NADH
dependent reductases.
Consequently, normal individuals have a methemoglobin concentration of 1%.
NADH dependent reductase, diaphorase I is absent in hereditary methemoglobinemia.
ii) Etiology of methemoglobinemia: Besides hereditary cause, other causes are:
1. Nitrites: Due to contaminated well water, food additives.
2. Aniline dyes: Laundry dyes, shoe dyes, red crayons and disinfectant.
3. Naphthalene and
4. Drugs (see Tables 12.4 and 12.5).
iii) Presentation
Slate gray cyanosis is appreciated when methemoglobin exceeds 10%, but the levels
between 20% and 25% are usually well tolerated.
OTHER SYMPTOMS 155
Table 12.4 Drugs causing methemoglobinemia
1. Anesthetics: Benzocaine, prilocaine

2. Analgesics: Acetophenetidin, phenacetin
3. Antimalarials
4. Nitrates: Amylnitrate, nitroprusside, ammonium nitrate
5. Sulfonamides
6. Vitamin K analogues
Table 12.5 Etiology of cyanosis and methemoglobinemia
Central cyanosis Peripheral cyanosis Mixed cyanosis Methemoglobinemia
1. TOF 1. CHF 1. Chronic 1. Hereditary

cor pulmonale
2. Eisenmenger syndrome 2. Septicemia 2. Nitrites
3. dTGA, TAPVC, DORV 3. Cold exposure 3. Aniline dyes
4. Truncus arteriosus 4. Peripheral vascular 4. Drugs (antimalarials,
disease analgesics, anesthetics)
5. Raynauds phenomenon
TAPVC: total anomalous pulmonary venous connection, TOF: tetralogy of Fallot, dTGA: dextro transposition of great
arteries, DORV: double outlet right ventricle, CHF: congestive heart failure.
At 3040% levels, patient becomes irritable, lethargic and develop exercise intolerance.
At 50% levels, severe CNS depression develops.
At 70% levels, it is incompatible with life.
However, symptoms may appear earlier in the anemic individuals.
iv) Diagnosis of methemoglobinemia

When a sample of venous blood is agitated in air for 15 min, a characteristic choco-
late brown color is formed.
Decreased O2 saturation despite normal levels of pO2.
Measurement of methemoglobin levels with spectroscope. In drug-induced methe-
moglobinemia, sulfhemoglobin is also detected.
v) Treatment of methemoglobinemia
Slow IV infusion of 12 mg/Kg body wt. of 1% freshly prepared methylene blue in
normal saline, which decreases methemoglobin levels (reduction via diaphorase II).
If there is no adequate response with methylene blue, investigate for G-6 phosphate
dehydrogenase deficiency.
Withdrawal of the offending drugs.
Neonatal At 13 months 6 months

1. ASD R-to-L TOF RVOTO in VSD
2. PPD (subpulmonary)
3. CNS
Childhood 2 years
Age of
1. TOF
At birth appearance
2. Eisenmenger VSD
1. TGA
2. Admixture lesions
>20 years
Eisenmenger ASD
Equal in UL and LL
1. Central cyanosis
More in UL
2. Peripheral cyanosis
TGA and COA with PDA
3. Methemoglobinemia
Distribution
More in LL More in LUL and both feet
1. PDA with PH PDA proximal to LSA
2. COA with PH with PH
Exertion
Cyanotic CHD
Aggravating Cold exposure
factors Peripheral cyanosis
More in the morning
TOF
Squatting 100% O2 inhalation

TOF Pulmonary disorders
Relieving factors
Beta blockers Hot bath
TOF Peripheral cyanosis
Central cyanosis Peripheral cyanosis

1. Clubbing Association 1. Low cardiac output
2. Polycythemia 2. Raynauds phenomenon
Methemoglobinemia
1. Hereditary
2. Drug exposure
Fig. 12.18 | Evaluation of cyanosisASD R-to-L: atrial septal defect with transient right to
left shunt, PPD: pulmonary parenchymal disease, CNS: central nervous sys-
tem depression, TGA: transposition of great arteries, TOF: tetralogy of Fallot,
RVOTO: increasing right ventricular outflow tract obstruction, COA: coarc-
tation of aorta, PH: pulmonary hypertension, LSA: left subclavian artery.
iii. Evaluation of Cyanosis

Again, history plays a key role in differentiating cardiac cause of cyanosis from other causes
(see Fig. 12.18).
a) Duration at What Age Cyanosis Appeared/Notice

At birth: CHD like dTGA, admixture lesions.
OTHER SYMPTOMS 157
Neonatal period: ASD with transient right to left shunt, pulmonary parenchymal
diseases, CNS depression.
13 months of age: TOF.
6 months of age: Progression of RVOTO in VSD (sub-pulmonary type).
Childhood: CHD including pulmonary AV fistula:
(i) 25 years of age: TOF, Eisenmenger syndrome due to VSD.
(ii) After 10 years of age: Eisenmenger syndrome due to VSD.
(iii) After 20 years of age: Eisenmenger syndrome due to ASD.
b) Distribution of Cyanosis
Equal on both sides or differential cyanosis is present:
Equal in upper limb (UL) and lower limb (LL): Central/peripheral/mixed cyanosis/
methemoglobinemia.
More in LL: PDA with PH, COA or interrupted aortic arch with PDA.
More in UL (Reversed differential cyanosis): TGA and COA with PDA.
More in left UL and both feet: If ductus is proximal to left subclavian artery in
PDA with PH.
c) Aggravating Factors
On exertion/exercise/playing
Eating
Defecation
More in the morning: Cyanotic congenital heart diseases especially in TOF, but not
in peripheral cyanosis
Swimming or cold exposure: Cyanosis appears or is aggravated in peripheral cyanosis,
including Raynauds phenomenon.
d) Relieving Factors
Cyanosis/cyanotic spells may decrease or get relieved by:
Squatting or squatting equivalents in TOF and other cyanotic CHDs as well.
Beta-blockers in TOF.
100% O2 inhalation in central cyanosis, and the relief is more prominent in pul-
monary disorders.
After hot bath: Peripheral cyanosis may decrease or disappear.
e) Associations
Central cyanosis is most often associated with CHD.
Central cyanosis is often associated with polycythemia and clubbing.
Raynauds phenomenon in peripheral cyanosis.
Low cardiac output in peripheral cyanosis.
Hereditary disorder without cardiac ailment: Methemoglobinemia.
Drug exposure in methemoglobinemia.
Cor pulmonale: Mixed cyanosis.
1 2 3 4 5
Fig. 12.19 | Squatting and its equivalents adopted by the patients to alleviate the cyan-
otic spells (line diagrams)1: typical squatting, 2: sitting in a chair with
legs drawn underneath, 3: legs crossed while standing, 4: mother holding
an infant with its legs flexed upon its abdomen, 5: simply lying down.
vi. Squatting
a) Squatting equivalents
Lying on left side.
Sitting with legs closely drawn beneath the trunk.
Sitting with legs drawn up on the seat of a chair.
Prune knee chest position.
Simply lying down (see Fig. 12.19).
Crossed their legs and squeezed them together when asked to stand or sit.
Babies sometimes soothed by being held with their legs flexed and knees squeezed
well into their abdomen.
b) How squatting alleviates the symptoms
In normal: Squatting increases systemic BP, systemic vascular resistance (SVR) and
venous return as well as an increase in O2 saturation. The increase in SVR is due to:
kinking of the iliac arteries.
squatting reduces the distending pressure of gravity on the lower limb vessels.
In TOF: Squatting increases SVR with PS remaining constant which results in
decrease of right to left shunt and increase in pulmonary blood flow with immediate
improvement in arterial O2 saturation, thereby alleviating hypoxic/cyanotic spells.
REFERENCES
1. Braunwald E. Cyanosis. In: Isselbacher KJ, Braunwald E, et al. eds. Harrisons Principles of Internal
Medicine. 13th ed. New York, McGraw-Hill, 1994:178182.
2. Buckley MJ, Mason DT, Ross J Jr, Braunwald E. Reversed differential cyanosis with equal desatura-
tion if the upper limbs. Syndrome of complete transposition of the great vessels with complete inter-
ruption of the aortic arch. Am J Cardiol 1965;15:111115.
3. Wedemeyer AL, Lucas RV, Castaneda AR. Taussig-Bing malformation, coarctation, and reversed patent
ductus arteriosus. Circulation 1970;42(6):10211027.
4. Waldman JD, Paul MH, Newfeld EA, Muster AJ, Idriss FS. Transposition of great arteries with intact
ventricular septum and patent ductus arteriosus. Am J Cardiol 1977;39(2):232238.
GENERAL PHYSICAL
EXAMINATION
13. General examination 161

14. Arterial pulse 225
15. Measurement of the blood pressure 249
CHAPTER 13
G ENERAL E XAMINATION
1. GENERAL BUILD AND STATURE 162 ix) Iris 179

i) Tall Stature 163 x) Pupils 181
ii) Short Stature 165 xi) Lens 181
iii) Build 166 xii) Retina 181
2. POSTURE OR ATTITUDE 169 6. NOSE 185
3. GESTURES AND SIGNS 170 7. EARS 185
4. FACIAL APPEARANCE 172 i) Ear Lobe Crease 185
i) Facial Dysmorphism 172 ii) Cauliflower (Floppy) Ear 185
ii) Facial Edema 172 iii) Low Set Ears 185
iii) Dull Expressionless Face with iv) Deafness 187
Periorbital Puffiness 173 8. ORAL CAVITY 187
iv) Dull Expressionless Face i) Lips 187
with Ptosis 173 ii) Mucous Membrane 188
v) Butterfly Rash on the Face 173 iii) Teeth 188
vi) Malar Rash (Brownish Tint iv) Gums 189
or Flush) 173 v) Tongue 189
vii) Flushing 174 vi) Palate 189
viii) Striking Premature Aging 174 9. NECK 190
ix) Facial Expression of Fright i) Short Neck 190
and Anxiety 174 ii) Webbed Neck 191
x) Moon Face 174 iii) Low Hair Line 191
xi) Ape Like Appearance 174 iv) Lymphadenopathy 192
xii) Mongoloid Facies 175 v) Thyromegaly 192
xiii) Grotesque Facial Features 175 vi) Parotid Enlargement 192
xiv) Elfin Facies 175 10. SPINE 192
xv) Distinctive Unilateral Lower 11. SKIN 193
Facial Weakness (7th Cranial i) Pigmentation 194
Nerve Palsy) 175 ii) Skin Texture 195
xvi) Midfacial Growth iii) Xanthomas 196
Deficiency 176 iv) Nodules 198
5. EYES 176 v) Cyanosis, Icteru, and
i) Hypertelorism 176 Pallor 200
ii) Exophthalmos 176 12. EXTREMITIES 200
iii) Enophthalmos 177 i) Digits 200
iv) Nystagmus 177 ii) Nails 205
v) Eye Lids 177 iii) Feet 210
vi) Conjunctiva 177 iv) Joints 212
vii) Sclera 178 13. PERIPHERAL EDEMA 215
viii) Cornea 178 i) Pathogenesis 216
162 GENERAL PHYSICAL EXAMINATION
ii) Causes 217 iv) Characteristics of Peripheral

iii) Types and Site of Peripheral Edema 221
Edema 218 REFERENCES 222
In the present-day high tech practice of medicine, the physical examination remains
a valuable and inexpensive tool for early detection of critical findings, which aid in the
early diagnosis of the cardiovascular diseases. It helps in the intelligent selection of
costly diagnostic tests, besides creating a closer bond with the patient at a time when the
medical care system is becoming often impersonal, which may be valuable in securing
patients compliance in following a diagnostic workup and treatment plan. Important
information concerning the patient with definite or suspected heart disease is often
obtained by a careful and deliberate physical examination from head-to-toe, which
includes general examination, examination of arterial pulses, measurement of blood
pressure and evaluation of the jugular venous pressure and pulsations, before thorough
examination of the cardiovascular system systematically to arrive at a definitive diagnosis.
An assessment of the patients general appearance begins with a detailed inspection
while the history is being obtained.
1. GENERAL BUILD AND STATURE
The general build and stature of the patient is usually assessed best by taking the
following measurements (see Table 13.1):
(i) Height of the patient: It includes upper and lower segments.
The upper segment of the body is measured from the top of the head to pubic
ramus, and the lower segment is measured from the pubic ramus to the floor,
(Pubic bone has 3 partsbody, superior and inferior rami. Here, reference is to
the superior remus which has 3 bordersobturator, pectineal and inferior. So,
it is not appropriate to use top of the pubic ramus)
Calculate the upper to lower segment ratio, which is equal after 10 yrs of age.
(ii) Arm span: It is the distance between the tips of the middle fingers of one hand to
the other. The arm span to height ratio is normally equal or 1.05.
(iii) Body mass index (BMI): It is the body weight of the individual in kg/height in
meters2 (wt/ht2). Normal BMI is 18.524.9 kg/m2.1
Table 13.1 Indices of build and stature
1. Height, lower and upper segments

2. Arm span
3. Body mass index
4. Waist circumference
GENERAL EXAMINATION 163
(iv) Waist circumference: It is measured at midway between lowest rib and iliac crest.
Normally, it should be 102 cm in males and 88 cm in females.2
i) Tall Stature
When the height of an individual is far in excess of the average normal for the age and
race (2 standard deviation of the mean height), the individual is considered to be tall
in stature (in India usually 6 ft). Causes of tall stature are as follows:
Tall stature with equal upper and lower segments or equal arm span to height ratio:
constitutional and pituitary giants.
Tall stature with upper to lower segment ratio of 0.8 or arm span to height ratio
of 1.05: Marfan syndrome (Fig. 13.1), homocystinuria, Klinefelters syndrome
(see Fig. 13.2).
Marfan Syndrome
Ghent diagnostic criterion for Marfan syndrome3 include (see Fig. 13.1 and Table 13.2):
1. With family history: 1 major criterion in an organ system involvement of second
organ system (11).
Fig. 13.1 | Tall stature with long extremities in Marfan Fig. 13.2 | Tall stature with gynecomastia
in Klinefelters syndrome.
syndrome.
Table 13.2 Syndromes with tall stature and cardivascular manifestations
Syndrome Diagnostic clinical features Cardivascular manifestations
1. Marfan Ghent diagnostic criteria3 i. Dilatation of ascending aorta AR

syndrome ii. Dissection of ascending aorta
iii. MVP valvular mitral regurgitation
iv. Calcification of mitral annulus
in 40 yrs of age
v. Dilatation of MPA in the absence of
valvular or peripheral PS or any other
obvious cause in 40 yrs of age
vi. Dilatation or dissection of descending
thoracic aorta or abdominal aorta in
50 yrs of age
2. Homocystinuria Due to deficiency of i. Aortic and pulmonary dilatation
cystathionine synthase4 ii. Intravascular thrombosis which may
Tall, long extremities, other cause MI, stroke or pulmonary
skeletal deformity, downward lens embolism5
subluxation and mental retardation
3. Klinefelters Tall, eunuchoid appearance, i. Venous thromboebolism
syndrome small testes, azoospermia, ii. Increased incidence of congenital
(47 XXX/XXY)6 gynecomastia, mild mental heart diseases, especially ASD
retardation (see Fig. 13.2)
AR: aortic regurgitation, MVP: mitral valve prolapse, MPA: main pulmonary artery, PS: pulmonary stenosis,
MI: myocardial infarction, ASD: atrial septal defect.
2. With no family history: major criteria in 2 different organ system involvement

of third organ system (21).
Usual organ systems involved are skeletal, ocular, cardiovascular system, lungs, skin
and duramater.
(1) Skeletal system: For major criterion in skeletal system, 4 major signs of the
following should be present. (FEW TAP 2S)
Flat foot (medial displacement of medial malleolus causing pes planus)
Reduced extension at the elbow (170)
Wrist (Walker-Murdock) and thumb (Steinberg) signs (due to arachnodactyly)
Tall stature (upper to lower segment ratio of 0.8 or arm span to height ratio of
1.05) (due to long arms and legs: dolichostenomelia)
Protrusio acetbulae of any degree (confirmed by radiography)
Pectus carinatum
Pectus excavatum requiring surgery and
Scoliosis of 20 or spondylolisthesis.
For organ involvement criterion: 2 major signs or 1 major sign 2 minor signs should
be present.
Minor signs include:

Pectus excavatum of moderate severity
Joint hyper mobility
High arched palate with crowding of teeth
Abnormal facial appearance (due to dolichocephaly, malar hypoplasia, enophthalmos,
retrognathia, down slanting palpebral fissures).
(2) Ocular system: For major criterion in ocular system, ectopia lentis is included.
For organ involvement criterion: 2 of the following signs must be present.
Abnormally flat cornea
Increased axial length of globe
Hypoplastic iris or hypoplastic ciliary muscle causing decreased miosis.
(3) Cardiovascular system: For major criterion in cardiovascular system, atleast one
of the following major signs should be present.
Dilatation of ascending aorta involving sinuses of Valsalva with or without aortic
regurgitation
Dissection of ascending aorta.
For organ involvement criterion: 1 major sign or 2 minor signs must be present.
Minor signs include:
Mitral valve prolapse with or without mitral valve regurgitation
Calcification of mitral annulus in 40 yrs of age
Dilatation of main pulmonary artery in the absence of valvular or peripheral pul-
monary stenosis (PS) or any other obvious cause in 40 yrs of age
Dilatation or dissection of descending thoracic or abdominal aorta in 50 yrs
of age.
(4) Lungs: Only organ involvement criterion: one of the following must be present.
Spontaneous pnuemothorax
Apical blebs.
(5) Skin: Only organ involvement criterion: one of the following must be present.
Stretch marks not associated with marked weight gain, pregnancy or repetitive
stress
Recurrent or incisional herniae.
(6) Dura: For major criterion, lumbosacral dural ectasia confirmed by CT scan or
MRI must be present.
Also for organ involvement criterion, lumbosacral dural ectasia must be present.
ii) Short Stature

When the height of an individual is far shorter than the average normal for age and
race (2 standard deviations of the mean height), the individual is considred to be
Table 13.3 Syndrome with short stature and cardiovascular manifestations
Cardiovascular
Syndrome Diagnostic clinical features
manifestations
1. Turner Short female, webbed neck, low hair line, Coarctation of aorta
syndrome (45X) low set ears, broad chest with widely spaced (post-ductal type),
(gonadal dysgenesis) nipples, sexual infantalism, deafness, bicuspid aortic
pigmented nevi, normal intelligence valve, PAVC7
2. Noonan syndrome8 Short, webbed neck, low hair line, Dysplastic PS,
(normal chromosomal hypertelorism, pectus excavatum, HCM
pattern) (male Turner cubital valgus, ptosis,
syndrome, but both sexes cryptorchidism, mental dullness
are affected) AD
inheritance
3. Ellis-van Creveld Short limbs, polydactyly, dysplastic Single atrium, ASD
syndrome.9 AR nails and teeth, genu valgum, lip tie
inheritance (common in due to multiple frenulum
Amish population)
AD: autosomal dominant, AR: autosomal recessive, PAVC: partial anomalous venous connection, PS: pulmonary
stenosis, HCM: hypertrophic cardiomyopathy, ASD: atrial septal defect.
short in stature. In the Indian subcontinent, 4 ft of height is considered as short

stature.
Causes of short stature are (see Table 13.3):
Constitutional (hereditary): Gurkhas, African pygmies. The individuals are normal
in all respects except the height. The growth hormone and gonodotropin levels
are normal.
Endocrine: Cretin (ratio between upper and lower segments is 1 with mental
retardation, see Fig. 13.3), pituitary dwarf (short limbed, normal intelligence but may
be associated with infantalism), Froehlichs syndrome (obese, diabetes insipidus,
hypogonadism), Cushing syndrome (obese, moon facies, abdominal striae, hyper-
tension and impaired glucose tolerance, see Fig. 13.4).
Genetic: Turner syndrome (phenotypic female: 45XO, see Fig. 13.5), Noonan syn-
drome (normal chromosomal pattern), Hurlers syndrome, Morquios syndrome,
Multiple lentigines syndrome.
Skeletal: Ellis van Creveld syndrome (chondrodystrophic dysplasia, short arms, and
legs see Fig. 13.6), achondroplasia (short and bowed legs and arms, waddling gait
see Fig. 13.7), osteogenesis imperfecta (4 types, autosomal dominance [AD]/autosomal
recessive [AR] inheritance).
Acquired: Acquired skeletal causes include: rickets, Potts spine (in children).
iii) Built
Excess fat lengthens the waist line but shortens the life line of an individual. Obesity
predisposes or aggravates hypertension, hyperlipidemia, diabetes mellitus, atherosclerosis,
Fig. 13.3 | Endocrine

cretin.
dwarf Fig. 13.4 | Endocrine dwarfcushing syndrome with
moon face, abdominal striae and obesity.
Fig. 13.5 | Genetic dwarfturner Fig. 13.6 | Skeletal dwarf

Ellis-van Creveld
Fig. 13.7 | Achondroplastic dwarf.
syndrome with wide set
nipples webbed neck syndrome.
and absent pubic hair.
Fig. 13.8 | Central obesitymainly Fig. 13.9 | Generalized obesity Fig. 13.10 | Obesity, polydactyly
and genu valgum
abdominal giving rise to mainly on the hips
an apple shaped body and thighs giving rise in Laurence Moon
and prone for coronary to a pear shaped Biedl syndrome.
artery disease (CAD). body.
restrictive lung disease, gout, cholelithiasis, infertility, and degenerative arthritis, besides
increasing the morbidity and mortality. Obesity, which can be defined as an excessive
accumulation of body fat, and since, it is difficult to determine the amount and loca-
tion of body fat, body mass index (BMI) and waist circumference have been used as
surrogate parameters.
(i) Depending upon BMI, there are three grades of over weight:1
Grade 1 over weight with BMI of 2529.9 kg/m .
2
Grade 2 over weight is known as obese with BMI of 3039.9 kg/m .

2
Grade 3 over weight is known as morbidly obese with BMI of 40 kg/m .
2
Obesity has been described as enviable for grade 1, regal for grade 2 and
pitiable for grade 3 over weight.

(ii) Depending upon the waist circumference: The individuals with central (abdom-
inal) obesity (as in metabolic syndrome, see Fig. 13.8) are more prone to coronary
artery disease as compared to generalized obesity (see Fig. 13.9). In central obe-
sity, the males have a measurement of 102 cm and females 88 cm of waist
circumference.2
(iii) The conditions in which the patients are obese are (see Figs 13.4 and 13.10,
Table 13.4):
Metabolic syndrome
Cushings syndrome
Table 13.4 Syndromes with obesity and cardiovascular manifestations
Cardiovascular
manifestations
1. Pickwickian Obese, somnolence, hypoventilation, Increased PVR,

syndrome10 cyanosis, secondary polycythemia (Dickens pulmonary hyper-
fat boy) tension
2. Laurence-Moon-Biedl Obese, retinitis pigmentosa, polydactyly and Variable congenital
syndrome syndactyly, mental retardation, hypogonadism heart disease11
3. Cushings Truncal obesity, moon face, buffalo hump Hypertension,
syndrome12 abdominal striae, fatigue, hirsutism, accelerated athero-
(hypercortisolism) osteoporsis, diabetes mellitus, acne sclerosis (MI, CHF,
stroke)
PVR: pulmonary vascular resistance, MI: myocardial infarction, CHF: congestive heart failure.
Table 13.5 Posture or attitude and cardiovascular manifestations
Posture/attitude Cause
1. Sitting quietly Angina pectoris

2. Sitting up posture Heart failure
3. Moving restlessly Acute myocardial infarction
4. Comfortable in sitting Left ventricular failure
5. Kneeling forward Pericarditis
6. Squatting Cyanotic congenital heart disease
Pickwickian syndrome
Laurence-Moon-Biedl syndrome, and
Myxedema.
(iv) An individual is described as underweight or thin with BMI of 18.5 kg/m2.

Malnutrition and cachaxia occur in severe chronic heart failure, which may be
confirmed usually by the triceps skin fold thickness (midway between the point
of acromian and olecranon process) by Schofields calipers.
2. POSTURE OR ATTITUDE
Posture or attitude of the patient can be observed on inspection which offers a great
diagnostic value (see Table 13.5).
(i) If the patient is in pain:
If the patient is sitting quietly, it is typical of angina pectoris.
If the patient is moving about, trying to find a more comfortable position, it is
suggestive of acute myocardial infarction.

Fig. 13.11 | Sitting up posture in left ventricular failure. Fig. 13.12 | Squatting
of fallot.
posture in tetrology
If the patient is comfortable in sitting up posture (see Fig. 13.11), it is seen as in

heart failure (LVF) (noncardiac conditions include: bronchial asthma, severe
ascitis, massive abdominal tumor, late pregnancy) or
kneeling forward (prayer posture) observed in pericarditis.
(ii) Squatting posture to get relief from dyspnea is seen in cyanotic congenital heart
diseases (see Fig. 13.12).
3. GESTURES AND SIGNS
Patients gestures while describing the symptoms should also be carefully observed (see
Table 13.6).
Levines sign:13 Clenching of the fist in front of the chest while describing the chest
discomfort is a strong indication of an ischemic chest pain (see Fig. 13.13).
Finger pointed to a small circumscribed area in the left inframammary region,
while describing the chest discomfort, is more likely of psychogenic origin (see
Fig. 13.14).
The cold sweaty palms with frequent sighing respirations are typical of neurcircula-
tory asthenia.
Patient is dyspneic in heart failure, pericardial effusion (massive) (see causes of dys-
pnea in symptomatology).
Gowers sign: It is observed in Duchene muscular dystrophy which may be associ-
ated with cardiomyopathy (posterobasal LV wall is involved, see Fig. 13.15).
Table 13.6 Gestures and diseases
Gestures/signs Cause
1. Levines sign Ischemic chest pain

2. Gowers sign Muscular dystrophy cardiomyopathy
3. Localized chest discomfort Psychogenic chest discomfort
4. Sighing respirations with sweating Neurocirculatory asthenia
5. Dyspneic Heart failure, pericardial effusion
Fig. 13.13 | Clenching of the fist in front of the Fig. 13.14 | Finger pointing to a small circumscribed
area in the left inframammary region
chest while describing the chest
discomfort (Levines sign) is typical while describing the chest discomfort is
of ischemic chest pain. usually of non-cardiac originmore of
a psychogenic origin.
1 2 3
4 5 6
7 8 9
Fig. 13.15 | Method of rising from supine to erect position i.e. Gowers sign in Duchene
muscular dystrophy which may be associated with cardiomyopathy.
4. FACIAL APPEARANCE
i) Facial Dysmorphism
Facial dysmorphism may be due to hypertelorism, epicanthic folds, broad flat nose,
low set ears, thick lips, abnormal teeth, short and webbed neck, low hair line and
mid facial hypoplasia.
It occurs in disorders due to genetic abnormalities such as Down syndrome, Turner
syndrome, Noonan syndrome (see Figs 13.16 and 13.17) and Williams syndrome
which may be associated with cardiovascular manifestations.
It may give rise to characteristic facies such as mongoloid facies of Downs syndrome (see
Fig. 13.18), elfin facies of Williams syndrome and grotesque facies of Hurlers syndrome.
ii) Facial Edema

It may be present in the patients with tricuspid valve disease or constrictive pericarditis
(see Table 13.7).
Figs 13.16 & 13.17 | Noonan syndromeshowing facial dysmor-

phism, low set ears hypertelorism and low
Fig. 13.18 | Down syndromeshowing
facial dysmorphism.
hairline.
Table 13.7 Abnormal facies and syndromes with cardiovascular manifestations
Facial expression Syndromes/cause
1. Hypertelorism, epicathic folds, broad flat nose, Turner and Noonan syndromes
low set ears and short neck
2. Moon face Cushings syndrome
3. Ape like face Acromegaly
4. Senile face Werners syndrome
5. Mongoloid facies Down syndrome
6. Grotesque facies Hurlers syndrome
7. Elfin facies Williams syndrome
8. Dull expression face Myxedema; Myotonic dystrophy
9. Frightened and staring Thyrotoxicosis
In SVC obstruction syndrome, upper part of the chest and face are involved with
edema and engorged veins.
iii) Dull Expressionless Face with Periorbital Puffiness

It is associated with loss of lateral eyebrows, large tongue, thickened skin and dry sparse
hair, cold intolerance, lethargy, constipation, menorrhagia, hoarse voice, increase in
weight, decreased intellectual and motor activity are characteristics of myxedema14
(which may have pericardial effusion and increased risk of atherosclerosis) (see Figs 13.19
and 13.20).
iv) Dull Expressionless Face with Ptosis

It is observed in myotonic dystrophy, which may be associated with cardiac manifesta-
tions (myocardial disease, conduction defects, arrhythmias).15
v) Butterfly Rash on the Face

It is associated with malar depigmentation, seen in systemic lupus erythematosis (SLE)
which may be associated with cardiovascular manifestations16 in 57% (see Fig. 13.21).
Pericarditis (up to 30%)17
Myocarditis (up to 10%)18
Libman-Sacks endocarditis (upto 50% in autopsy series, commonly leading to AR
and MR, less frequently to AS, MS, TS and TR).19
Congenital heart blocks in offsprings of affected mother, and
CAD (may be due to steroids or antiphosphlipid antibody syndrome).20
vi) Malar Rash (Brownish Tint or Flush)

It is seen on face, cheeks, nose and ears, and is observed in patients with chronic MS
(due to venocapillary stasis caused by low cardiac output, see Fig. 13.22).
Fig. 13.19 | Dull expressionless

face in myxedema.
Fig. 13.20 | Periorbital edema in
acute nephritis.
Fig. 13.21 | Butterfly rash in systemic

lupus erythematosis.
Fig. 13.22 | Malar flush in chronic
mitral stenosis.
vii) Flushing
It occurs in carcinoid syndrome (due to metastasizing carcinoid tumor of ileum),
accompanied by facial and periorbital edema, diarrhea, bronchial constriction and
valvular lesions (usually TR and PS/PR).21
viii) Striking Premature Aging

It is often seen in Werners syndrome22 and is characterized by:
Loss of subcutaneous tissue (scleroderma-like changes)
Graying of hair and baldness
Cataract and leg ulcers
It is often associated with severe coronary atherosclerosis.
ix) Facial Expression of Fright and Anxiety

Staring eyes (other ocular signs: lid lag, lid retraction, infrequent blinking, oph-
thalmplegia) and moist skin with fine and silky hair, Plummers nail especially in
ring fingers (separation of nail from nail bed) seen in thyrotoxicosis (see Fig. 13.23).
It is often associated with arrhythmias (sinus tachycardia, atrial fibrillation), wide
pulse pressure, high output failure and Means-Lerman scratch, a to and fro high
pitched sound in the pulmonary area, simulating pericardial rub.23
x) Moon Face
Associated with central obesity and hirsutism is observed in Cushings syndrome12 (see
Fig. 13.24).
xi) Ape Like Appearance

Coarse features with broad nose, thick lips, prominent forehead and cheek bones,
prognathism, enlarging hands and feet, hypertrichosis, and weight gain are charcter-
istic of acromegaly (see Fig. 13.25).
Fig. 13.23 | Facial expression of

fright and anxiety
Fig. 13.24 | Moon face of Cushings
syndrome.
Fig. 13.25 | Ape like face
with borad nose
with exophthalmos in acromegaly.
in hyperthyroidism.
It is often associated with hypertension, cardiomyopathy, arrhythmias (premature

ventricular contractions, atrial fibrillation, atrial flutter, interventiclar conduction
defects), and atherosclerosis.24,25
xii) Mongoloid Facies

Broad flat nose, inner epicanthic folds, Brushfields spots in iris, lenticular opacities,
low set ears, large protuberant tongue, mental retardation, broad and short hands
with a single transverse palmar crease, short and incurved little fingers (clindactyly)
are charcteristic of Downs syndrome (trisomy 21) (see Fig. 13.18).
It may be associated with endocardial cushion defect26, less frequently with TOF,
ASD, PDA.27
xiii) Grotesque Facial Features

Prominent supraorbtal ridges, depressed nasal bridge, thick lips and peg shaped
teeth, corneal clouding, hepatosplenomegaly and mental retardation, seen in Hurlers
syndrome [mucopolysaccharidosis (MPS)-I, autosomal recessive inheritance ]28 due
to
iduronidase deficiency and
It is associated with CAD, AR, MR (mitral annulus calcification) and hypertrophic
cardiomyopathy.
xiv) Elfin Facies

Hypertelorism, epicanthic folds, strabismus, low set ears, depressed nasal bridge,
anomalies of dentition, hoarse voice and hypercalcemia are charcteristic of cardiofacial
syndrome II (William syndrome, see Fig. 13.26).29
It is often associated with supravalvular AS and peripheral PS.
xv) Distinctive Unilateral Lower Facial Weakness

(7th Cranial Nerve Palsy)
In cardiofacial syndrome I, seventh cranial nerve palsy is associated with VSD.
Fig. 13.26 | Elfin facies with broad flat nose in William syndrome.
xvi) Midfacial Growth Deficiency
Hypoplastic upper lip, thin or absent philtrum, short palpebral fissures, microg-
nathia and microcephaly are charecteristic of fetal alcohol syndrome.30
It is associated with VSD and ASD.
5. EYES
Eyes are examined for:
i) Hypertelorism
This refers to wide set eyes i.e. distance between the two eyes is more than the size of
one eye. It is observed in:
Noonan syndrome often associated with PS (see Fig. 13.16).
Turner syndrome often associated with coarctation of aorta.
LEOPARD (multiple lentigines) syndrome often associated with PS and HCM.
Hurler syndrome associated with arrhythmias and valvular regurgitation.
William syndrome associated with nonfamilial supravalvular AS and PS.
Klippel-Feil syndrome often associated with VSD (see Table 13.8).
ii) Exophthalmos
Exophthalmic ophthalmoplegia and staring with lid lag seen in thyrotoxicosis (see
Fig. 13.23).
Pulsatile exophthalmos31 and pulsating earlobes occur in severe TR.32
It is rarely seen in severe myopia, chronic cor pulmonale and in normal individuals
as congenital anomaly.
Table 13.8 Syndromes with cardiovascular manifestations
Cardiovascular
manifestations
1. LEOPARD Lentigines (basal cell nevi), ECG Pulmonary stenosis,

(multiple lentigenes) defects, broad facies with ocular hypertrophic cardiomyopathy,
syndrome (AD hypertelorism, growth retardation, AV blocks, left axis deviation
inheritance) deafness, genital and rib anomalies or superior axis
2. Klippel-Feil Facial asymmetry with short webbed Ventricular septal defect34
syndrome neck, low hairline, small jaw, cleft (most common, dextrocardia
palate, torticollis, scoliosis, deafness may also occur)
and strabismus
3. Kearns-Sayre Ptosis, progressive external Progressive AV block,
syndrome35,36 ophthalmoplegia, pigmentary dilated cardiomyopathy,
retinopathy, ataxia, deafness and hypertrophic cardiomyopathy
diabetes mellitus
iii) Enophthalmos
It occurs in cachexia.
iv) Nystagmus
It may be noted in Friedrichs ataxia33 (autosomal recessive inheritance of spinocerebel-
lar degeneration) which is associated with kyphoscoliosis, HCM, SA node artery
occlusion and arrhythmias.
v) Eye Lids
Examine lids for:
Lid lag with other signs in hyperthyroidism.
Ptosis: It is often associated with external ophthalomoplegia, pigmentary retinopathy,
myocardial diseases and complete heart block in Kearns-Sayre syndrome (see Fig.
13.27). Ptosis also occurs in Klippel-Feil syndrome and multiple lentigines syndrome.
Xanthelasma (soft yellowish nodules of cholesterol) near inner canthus in dyslipidemia
(other signs of dyslipidemia include: corneal arcus, xanthomas and heptosplenomegaly)
which often leads to atherosclerotic CAD (see Fig. 13.28).
vi) Conjunctiva
It is examined for pallor, cyanosis, inflammation and presence of any petechial
hemorrhages.
Pallor of anemia
Suffusion of cyanosis
Petechiae (lower eye lid)/subconjuctival hemorrhages in infective endocarditis
(see Fig. 13.29).
Fig. 13.27 | Ptosis in Kearns- Fig. 13.28 | Xanthelasma (with left eye cataract).
Sayre syndrome.
Fig. 13.29 | Petechiae

endocarditis.
in infective Fig. 13.30 | Blue sclera in osteogenesis imperfecta.
Conjunctivitis with arthritis and urethritis observed in Reiters disease, which is

associated with pericarditis37 and abnormal AV conduction38 in acute stage and AV
block and AR in chronic stage.
vii) Sclera
It is examined for:
Jaundice or icterus, which is observed in CHF, large pulmonary infarct, hemolysis
due to prosthetic valves, sometimes in calcified valves.
Blue sclera noted in osteogenesis imperfecta (see Fig. 13.30 and Table 13.10), Marfan
synfrome, Ehlers-Danlos syndrome, and may also be familial.
viii) Cornea
Examine cornea for clouding and arcus.
Corneal arcus (or arcus juvenalis) is one of the signs of dyslipidemia. It is a well
defined yellowish white ring in the outer margin of the cornea (see Fig. 13.31).
Fig. 13.31 | Corneal arcusa well-defined yellow white Fig. 13.32 | Arcus senilisan ill grayish white
ring is seen in elderly individuals.
ring, one of the signs of dyslipidemia.
Table 13.9 Mucopolysacharidosis (MPS) and cardiovascular manifestations
Cardiovascular
manifestations
1. MPS II-Hunter X-linked due to idurate sulfatase deficiency, Similar to Hurler

syndrome28 grotesque (coarse) facies, clear cornea, syndrome
growth and mental retardation
2. MPS IV-Morquios Autosomal recessive inheritance due to Aortic regurgitation
disease39 N-acetyl-galactoseamine-6-sulfatase
deficiency, short trunk dwarf, coxa valga,
cloudy cornea, normal intelligence
3. MPS VI-Maroteaux- Due to arylsulfatase B deficiency, coarse Aortic regurgitation and
Lamy syndrome40 facies, cloudy cornea, multiple skeletal dilated cardiomyopathy
changes and normal intelligence (AS, MR or MS are less
common)
Arcus senilis is an ill defined grayish white crescent or rarely circle in the outer mar-
gin of the cornea due to degenerative condition of the cornea often associated with
old age (see Fig. 13.32).
Corneal clouding is observed in Hurler syndrome, type IV and VI mucopolysachari-
dosis (see Table 13.9) but clear cornea is seen in Hunter syndrome.
ix) Iris
Iris is examined for spots and fissures.
(i) Brushfields Spots

It is grayish white spots at the periphery of the iris, but well appreciated in dark pig-
mented iris are characteristic of Downs syndrome (see Fig. 13.33).
Fig. 13.33 | Brushfileds spots in the iris Fig. 13.34 | Colobomamay be associated with complex
congenital heart diseases such as TOF, TAPVC
(arrows)characteristic of
Down syndrome. or VSD.
Table 13.10 Syndromes with cardiovascular manifestations
Cardiovascular
manifestations
1. Ehlers-Danlos Hyper extensible and fragile skin with poor wound Arterial dilatation and
syndrome42 healing, cigarette paper scarring, hyper extensible rupture, AR or mitral
(type I to IV) joints, hyper mobile ears (lop ears), scoliosis, valve prolapse
umbilical and diaphragmatic hernias
2. CHARGE Coloboma, congenital heart disease, TOF, conotruncal
syndrome43 choanal atresia, retarded growth, genital anomalies
hypoplasia, ear anomalies
3. Osteogenesis Brittle bone disease (severe osteoporosis,
imperfecta bone fragility, repeated fractures, bowing of long AR,44 aortic root
(autosomal bones), short stature, deafness, blue sclerae and dilatation,45 MR46
dominance angiod streaks in the retina. Blue sclera is due to
inheritance) thinness of the collagen layers of the sclera that
allow the choroids layers to be seen
(ii) Congenital Coloboma

It is (fissures of iris) (which change the pupillary shape from normal circular to oblong
giving an appearance of cat eye)
Noted in cat eye syndrome41 (chromosomal trisomy or tetrasomy 22) in which 50%
of the affected patients may be associated with complex congenital heart diseases
such as TAPVC, VSD, TOF (see Fig. 13.34).
Coloboma also occurs in CHARGE syndrome, which is associated with conotruncal
anomalies or TOF (see Table 13.10).
Fig. 13.35 | Premature cataract may be associated with

cardiomyopathy.
Fig. 13.36 | Upward subluxation of lens in
Marfan syndrome.
x) Pupils
Pupils are examined for the presence of Argyll Robertson pupil (small irregular unequal
pupils with absent light reflex but sparing accommodation and convergence) which is
noted in neurosyphilis and may be associated with cardiovascular lesions such as AR.
xi) Lens
Lenses are examined for cataracts and for dislocation.
(i) Premature Cataracts

These are noted in:
Myotonic muscular dystrophy (which is associated with cardiomyopathy, see
Fig. 13.35).
Refsums disease47 (autosomal recessive inheritance due to
hydroxylase deficiency
and is associated with cerebellar ataxia, deafness, peripheral neuropathy, retinitis
pigmentosa and dilated cardiomyopathy and/or hypertrophic cardiomyopathy),
Werners syndrome (associated with premature coronary atherosclerosis) and
Rubella (1st trimester infection and may be associated with congenital heart disease,
especially PDA).
(ii) Subluxation of the Lens

Upward lens dislocation in Marfan syndrome (see Fig. 13.36) and
Downward lens dislocation in homocystinuria (which may be associated with arte-
rial and venous thrombosis, myocardial infarction or pulmonary embolism).
xii) Retina
Fundus examination is helpful for diagnosis (coarctation of aorta, infective endocardi-
tis) and prognosis of the cardiovascular conditions (hypertension) (see Table 13.11
and Fig. 13.37). The cotton wool spots are usually found around the optic disc,
Table 13.11 Fundus examination in patients with cardiovascular manifestations
Findings Disease
1. Hypertensive retinopathy Hypertension

2. Arteriosclerotic retinopathy Atheroclerosis
3. Wreathlike AV anastomosis Takayasus disease
4. Corkscrew tortuous retinal arteries Coarctation of aorta
5. Roth spots Infective endocarditis
6. Papilledema Malignant hypertension
7. Angiod streaks Pseudoxanthoma elasticum
Fig. 13.37 | Normal fundus.

Table 13.12 Helpful guidance for fundus examination
Lesions Most common site in the retina
1. Arteriovenous crossings Upper temporal quadrant

2. Cotton wool spots Around the optic disc
3. Hard exudates Between the disk and fovea
4. Microaneurysms Temporal to fovea
5. Emboli Arterial bifurcation
6. Diabetic new vessels Nerve head and arcades
microaneurysms temporal to the fovea and new vessels around the nerve head (see
Table 13.12). Fundus examination is done for:
(i) Hypertensive retinopathy: The duration and severity of hypertension can be
judged from fundus examination. Hemorrhages and exudates are described in
grade 3 fundus changes, while the presence of papilledema indicates grade 4
fundus changes (see Fig. 13.38 and Table 13.13).48
(ii) Arteriosclerotic retinopathy: Similarly the state of arteriosclerotic changes can be
determined from fundus examination. The occurrence of copper wire and silver
wire indicates grade 2 and 3 fundus chages respectively (see Table 13.14).48
(iii) Wreath-like AV anastamosis around the disc, characteristic of Takayasus disease.
Fig. 13.38 | Hypertensive retinopathycharacteristic flame shaped hemorrhages and

cotton wool exudates (arrow).
Table 13.13 Hypertensive retinopathy (Keith-Wagener-Barker classification)48
Arteriolar/venous
Focal spasm (ratio
Degree/ diameter ratio
of region/proximal Hemorrhages Exudates Papilledema
severity (narrowing of
arterioles diameter)
arterioles)
Normal 3:4 1:1 0 0 0

Grade I 1:2 1:1 0 0 0
Grade II 1:3 2:3 0 0 0
Grade III 2:3 1:3 0
Grade IV Fine fibrous cords Obliteration of distal flow
Table 13.14 Fundus in arteriosclerosis (Keith-Wagener-Barker classification)48
AV crossing defects (arteriolar length

Degree/severity Arteriolar light reflex
and tortuosity increase with severity)
Normal Fine yellow line, red blood column 0

Grade I Broadened yellow line, Mild depression of vein
red blood column
Grade II Broad yellow line, copper wire, Depression or hump of vein
blood column not visible
Grade III Broad white line, silver wire, Right angle deviation, tapering and
blood column not visible disappearance of vein under arteriole
Grade IV Fibrous cords, blood column Same as grade III and distal dilatation
not visible of vein
(iv) Cork-screw tortous retinal arteries with no changes of hypertensive retinopathy

seen in coarctation of aorta (see Fig. 13.39).
(v) Roth spots (retinal hemorrhages with pale centers near the disc, (see Fig. 13.40).
These are seen due to perivascular collections of lymphocytes in the nerve layer
of the retina, and are observed in 410% of infective endocarditis patients.

Fig. 13.39 | Cork-screw retinal arteries in

coarctation of aorta.
Fig. 13.40 | Roth spotsretinal hemor-
rhages with pale centers.
It is considered as one of the minor diagnostic criteria (immunological phe-

nomenon), but can be found in leukemia and anemia.49
(vi) Large retinal veins
These extend to the periphery due to the increased red cell mass and are occa-
sionally associated with papilledema and retinal edema (in response to low
systemic arterial O2 saturation).
These are observed in cyanotic congenital heart disease.
(vii) Papilledema (grade 4 changes, see Fig. 13.41) may be seen in:
Severe hypertension (malignant hypertension) and
Chronic severe cor-pulmonale
(viii) Embolic retinal occlusions may occur in patients with:

Rheumatic heart disease, left atrial myxoma and atherosclerosis of aorta or
arch vessels.
Calcific emboli are white, dull and near the optic disc.
Cholesterol emboli (Hollen horst plaques) are yellowish white and are highly
refractile (see Fig. 13.42).

Fibrin platelet emboli appear as whitish plugs that are sometimes seen moving
through the retinal arteries.

(ix) Angiod streaks (reddish brown lines, which are wider than retinal vessels and
radiate from the optic disc) are observed in:
Pseudoxanthoma elasticum:
50
There are raised yellowish papules (pseudox-
anthoma) on the skin of neck, groin, cubital and popliteal fossae and the skin
is also associated with premature calcification of systemic and coronary arteries,
systemic hypertension, and retinal artery involvement.
Pagets disease of the bone which is often associated with high output failure.
Sickle cell anemia, which is associated with pulmonary hypertension and
occlusion of small intracardiac arteries.

Osteogenesis imperfecta.
Fig. 13.41 | Papilledema. Fig. 13.42 | Retinal embolicholesterol emboli.
6. NOSE
Broad flat nose is a part of facial dysmorphism and is observed in Cornelia de Lange
syndrome, Down syndrome, Williams syndrome and Hurlers syndrome (see Tables
13.15 and 13.16 and Fig. 13.26).
Broad nose is seen in acromegaly (see Fig. 13.25).
Thin beaked nose is seen in Rubinstein Taybi syndrome.
7. EARS
Examine ears for distorted shape, low set ears and for the ear lobe crease (see Table 13.16).
i) Ear Lobe Crease

Individuals with ear lobe crease (i.e. a crack in the pinna, Frank sign) more frequently
have CAD51 (see Fig. 13.43).
ii) Cauliflower (Floppy) Ear
It is seen in polychondritis which is associated with arthritis, saddle shaped nose, and
cardiovascular manifestations such as pericarditis (in 30%), AR and TR (in 12%)52
(see Fig. 13.44).
iii) Low Set Ears

If 1/3rd of the ear lobe present above a line drawn from the outer canther of each
eye. It is a part of facial dysmorphism which is often associated with cardiovascular
manifestations. Low set ears are common in:
Noonan syndrome (see Fig. 13.45),
Turner syndrome,
Table 13.15 Syndromes and CV manifestations
Cardiovascular
manifestations
1. Cornelia de Short stature, hirsutism, bushy eye brows, downward VSD

Langes slanting eyes, long eye lashes, low set ears, broad Others: PDA, ASD,
syndrome flat nose, growth and mental retardation, phocomelia, PS, anomalous
and a single thumb like digit (chicken-wing extremity) venous return
2. Rubinstein Broad thumbs and toes, slanting palpebral PDA, VSD
Taybi fissures, thin beaked nose, large low set ears,
syndrome53 short stature and microcephaly
Table 13.16 Ear, nose and teeth abnormalities and syndromes with cardiovascular manifestations
Ear abnormalities Nose abnormalities Teeth abnormalities
1. Low set ears: 1. Broad flat nose: 1. Peg shaped teeth:

i. Noonan syndrome i. Down syndrome i. Hurlers syndrome
ii. Turner syndrome ii. Williams syndrome ii. Williams syndrome
iii. Klippel-Feil syndrome iii. Cornelia de Langes syndrome iii. Congenital syphilis
iv. Down syndrome iv. Hurlers syndrome
v. Cornelia de Langes syndrome
vi. Rubinstein-Taybi syndrome
2. Deformed ears: 2. Broad nose: 2. Widely spaced teeth:
Polychondritis Acromegaly i. Morquios syndrome
ii. Acromegaly
3. Ear lobe crease: 3. Thin beaked nose: 3. Malformed teeth:
CAD Rubinstein-Taybi Non hereditary form of
syndrome supravalvular AS with PS
Fig. 13.43 | Ear lobe crease (Frank sign)

more prone to coronary artery
Fig. 13.44 | Cauliflower ear.
disease.
Fig. 13.45 | Low set ears and hypertelorism in Noonan syndrome.

Klippel-Feil syndrome,
Downs syndrome,
Cornelia de Langes syndrome, and
Rubinstein-Taybi syndrome (see Table 13.15).
iv) Deafness
It is associated with Turners syndrome, Klippel-Feil syndrome, Rubella and multiple
lentigines syndrome.
8. ORAL CAVITY
i) Lips
Examine for pallor, cyanosis, thickening, fissures and capillary pulsations.
Pallor of anemia.
Cyanosis is detected early except in dark-skinned individual and in those using cos-
metics.
Thick lips noted in Hurler syndrome, acromegaly, myxedema and cretin.
Absent philtrum seen in fetal alcohol syndrome (see Fig. 13.46).
Capillary pulsations can be observed by gently pressing a slide on the mucous
membrane of the lips, which is noted in AR (Quinkes sign).

Other sites of demonstration of capillary pulsations:
By rubbing the skin of the forehead and observing the alternate blushing and
blanching of the hyperemic area.
Gentle pressure is applied at the tip of the nail and the nail bed is observed for a
rhythmic flush.
Transilluminate the ear tip, finger or thumb tip by a torch light.
Rhagades are ulcerative fissures at the angles of the mouth. These are observed in
congenital syphilis (see Fig. 13.47) and need to be differentiated from angular stom-
atis of riboflavin deficiency (see Fig. 13.48).
Fig. 13.46 | Absent philtrum Fig. 13.47 | Rhagades, saddle-nose

and interstitial keratitis
Fig. 13.48 | Angular stomatis and
glossitis in riboflavin
in feotal alcohol
syndrome. in congenital syphilis. deficiency.
ii) Mucous Membrane

It is examined for petechiae and telangiectasia.
(i) Petechiae occur in infective endocarditis.
(ii) Clusters of small ruby patches are telangiectasia present on lips, mucous mem-
brane, palate tongue and fingertips in Osler-Rendu-Weber syndrome,54 which
may be associated with:
Arteriovenous fistulas in lungs (which may result in hyperdynamic circulation,
hemoptysis, hypoxemia, polycythemia, clubbing, paradoxical emboli through

right to left shunt).
And less commonly in liver, brain and kidneys.
iii) Teeth
Examine teeth for dentition, malformation and for wide spacing (see Table 13.16).
(i) Delayed dentition occurs in cretins, mongolism and rickets.
(ii) Malformed and premature dentition at birth with gingival hypertrophy, lip tie
and multiple frenulums observed in Ellisvan Crevald sydrome.9
(iii) Peg shaped teeth occur in:
Hurler syndrome
Williams syndrome (see Fig. 13.49) and
Characteristic of Hutchinsons teeth (upper central permanent incisors are peg
shaped or rounded; interstitial keratitis, deafness and Hutchinsons teeth com-

plete the diagnostic triad of congenital syphilis, see Fig. 13.50).
(iv) Malformed teeth erupt in nonhereditary form of supravalvular AS with PS.
(v) Widely spaced teeth may be seen in:
Acromegaly
Morquios syndrome and
Williams syndrome.
Fig. 13.49 | Small and widely spaced teeth in Fig. 13.50 | Hutchinsons
syphilis.
teeth in congenital
Williams syndrome.
iv) Gums
Look for cyanosis and gum hypertrophy.
Cyanosis can be appreciated in the gums.
Gingival hypertrophy can be seen in Ellisvan Crevald syndrome and phenytoin
intake (see Fig. 13.51).
v) Tongue
Examine for colour and size.
(i) Color of the Tongue

Blue tongue in cyanosis
Magenta (or dark red) tongue in riboflavin deficiency
Bright or scarlet red tongue (angry tongue) in niacin deficiency
Black tongue from fungal infection (actinomycosis)
Brown tongue may be seen in uremia and
Pale tongue in anemia.
(ii) Macroglossia
It is seen in acromegaly (see Fig. 13.52), myxedema, large protruding tongue observed
in Downs syndrome, Hurler syndrome and in cretin.
(iii) Glossoptosis (Retracted Tongue)

It occurs in Pierre Robin syndrome which is associated with shrew like face (hypoplas-
tic mandible, high arch/cleft palate) and VSD.
vi) Palate
It is examined for cleft/perforation and for the presence of high arched palate.
Fig. 13.51 | Gum hypertrophy in phenytoin intake. Fig. 13.52 | Macroglossia in acromegaly.
Fig. 13.53 | Perforated palate in tertiary syphilis. Fig. 13.54 | Cleft palate in velo cardiofacial syndrome.
High arched palate observed in Marfan syndrome, and Pierre Robin syndrome.
Cleft/perforated palate may be due to tertiary syphilis (see Fig. 13.53), velocardio-
facial syndrome (see Fig. 13.54) and tuberculosis.
9. NECK
Examine neck for low hair line, short and webbed neck (see Table 13.17), lymphadenopa-
thy, thyromegaly and for any parotid gland enlargement.
i) Short Neck
The ratio of height to the distance between external occipital protuberance and C7
spinous process (Birds index): 12.8 is normal, while 13.6 indicates short neck,
which is seen in:
Klippel-Feil syndrome
Morquios syndrome (MPS IV).
Table 13.17 Neck abnormalities and low hair line in syndromes with cardiovascular manifestations
Short neck Webbed neck Low hair line
1. Klippel-Feil syndrome 1. Noonan syndrome 1. Noonan syndrome

2. Morquios syndrome 2. Turner syndrome 2. Turners syndrome
3. Edwards syndrome 3. Klippel-Feil syndrome
4. Cornelia de Langes syndrome
Fig. 13.55 | Webbed neck in Turner syndrome.
ii) Webbed Neck

Noted in:
Noonan syndrome
Turners syndrome (see Fig. 13.55)
Trisomy 18 (Edwards) syndrome55 which is characterized by a small triangular
mouth with receding chin, small mandible, clenched hand (tightly clenched fist
with index finger overlapping 3rd finger and 5th over the 4th finger), low arch dermal
ridge pattern on finger tips, short sternum, rocker bottom feet and mental retardation
besides webbed neck. It is associated with VSD, PDA and poly-valvular dysplasia.
iii) Low Hair Line

When the posterior hairline extends below the level of C5 spinous process or the ratio
of the distance from the external occipital protuberance to the hair line and the dis-
tance from the hair line to C7 spinous process is 1/6 in males and 1/4 in females,
it is defined as low hair line which is observed in
Noonan syndrome (see Fig. 13.17)
Turner syndrome
Klippel-Feil syndrome
Cornelia de Langes syndrome.
Fig. 13.56 | Thyromegaly in goiter. Fig. 13.57 | Parotid enlargement in mumps.
iv) Lymphadenopathy
Cervical lymphadenopathy may be due to:
Tuberculosis
Syphilis
Sarcoidosis.
v) Thyromegaly
It may be due to thyrotoxicosis (see Fig. 13.23) or goiter (see Fig. 13.56).
vi) Parotid Enlargement

It occurs in mumps, which may be associated with myocarditis (see Fig. 13.57).
10. SPINE
Normally, there is a mild convexity (kyphosis) of thoracic spine, a mild concavity of

cervical spine and a definite concavity (lordosis) of lumbar spine without any lateral
curvature (scoliosis) (see Table 13.18). Examine the spine for scoliosis and loss of
thoracic kyphosis and lumbar lordosis.
Kyphoscoliosis, pectus excavatum and pectus carnitum are observed in Marfan
syndrome.
Loss of thoracic kyphosis (resulting in straight back) (best observed in sitting pos-
ture) with a decrease in the anteroposterior chest dimensions results in parasternal
systolic impulse and a pulmonary mid systolic murmur mimicking ASD.
Ankylosing spondylitis56 is a seronegative spondyloarthropathy characterized by
progressive inflammation of spine leading to chronic backache, deforming dorsal
kyphosis and in advanced stage, there is a fusion of the costovertebral and sacroiliac
Table 13.18 Spine abnormalities in diseases

with cardiovascular manifestations
1. Marfan syndrome
2. Ankylosing spondylitis
3. Straight back syndrome
Fig. 13.58 | X-ray of spineshowing

ankylosing spondylitis.
Fig. 13.59 | Scoliosis with convexity to the
right.
joints with immobilization of the spine (see Fig. 13.58). It may be associated with
HLA-B27 histocompatibility antigen and AR (in 10%) and the extension of inflam-
mation results in MR and complete heart block.
Functional scoliosis disappears on bending forward while structural scoliosis persists
and is associated with the rotation of the vertebral bodies and with the systolic
murmurs, which may lead to faulty diagnosis.
Minor degrees of scoloisis can be better identified with chest X-ray.
Scoliosis with convexity to the left is usually due to poliomyelitis or neuro-muscular
diseases while the structural changes in the spine give rise to scoliosis with convexity
to the right (see Fig. 13.59).
Angle of curvature is known as Cobb angle: More the angle, the worst is the prognosis.
11. SKIN
The skin lesions are the alphabets of systemic diseases (see Table 13.19) and should be
examined for nature, evolution and their distribution.
Table 13.19 Skin lesions in systemic diseases with cardiovascular (CV) manifestations
Skin lesions Systemic disease CV manifestations
1. Bronze pigmentation Hemochromatosis, Cardiomyopathy

2. Caf au luit spots Von Recklinghausens Pheochromocytoma
disease hypertension and myocarditis
3. Multiple lentigines LEOPARD syndrome Hypertrophic cardiomyopathy
4. Angiofibromas Tuberous sclerosis Rhabdomyoma and arrhythmias
5. Erythema marginatum Rheumatic fever Carditis
6. Janeway lesions Infective endocarditis Valvular lesions and embolism
i) Pigmentation
(i) Bronze pigmentation
Bronze pigmentation on exposed areas of the skin (due to melanin and iron
in dermis) with loss of axillary and pubic hair, hepatomegaly, DM, arthritis,
testicular atrophy and loss of libido occur in hemochromatosis.
It is associated with cardiomyopathy (restrictive or dilated) in about 15%.
(ii) Caf au luit spots (on the trunk), freckles (especially axillary: crowes sign) and
neurofibromas (on the trunk and face) occur in von Recklinghausens disease that
may be accompanied by pheochromocytoma (see Fig. 13.60).
(iii) Multiple lentigines or large wide spread freckling characteristic of LEOPARD
syndrome, which may be associated with hypertrophic cardiomyopathy especially
when the lentigines are present from the first year of life.
(iv) Angiofibromas (usually referred by a misnomer adenoma sebaceum):
These are yellow to orange red nevi of a few mm to a cm on the face (symmetrically
distributed on malar and nasal skin) and occur in tuberous sclerosis (see Fig. 13.61).
Tuberous sclerosis is characterized by autosomal dominance inheritance and
consists of triad of mental retardation, seizures and skin lesions.

Other cutaneous lesions include subungual fibromas around the finger nail,
caf au lait spots and subcutaneous nodules.

Seizures are due to intracranial hamartomatous lesions and calcification primarily
in the basal ganglia.57

The associated cardiovascular manifestations consist of rhabdomyoma,
58
Wolff-
Parkinson-White syndrome and supraventricular tachycardia.59
(v) Erythema marginatum
It is an erythematous, macular non-pruritic, non-indurated rash with pale centers
and rounded or serpiginous margins, which blanches completely on pressing,

mainly occurring on the trunk and proximal extremities but not on the face or
below elbows and knees.
It is a rare manifestation of rheumatic fever, occurring in 3% of the patients
(see Fig. 13.62).

It is induced by heat application, is non-specific and not related to rheumatic
activity.
Fig. 13.60 | Neurofibromas in von Fig. 13.61 | Angiofibromas (orange red nevi) on the face
of a patient with tuberous sclerosis.
Recklinghausens disease.
Fig. 13.62 | Erythema marginatumin rheumatic fever.

It is considered as one of the major criteria for diagnosis of rheumatic fever,60
but it is rare or difficult to visualize in dark skinned individuals (Indian sub-
continent), and could be of idiopathic etiology or could be due to drug reactions,
staphylococcus infection or nephritis.
(vi) Janeway lesions
These lesions are one of the classical signs of infective endocarditis.
They are small erythematous or hemorrhagic, non tender and non painful
macular lesions on the palms of the hands or soles of the feet due to septic
emboli, observed in 610% of the patients.
They constitute one of the minor criteria (vascular phenomena) of Dukes criteria
of diagnosis of infective endocarditis.61

(vii) Symmetric vitiligo, especially on distal extremities, is seen in Gravess disease.
ii) Skin Texture

Skin is coarse, thick and dry with brittle, sparse and coarse hair in myxedema.14
Hyperextensible and rubber like skin with cigarette paper scars (due to fragility and
poor wound healing) occur in Ehlers Danlos syndrome (see Fig. 13.63).
Fig. 13.63 | Hyperextensible

syndrome.
skin in Ehlers-Danlos
Fig. 13.65 | Palmar xanthoma producing

pink discoloration of the palm
and digital creases.
Fig. 13.64 | Grooved skin in axilla in pseudoxanthoma

elasticum.
Plucked chicken appearance/grooved skin over the neck and axillae occurs in pseu-
doxanthoma elasticum as the skin is reticular and telangiectatic with small tarnish
yellow papules (see Fig. 13.64).
Moist skin with fine silky hair and staring eyes occurs in hyperthyroidism.23
iii) Xanthomas
They are small yellowish orange papules or nodules associated with hyperlipidemias in
those patients whose premature atherosclerosis develops frequently.
(i) Tuberous xanthomas are yellowish orange papules erupting over the elbows,
knees, buttocks and heels. These are often associated with hyperlipidemia, but
can occur in myxedema and liver disorders.
(ii) Xanthoma striatum palmare
It produces yellowish, orange or pink discoloration of the palmar and digital
creases (see Fig. 13.65).
Table 13.20 Xanthomas and hyperlipidemia
Xanthomas Hyperlipoproteinemia type
1. Palmar xanthomas Type III

2. Tendinous xanthomas Type II
3. Eruptive xanthomas Types I and V
Fig. 13.66 | Achilles tendon xanthomata. Fig. 13.67 | Tendinous xanthomas over the knees.
It occurs most commonly in type III hyperlipoproteinemia (familial dysbeta

lipoproteinemia, autosomal recessive inheritance, see Table 13.20) which is due
to the elevated levels of intermediate density lipoprotein, total cholesterol and
triglycerides (300 mg/dl).
They are associated with premature atherosclerosis, diabetes mellitus, and in
turn with CAD, peripheral vascular disease and stroke.

(iii) Xanthoma tendinosum (tendinous xanthomas)
These are yellowish nodular swellings of the tendons, especially of the elbows,
extensor surfaces of the hands and Achilles tendons (see Figs 13.66 and 13.67).
They are commonly associated with type II hyperlipoproteinemia (familial
hypercholesterolemia, due to low-density lipoprotein (LDL) receptor defect,

and autosomal dominance inheritance (see Table 13.20). Heterozygous form
occurs in 1:500 population and homozygous form in 1:10).
These are characterized by elevated levels of LDL and total cholesterol but have
normal levels of triglyceride.

They are associated with corneal arcus and premature atherosclerosis.
(iv) Eruptive xanthomas

These are tiny yellowish nodules of 12mm in diameter on an erythematous
base, which frequently occur on arms, legs, thighs and buttocks (but can occur
anywhere on the body) (see Fig. 13.68).
These are usually associated with hyperchylomicronemia and hence with Type I
and V hyperlipoprotemia, DM, pancreatitis, myxedema and nephrotic syndrome

(see Table 13.20).
Fig. 13.68 | Eruptive xanthomas on the elbow.
Table 13.21 Nodules associated with cardiovascular manifestations
Nodules Disease
1. Waxy flat nodules Amyloidosis restrictive cardiomyopathy

2. SC nodules Rheumatic fever, systemic lupus erythematosis
and rheumatoid arthritis
3. Oslers node Infective endocarditis
Type I Hyperlipoproteinemia or Familial Chylomicronemia

It is due to lipoprotein lipase or apoprotein C II deficiency with autosomal recessive
inheritance.
It is characterized by increased levels of chylomicrons, triglycerides and normal to
mildly elevated total cholesterol level.
It is associated with recurrent abdominal pain, pancreatitis, hepatosplenomegaly but
not with premature atherosclerosis.
Type V Hyperlipoproteinemia or Familial Mixed Triglyceridemia

It is characterized by elevated levels of very low-density lipoproteins (VLDL), chy-
lomicron, total cholesterol and triglycerides.
It is associated with pancreatitis and possibly premature atherosclerosis.
iv) Nodules
(i) Subtle small translucent waxy flat top nodules (better visualized with hand lens).
These occur in systemic amyloidosis, which may be associated with restrictive car-
diomyopathy and conduction defects. They are usually clusterd in the folds of
axillae, anal or inguinal regions, face and neck, ear or tongue (see Table 13.21).
(ii) Subcutaneous nodules:
These are firm painless freely movable nodules of 0.52 cm size seen in about
3% of rheumatic fever patients with carditis.

Fig. 13.69 | Rheumatic nodules over the knuckles Fig. 13.70 | SC nodules over the elbow.
of the hand.
Fig. 13.71 | SC nodules on the occipital protu-

berance in a rheumatic fever.
Fig. 13.72 | Rheumatic nodules over the spinous
process of thoracic vertebrae.
They are located over the extensor surfaces of the joints (on the tendons of the
extensors of the fingers and toes and flexors of the wrist and ankle, see Figs 13.69
and 13.70), on the occipital protuberance (see Fig. 13.71), or over the spinous
processes of thoracolumbar vertebrae (see Fig. 13.72).
They occur in crops, and are symmetrical in distribution (when in large number).
They heal without scar formtion and last for 12 weeks, rarely one month.
SC nodules are considered as one of the five major criteria for the diagnosis of
rheumatic fever;60 however, they can also occur in rheumatoid arthritis and SLE.
(iii) Oslers nodes
Oslers nodes are small, tender subcutaneous nodules on the pads of fingers or
toes and palms or soles, seen in 710% of infective endocarditis (see Fig. 13.73).
They occur due to the deposits of immune complex in mucocutaneous vessels
and infected microemboli.

They constitute one of the minor criteria (immunological phenomena) of
Dukes criteria of the diagnosis of infective endocarditis.61

Fig. 13.73 | Oslers node in infective endocarditis (arrow mark).

(iv) Peripheral emboli: Emboli from prosthetic valve, LV mural thrombus or marantic
endocarditis occur on the tips of fingers and toes as small tender, painful areas that
suddenly become pallid or cyanotic.
v) Cyanosis, Icteru, and Pallor

(i) Cyanosis: See chapter 12.
(ii) Icterus: Yellowish discoloration of skin, mucous membrane and sclerae is due to
the deposition of bilirubin (see also sclera).
(iii) Pallor of the skin and mucous membrane is often due to anemia, and sometimes
due to:
The accumulation of myxematous substance in the skin as in myxedema
Could be racial as in Chinese or
Occupational as in radium or lead workers.
12. EXTREMITIES
Varieties of congenital and acquired cardiac malformations are associated with charac-
teristic changes in the extremities including digits.
i) Digits
Examine for:
(i) Arachnodactyly: (spider fingers)
Unduly long and thin fingers and toes with positive wrist (Walker-Murdock)
and thumb (Steinberg) signs are characteristics of Marfan syndrome (see

Figs 13.74 and 13.75).
In sickle cell anemia, bones of hands and feet (especially in young adults) are elon-
gated with increased metacarpal index (MCI, a pseudo-Marfan syndrome sign).

Fig. 13.74 | Arachnodactyly and wrist (Walker- Fig. 13.75 | Thumb (Steinberg) sign in Marfan
syndrome.
Murdock) sign in Marfan syndrome.
Fig. 13.76 | Polydactyly, syndactyly, and clindactyly in

Ellis-van Creveld syndrome. Fig. 13.77 | Polydactyly in Laurence-Moon-
Biedl syndrome.
Arachnodactyly is assessed by the ratio of the middle finger length to the total
hand length or radiologically by the metacarpal index.62
Metacarpal index (MCI) (In L/WMi L/WRi L/WLi L/W)4
Postivie if MCI is 8.4 In index finger, Mi middle finger, Ri ring finger,
Li little finger, L length of the bone, W width of the bone.
(ii) Polydactyly is the presence of extra or supernumerary fingers or toes which may
be familial or associated with Ellis-van Creveld syndrome, Laurence-Moon-Biedl
syndrome (see Figs 13.76 and 13.77).
(iii) Syndactyly (webbed fingers): Fusion between the adjacent fingers or toes may be
dermal or osseous and etiology is similar to that of polydactyly.
(iv) Clindactyly: (incurved fingers)
th
Clindactyly of little finger, with increased space between 4 and 5th fingers is
seen in Down syndrome.
Fig. 13.78 | Fingerized thumb in Holt-Oram syndrome.
Table 13.22 Abnormal thumbs and cardiovascular manifestations
Abnormal thumbs Disease
1. Fingerized thumbs Holt-Oram syndrome

2. Single thumb like digit Cornelia de Lange syndrome
3. Broad thumbs Rubinstein-Taybi syndrome
Clindactyly of 4th and 5th fingers resulting in a claw like appearance of hands
also occurs in Hurlers syndrome.
(v) Fingerized thumbs
Thumb with an extra phalanx (triphalangeal thumb) lies in the same plane as
rest of the fingers which makes it difficult to appose with the fingers, a charac-
teristic of Holt-Oram syndrome63 (see Fig. 13.78).
Other manifestations include radial aplasia, hypoplasia of clavicles and shoulders,
phocomelia and mental retardation that is inherited by autosomal dominance.

It is associated with ASD, VSD and conduction defects.
(vi) Single thumb like digit (chicken wing extremity) occurs in Cornelia de Lange
syndrome (see Table 13.22).
(vii) Broad thumbs and toes are seen in Rubinstein-Taybi syndrome (see Figs 13.79,
13.80 and Table 13.23).
(viii) Brachydactyly is the presence of shortened fingers, which results in short hands.
Broad and short hands are noted in Down syndrome.
Short and trident hands of achondroplasia: The middle finger is not longer
than the others (i.e. fingers are of equal length) and fingers are divergent like
the spokes of a wheel.
Brachydactyly due to shortened 4
th
metacarpal occurs in Turner syndrome.
Shortened fingers due to the absence of one of the phalanges occur in pseudo-
hypoparathyriodism (autosomal dominance inheritence).

Fig. 13.79 | Broad thumbs in Rubinstein-Taybi syndrome.
Fig. 13.80 | Broad toes in Rubinstein-Taybi syndrome.

Table 13.23 Abnormal digits and diseases with cardiovascular manifestations
Digits description Disease
1. Arachnodactyly Marfan syndrome

2. Polydactyly Ellis-van Creveld and Laurence-Moon-Biedl syndromes
3. Syndactyly Ellis-van Creveld and Laurence-Moon-Biedl syndromes
4. Clindactyly Down, Ellis-van Creveld and Hurlers syndromes
5. Brachydactyly Down and Turner syndromes, hyperparathyroidism
6. Sclerodactyly Scleroderma
Fingers appear stubbed with bulbous ends due to the collapse of the distal pha-
langes in hyperparathyroidism.
(ix) Clenched hand with index finger overlapping the 3rd finger and 5th overlapping
the 4th finger, is seen in Edwards syndrome (Trisomy 18).
(x) Phocomelia (limb without hand, like flipper) may be associated with Holt-Oram
syndrome and Cornelia de Lange syndrome (see Fig. 13.81).
Fig. 13.81 | Phocomelia in Cornelia de Lange Fig. 13.82 | Raynauds phenomenon with peripheral
cyanosis and digital ulcers.
syndrome.
Fig. 13.83 | Sclerodactyly in scleroderma.

(xi) Raynauds phenomenon
It is defined as episodes of white blue color changes of the digits (fingers
more often involved than toes while thumbs are often spared) followed by reactive
hyperemia (ruber) during recovery, and often induced by cold or emotional
stimuli (see Fig. 13.82).
The recovery time is usually 310 min but can exceed 1h in advanced cases,
especially of secondary origin.

Raynauds phenomenon is sometimes seen in primary pulmonary hypertension.
It is also an early manifestation of progressive systemic sclerosis (scleroderma) and

CREST syndrome (calcinosis, Raynauds phenomenon, esophageal dysmobility,
sclerodactyly (see Fig. 13.83), and telangiectasia).
(xii) Sclerodactyly
Sclerodactyly is tightening of the skin of the fingers with hair loss and disappear-
ance of subcutaneous tissue and skin creases, with the development of flexion con-
tractures leading to claw hand deformity which is characteristic of scleroderma.64
Proximal nail fold

Nail plate
Lateral nail fold
Nail bed
Nail plate
Lunule Cuticle
Cuticule
Nail matrix
Proximal
nail fold
Fig. 13.85 | Structure of the nail-lateral view.
Fig. 13.84 | Normal structure of the nail-dorsal view.
Table 13.24 Abnormal nails and cardiovascular manifestations
Abnormal nails Disease
1. Nail stripes Chronic constrictive pericarditis

2. Dysplastic nails Ellis-van Creveld syndrome
3. Plummer nails Hyperthyroidism
4. Square/broad nails Acromegaly, cretin
5. Koilonychias Iron deficiency anemia
6. Clubbing Cyanotic congenital heart disease,
infective endocarditis, myxoid tumor
Tightening of the skin (scleroderma) may also extend to hands, forearms,

upper chest and face.
It is often associated with myocardial fibrosis (see Table 13.23).
ii) Nails
Normally, nail consists of proximal nail fold, cuticle, lunule, nail plate and lateral nail
fold (see Figs 13.84 and 13.85). Examine nails for (see Table 13.24):
Cyanosis: See symptomatology, chapter 12.
Tuft erythema of the finger tips. It is a minor variation in the theme of cyanosis,
which sometimes precedes cyanosis in patients with small or intermittent right to
left shunts (see Fig. 13.86).
Nail stripes: Alternating dark and light lines parallel to the tips of the nails occur in
chronic constritive pericarditis (due to protein losing enteropathy). Nail strips are
more common in Laennecs cirrhosis.
Dysplatic nails occur in Ellis-van Creveld syndrome (see Fig. 13.87).
Plummers nail is onycholysis (separation of nail from nail bed) and occurs in hyper-
thyroidism or trauma. Onycholysis is also a classic feature of psoriasis (see Fig. 13.88).
Square or broad nails: These occur in acromegaly (see Fig. 13.89) and cretinism.
Koilonychia are spoon shaped nails (see Fig. 13.90). They occur when the normal trans-
verse convex curvature of the nail plate becomes flattened or concave, a characteristic
Fig. 13.87 | Brachydactyly and dysplastic nails in Ellis-van

Creveld syndrome.
Fig. 13.86 | Tuft erythema of the fin-
gertips in a patient with a
small right-to-left shunt.
Fig. 13.88 | Onycholysis in psoriasis. Fig. 13.89 | Broad nails in acromegaly.

of iron deficiency anemia which in turn may cause heart failure (high output) when
Hb levels are 5 gm%.
Splinter (subungual) hemorrhages are one of the non-specific signs of infective
endocarditis, as trauma can also produce them (see Fig. 13.91).
Capillary pulsations (Quinkes sign): It is seen in AR (see lips for methods of
demonstration).
Clubbing of fingers and toes (Hippocratic fingers): Clubbing is probably due to
hypervascularity and opening of the anastomotic channels in the nail bed, which
increases the hydrostatic pressure in the capillaries and venules promoting intersti-
tial edema and hypertrophy of the soft tissue (see Fig. 13.92).
The stages and severity of the clubbing can be divided into 4 grades:
Grades of Clubbing
Grade 1 clubbing is characterized by an increased glossiness and cyanotic tinge of the
skin at the root of the nails.
Fig. 13.90 | Koilonychia.
Fig. 13.91 | Splinter

carditis.
hemorrhages in infective endo-
Fig. 13.92 | Clubbing of a finger compared with a
normal digit.
Grade 2 clubbing: The normal angle of the nail bed (120 160 140) is lost and
may exceed 180 with hypertrophy of the subungual tissue and freely floating root i.e.
increased ballotability or fluctuation of the nail on its bed.
Obliteration of the angle is demonstrated by:

(i) Profile sign: by viewing the side of the flexed distal index or thumb (see Fig. 13.93).
(ii) Schamroths window test: In normals when both two fingers are placed in appo-
sition, there is a lozenge shaped gap between the nails, while in clubbed fingers
there is a reduction in this gap (see Fig. 13.94).
Fluctuation of nail on its bed: Palpate the dorsum of the finger immediately proximal
to the base of the nail with both index and middle fingers. A sensation of fluctuation
or rocking movement can be detected. However; in the presence of marked fluctua-
tion, palpation of the nail itself may give the impression of nail floating on its bed.
L R L R
Normal nail Clubbed nail
Fig. 13.93 | Profile sign in a clubbed

pared with a normal digit.
finger com- Fig. 13.94 | Schamroths window testL: left,
R: right hand digits.
Fig. 13.95 | Parrot beak like clubbing. Fig. 13.96 | Drumstick clubbing with cyanosis.
Grade 3 clubbing
It is characterized by grade 2 changes and increased curvature of the nails in both
planes resulting in parrot beak (see Fig. 13.95) or watch glass like clubbing or
Grade 2 changes, increased curvature of the nails and excessive swelling of the finger
ends resulting in drumstick clubbing (see Fig. 13.96) or serpent head deformity, which
is also known as Hippocratic fingers and is often associated with cyanosis.
Grade 4 clubbing or hypertrophic osteoarthropathy: It is a severe form of clubbing,
characterized by clubbing of the nails and bony changes in the terminal digits, which
may rarely extend to wrists and elbows, ankles and knees (see Fig. 13.97).
In early stages, it is radiologically demonstrated by thickening of the periostium of
the radius, ulna, tibia and fibula or subperiostal new bone formation.
Causes of Clubbing
(i) Cardiovascular causes:
Cyanotic congenital heart disease: TOF, TGA, Tricuspid atresia, TAPVC
Infective endocarditis (within a few weeks of IE)
Acyanotic congenital heart disease: Myxoid tumor.

Fig. 13.97 | Grade IV clubbingclubbing of the nails with bony changes extending into
the wrists and ankles.
(ii) Pulmonary diseases with hypoxia:

Bronchiectasis
Chronic fibrosing alveolitis
Emphysema
Empyma
Lung abscess
Bronchogenic carcinoma
Pulmonary tuberculosis.
(iii) GIT causes:

Crohns disease
Ulcerative colitis
Polyposis of the colon
Biliary cirrhosis.
(iv) Harmless familial condition.
Unilateral Clubbing of Fingers

It is rare and can occur in:
Aortic aneurysm (and aneurysm of its branches) that interferes with arterial supply
to one arm
It is also observed in brachial arteriovenous fistula
Pan coast tumors
Erythromelalgia and
Lymphangitis.
Subungual fibromas of the fingers which in tuberous sclerosis may be mistaken for
unilateral clubbing of the fingers.
Unidigital clubbing
It may occur due to various factors:
Hereditary if bilateral and involves the thumbs
Median nerve injury
Tophaceous gout
Sarcoidosis, or
Trauma.
Differential Clubbing
Toes may be clubbed (independent of the fingers) in PDA with reverse shunt.
iii) Feet
Examine feet for:
(i) Pes cavus (claw foot)
Pes cavus is the exaggeration of the longitudinal arch of the foot resulting in a
marked upward convexity of the instep and drawing up of the toes (see Fig. 13.98).
It occurs in Friedrichs ataxia (see Fig. 13.99), muscular atrophy (peroneal) and
poliomyelitis.
(ii) Rocker bottom foot due to protruding heel is characteristic of Edward syndrome
(see Fig. 13.100).
(iii) Bow-legs (genu varum): Outward bowing of the legs with the knees wide apart
(see Fig. 13.101), is seen in:
Achondroplasia and osteogenesis imperfecta
Fig. 13.98 | A:C: normal,

flat foot.
B: claw and
Fig. 13.99 | Pes cavus in Friedrichs ataxia.
Fig. 13.100 | Rocker bottom foot in Edward syndrome.
Fig. 13.101 | Genu varum. Fig. 13.102 | Sabre tibiae in congenital syphilis.
Rickets and osteomalacia

Sabre tibiae (bowing of the tibiae) are seen in congenital syphilis (see Fig. 13.102),
and can also be seen in rickets, osteomalacia and osteitis deformans or old multiple
fractures.
(iv) Genu valgum (knock-knees): It is observed in Ellis-van Creveld syndrome,
Laurence-Moon-Biedl-syndrome and rickets (see Figs 13.103, 13.104 and 13.105).
Fig. 13.104 | Genu valgum in

Laurence-Moon-
Biedl syndrome.
Fig. 13.103 | Genu valgum in Ellis-van Fig. 13.105 | Genu valgum

in rickets.
Creveld syndrome.
iv) Joints
Examine the joints for inflammation, deformity or loss of function.
(i) Hypermobility of the joints (lax joints) is observed in Ehlers-Danlos syndrome
(see Fig. 13.106) and in few cases of Marfan syndrome.
(ii) Arthritis could be due to rheumatic polyarthritis, Jaccords arthritis, polychondritis,
rheumatoid arthritis, gouty arthritis, Reiters syndrome, infective endocarditis,
and polyarteritis nodosa.
Migrating Polyarthritis
It occurs in 58% of rheumatic fever, which spontaneously abates in 24 weeks with-
out leaving any residual deformity.
It affects the large joints: knee, ankle, elbow and wrist.
With salicylates, it produces dramatic response within 2448 hours.
It can be associated with carditis but not with rheumatic chorea.
It is considered as one of major diagnostic criteria (Jones criteria), however polyarthral-
gia (pian in the joints, not in the muscles and other periarticular tissues with no evidence
of inflammation) is more common than polyarthritis in the Indian sub-continent and
should be considered as one of the major criteria than as the minor diagnostic criteria.
Fig. 13.107 | Proximal interphalangeal arthritis in rheu-

Fig. 13.106 | Hypermobility (laxity) of the joints
in Ehlers-Danlos syndrome.
matoid arthritis.
Jaccords Arthritis
Jaccords arthritis is the post-streptococcal reactive arthritis, characterized by similar
clinical picture as that of rheumatic polyarthritis but with no other evidence of diag-
nostic criteria of rheumatic fever.
It does not dramatically respond to salicylates.
The deformity can be voluntarily corrected as it is due to sub-luxation of the joints
than due to the erosion and fusion of their articular surfaces.
Polychondritis
Polychondritis is characterized by cartilaginous inflammation, auricular chondritis
in 40% (resulting in floppy ears, deafness, vertigo and ataxia due to inflammation of
internal auditory artery or its cochlear branch), nasal chondritis in 50% (producing
saddle nose) and eye inflammation in 50% (producing conjunctivitis, episcleritis,
scleritis and cataracts).
Arthritis occurs in 1/3rd, which is asymmetric oligo or poly-articular involving both
large and small joints, but more likely to involve costochondral, sternomanubrial
and sternoclavicular cartilages, destruction of which may result in pectus excavatum
or flial anterior chest.
Rheumatoid Arthritis
It is a symmetrical polyarthrtis (but it may be asymmetric in few) affecting any of the
diarthrodial joints but characteristically, proximal interphalangeal and metacarpo-
phalangeal joints are involved with morning stiffness of 1 hour (see Fig. 13.107).
Persistent inflammation leads to characteristic joint deformities in hands and feet.
(i) Deformities in hands:
Z deformity: It is the radial deviation at the wrist with ulnar deviation of
the digits often associated with palmar subluxation of proximal phalanges (see
Fig. 13.108).
Fig. 13.108 | Zdeviation

deformity of the hand-radial
at the wrist with Fig. 13.109 | Swan neck deformity in rheumatoid arthritis.
ulnar deviation of the digits
in rheumatoid arthritis.
Swan neck deformity: There occurs hyperextension of the proximal interpha-

langeal joints with compensatory flexion of the distal interphalangeal joints
(see Fig. 13.109).
Boutonniere deformity: It involves flexion contracture of the interphalangeal
joints and extension of the distal interphalangeal joints.

Hyperextension of the first interphalangeal joint and flexion of the first metacar-
pophalangeal joint with a consequent loss of thumb mobility and pinch.

(ii) Deformities in feet:
Eversion at the subtalar joint (hind foot)
Plantar subluxation of metatarsal heads
Widening of the forefoot
Hallux valgus and
Lateral deviation of dorsal subluxation of the toes.
It can also involve wrist, elbow, knee (give rise to Bakers cyst if extends to popliteal
space) and upper cervical spine.
Extra articular manifestations include:
Rheumatoid nodules (2030%) on extensor surfaces (but may be seen in pleura,
meninges) most commonly on olecranon bursa, proximal ulna, Achilles tendon
and occiput in patients with circulatory rheumatoid factor (see Fig. 13.110).
Pneumonitis, pulmonary nodules and pleuritis.
Feltys syndrome with splenomegaly, neutropenia (occasionally, anemia and
thrombocytopenia).
Diffuse necrotizing vasculitis resulting in digital gangrene, cutaneous ulcerations,
visceral infarction (lungs, bowel, liver, spleen, pancrease, MI).
Cardiovascular manifestations include pericarditis (50% of autopsy) which rarely
leads to cardiac tamponade and constrictive pericarditis,65 valvular infiltration
of rheumatoid nodules (12%) which may result in AR, MR66 and conduction
defects when conduction tissue is involved.67
Fig. 13.110 | Rheumatoid nodule over the Fig. 13.111 | Classical metatarso-phalangeal joint arthritis
of greater toe in gouty arthritis.
elbow.
Fig. 13.112 | Gouty tophi in the ear helps in the diagnosis.

Gouty Arthritis
Monosodium urate arthritis:
Usually one joint i.e. metatarsophalangeal joint of the first toe is involved (see
Fig. 13.111) but may be polyarticular (tarsal joints, ankles and knees) especially in
hypertensive males with ethanol abuse and in postmenopausal woman.
The tophi in the ear (small hard nodules over the helix and antihelix) containing
biurate crystals are pathognomonic of gout (see Fig. 13.112).
Atherosclerosis and CAD are the most common cardiovascular manifestations, but
conducting system, mitral, aortic and tricuspid valve leaflets may also be involved.
13. PERIPHERAL EDEMA
Edema is defined as the excess accumulation of fluid in the subcutaneous tissues due
to increase in the interstitial fluid volume.
i) Pathogenesis
Water constitutes about 50% of body weight in women and 60% in men. This total
body water is distributed in two major compartments:
5575% (approximately 3/4th) is intracellular (i.e. intracellular fluid, ICF).
2545% (approximately 1/3rd) is extracellular (i.e. extracellular fluid, ECF).
The ECF is distributed in the ratio of 1:3 between
Intravascular i.e. plasma and
Extravascular i.e. interstitial fluid
which is regulated by Starling forces i.e.
Liquid Accumulation K (PcPi)(ci)Qlymph

Where K is the filtration coefficient across the capillary membrane, Pc is the mean
intracapillary hydrostatic pressure, Pi is the mean interstitial hydrostatic pressure, c
is the oncotic (colloid osmotic) pressure of plasma, i is the interstitial oncotic (col-
loid osmotic) pressure and Q lymph is the lymphatic flow.
The intracapillary hydrostatic pressure and interstitial oncotic pressure tend to promote
the movement of fluid from the capillaries to the interstitium (i.e. extravascular
spaces), while the oncotic pressure of the plasma (mainly due to plasma proteins)
and interstitial hydrostatic pressure promote the movement of fluid into the vascular
compartment (i.e. into the capillaries).
Fluid is returned from the interstitial spaces into the vascular system at the venous
end of the capillary network through the lymphatics. And in an average adult (70 kg),
the lymphatic flow is about 20 ml/h.68
Hence, edema occurs when one or more Starling forces are altered, to increase the
flow of fluid from the vascular system into the interstitium (or into a body cavity)
which exceeds the capacity of lymphatic drainage away from the interstitial spaces
(i.e. lymphatic insufficiency).
When the fluid moves from the vascular system into the interstitium, secondary con-
sequences occur, i.e. there is a fall in the plasma volume (i.e. decrease in cardiac output)
which activates renin angiotensin and sympathetic systems and thereby the kidneys
retain Na and water in an attempt to maintain the blood (intravascular) volume.
However, this increased blood volume results in an increased venous capillary hydro-
static pressure, promoting crossing over of large amount of fluid into the interstitial
tissues and thus causing edema.
However, in some cases of primary renal diseases, hepatic failure and certain drugs
(side effects), the primary event itself is the renal retension of Na and salt, which results
Table 13.25 Pathogenesis of peripheral edema
1. Capillary hydrostatic pressure

2. Plasma oncotic pressure
3. Interstitial oncotic pressure
4. Capillary endothelial damage
in an increased plasma volume, thereby increasing the venous capillary hydrostatic

pressure and thus forming edema (see Table 13.25 and Fig. 13.113).
ii) Causes
(1) Imbalance of Starling Forces
(i) Increased capillary hydrostatic pressure is due to an increased blood volume or
venous obstruction.
Increased blood volume due to renal Na and salt retention (secondary consequence)
as in CHF.
Increased blood volume due to primary renal Na and salt retention as in:
Renal failure
Glomerulonephritis
Early hepatic failure
Hypothyroidism
Lyphatic Capillary
obstruction/ i
permeability
insufficiency
Venous obstruction: Protein loss:

Hepatic cirrhosis, Nephrotic syndrome
Local venous obst. Protein losing enteropathy
Imbalance
Blood volume Pc c
of Starling
(secondary): CHF
forces
Blood Albumin synthesis:

volume (primary): Malnutrition
1. Renal failure, liver disease
glomerulonephritis EDEMA
2. Vasodilators, NSAID,
steroids, cyclosporine
3. Pregnancy
Capillary
Endothelial
damage
Trauma: Mechanical, thermal Inflammation: Viral, bacterial
Hypersensitivity Drugs: Interleukin-2
Fig. 13.113 | Pathogenesis of peripheral edema : interstitial oncotic pressure, :

i
plasma oncotic pressure, P : capillary hydrostatic pressure, NSAID: non-
c
c
steriodal anti inflammatory drugs, CHF: congestive heart failure, obst.:
obstruction.
Drugs:
1. Direct arterial/arteriolar vasodilators: Minoxidil, hydralazine, clonidine,
methyldopa, guanethidine
2. Ca channel blockers
3.
adrenergic blockers
4. Non-steroidal anti-inflamatory drugs
5. Steroid hormones: Glucocorticoids, anabolic steroids, estrogens, progestins
6. Cyclosporine.
Pregnancy and premenstrual edema
Idiopathic edema (in young menstruating women).
Venous obstruction:
Hepatic cirrhosis or hepatic venous obstruction
Local venous obstruction.
(ii) Decreased plasma oncotic pressure due to protein loss or reduced albumin synthesis:
Protein loss:
Nephrotic syndrome
Protein losing enteropathy.
Reduced albumin synthesis:
Malnutrition
Liver disease.
(iii) Increased interstitial oncotic pressure due to:
Lymphatic obstruction (lymphatic insufficiency)
Hypothyroidism and
Increased capillary permeability.
(2) Capillary Endothelial Damage

Increases its permeability and permits the transfer of proteins into the interstitial com-
partment. This occurs in:
Inflammation due to viral or bacterial agents
Trauma: Mechanical or thermal (burns)
Hypersensitivity reaction: Allergic reactions, characteristic of immune injury and
Drugs used for immunotherapy: Interleukin-2, OKT3 monoclonal antibody.
iii) Types and Site of Peripheral Edema

(i) Localized
Edema is limited to one leg or one/both arms usually due to venous and/or lymphatic
obstruction (trauma, inflammation or hypersenstivity).
It may be limited to a body cavity as in ascitis, pleural effusion or pericardial
effusion.
(ii) Anasarca
It is a gross generalized edema characterized by periorbital edema (soft tissues of eye-
lids & face) and bilateral leg edema. Common causes include nephrotic syndrome,
hypoproteinemia and severe congestive heart failure.
(iii) Leg Edema

It could be bilateral or unilateral (see Table 13.26); pitting or non-pitting.
For pitting edema, a firm pressure is applied for 1020 sec (30 sec) for detection.
It is frequently detected in:
The region of ankles ( especially in ambulatory patients)
The presacral region, trochanters, or the back of the thighs (especially in patients
confined to bed/recumbent patients) and
The region of the genital organs (particularly, the scrotum).
Bilateral pitting leg edema: occurs in
Congestive heart failure (see Fig. 13.114)
Constrictive pericarditis (may be associated with ascites)
Renal causes: glomerulonephritis, nephrotic syndrome (may have ascites)
Cirrhosis of liver (associated with ascites)
Protein-losing enteropathy
Nutritional causes: hypoproteinemia, anemia (when Hb is 5 g/dl), wet beriberi,
epidemic dropsy
Physiological: pregnancy and premenstrual edema
Idiopathic edema.
Table 13.26 Causes of leg edema
Bilateral Unilateral
Bilateral pitting Unilateral pitting
non-pitting non-pitting
1. CHF 1. Trauma 1. Myxedema 1. Lymphatic obstruction:

filariasis radiation
trauma, malignancy
2. Constrictive pericarditis 2. Inflammation 2. Milroys disease
3. Renal: glomerulonephritis, 3. Bakers cyst
nephritic syndrome
4. Cirrhosis of liver 4. Varicose veins
(later stages)
5. Protein losing 5. Deep vein
enteropathy thrombophlebitis
6. Nutritional: anemia, 6. Congenital venous
hypoproteinemia malformations
7. Pregnancy, pre-
menstrual edema
8. Idiopathic
Fig. 13.114 | Bilateral

failure.
pitting leg edema in congestive heart Fig. 13.115 | Pretibial
disease.
myxedema in Graves
Bilateral nonpitting leg edema may occur in

Myxedema (see Fig. 13.115).
Unilateral pitting leg edema could be of:
(i) Acute onset (72 hours): due to
Trauma: Mechanical or thermal (burns).
Inflammation:69
Bacterial cellulitis (see Fig. 13.116)
Acute deep venous thrombophlebitis
Popliteal (Bakers) cyst
Erythema nodosum.
(ii) Late onset (72 hours): as in
Chronic venous insufficiency: It may also cause bilateral leg edema. The most common
causes are:
Varicose veins
Deep venous thrombosis
Congenital venous malformations.
Reflex sympathetic dystrophy due to trauma, infection and vascular insufficiency,
which is characterized by burning pain, hyperesthesia, hyperhydrosis, trophic changes

of skin and swelling of the affected limb.
Bone and soft tissue tumors may also cause unilateral leg edema.
Paralysis can reduce lymphatic and venous drainage of the affected side and produce
edema.
Unilateral non-pitting leg edema is usually due to lymphedema. Initially, it may be pitting
but later, the limb develops a woody texture and edema is no longer pitting. This occurs in:
Lymphatic obstruction due to infection (classical example being filariasis which often
involves scrotum and penis, see Fig. 13.117 and Table 13.27), radiation, surgery,
trauma, or malignancy.
Elephantiasis of penis
Rams horn penis
Lymphoedema scrotum
Lymphoedema leg
Fig. 13.116 | Unilateral

cellulites.
leg in acute Fig. 13.117 | Unilateral non-pitting edema of the leg in filariasis
with scrotum and penis involvement.
Table 13.27 Stages/grades of filarial lymphedema
Stages Edema Other characters
1. Stage-I Pitting Edema completely relieved on rest

and leg elevation. No skin changes
2. Stage-II Pitting Edema partially relieved on rest
and leg elevation. No skin changes
3. Stage-III Non-pitting Thickening of the skin and subcutaneous tissue
4. Stage-IV Non-pitting Lymphorrhea and elephantiasis present
Congenital lymphatic malformation: Milroys disease (chronic hereditary edema, a rare

familial disorder).
iv) Characteristics of Peripheral Edema

In hypoproteinemia, edema is most pronounced in the morning,
Edema associated with CHF tends to be more extensive in the legs and is accentuated
in the evenings. However, edema is most prominent in the presacral region in CHF
in bed-ridden patients.
Edema due to renal causes (glomerulonephritis, nephritic syndrome) is initially most
prominent in the periorbital area (puffiness of face) followed by leg edema.
In cirrhosis of liver: Initially, the patient has ascites, and edema occurs in other parts
of the body including lower extremities because of hypoalbuminemia, and impedence
of venous return from the lower limbs due to increased intrabdominal pressure from
ascites.
REFERENCES
1. National Institute of Health. Clinical guidelines on the identification, evaluation, and treatment of
overweight and obesity in adults: the evidence report. Obes Res 1998;6(Suppl 2):51S209S.
2. Third report of the National Cholesterol Education Program (NCEP). Expert panel on Detection,
Evaluation, and Treatment of High blood cholesterol in adults (Adult Treatment Panel III). JAMA
2001;285(19):24862497.
3. De Paepe A, Deitz HC, Devereux RB, et al. Revised diagnostic criteria for the Marfan syndrome.
Am J Med Genet 1996;62(4):417426.
4. Kraus JP. Molecular basis of phenotype expression in homocytinuria. J Inherit Metab Dis
1994;17:383390.
5. Mudd SH, Shovby F, Levy HL, Pettigrew KD, Wilcken B, Pyeritz RE, et al. The natural history of
homocystinuria due to cystathionine -synthase deficiency. Am J Hum Genet 1985;37:131.
6. Rosenthal A. Cardiovascular malformations in Klinefelters syndrome: report of three cases. J Pediatr
1972;80(3):471473.
7. Lin AE, Garver KL. Genetic council for congenital heart defects. J Pediatr 1988;113:11051109.
8. Mendez HM, Opitz JM. Noonan syndrome: a review. Am J Med Genet 1985;21(3):493506.
9. McKusick VA, Egeland JA, Eldridge R, et al. Dwarfism in the Amish: I. The Ellis-van Creveld syn-
drome. Bull Johns Hopkins Hosp 1964;115:306336.
10. Burwell CS, Robin ED, Whaley RD, Bickelmann AG. Extreme obesity associated with alveolar
hypoventilation-A Pickwickian syndrome. Am J Med 1956;21(5):811818.
11. Green JS, Parfrey PS, Harnett JD, Farid NR, Cramer BC, Johnson G, et al. The cardinal manifesta-
tions of Bardet-Biedl syndrome, a form of Laurence-Moon-Biedl syndrome. N Engl J Med
1989(15);321:10021009.
12. Cushing H. The basophil adenomas of the pituitary body and their clinical manifestations (pituitary
basophilism). Bull Johns Hopkins Hosp 1932;50:137195.
13. Levine HJ. Difficult problems in the diagnosis of chest pain. Am Heart J 1980;100(1):108118.
14. Zimmerman J, Yahalom J, Bar-On H. Clinical spectrum of pericardial effusion as the presenting
feature of hypothyroidism. Am Heart J 1983;106(4 Pt 1):770771.
15. Hiromasa S, Ikeda T, Kubota K, et al. Myotonic dystrophy: ambulatory electrocardiogram, electro-
physiologic study, and echocardiographic evaluation. Am Heart J 1987;113(6):14821488.
16. Cervera R, Font J, Pare C, et al. Cardiac disease in systemic lupus erythematosis: prospective study
of 70 patients. Ann Rheum Dis 1992;51(2):156159.
17. Roberts WC, Bulkley BH. The heart in systemic lupus erythematosis and the changes induced in it
by corticosteroid therapy: a study of 36 necropsy patients. Am J Med 1975;58(2):243264.
18. Bornstein DG, Fye WB, Arnett FC, Stevens MB. The myocarditis of systemic lupus erythematosis:
association with myositis. Ann Intern Med 1978;89(5 Part I):619624.
19. Libman E, Sacks B. A hitherto undescribed form of valvular and mural endocarditis. Arch Intern
Med 1924;33:701737.
20. Nihoyannopoulos P, Gomez PM, Joshi J, et al. Cardiac abnormalities in systemic lupus erythemato-
sis: association with raised anticardiolipin antibodies. Circulation 1990;82(2):369375.
21. Pellikka PA, Tajik AJ, Khandheria BK, et al. Carcinoid heart disease. Clinical and echocardiographic
spectrum in 74 patients. Circulaton 1993;87(4):11881196.
22. Cohen JI, Arnett EN, Kolodny AL, Roberts WC. Cardiovascular features of the Werner syndrome.
Am J Cardiol 1987;59(5):493495.
23. Woeber KA. Thyrotoxicosis and the heart. N Engl J Med 1992;327(2):9498.
24. Sacca L, Cittadini A, Fazio S. Growth hormone and the heart. Endocr Rev 1994;15(5):555573.
25. Fazio S, Cittadini A, Cuocolo A, et al. Impaired cardiac performance is a distinct feature of uncom-
plicated acromegaly. J Clin Endocrinol Metab 1994;79(2):441446.
26. Tandon R, Edwards JE. Cardiac malformations associated with Downs syndrome. Circulation
1973;47(6):13491355.
27. Lewandowski RC Jr, Yunis J. New chromosomal syndromes. Am J Dis Child 1975;129(4):515529.
28. Neufeld EF, Muenzer J. The mucopolysaccharidosis. In: Scriver CR, Beaudet AL, Sly NS, Valle D,
eds. The Metabolic and Molecular Bases of Inherited Diseases, 7th ed. New York: McGraw-Hill,
1995:24652494.
29. Williams JCP, Barratt-Boyes BG, Lowe JB. Supravalvular aortic stenosis. Circulation 1961;24:
13111318.
30. Sandor GG, Smith DF, McLeod PM. Cardiac malformations in the fetal alcohol syndrome. J Pediatr
1981;98(5):771773.
31. Allen SJ, Naylor D. Pulsation of the eye balls in tricuspid regurgitation. Can Med Assoc J 1985;
133(2):119120.
32. Byrd MD. Lateral systolic pulsation of the earlobe: a sign of tricuspid regurgitation. Am J Cardiol
1984;54(1):244.
33. Barbeau A. Friedreichs ataxia 1978. An overreview. Can J Neurol Sci 1978;5(1):161165.
34. Helmi C, Pruzansky S. Craniofacial and extracranial malformations in the Klippel-Feil syndrome.
Cleft Palate J 1980;17(1):6588.
35. Kearns TP, Sayre GP. Retinitis pigmentosa, external ophthalmoplegia, and complete heart block.
Arch Ophthalmol 1968;60:280289.
36. Lowes M. Chronic progressive external ophthalmoplegia, pigmentary retinopathy and heart block
(Kearns-Sayre syndrome). Acta Ophthalmol 1975;53(4):610.
37. Csonka GW, Oates JK. Pericarditis and electrocardiographic changes in Reiters syndrome. Br Med
J 1957;1(5023):866869.
38. Deer T, Rosencrance JG, Chillag SA. Cardiac conduction manifestations of Reiters syndrome.
South Med J 1991;84(6):799800.
39. Morquio L. Sur une forme de dystrophie osseuse familiale. Bull Soc Pediatr Paris 1929;32:129135.
40. Jackson CE, Yuhki N, Desnick R, Haskins ME, OBrien SJ, Schuchman EH. Feline arylsulfatase B
(ARSB): isolation and expression of the cDNA, comparison with human ARSB, and gene localiza-
tion to feline chromsome A1. Genomics 1992;14:403411.
41. Ho CK, Kaufman RL, Podos SM. Ocular colobomata, cardiac defect, and other anomalies. J Med
Gen 1975;12(3):289293.
42. Takahashi T, Koide T, Yamaguchi H, Nakamura N, Ohshima Y, Suzuki J, et al. Ehlers-Danlos syn-
drome with aortic regurgitation, dilation of the sinuses of Valsalva, and abnormal dermal collagen
fibrils. Am Heart J 1992;123(6):17091712.
43. Cyran SE, Martinez R, Daniels S, Dignan P, Kalpan S. Spectrum of congenital heart disease in
CHARGE association. J Pediatr 1987;110(4):576578.
44. Wong RS, Follis FM, Shively BK, Wernly JA. Osteogenesis imperfecta and cardiovascular diseases.
Ann Thorac Surg 1995;60(5):14391443.
45. Hortop J, Tsipouras P, Hanley JA, Maron BJ, Shapiro JR. Cardiovascular involvement in osteogen-
esis imperfecta. Circulation 1986;73(1):5461.
46. Stein D, Kloster FE. Valvular heart disease in osteogenesis imperfecta. Am Heart J 1977;94:
637641.
47. Leys D, Petit H, Bonte-Adnet C, Millaire A, Fourier F, Dubois F, et al. Refsums disease revealed by
cardiac disorders (letter). Lancet 1989;1:621.
48. Keith NM, Wagener HP, Barker NW. Some different types of essential hypertension: their course
and prognosis. Am J Med Sci 1939;268(6):336345.
49. Cogan DG. Significance of fundus signs. In: Cogan DG, Ophrhalmic manifestations of systemic
vascular disease. Vol. 3 of Major problems in internal medicine. Philadelphia: W.B. Saunders,
1974:52.
50. Goodman RM, Smith EW, Paton D, et al. Pseudoxanthoma elasticum: a clinical and histopatholog-
ical study. Medicine 1963;42:297334.
51. Kirkham N, Murrells T, Melcher SH, Morrison EA. Diagonal earlobe creases and fatal cardiovascu-
lar disease: a necropsy study. Br Heart J 1989(4);61:361364.
52. Bowness P, Hawley JC, Morris T, Dearden A, Walport MG. Complete heart block and severe aortic
incompetence in relapsing polychondritis. Arthritis Rheum 1991;34:97100.
53. Gellis SS, Feringold M. Rubinstein Taybi syndrome. Am J Dis Child 1971;121(4):327328.
54. Guttmacher AE, Marchuk DA, White RI Jr. Hereditary hemorrhagic telangiectasia. N Engl J Med
1995;333:918926.
55. Van Praagh S, Truman T, Firpo A, et al. Cardiac malformations in trisomy 18: a study of 41 post-
mortem cases. J Am Coll Cardiol 1989(7);13:15861597.
56. Bergfeldt L, Edhag O, Rajs J. HLA-B27-associated heart disease. Clinicopathologic study of three
cases. Am J Med 1984;77(5):961967.
57. Konishi Y, Ito M, Okuno T, Hojo H, Okuda R, Nakano Y, et al. Tuberous sclerosis: early neurolog-
ical manifestations and CT features in 18 patients. Brain Dev 1979;1(1):3137.
58. Tsakraklides V, Burke B, Mastri A, Runge W, Roe E, Anderson R. Rhabdomyomas of heart.
A report of four cases. Am J Dis Child 1974;128(5):639646.
59. Jayakar PB, Stanwick RC, Seshia SS. Tuberous sclerosis and Wolf-Parkinson-White syndrome.
J Pediatr 1986;108:259260.
60. Special Writing Group of the Committee on Rheumatic Fever, Endocarditis and Kawasaki
Disease of the Council on Cardiovascular Disease in the Young of the American Heart Association.
Guidelines for the diagnosis for rheumatic fever: Jones Criteria, 1992 update. JAMA 1992;
268:20692073.
61. Durack DT, Bright DK, Lukes AS. Duke Endocarditis Service. New criteria for diagnosis of infec-
tive endocarditis: utilization of specific echocardiographic findings. Am J Med 1994;96:200209.
62. Eldridge R. The metacarpal index: the useful aid in the diagnosis of Marfan syndrome. Arch Intern
Med 1964;113:248254.
63. Smith AT, Sack GH, Taylor GJ. Holt-Oram syndrome. J Pediatr 1979;95:538543.
64. Smiley JD. The many faces of scleroderma. Am J Med Sci 1992;304(5):319333.
65. Bacon PA, Gibson DG. Cardiac involvement in rheumatoid arthritis: an echocardiographic study.
Ann Rheum Dis 1974;33(1):2024.
66. Ahern M, Lever JV, Cosh J. Complete heart block in rheumatoid arthritis. Ann Rheum Dis
1983;42(4):389397.
67. Roberts WC, Dangel JC, Bulkley BH. Nonrheumatic valvular cardiac disease: a clinicopathologic
survey of 27 different conditions causing valvular dysfunction. Cardiovasc Clin 1973;5(2):333446.
68. Staub NC. Pulmonary edema due to increased microvascular permeability to fluid and protein. Cir
Res 1978;43(2):143151.
69. Merli GJ, Spandorfer J. The outpatient with unilateral leg swelling. Med Clin North Am 1995;
79(2):435447.
CHAPTER 14
A RTERIAL P ULSE
1. DEFINITION 225 iv.Volume of the Pulse 244

2. GENESIS OF THE ARTERIAL v.Condition of the Vessel Wall 245
PULSE 225 vi.Radial Pulse Synchronocity 245
3. PULSE WAVE PATTERN 226 vii.Absent or Delayed Femoral
i. In Ascending Aorta 226 Pulsations 245
ii. In Peripheral Arterial Pulse 226 5. CHARACTERISTIC FEATURES OF
4. EXAMINATION OF THE ARTERIAL PULSE IN COMMON CLINICAL
PULSE 228 CONDITIONS 246
i. Rate of the Pulse 231 i. Aortic Stenosis 246
ii. Rhythm 232 ii. Aortic Regurgitation 246
iii. Character of the Pulse 233 REFERENCES 248
1. DEFINITION
Pulse is a Greek word meaning move to and fro. Arterial pulse is a wave produced by
cardiac systole traversing in the peripheral direction in the arterial tree at a rate faster
than the column of blood (speed of the pulse wave is 5 m/sec or 18 km/h, while the
blood flows at a speed of 0.5 m/sec or 1.8 km/h).
2. GENESIS OF THE ARTERIAL PULSE
Despite early significance attached to the pulse, its origin in the heart was not
considered till Herophilus in 344 BC.
The arterial pulse wave (first described by Broadbent in 1890) begins with the aor-
tic valve opening and onset of left ventricular (LV) ejection, when the LV pressure
exceeds the aortic pressure and the LV pressure becomes the driving force for the
movement of blood into the ascending aorta.1
The pulse wave consists of two positive deflections during systole (upstroke) and
one deflection during diastole (descending limb). The first shoulder during systole
is the percussion wave due to the arrival of the impulse generated by LV ejection; the
second is the tidal wave due to reflection from upper part of the body. Whereas the
dicrotic or diastolic wave is due to reflection from the lower part of the body.2
Tidal wave
Dicrotic notch
Dicrotic
wave Anacrotic
notch
Percussion wave
S1 S2
Fig. 14.1 | Normal arterial pulse.

The peripheral arterial pulse wave recorded is the summation of initial generated
wave (in the ascending aorta) and reflected waves from upper and lower parts of the
body (see Fig. 14.1).
The driving force of the LV is dependent on:
The intrinsic contractility of the ventricular muscle
The size and shape of the LV
The heart rate.
However, the forward flow of the blood (LV ejection) also depends on:
Resistance offered by the blood viscosity and geometry of the vasculature
Inertia produced by the mass of the blood column and
Compliance of the vasculature.
3. PULSE WAVE PATTERN
i. In Ascending Aorta
Pulse wave normally rises rapidly to a rounded dome (percussion and tidal waves)
which reflects the peak velocity of the blood ejected from the LV.
A slight anacrotic notch (ana: up, again, krotos: to beat) is occasionally felt but
frequently recorded on the ascending limb of the pulse.
The descending limb is less steep than the ascending limb and is interrupted by an
incisura, a sharp downward deflection due to closure of the aortic valve.
The pulse wave then rises slightly (dicrotic wave) and thereafter declines gradually
throughout the diastole.
Ascending aorta, innominate and carotid arteries represent the central arterial pulse
(see Fig. 14.2 and Table 14.1). However, clinically the carotid arterial pulse provides
the most accurate representation of the central aortic pulsation.
ii. In Peripheral Arterial Pulse

Brachial, radial and femoral arteries represent the peripheral arterial pulse (see Fig.
14.2 and Table 14.1). However, the brachial artery is most suitable for appreciating
ARTERIAL PULSE 227
Ascending aorta High descending aorta Innominate artery
Subclavian artery Brachial artery
Fig. 14.2 | Pulse wave pattern in central and peripheral arteries.

Table 14.1 Pulse wave pattern
Central artery (aorta) Peripheral artery (brachial)
1. Upstroke rises to a rounded dome Upstroke is steeper

2. Ascending limb has an anacrotic notch Anacrotic notch in the ascending
limb disappears
3. Descending limb has incisura followed Incisura in descending limb is
by dicrotic wave replaced by dicrotic notch followed
by dicrotic wave
the rate of rise of pulse, contour, volume and consistency of the peripheral
vessels.
As the normal aortic pulse wave is transmitted peripherally (reaches carotid at 30 ms,
brachial 60 ms, radial 80 ms, and femoral at 75 ms), significant changes in its con-
tour occur due to:
Distortion and damping of the pulse wave components.
Different rates of transmission of various components.
Distortion or exaggeration by reflected waves.
Conversion of kinetic energy into hydrostatic or potential energy.
Differences in distensibility and caliber of the arteries and
Changes in the vessel wall due to age and/or disease.3
As the pulse wave travels peripherally; the pulse pressure increases, upstroke (ascend-
ing limb of the pulse wave) becomes steeper, and systolic peak (percussion wave)
becomes higher but the tidal wave is less significant.
The anacrotic shoulder disappears, and the sharp incisura is replaced by a smoother
and later dicrotic notch, followed by a dicrotic wave, which probably results from the
summation of the forward pulse wave and reflected waves from the peripheral vessels.
Normally, anacrotic notch, tidal wave, dicrotic notch and dicrotic wave are not
palpable.
Normally, percussion wave is more prominent than tidal wave. However; in older
patients with increased systemic vascular resistance, arteriosclerosis and diabetes mellitus,
the tidal wave may be somewhat higher than the percussion wave (i.e. late systolic peak).
The height of the dicrotic wave decreases with age, hypertension and arteriosclerosis.
4. EXAMINATION OF THE ARTERIAL PULSE
Ejection of blood with every cardiac contraction is converted into:

i. Flow pulsations: i.e. longitudinal movement of blood along the arterial lumen which
can be measured by electromagnetic flow meters and Doppler ultrasonic probe.
ii. Pressure pulsations: The amplitude of the arterial pulse perceived by the clinician
in a large accessible artery is the pressure pulse.
Clinicians perception of pulse is formed by the tactile receptors (Meisseners corpus-
cles, Pacinian corpuscles and Merkels discs) that mediate the tactile sensation on the
finger-tips. Varying degrees of pressure (which is known as trisection method ) should
be applied to assess the upstroke, systolic peak and diastolic slope of the pulse.3
All major arterial pulses should be bilaterally examined for:
Rate of the pulse
Rhythm
Character
Volume
Condition of the arterial wall (thickness)
Equal (synchronous) or inequality of the radial pulses and
Presence or absence of delay of the femoral pulses compared with radials.
The radial pulse is felt with the tips of the fingers (preferably three: index, middle,
and ring) compressing the vessel against the head of the radius, with the patients fore-
arm slightly pronated and the wrist slightly flexed (see Fig. 14.3).
The brachial artery is compressed against the humerus just above the antecubital
fossa. The examiner should use either the left thumb or fingertips when examining the
patients right brachial artery and vice versa (see Fig. 14.4).
The carotid (common carotid) is gently examined one at a time best with the thumb
(left thumb for patients right carotid and vice versa) with the sternocleidomastoid
muscles relaxed and the head rotated slightly towards the examiner. It should be palpated
Fig. 14.3 | Examination of the radial pulse.

ARTERIAL PULSE 229
Fig. 14.4 | Examination of the brachial pulse. Fig. 14.5 | Examination of the carotid pulse.
Fig. 14.6 | Examination of the femoral pulse.

in the lower half of the patients neck in order to avoid carotid sinus compression
(see Fig. 14.5).
The femoral arteries lie midway between the iliac crest and pubic ramus and are
palpable against the underlying femur (see Fig. 14.6).
The popliteals are best examined with the patients knee flexed at an angle of 120.
The fingertips of both hands are placed in the popliteal fossa with the thumbs resting
on the patients patella (see Fig. 14.7).
The posterior tibial pulse is found 1 cm behind the medial malleolus of the tibia.
The patients foot should be relaxed between plantar and dorsiflexion (see Fig. 14.8).
The dorsalis pedis pulse is commonly felt between the tendons of 1st and 2nd toes,
57.5 cm below the joint crevice. It is compressed against the tarsal bones and the
patients left dorsalis pedis is mostly examined with the fingers of the right hand and
vice versa (see Fig. 14.9).
The dorsalis pedis and posterior tibial are impalpable in about 2% of normal indi-
viduals due to anomalous course.
Fig. 14.7 | Examination of the popliteal pulseflex the patients knee at an angle of 120
and place fingers of both hands in the popliteal fossa with thumbs resting on
the patients patella.
Fig. 14.8 | Examination of the posterior tibial pulse Fig. 14.9 | Examination
pulse.
of the dorsalis pedis
patients foot relaxed between plantar and
dorsiflexion.
Sublingual nitroglycerine often resolves the doubt by rendering a temporarily absent

dorsalis pedis or posterior tibial pulse readily palpable.
In peripheral arterial occlusion, passive leg elevation intensifies the pallor in the
affected limb.
The examination of the arterial pulses is tabulated using a scale as follows:
0 Complete absence of pulsation.
1 Small or feeble/reduced pulsation.
2 Palpable but diminished as compared to other side.
3 Normal pulsation.
4 Large or high volume/bounding pulsation.
ARTERIAL PULSE 231
Besides palpation, auscultation over the major arteries should be performed as audible
bruit may give a clue to partial occlusion or transmission of a cardiac murmur (e.g.
mid systolic murmur of AS may be conducted to the carotids).
50% obstruction of an artery may produce a short systolic bruit.
80% obstruction of an artery may produce a continuous bruit.
80100% obstruction of an artery may produce no audible bruit.
i. Rate of the Pulse

Examine whether the patient has tachycardia, bradycardia or pulse deficit.
The range of rates of normal sinus rhythm in an adult person is between 60 and
100 beats per minute.
However, the average rate of pulse in children depends upon the age and is as
follows: 1 week of age 140/min, 1 yr of age 120/min, 6 yrs of age 100/min
and at puberty 80/min.
(1) Tachycardia
i) Sinus tachycardia: A sinus rate above 100 beats per minute is defined as sinus
tachycardia.
Causes of sinus tachycardia:
Physiological: It occurs in infancy and early childhood and in response to exercise,
excitement, anxiety and other emotional stresses.
Pharmacological: It results from medications or drugs.
Medications: Amyl nitrate, epinephrine, isoproterenol, ephedrine, atropine
Intoxicants: Exposure to alcohol, nicotine or caffeine.
Pathological:
Cardiovascular causes include congestive heart failure, acute myocardial infarction,
pulmonary embolism, myocarditis or shock.
Non-cardiac causes include fever, anemia, thyrotoxicosis, hemorrhage, hypotension
and hypoxemia.
ii) Tachyarrhythmias
Most tachycardias associated with a regular pulse are of supraventricular origin.
Tachycardia with irregular pulse may be due to ventricular tachycardia and AV dis-
sociation with variation in atrio-ventricular sequence of contraction. The resulting
variation in pulse amplitude may often be detected by palpation.4
An irregularly irregular pulse with varying pulse pressure is usually due to atrial
fibrillation or multifocal atrial tachycardia.
(2) Bradycardia
i) Sinus bradycardia: A sinus rate of 60 beats per minute is defined as sinus
bradycardia.
Causes of sinus bradycardia:

Physiological (asymptomatic bradycardia) occurs usually in athletes (training effect)
and during sleep.
Pharmocological: Bradycardia resulting from medications include beta-blockers,
amiodorone, propafenone, lithium, and other parasympathomimetic drugs.
Pathological (symptomatic bradycardia):
Cardiovascular causes: Bradycardia occurs in inferior wall MI., SA block, during
coronary angiography, following cardiac transplantation and in vasovagal syncope.
Non-cardiac causes include myxedema, increased intracranial pressure (due to
meningitis, intracranial tumors), Chagas disease, hypothermia, mental depression,
obstructive jaundice, enteric fever, gram negative sepsis and eye surgery.
ii) Bradyarrhythmias: They are usually due to AV conduction abnormalities espe-
cially with second degree AV block and complete heart block.
(3) Pulse Deficit

The difference between the radial pulse rate and the heart rate (usually counted by
auscultation) is defined as pulse deficit.
It occurs in tachyarryhthmias. A pulse deficit of 6/min is diagnostic of atrial fibril-
lation and 6/min can occur in premature ventricular contractions (PVCs).
Mechanism of pulse deficit
In tachyarrhythmias, the diastole is shortened and subsequent systolic stroke volume
is insufficient to cause opening of the aortic valve therefore, the arterial pulse will be
non-existent inspite of the cardiac contraction.
As diastole becomes longer in subsequent cardiac cycles, the stroke volume gradually
increases and arterial pulse is felt.
ii. Rhythm
The normal pulse is regular in rhythm. If the pulse is irregular, note whether it is regularly
irregular or irregularly irregular.
(1) Regularly Irregular Pulse

It occurs in: (see Table 14.2)
i) Sinus arrhythmia: Sinus arrhythmia is present when the variation between the
longest and the shortest cycle (PP interval) exceeds 0.12 s.
Table 14.2 Causes and types of irregular pulse
Regularly irrregular pulse Irregularly irregular pulse
1. Sinus arrhythmia 1. Atrial fibrillation

2. Pulsus bigeminus (due to PVCs) 2. Multifocal atrial tachycardia
3. Pulsus alternans 3. Frequent PVCs
4. Partial (1st and 2nd degrees) heart blocks
ARTERIAL PULSE 233
It is defined as phasic sinus arrhythmia if the cycle lengths shorten with inspiration
(pulse rate increases) and lengthen with expiration (pulse rate decreases).
It is referred as nonphasic sinus arrhythmia if it is unrelated to the respiration, and it
may related to digitalis intoxication.
Normally, it is most common in children.
It decreases with age and in autonomic dysfunction and hence is considered as a risk
factor for sudden cardiac death.
ii) Premature ventricular contractions (PVCs): PVCs at regular intervals (bigemini or
trigemini pattern) cause regularly irregular pulse.
Causes of PVCs include:
Physiological: exercise
Pharmacological: Either medications or intoxicants
Medications: Digoxin toxicity

Intoxicants: Intake of alcohol and coffee (caffeine) or smoking (nicotine).
Cardiovascular causes (usually with structural heart diseases): Coronary artery disease
(CAD) including acute myocardial infarction, post thrombolysis or percutaneous

trans-coronary angioplasty (PTCA), myocarditis, pericarditis, cardiomyopathy,
hypertensive heart disease and mitral valve prolapse.
iii) Partial (1st and 2nd degree) heart blocks: Partial heart blocks usually produce
regularly irregular pulse. They can occur during exercise, in CAD especially in AMI and
in myocarditis. Drugs such as digitalis and propronolal may also produce partial heart
blocks.
(2) Irregularly Irregular Pulse

Atrial fibrillation, multifocal atrial tachycardia and frequent PVCs produce irregularly
irregular pulse.
iii. Character of the Pulse

It is best evaluated by palpation of the carotid pulse. Following are the abnormal types
of pulses depending upon the character of the pulse:
(1) Pulsus Tardus (Slow Rising Pulse)

Slow rising pulse with delayed systolic peak (nearer to S2) and upstroke, frequently
associated with a thrill in the carotids (carotid shudder) is characteristic of AS, and
often occurs with pulsus parvus (i.e. pulsus parvus et tardus) (see Fig. 14.10).
It is better appreciated by simultaneous auscultation and carotid palpation, and the
presence of pulsus tardus indicates atleast 70 mmHg of pressure gradient in AS.
(2) Water-Hammer (Collapsing) Pulse or Corrigan Pulse or

Pulsus Celer
It is characterized by rapid upstroke (percussion wave) followed by rapid descent (col-
lapse) of the pulse wave without dicrotic notch, which reflects low systemic vascular
resistance (see Fig. 14.11).5
EIOQ
ESM A ESM
B4 B1 EC 2 S4 S1 EC A2
Phono
Carotid Pulsus parvus et tardus
Fig. 14.10 | Pulsus parvus et tardus in aortic stenosis.
150
100
50
Fig. 14.11 | Water hammer pulse in aortic regurgitation.
Rapid upstroke is due to the rapid ejection of greatly increased stroke volume.
The rapid descent or collapsing character is due to:
(i) Diastolic run-off (back flow) into the left ventricle
(ii) Reflex vasodilatation mediated by carotid baroreceptors secondary to large
stroke volume
(iii) The rapid run-off to the periphery due to decreased systemic vascular
resistance.
Water-hammer pulse
Thomas Watson (1844), an English Physician, named this term after a Victorian
toy, which refers to the rapid and forceful ascending limb of the arterial pulse.
Water-hammer consisted of a sealed glass tube containing water in a vacuum.
As solids and liquids fall at the same rate in vacuum, so when this glass tube is
quickly inverted, water column falls abruptly from one end of the tube to the other
and finger tip holding the inverted end senses a sudden impact or jolt.
Detection: It is best appreciated at the radial pulse with the palmer side of the
patients wrist held in the examiners hand and with the patients arm suddenly ele-
vated above the shoulder. This may be related to the artery becoming more in line
with the central aorta, allowing direct systolic ejection and diastolic backward flow
(see Figs 14.12A and 14.12B).
ARTERIAL PULSE 235
A B
Fig. 14.12 | Detection of water hammer pulse. (A) The palmer side of patients wrist is
held in the examiners hand. (B) The patients arm elevated suddenly above
the shoulder.
Table 14.3 Causes and types of pulse depending upon the character
Pulsus tardus Collapsing pulse
1. Aortic stenosis 1. Hyperkinetic circulatory states

2. Aortic regurgitation, patent ductus arteriosus,
aortopulmonary window, RSOV into right heart,
arteriovenous fistula
3. Truncus arteriosus with truncal sufficiency, PAt
with bronchopulmonary collaterals, TOF with
bronchoplumonary collaterals, TOF after BT shunt
RSOV: rupture of sinus of Valsalva, PAt: pulmonary atresia, TOF: tetrology of Fallot, BT: Blalock-
Taussig.
Causes
i) Conditions with aortic run-off: AR, PDA, AP window, rupture of sinus of
Valsalva into the right chambers and arteriovenous fistula.
ii) Cyanotic congenital heart diseases: Truncus arteriosis with truncal run-off into
PA or truncal insufficiency, pulmonary atresia with bronchopulmonary collaterals,
TOF with bronchopulmonary collaterals/associated PDA/associated AR or after
Blalock Taussig (BT) shunt (systemic artery to pulmonary artery).
iii) Hyperkinetic circulatory states: Pregnancy, anemia, thyrotoxicosis, Beriberi, fever
and Pagets disease of the bone (see Table 14.3).
(3) Twice Beating Pulse

It includes anacrotic pulse, pulsus bisferiens, and dicrotic pulse (see Table 14.4).
Table 14.4 Causes of twice beating pulse
Anacrotic pulse Bisferiens pulse Dicrotic pulse
1. AS 1. Hyperkinetic circulatory states 1. Enteric fever

2. AR, PDA 2. Cariomyopathy, cardiac
tamponade, myocarditis
3. ARAS 3. Hypovolemic shock
4. Hypertrophic obstructive 4. During intraoartic
cardiomyopthy balloon pump
A B
S4 P2 S4 P2
S1 A2 S1 A2
Dicrotic notch Dicrotic notch
Fig. 14.13 | Anacrotic pulse. (A) Normal pulse, (B) anacrotic pulse in AS with distinct
anacrotic and percussion waves on the upstroke.
(a) Anacrotic pulse

In the slow rising pulse (pulsus tardus), a distinct notch (anacrotic) on the upstroke
of the carotid pulse with two separate waves (anacrotic and percussion) can be pal-
pated. This is characteristically found in AS (see Fig. 14.13).
Lower the notch, severe is the AS, and the presence of anacrotic pulse indicates
70 mmHg pressure gradient.
(b) Bisferiens Pulse (Bisferiens is a Latin word, Bis two, ferise to beat): It is
characterized by two systolic peaks (percussion and tidal waves) separated by a distinct
midsystolic dip (see Fig. 14.14).
Causes and mechanism of bisferiens pulse:
i) Conditions with large stroke volume:
It occurs in conditions in which a large stroke volume is rapidly ejected from
the LV as in severe AR, PDA, hyperkinetic circulatory states.

Normally, the percussion wave is felt but not the tidal wave (these waves are due
to the elastic recoil of aorta and reflected wave from the periphery respectively).
Hence in situations where the initial percussion wave is exaggerated due to large
stroke volume (as in severe AR), the tidal wave also becomes prominent.
ii) Combination of slow rising and collapsing pulse:
Bisferiens pulse also occurs in patients with combined AS and AR, a combination
of slow rising and collapsing pulses.

ARTERIAL PULSE 237
A B C
S4 P2 S4 P2 S4 P2
S1 A2 S1 A2 S1 A2
P T
P T
Dicrotic notch Dicrotic notch Dicrotic notch
Fig. 14.14 | Pulsus Bisferiens. (A) Normal pulse, (B) pulsus bisferiens in AR with equal
percussion (P) and tidal (T) waves, (C) pulsus bisferiens (Spike and dome
pulse) in HOCM with prominent percussion (P) wave.
The stenosis permits a jet lateral to the increased velocity of jet which causes a fall
in pressure (Bernoulli phenomenon) and results in a dip in the pulse wave with
a secondary outward movement (prominent tidal wave).
iii) Hypertrophic obstructive cardiomyopathy (HOCM): Bisferiens pulse may also
occur in HOCM.6 However, it is usually recordable but not palpable.
The initial percussion wave is due to rapid ejection of blood into the ascending
aorta during early systole.
The midsystolic dip (negative wave) coincides with marked decrease in the rate
of LV ejection, as the left ventricular outflow tract obstruction becomes mani-
fest due to the thickening of interventricular septum and the systolic anterior
motion (SAM) of anterior mitral leaflet.
The second systolic (tidal) wave is most likely produced by reflected waves from
the periphery.
Hence, pulse of HOCM behaves partly like AR (initial component) and partly
as AS (second component), but percussion wave is more prominent than the
tidal wave.
iv) Normals: Rarely seen in normal individuals.
Other characteristic features
The two waves are equal or tidal wave is prominent in AR, ARAS.
In HOCM, percussion is more prominent than tidal wave.
Bisferiens pulse disappears when the heart failure supervenes.
Detection: It is readily detected by palpating the carotids.
However, the presence of carotid systolic thrill may mask the features of bisferiens
pulse, in which case peripheral pulses like the radial or brachial are suitable for
detection of this pulse.
Apply graduated pressure or completely obliterate the pulse and gradually release it
to appreciate the two waves.
A B
S4 P2
S1 A2 S4 P2
S1 A2
Dicrotic
wave
Dicrotic notch Dicrotic notch
Fig. 14.15 | Dicrotic pulse. (A) Normal pulse, (B) dicrotic pulse in hypovolemics shock
with prominent dicrotic wave.
(c) Dicrotic pulse (Dicrotic is a Greek Word, di two, krotos beat): It is character-
ized by two peaks, one in systole (percussion wave) and the other in diastole (dicrotic
wave) immediately after S2, which is due to accentuated and palpable reflected wave
from the periphery7 (see Fig. 14.15).
Commonly seen in low output states such as:
Enteric fever or any fever with vasodilatation due to the circulating vascular toxins.
Cardiomyopathy
Cardiac tamponade
Myocarditis
Hypovolemic shock and
During intraoartic balloon pump (IABP).
Detection: It can be felt in carotids, but can be better appreciated in the radial artery.
It is better appreciated during inspiration and with the inhalation of amylnitrate.
But it is unusual when the systolic pressure is 130 mmHg.
Simultaneous auscultation is helpful as it occurs immediately after S2.
(4) Irregularly Regular Pulse

It consists of pulsus bigeminus and pulsus alternans.
(i) Pulsus bigeminus: It is an irregular rhythm caused by premature contractions
(usually PVCs) resulting in the alteration of the strength of the pulse which may be
confused with pulsus alternans (see Fig. 14.16).
However, in pulsus bigeminus, the weak beat always follows the short interval and
the long compensatory pause following a premature beat is followed by a stronger
than normal pulse in normal individuals or in states of fixed left ventricular outflow
tract obstruction such as AS.
Stronger pulse is due to more diastolic filling following long compensatory pause
and extrasystolic potentiation of ventricular contraction.
Pulsus bigeminus may also be seen in AV blocks and atrial flutter with block.
ARTERIAL PULSE 239
EKG VPC VPC
Carotid Pulse bigeminy
Fig. 14.16 | Pulsus bigeminus and ventricular premature contraction (VPC).
120
Strong Weak beat
beat
mmHg
80
Fig. 14.17 | Pulsus alternans.
Brockenbrough sign is fall or failure to increase the pulse volume in the post extra sys-
tolic beat. This sign occurs in:
HOCM due to post extra systolic potentiation of dynamic left ventricular outflow tract
obstruction
Constrictive pericarditis due to failure to fill the ventricles more even after longer
diastolic periods due to constriction
Severe LV dysfunction due to failure to augment contraction inspite of more
preload.
(ii) Pulsus alternans: (Traube, 1872) It is a regular rhythm in which a strong beat
alternates with a weak beat and is related to alternating more number of contractile
elements and loss of contractile elements participating in each contraction8 (see
Fig. 14.17).
It is frequently precipitated by PVCs and is a sign of severe LV dysfunction.
Types
Total: When the weak beat is not perceived at all or when involving both sides of
the heart.
Partial: When involving only RV (as in PE) or LV (as in AS).
Right atrial pulsus alternans: Severe right ventricular failure rarely associated with
tall a and v waves that alternate with short a and v waves of right atrial pressure.
Compound pulsus alternans: Additional alteration involving the weak beats in
association with a usual alteration of strong and weak beats is said to have compound
pulsus alternans.
Causes
Severe AS (often with failure)
Dilated cardiomyopathy, myocarditis
Acute pulmonary embolism and severe pulmonary stenosis.
Detection: It is better appreciated in the peripheral pulses (radial and femoral).
Readily recognized and confirmed by sphygmomanometry, generally accompanied
by alteration in the intensity of Korotkoff s sounds and occasionally by alteration in
the intensity of heart sounds and murmurs.
When systolic pressure alternates by 20 mmHg, it can be readily detected by pal-
pation of a peripheral pulse (radial or femoral) than a central pulse (like carotid).
Palpation should be carried out with light pressure and with patients breath held in
mid expiration to avoid the superimposition of respiratory variation on the ampli-
tude of the pulse.
It is accurately quantified by the determination of intra-arterial pressure by
catheterization.
The maneuvers, which exaggerate the pulsus alternans, help in its detection. It is
exaggerated:
By decreasing the venous return by adopting upright posture or by infusion of
nitroglycerine
And in the presence of aortic regurgitation or systemic hypertension.
(5) Pulsus Paradoxus

It is defined as an exaggerated decrease in the strength (amplitude) of the arterial
pulse during normal quiet inspiration due to the exaggeration of normal inspiratory
decline in the systolic arterial pressure of 10 mmHg, reflecting an exaggerated
inspiratory decline of 7% in the LV stroke volume9 (see Table 14.5).
The term pulsus paradoxus was coined by Kussmaul (1873). It is defined as the
apparent paradox of disappearance of pulse during inspiration despite the presence
of heart beat.
Detection:
When the inspiratory decline of systolic arterial pressure is 20 mmHg, pulsus
paradoxus is easily detected by the palpation of radial or brachial artery as an inspi-
ratory decline in the amplitude of the pulse.
Milder degrees of paradoxical pulse can be readily detected by sphygmomanometry.
The cuff should be inflated 20 mmHg above the systolic pressure and slowly
deflated at a rate of 2 mmHg/heart beat, when the Korotkoff sounds are heard only
during expiration (i.e. peak systolic pressure during expiration). The cuff is further
deflated more slowly to the point at which Korotkoff sounds are heard equally well
in both inspiration and expiration. The difference between these two pressures is the
estimated magnitude of pulsus paradoxus. The patient should be breathing nor-
mally and should not take a deep breath as normal individuals can have pulsus para-
doxus with deep breathing.
ARTERIAL PULSE 241
Table 14.5 Pulsus paradoxus
Absence of pulsus
Cardiovascular Pulmonary
paradoxus when CT
causes causes
is associated with
1. Cardiac tamponade 1. COPD 1. ASD

2. Effusive constrictive pericarditis 2. VSD
3. Restrictive cardiomyopathy 3. AR
4. Massive pulmonary embolism 4. Pericardial adhesions
5. Severe hypovolemic shock
The magnitude of the paradoxical pulse can be accurately quantified by means of an

intra arterial catheter, but cuff sphygmomanometry is sufficient for bed side evaluation.
Causes
Physiological:
Pregnancy
Extreme obesity
Students paradox (exaggerated inspiration voluntarily).
Cardiovascular:
Cardiac tamponade
Effusive constrictive pericarditis (in 50%)
Massive pulmonary embolism
Severe hypovolemic shock (due to hemorrhage or septic shock)
Restrictive cardiomyopathy
Pulmonary:
COPD: Severe emphysema, acute severe bronchial asthma, upper airway obstruction
Mechanism of pulsus paradoxus
Normally, inspiration results in fall of intrapericardial pressure (IPP, from 3 mmHg
to 6 mmHg) which causes increase of right ventricular transmural pressure and
venous return with slight changes in right and left ventricular sizes (see Fig. 14.18).
In pulsus paradoxus inspiration causes a decline in elevated intrapericardial pressure
(often from 20 mmHg to 18 mmHg) and right atrial pressure that results in the
increase of RV transmural (distending) diastolic pressure which augments the venous
return and the filling of the right heart. This in turn results in:
(1) The increase in RV (diastolic) dimensions producing flattening and leftwards
shift of the interventricular septum thereby compressing the LV (i.e. LV
dimensions and compliance) that impedes LV filling and decreases LV output
and systolic arterial pressure.10
(2) The increase of intrapericardial pressure and fall of the LV transmural diastolic
pressure which further impedes LA and LV filling, fall in LV output and decrease
of systolic arterial pressure11 (see Figs 14.19 and 14.20).
This can be substantiated by echocardiography.12
Pericardium
Pericardial
space
Normal expiration-IPP: -3 mmHg Normal inspiration-IPP: -6 mmHg
Fig. 14.18 | Normal hemo-dynamic effects of respiration: Inspiration results in fall of

IPP, which causes an increase of RV transmural pressure (RVTP
RVEDP IPP) and increase in venous return. This in turn, results in slight
increase in RV size at the expense of a slight decrease in LV size due to dis-
placement of IVS from right to left. (IPP: intrapericardial pressure, RVTP:
right ventricular transmural pressure, RVEDP: right ventricular end diastolic
pressure, IVS: interventricular septum).
Fig. 14.19 | Mechanism of pulsus paradoxus in Cardiac tamponade: Inspiration results

in the fall of elevated intrapericardial pressure (often from 20 mmHg
to 18 mmHg) which causes an increase in RV transmural pressure and
augments venous return. This in turn further increase in RV size and causes
septal bulging towards LV, which further decreases LV size, LV output and
arterial pressure.
Additional factors for pulsus paradoxus

Inspiratory pooling of blood in the pulmonary bed (pulmonary veins and capillaries)
(i.e. increase of hang out interval) produces decline in LA and LV filling and LV
stroke volume and systolic arterial pressure.11
The underfilled LV (LV volume is decreased in cardiac tamponade) may be oper-
ating in the steep ascending limb of Starling curve so that any inspiratory reduction
ARTERIAL PULSE 243
Systolic arterial
Pulsus paradoxus
pressure
Pulmonary
Inspiration LV filling & output
vascular pooling
LV dimensions &
Elevated IPP LVTP
compliance
RVTP IPP LV compression
RA & RV filling RV volume & size Left shift of IVS
Fig. 14.20 | Mechanism of pulsus paradoxusIPP: intrapericardial pressure, RVTP: right

ventricular transmural pressure, LVTP: left ventricular transmural pressure,
IVS: interventricular septum.
of LV filling results in marked depression of the LV stroke volume and the systolic
pressure.13
Pulsus paradoxus in COPD: The decrease in lung compliance magnifies the nor-
mal inspiratory decrease in LV volume and systolic arterial pressure and expiration
may be accompanied by an excessive rise in the systolic pressure above normal.
Absence of pulsus paradoxus: Pulsus paradoxus is absent, when cardiac tamponade (CT)
occurs in a condition which permits equal filling of both ventricles (e.g. shunt) or more
filling of LV (e.g. AR). CT without pulsus paradoxus occurs when associated with:
ASD due to equal filling of both ventricles in both phases of respiration
VSD due to free communication between the ventricles preventing differential
filling
AR as filling of LV is maintained irrespective of respiration
Pericardial adhesions especially over the right side of the heart.
Types
(i) Total paradox is the complete disappearance of palpated pulse during inspiration,
which occurs during very severe CT or CT combined with hypovolemia (see
Table 14.6).
(ii) Reversed pulsus paradoxus: There is an inspiratory increase and an expiratory
decrease of systolic arterial pressure. It occurs in:
Positive pressure breathing with artificial ventilators: Intrathoracic pressure is
higher during inspiration and lower during expiration i.e. reversal of the normal.
If CT occurs in this setting, reversal of pulsus paradoxus is noted.
Isorhythmic AV dissociation: (atrial activity precedes QRS during inspiration

and marches into QRS during expiration) The atrial activity during inspiration
increases the stroke volume and its lack during expiration decreases the stroke
volume and systolic pressure.
HOCM: Reversed pulsus paradoxus occurs in HOCM,14 but the mechanism is
not known.
iv. Volume of the Pulse

It gives an idea of the pulse pressure, which depends on the stroke volume and the com-
pliance of the arteries. The pulse volume could be normal, low or high. Pulsus parvus,
pulsus magnus and hyperkinetic pulse are the types of pulse depending upon its volume
(see Table 14.7).
i) Pulsus Parvus
It is a low volume small amplitude pulse (a small weak pulse) that occurs because of
the decreased stroke volume, characteristically seen in AS with pulsus tardus.
Pulsus parvus et tardus refers to a small pulse with a delayed systolic peak charac-
teristic of severe AS.
Pulsus parvus is also observed in severe heart failure.
It is best detected by palpating the carotids.
Table 14.6 Causes and types of pulsus paradoxus
Total pulsus paradoxus Reversed pulsus paradoxus
1. Severe cardiac tamoponade 1. Positive pressure breathing with ventilators

2. Isorhythmic AV dissociation
3. HOCM
Table 14.7 Causes and types of pulse depending upon the volume
Pulsus parvus Pulsus magnus Hyperkinetic pulse
1. Aortic stenosis 1. Aortic regurgitation 1. Pregnancy

2. Severe congestive heart failure 2. Anemia
3. Thyrotoxicosis
4. Beriberi
5. Fever
6. Pagets disease
of the bone
ARTERIAL PULSE 245
ii) Pulsus Magnus

It is a high volume large amplitude pulse because of an increased stroke volume, char-
acteristically seen in AR.
iii) Hyperkinetic or Bounding Pulse

It is characterized by a large bounding pulse due to an increased stroke volume and
rapid ejection from the left ventricle.
It occurs in patients with elevated stroke volume, sympathetic hyperactivity,
and in patients with a rigid sclerotic aorta. It is typically seen in hyperkinetic
circulatory states.
In MR and VSD, the forward stroke volume (from LV into aorta) is usually
normal, but the fraction ejected during early systole is greater than normal.
Therefore, the pulse is of normal volume but may rise briskly (also described
as abnormally rapid).
v. Condition of the Vessel Wall

It is examined by flattening the artery by digital pressure and sliding it sideways.
Atherosclerotic vessel is thickened, rigid and tube like.
It is hard and calcified in Monckebergs degeneration (medial calcification).
vi. Radial Pulse Synchronicity

Examine whether the radial pulses are equal on both sides. Radial pulse on one side
may be diminished or absent in patients with:
Takayasu arteritis
Thoracic outlet syndrome (commonly a cervical rib, scalenus anticus syndrome)
Subclavian steal syndrome
Chronic atherosclerosis (predominantly involves innominate, more commonly the
left subclavian artery)
Acute microemboli to the arm from the heart or from proximal aneurysmal lesion
(including aortic aneurysm)
Coarctation of aorta (if proximal vessels are also involved) and
Dissection of aorta.
vii. Absent or Delayed Femoral Pulsations

While palpating radial pulse, place fingers of the other hand over the femoral pulse
(below inguinal ligament, one third of distance from pubic tubercle) (see Fig. 14.21).
A noticeable delay in the arrival of femoral pulse is suggestive of:
Coarctation of aorta (COA): In COA, the radiofemoral delay is not due to the delay
in arrival time but due to the delay in its rate of rise (amplitude).
Occlusive disease of the bifurcation of the aorta, common iliac or external iliac
arteries.
Fig. 14.21 | Simultaneous

delay.
palpation of radial and femoral pulse to detect any radiofemoral
5. CHARACTERISTIC FEATURES OF PULSE IN

COMMON CLINICAL CONDITIONS
The examination of arterial pulse is specially valuable in aortic valve disease.
i. Aortic Stenosis (AS)

Following are the characteristic features of the pulse in aoric stenosis:
Pulsus parvus et tardus: This is a low volume and slow rising pulse with delayed
systolic peak characteristic of severe AS (see Fig. 14.10).
Anacrotic pulse: In slow rising pulse, a distinct notch (anacrotic) on the upstroke of
the carotid pulse with two separate waves (anacrotic and percussion) can be felt (see
Fig. 14.13).
Pulsus alternans: It occurs in severe AS (see Fig. 14.17).
Pulsus bisferiens: It occurs in patients with combined AS and AR, a combination of
slow rising and collapsing pulses in which the two waves (percussion and tidal) are
equal or tidal wave may be prominent.
ii. Aortic Regurgitation (AR)

Following are the characteristic features of the pulse and peripheral signs in AR: These
signs are mostly due to wide pulse pressure.
(i) Pulse
Water hammer (collapsing) pulse: Thomas Watson first described it in 1844. It is
characterized by rapid upstroke followed by rapid descent of the pulse wave and is
best appreciated at the radial pulse (see Figs 14.11 and 14.12).
Pulsus bisferiens: It is characterized by two systolic peaks separated by a distinct mid
systolic dip. Either the percussion and tidal waves are equal or the tidal waves is
ARTERIAL PULSE 247
prominent. It is readily detected by palpating the carotids. Its presence indicates

severe AR (see Fig. 14.14).
Pulsus magnus: It is a high volume large amplitude pulse, and is best detected at the
radial pulse. Its presence indicates mod-severe AR.
(ii) BP
Diastolic BP is 40 mmHg and pulse pressure is 70 mmHg or 50% of systolic
BP in severe AR. BP is normalized in the presence of heart failure or LV dysfunc-
tion. In acute AR pulse pressure is narrow with high systolic and diastolic blood
pressures.
Hills sign: Hill and Rowlands in 1912 described the peak systolic pressure gradient
between posterior tibial and radial arteries. It is due to greater velocity of blood in
lower limb artery, which arises from the aorta in a straight course. Severity of AR
from Hills sign may be deduced: Systolic pressure difference of 2040 mmHg
angiographic 2AR, 4160 mmHg systolic pressure difference angiographic 3
AR, 60 mmHg systolic pressure difference angiographic 4AR.
(iii) Eyes
Landolfis sign (Landolfi, 1909): Due to the hyperemia of iris, there is contraction
and dilatation of pupil in systole and diastole respectively, which is known as
Landolfis sign.
Beckers sign: It presents as prominent retinal artery pulsations.
(iv) Head and Neck

de Mussets sign (de Musset was a French poet suffering with AR, described by
Delpinch in 1900): It is the synchronous nodding of head with heart beat.
Corrigans sign (Sir Dominic John Corrigan, 1932): It presents as the visible (danc-
ing) carotid pulsations.
Mullers sign (Muller, 1898): This sign presents as the pulsation of the uvula.
Minervinis sign (Minervini, 1910): Strong lingual pulsations are described as
Minervinis sign. The tongue depressor moves up and down when the tongue is
lightly depressed.
Logues sign (Logue, 1952): It is the pulsation of the sternoclavicular joint when AR
is associated with aortic dissection.
(v) Upper Limb

Locomotor brachialis: It is worm like visible pulsations of the brachial artery.
Quinckes pulse/sign (Heinrich Quinke, 1868): It is visible capillary pulsations.
Alternating blanching and reddening in the nail bed can be visualized by transmit-
ting light on the pateints finger tips. The capillary pulsations can also be visualized
by pressing a glass slide on the patients lips.
Palfreys sign (Palfrey, 1952) is the pistol shot sounds heard over the radial artery.
See above for various types of pulses.
BP: See above.
(vi) Lower Limb

Traubes sign: Booming of systolic sounds (pistol shots) heard over the femoral artery
due to sudden distension of arterial wall is described as Traubes sign.
Duroziezs sign (murmur) is more specific of all the peripheral signs of AR Paul
Louis Duroziez described it in 1861. It is a brui de tambour and consists of:
Systolic murmur: A forward murmur perceived by pressing the femoral artery
2 cm above the stethoscope, which is due to powerful contraction of LV and
increased stroke volume.
Diastolic murmur: A backward murmur perceived by pressing the femoral artery
2 cm below the stethoscope, which is due to the arterial recoil and back flow.
Hills sign: See above.
(vii) Abdomen
Rosen bachs sign is the pulsations in liver.
Gerhardts sign is the pulsations in spleen.
Dennisons sign (Dennison, 1959): Presence of pulsations in the cervix in female
patients is known as Dennisons sign.
REFERENCES
1. Murgo JP, Altobelli SA, Dorethy JF. Normal ventricular ejection dynamics in man during rest and
exercise. AHA Monogr 1975;46:92101.
2. ORourke MF. The arterial pulse in health and disease. Am Heart J 1971;82(5):687702.
3. Schlant RC, Felner JM. The arterial pulse- Clinical manifestations. Curr Prob Cardiol 1977;2(5):
150.
4. Garratt CJ, Griffith MJ, Young G, Curzen N, Brecker S, Richards AF, et al. Value of physical signs
in the diagnosis of ventricular tachycardia. Circulation 1994;90(6):31033107.
5. Corrigan DJ. On permanent patency of the mouth of the aorta, or inadequacy of the aortic valves.
Edinburg Med Surg 1832;37:225245.
6. Talley JD. Recognition, etiology and clinical implications of pulsus bisferiens. Heart Dis Stroke 1994;
3(6):309311.
7. Dow P. The development of the anacrotic and tardus pulse of aortic stenosis. Am J Physiol 1940;
131:432436.
8. Cohn KE, Sandler H, Hancock EW. Mechanism of pulsus alternans. Circualtion 1967;36(3):
372380.
9. Fowler NO. Pulsus paradoxus. Heart Dis Stroke 1994;3(2):6869.
10. Spodick DH. Pulsus paradoxus. In: Spodick DH. The Pericardium: A Comprehensive Textbook.
New York, Marcel Dekker, 1997:191199.
11. Shabetai R, Fowler NO, Guntheroth WG. The hemodynamics of cardiac tamponade and constrictive
pericarditis. Am J Cardiol 1970;26(5):480498.
12. Hoit et al. Echocardiographic correlates of pulsus paradoxus. Echocardiography 1996;11(3):265.
13. Friedman HS, Sakurai H, Choe SS, Lajam F, Celis A. Pulsus paradoxus: A manifestation of marked
reduction of left ventricular end diastolic volume in cardiac tamponade. J Thorac Cardiovasc Surg
1980;79(1):7482.
14. Massumi RA, Mason DT, Vera Z et al. Reversed pulsus paradoxus. N Eng J Med 1973;289(24):
12721275.
CHAPTER 15
M EASUREMENT OF THE
B LOOD P RESSURE
1. DEFINITION AND COMPONENTS Indirect Methods 251

OF ARTERIAL BLOOD PRESSURE 249 4. HYPERTENSION 262
2. DETERMINANTS OF ARTERIAL Causes of Hypertension 262
BLOOD PRESSURE 250 Mechanisms of Primary
3. MEASUREMENT OF ARTERIAL Hypertension 265
BLOOD PRESSURE 250 Complications of Hypertension 267
Direct Methods 250 REFERENCES 267
1. DEFINITION AND COMPONENTS OF ARTERIAL BLOOD PRESSURE
The arterial blood pressure is a measure of its potential energy or lateral force per unit
area of vascular wall, which is expressed in units of dynes per cm2 (in the metric system).
However physiologically and clinically, measurements of arterial pressure are usually
obtained by mercury manometer, which is expressed in mmHg. i.e. 1 mmHg 1.332
dynes/cm2, 120/80 mmHg 160/106.5 dynes/cm2.
The systemic arterial blood pressure consists of (see Table 15.1):
(i) Systolic blood pressure (SBP) is the maximum pressure exerted during systole.
Table 15.1 Definitions of the components of blood pressure
Pressure Definition
1. Systolic blood pressure Maximum pressure exerted during systole and indicates the
extent of work done by the heart
2. Diastolic blood pressure Minimum pressure exerted during diastole and indicates the
load against which heart has to work
3. Pulse pressure Difference of systolic and diastolic blood pressure, which
determines the pulse volume
4. Mean blood pressure Average blood pressure throughout the cardiac cycle, which
determines the pressure head. Sum of diastolic blood pressure
and 1/3rd of pulse pressure gives the mean blood pressure
5. Proportional pulse pressure Pulse pressure/systolic blood pressure
It indicates the extent of work done by the heart or the force with which the heart is
working and the degree of pressure that the arterial walls have to withstand.
Normal SBP is 120 mmHg.1
(ii) Diastolic blood pressure (DBP) is the minimum pressure exerted during diastole.
It is the measure of the total peripheral resistance and indicates the constant load
against which the heart has to work.
Normal DBP is 80 mmHg.1
(iii) Pulse pressure (PP) is the difference of systolic and diastolic blood pressure (PP
SBP DBP). It determines the pulse volume and normal average PP is 40 mmHg.
(iv) Mean blood pressure (MBP) is the average blood pressure throughout the cardiac cycle.
It is the sum of DBP and 1/3rd of PP (MBP DBP 1/3 PP).
It is same for each organ and determines the pressure head i.e. regional blood flow
through an organ depends on it.
Normal MBP ranges between 95100 mmHg with an average of 96 mmHg.
(v) Proportional pulse pressure (PPP) is the pulse pressure/systolic blood pressure
(PPP PP/SBP) PPP of 25% identifies 90% of patients with left ventricular
failure (LVF) and cardiac index of 2.21/min/m2.
2. DETERMINANTS OF ARTERIAL BLOOD PRESSURE
Arterial BP is the product of cardiac output (CO) and peripheral resistance (PR) i.e.
BP CO PR. Hence, any condition, which alters the CO or the PR or both, will
cause a change in arterial BP.
CO is the functional product of heart rate (HR) and stroke volume (SV) i.e.
CO HR SV.
SBP increases if the increase in CO is due to increase in SV and DBP increases if the
increase is due to increased HR.
If increase of CO is due to increase of both SV and HR, both SBP and DBP
increase.
Arterioles are the chief seat of PR, which depends on the elasticity of the vessel wall,
velocity, viscosity and total blood volume in the arterial system.
3. MEASUREMENT OF ARTERIAL BLOOD PRESSURE
Direct Methods
Stephen Hales (1783) first recorded the arterial pressures in mares and other animals
by cannulation and by the use of blood-filled glass column.2
Current techniques for the direct and continuous measurement of arterial pressure
utilize electromanometer, a transducer that converts mechanical energy into an elec-
trical signal suitable for amplification, display and recording.
MEASUREMENT OF THE BLOOD PRESSURE 251
The artery is cannulated with a saline filled catheter or needle that machanically couples
the circulation to the arterial manometer.
The use of side-hole catheter (instead of end-hole catheter) positioned in a large, patent
artery allows the measurement of true arterial pressure with less measurement errors.
Miniature, self-flushing strain gauge manometers that are directly attached to an
intravascular catheter or needle eliminate many of the problems related to transducer
mounting and flushing and overdamping by connecting tubes.
However, the use of intravascular electromanometers mounted on cardiac catheters
or the ones that are surgically implanted in vessel walls are the best method of direct
measurement of the arterial pressures.
Indirect Methods
History
Karl Vierdot (18181884) introduced the first sphygmographic method for indirect
measurement of BP, and Samuel Siegfried von Basch (in 1881) developed the first
non-invasive sphygmomanometer.3
This led to further work by Scipione Riva-Rocci in 1896, who developed the prototype
of the present day instrument.4 The invention of inflatable manometer permitted
the clinical, non-invasive and indirect measurement of the arterial pressure.
The original method of measuring SBP was the palpation of radial pulse. With
the discovery of arterial sounds (Nikolai Korotkoff, a Russian surgeon in 1905)5
and exhaustive description of these sounds (as Ki and Kc by McCutcheon and
Rushmer in 1967), the auscultatory method became the most common and popular
non-invasive method of measurement of arterial pressure.6 The various indirect
methods are:
Sphygmomanometric measurement: palpatory, ausculatatory and flush methods
Ultrasound Doppler method
Oscillometric method
Self measurement (home BP recordings)
Ambulatory BP monitoring.
(i) Palpatory Method

With sphygmomanometer
After the standard cuff inflation (30 mmHg above the anticipated SBP) which oblit-
erates the brachial pulse, the cuff is slowly deflated and the approximate peak systolic
pressure is the point at which the brachial pulse first reappears consistently.
The diastolic pressure is estimated by a distinct snapping quality of the palpable
pulse as the cuff is further deflated.
Without sphygmomanometer
Approximation of the systolic pressure without sphygmomanometer may be done
by the amount of brachial artery compression required to obliterate the ipsilateral
radial pulse.
When relatively mild brachial artery compression obliterates the radial pulse, the SBP
is 120 mmHg, and it usually may be 160 mmHg when considerable compression
is required.
(ii) Auscultatory Method

This method of blood pressure measurement requires proper understanding of Korotkoff
sounds and phases, proper technique and adequate cuff size.
Korotkoff sounds: Korotkoff sounds consist of two major components:6
The initial transient sound (Ki): The initial clear tapping sound occurs at the instant the
cuff pressure reaches the arterial systolic pressure and is probably caused by the oscilla-
tion of the arterial wall as the occluded segment is suddenly opened by systolic pressure.
The compression murmur (Kc) is caused by a turbulent jet of flow distal to the
partially compressed segment.
The audibility of the Korotkoff sounds is improved by opening and closing of the
fist vigorously, a dozen times.
Vasodilatation increases the intensity of Ki, while vasoconstriction or circulatory
collapse decreases its intensity.
Korotkoff phases: The Korotkoff sounds (sound and murmur) have been divided into
five phases occurring in sequence as the occluding pressure declines (see Fig. 15.1).
PHASE-I consists of clear tapping sounds (K ) which occur when the cuff pressure
i
has reached the arterial peak systolic pressure.
Phase of silence
Systolic
pressure Phase I
Tapping sounds (Ki)
Phase II
Soft murmurs (Kc)
Phase III
Loud slapping sounds
Phase IV
Muffled sounds
Diastolic
pressure Phase V
Phase of silence
Fig. 15.1 | Korotkoff phases.

PHASE-II consists of Ki sounds followed by soft murmurs (Kc), 510 mmHg lower
than the peak systolic pressure. Auscultatory silent gap occurs when phase II sounds
and murmurs are faint or not heard. This phenomenon tends to occur when there is
a venous distension or reduced velocity of arterial flow into the arm.
PHASE-III is an augmentation of phase II sounds and murmurs, 510 mmHg below
phase II, as increased volume of blood passes through the partially compressed artery.
PHASE-IV is sudden muffling of sounds due to loss of Ki and diminution of Kc com-
ponents, resulting in a blowing quality as the cuff pressure approaches arterial diastolic
levels, 510 mmHg higher than the phase V. In severe AR and hyperkinetic circula-
tory states, this phase represents the diastolic pressure.
PHASE-V is complete disappearance of Korotkoff sounds (Kc) when the artery is
no longer compressed to produce turbulent flow, occurring 510 mmHg lower than
phase IV and represents the diastolic pressure.
Correlation of Korotkoff phases and blood pressure:
SBP is the point at which phase I occurs and onset of phase V is used to define
as DBP.
Correlation of phases I and V with direct measurement of systolic and diastolic
pressures respectively was good,7 even though the indirect methods have the ten-
dency to underestimate the systolic pressure and overestimate the diastolic pres-
sure (when phase IV is used as an end point).
However, diastolic pressure should be recorded both at phase IV and V in severe
AR and hyperkinetic circulatory states.
Failure to detect auscultatory gap when the second appearance of sounds is taken as
systolic pressure, may result in an erroneously low systolic pressure, and the gap will
be over estimated if the first muffling of sounds (silent gap) is considered as diastolic
pressure.
Sounds transmitted from the prosthetic valves may be responsible for falsely high
readings.
Adequate equipment and cuff size
The width of the cuff should be 20% more than the limb diameter or 40% of the
limb circumference, and length of the cuff should be adequate to encircle atleast
80% of the limb,1 with a ratio of 1:2 between the width and the length (see
Fig. 15.2).
The standard cuff size is 5 with a length of 10 (see Fig. 15.3).
When this cuff is applied to a large arm in an obese or to a normal adult thigh, arterial
systolic pressure is overestimated, and when it is applied to a small arm, the systolic
pressure is underestimated.
In patients with arteriosclerosis (with rigid sclerotic arteries), the systolic pressure
may also be overestimated by as much as 30 mmHg.
If the thigh cuff is too small, a higher diastolic pressure is recorded in the legs than
in the arms.
This cuff mismatch may be corrected to some extent by the following formula: If
cuff is relatively smaller: 32 (1.05 arm circumference in cm), if () add to the
BP recording and if () subtract from the BP recording.
Fig. 15.2 | Pediatric and adult cuffs. Fig. 15.3 | Standard cuff size for an adult (width 5
and length 10).
Fig. 15.4 | Usual cuff size for children (width 3).

The cuff width should be approximately 1.5 in infants and small children, 3 in
young children (25 years of age) and 8 in obese adults (see Fig. 15.4).
Mercury manometers (see Fig. 15.5) in general are more accurate and reliable than
the aneroid type (see Fig. 15.6) and other electronic equipments.
BP recordings using manual or automatic inflation and deflation of the cuff and detec-
tion of Korotkoff sounds by a stethoscope, microphone or ultrasonic transducer are
being increasingly used for home blood pressure recordings (see Fig. 15.7) and ambu-
latory assessment. As mercury manometers are being replaced by new equipment due
to environmental contamination (by mercury spillage), the new equipment should be
appropriately validated and regularly checked for accuracy.8
Proper technique
Patient should avoid caffeine, exercise and smoking atleast 30 min prior to BP mea-
surement. If patient had caffeine, exercise and smoking, BP will be elevated which
may return to the baseline in about 1530 min.
Fig. 15.5 | Mercury manometer. Fig. 15.6 | Aneroid manometer.
Fig. 15.7 | Automatic digital manometer in which systolic, diastolic and pulse readings
are displayed once the cuff is inflated.
Patient should be seated for atleast 5 min quietly and comfortably in a chair with
feet on the floor and arm supported at the heart level. Anxiety may give rise to white
coat hypertension. Ambulatory or self-monitoring of BP may be recommended in
such cases.
The cuff should be snuggly applied over the artery, at the level of the heart, with its
lower edge atleast 1 above the antecubital fossa (see Fig. 15.8).
Inflate the cuff to a pressure of 20 mmHg above the anticipated systolic pressure, as
indicated by the obliteration of radial pulse. Stethoscope is then applied lightly but
firmly over the artery, and auscultatory pressures are determined as the cuff is deflated
at a rate of 2 mmHg/sec. A rapid deflation of the cuff may cause the sounds to be
Fig. 15.8 | BP recording in upper limb.

missed especially in the presence of bradycardia or irregular rhythm and arterial
pressure may be underestimated.
When the cuff is deflated too slowly or is immediately re-inflated for repeat pressure
recordings, the resultant venous congestion may artificially elevate the diastolic pres-
sure and falsely decrease the systolic pressure by decreasing the intensity of phase I
or II sounds to inaudible levels.
The cuff should be deflated rapidly and completely after the diastolic pressure is
noted and a full minute is allowed to elapse before the pressure is re-measured in the
same limb.
Excessive pressure on the stethoscope head may not affect the systolic pressure record-
ing but it may give erroneously low diastolic readings.
Determination of BP in both arms and atleast one lower limb is recommended.
BP measurement in the lower limbs
The patient lies on the abdomen and preferably, 8 wide cuff is applied with com-
pression over the posterior aspect of the mid thigh. Auscultation is carried out in the
popliteal fossa (see Fig. 15.9).
To measure pressure in the lower leg (when 8 wide cuff is not available), an arm cuff is
placed over the calf and auscultation is done over the posterior tibial artery (or over
the dorsalis pedis).
Exercising the limb improves the audibility of the Korotkoff sounds.
BP recording in special circumstances
In severe aortic regurgitation and hyperkinetic circulatory states, diastolic pressure
should be recorded both at phase IV and V.
Patients with atrial fibrillation have a significant beat-to-beat variation in their arterial
pressure, which may result in underestimation of their BP. Hence, several recordings
should be taken (atleast 3 recordings) and the average is noted in each limb.
Fig. 15.9 | BP recording in lower limb.

Table 15.2 Variations in arm and leg systolic pressures
Pressure difference of 10 mmHg Pressure difference of 20 mmHg

between the two arms between arm and leg
1. Aortic arch syndrome, coarctation 1. Coarctation of aorta, aortic dissection,

of aorta aortic arch syndrome
2. Thrombosis/aneurysm of innominate 2. Subclavian steal syndrome
or subclavian arteries 3. Severe aortic regurgitation
3. Subclavian steal syndrome
4. Supravalvular aortic stenosis
5. Scalenus anticus syndrome,
cervical rib
Varible BP recordings
Differences in systolic pressures between the two arms that exceed 10 mmHg
(see Table 15.2): When measurements are made simultaneously or in rapid
sequence9 (switch the limbs and re-measure the pressures for confirmation) and the
difference in systolic pressures between the two arms exceeds 10 mmHg, it suggest
the presence of:
Obstructive lesions in the aorta, origin of the innominate and subclavian arteries
(due to arotic arch syndrome, coarctation, aneurysm and thrombosis)
Supravalvular AS10 (right arm pressure exceeds that in the left arm, see Fig. 15.10)
Subclavian steal syndrome in adults (lower or absent ipsilateral brachial artery
pressure accompanied by cerebrovascular symptoms in patients with vertebro-
basilar artery insufficiency)
Scalenus anticus syndrome and cervical rib.
Difference in arm and leg pressures: Normally, a progressive increase in systolic pres-
sure occurs as the point of BP measurement is moved from the central aorta to the
Coarctation
High pressure
Low pressure
Supravalvular
aortic stenosis
Possible
bicuspid
aortic valve
Left
ventricular
hypertrophy
Fig. 15.10 | Insuresupravalvular AS, right arm pres-

exceeds that in left arm.
Fig. 15.11 | Coarctation of aortaA high brac-
hial arterial pressure is detected.
periphery and increment is equal in large arteries of both arm and thigh. However, the
direct measurement of brachial and femoral arterial pressures11 and indirect measure-
ment of brachial and popliteal pressures by using appropriate cuffs,12 have shown
that the mean BP is equal in all the sites.
A difference in arm and leg pressures (a difference of 20 mmHg usually of the sys-
tolic pressure) may occur in the following conditions (see Table 15.2):
A relative high brachial systolic pressure occurs in coarctation of aorta or aortic
dissection (see Fig. 15.11).
A relative high crural systolic pressure occurs in aortic arch syndrome, subclavian
steal syndrome and severe AR (Hills sign13, see Fig. 15.12).
A higher diastolic pressure in the legs than in the arms, suggests that the thigh cuff
is too small.
An increase in arterial pulse pressure usually results from an increase in stroke
volume and ejection velocity, often with a decreased PR. A wide PP is commonly
observed in:
Hyperkinetic circulatory states such as pregnancy, hot weather, exercise, anemia,
hyperthyroidism, arteriovenous fistulas
AR, PDA, truncus arteriosus
Complete heart block and marked sinus bradycardia.
A narrow pulse pressure may result from (see Table 15.3):
An increased PR, e.g. in heart failure due to increased circulating catecholamines
Decreased stroke volume, e.g. severe AS
Markedly decreased intravascular volume, e.g. diabetic ketoacidosis.
Variation with respiration (also see pulsus paradoxus): With normal respiration, the
peak SBP is greater during expiration by as much as 10 mmHg and falls during
Dilated aorta
Aortic valve
Dilated left
ventricle
Fig. 15.12 | Aortic regurgitationA high crural systolic pressure is found (i.e. Hills sign).
Table 15.3 Conditions with wide and narrow pulse pressures
Wide pulse pressure Narrow pulse pressure
1. Hyperkinetic circulatory states 1. Heart failure

2. Aortic regurgitation 2. Severe aortic stenosis
3. PDA, truncus arteriosus 3. Diabetic ketoacidosis
4. Complete heart block
inspiration by 10 mmHg. A fall in systolic pressure by 10 mmHg during inspiration
(pulsus paradoxus) occurs:
During hyperventilation
In patients with pericardial tamponade, restrictive cardiomyopathy and COPD
which may be detected by the examination of pulse, but is best detected by
sphygmomanometry.
Variation with exercise
Isotonic exercise (both supine or upright) produces moderate increase in BP
(systolic mean diastolic pressure).
While sustained isometric exercise produces an abrupt increase in all pressures
(systolic, mean and diastolic).14
BP in pulsus alternans
Pulsus alternans can be detected by palpating a peripheral artery (femoral or
radial).
However, sphygmomanometer can be used to accurately measure the beat-to-
beat variation in the pressure that characterizes pulsus alternans.
Orthostatic hypotension (OH) is present when there is a supine to standing BP

decrease by 20 mmHg systolic or 10 mmHg diastolic pressure.
Severe volume depletion, baroreflex dysfunction, autonomic insufficiency and
venodilators (
blockers, blockers, nitrates and diuretics) may cause OH.
OH is more common in DM and in elderly individuals (70 years of age).
There is a strong correlation between the severity of OH, premature death and
increased morbidity from falls and fractures.15,16
In children, average SBP at 1 year of age is 90 mmHg and increases by 5 mmHg
every 3 years and reaches 120 mmHg (adult level) by 1213 years of age, while the
DBP is usually 60 10 mmHg. Following simple formula gives the expectant sys-
tolic pressure in children: SBP 90 (age 5)/3.
(iii) Flush Method of BP Recording

Snuggly apply the BP cuff to the limb (arm or thigh), elevate the limb and an elastic
bandage is applied from fingertips or toes proximally to eliminate the blood from
the skin capillaries and veins and to blanch the distal forearm and hand or leg
and foot.
With the bandage still in position, the cuff is inflated 20 mmHg above the antici-
pated systolic pressure, and then the bandage is removed.
The distal limb should now be pale and white, and cuff should be deflated at a rate of
2 mmHg/sec.
The pressure at which first blush appears in the limb is recorded which is closer to
the mean pressure than to peak systolic pressure. The reading is 1030 mmHg lower
than the systolic pressure obtained by the auscultatory method.
This method is helpful in suspected coarctation of aorta where auscultatory and
palpated pressures in the lower limb are not obtainable.
(iv) Ultrasound Doppler Method

The transducer is placed over the artery, which requires the recording of pressures.
The arterial wall oscillations are transformed into an audible signal (sounds) at the
peak intravascular systolic pressure and the sounds terminate when the intravascular
pressure dips below the end diastolic pressure.
With this method, systolic pressure is accurately recorded, while diastolic pressure
recording is not very reliable.
(v) Continuous Non-invasive BP Monitoring by Oscillometric

Method or Arterial Tonometry
In the arterial tonometry method, a probe with a micromanometer in its tip which
operates on the principle of a piezo-resistive transducer of cantilever construction, is
used.17,18
In oscillometric technique, a special cuff that senses the arterial waves is used.
Systolic, diastolic and mean arterial pressures as well as HR are digitally displayed
(see Fig. 15.13). The mean pressure is the most accurate.
Fig. 15.13 | Continuous BP monitoring by oscillometric method in ICU by which

systolic, diastolic and mean pressures as well as HR are digitally displayed.
(vi) Self-monitoring of BP
Self-monitoring of BP at home or work using manual or automatic inflation and
deflation of the cuff, and detection of Korotkoff sounds by stethoscope, microphone
or ultrasound transducer is a practical approach:
To assess the difference between office (clinic/hospital) and out of office BP
and to assess BP in smokers prior to consideration of ambulatory monitoring or drug
therapy.
(vii) Ambulatory BP Monitoring (ABPM)

This provides the information about BP during daily activities and sleep,19 and either
arterial tonometry or oscillometric technique is used.
BP has a reproducible circadian profile with higher values:
While awake
When mentally and physically active
And during early morning for 3 hrs during the transition of sleep to wakefulness.20
BP has much lower values during rest and sleep (drops by 1020% during sleep).
Hence, ABPM may be indicated and could be helpful in the following (see
Table 15.4):
Suspected white coat hypertension with no target organ damage which may be
noted in 2035% of patients diagnosed with hypertension.21
Apparent drug resistance in hypertensive patients
Hypotensive symptoms with antihypertensive drugs
Episodic hypertension
Autonomic dysfunction
Assessing BP in smokers: Smoking causes an acute rise in the BP and it returns to
the baseline in about 15 min of stopping the smoking.
Table 15.4 Indications of ambulatory BP monitoring
1. Drug resistance hypertension

2. Episodic hypertension
3. White coat hypertension
4. Drug induced hypotension
5. Autonomic dysfunction
The level of BP measurement using ABPM correlates better in a given clinical con-
dition than the clinic/hospital BP measurement.22
Individuals in whom BP does not fall (by 1020%) during night, are at increased
risk of the cardiovascular events.
In ABPM patients with 24 hr BP exceeding 135/85 mmHg, are likely to have a
cardiovascular event twice as those with 24 hr BP 135/85 mmHg, irrespective of
the level of the clinic/hospital BP.23
4. HYPERTENSION
The term hyperpiesia was introduced by Albutt (in 1896) to distinguish patients
with elevated BP alone from those with Brights disease, which was later renamed as
essential hypertension.24
Causes of Hypertension
An adult individual has normal BP when SBP is 120 mmHg and DBP 80 mmHg.
Hypertension is defined as SBP of 140 mmHg or DBP of 90 mmHg1 (see
Table 15.5).
(i) Primary or essential hypertension: about 89.50%25
(ii) Secondary hypertension: 510% (see Table 15.6).
(a) Renovascular hypertension (about 13.3%): 25 Two major types are (causes):
Atherosclertic renal artery disease (2/3rd, males)
Non-atherosclerotic: Fibro-muscular dysplasia (1/3rd, young females).
Other uncommon causes of Renovascular hypertension are:
Aneurysm of renal artery
Embolism of renal artery
Extravascular compression of renal artery by tumor or fibrosis.
(b) Renal parenchymal disease (25%)
Acute glomerulonephritis
Chronic glomerulonephritis (1.8%)25
Diabetic nephropathy
Polycystic renal disease
Table 15.5 Classification of BP for adults (JNC 7)1
BP classification Systolic BP (mmHg) Diastolic BP (mmHg)
1. Normal 120 and 80

2. Pre-hypertension 120139 or 8089
3. Stage 1 hypertension 140159 or 9099
4. Stage 2 hypertension 160 or 100
Table 15.6 Secondary hypertension
Cause Incidence
1. Renovascular disease 13.3%

2. Renal parenchymal diseases 25%
3. Coarctation of aorta 0.2%
4. Endocrinal diseases 1%
5. Neurological diseases 1%
6. Drugs and other substances 1%
induced hypertension
7. Pregnancy induced hypertension 10% of primi
Hydronephrosis
Hypertension during dialysis (blood pressure increases during the 2nd day as a result
of excessive fluid retention)26
After renal transplantation (within one year due to renal artery stenosis or drugs).27
Other causes:
Renin producing tumors
Primary sodium retention (Liddle syndrome, Gordon syndrome).
(c) Coarctation of aorta (0.2%)28
(d) Endocrinal diseases
Adrenal causes of hypertension (1%)
Adrenal cortical disease
Cushings syndrome (0.6%)25
Primary aldosteronism (1.5%)25 due to adenoma or bilateral adrenal hyperplasia.
Adrenal medullary disease
Pheochromocytoma (0.3%)25 (predominantly epinephrine)
Extra-adrenal chromoffin tumors (predominantly nor-epinephrine).
Thyroid gland related hypertension
Hyperthyroidism
Hypothyroidism
Hashimotos thyroiditis.
Hyperparathyroidism
Hypercalcemia.
Pituitary disease: Growth hormone excess
Acromegaly.
(e) Neurological disorders: Causing hypertension (uncommon causes)
Increased intracranial tension: Brain tumors, encephalitis
Sleep apnea
Acute porphyria
Familial dysautonomia
Guillian-Barre syndrome.
(f) Acute stress including surgery
Post-operative
Hypoglycemia
Burns
Pancreatitis
Sickle cell crisis
Alcohol withdrawal.
(g) Hypertension in pregnancy: 29 Hypertension may occur in 10% of the previously
normotensive women after 20 weeks of gestation of the first pregnancy. Following types
of hypertension have been described during pregnancy:
Chronic hypertension: 140 mmHg SBP or 90 mmHg DBP prior to pregnancy
or before 20 weeks of gestation and persists for 12 weeks postpartum.
Pregnancy induced hypertension: preeclampsia, eclampsia (140 mmHg SBP or
90 mmHg DBP with proteinuria after 20 weeks of gestation).
Chronic hypertension with superimposed preeclampsia.
Gestational hypertension without proteinuria occurring after 20 weeks of gestation:
It may be a temporary phenomenon or a pre-proteinuric phase.
Transient hypertension: BP is normalized by 12 weeks of postpartum. But it may
recur in subsequent pregnancies and may predict future primary hypertension.
(h) Common substances associated with hypertension1
Drugs:
Exogenous hormones: Estrogen (oral contraceptives: 1%),30 glucocorticoids (cortisone),
mineralocorticoids, ACTH
Nonsteroidal anti-inflammatory drugs
Drugs used for cold: Phenylpropanolamines and analogues (used as nasal decon-
gestants)
Immunosupressives: Cyclosporine and tacrolimus
Antidepressants: Tricyclics, MAO inhibitors (especially with venlafaxine)
Erythropoietin
Sibutramine
Others: Metclopramide, ketamine, carbamazepine, bromocriptine, clozapine, ergo-

tamine and other ergot containing herbal preparations.
Addictions (street drugs):
Cocaine and its withdrawal
Nicotine and its withdrawal
Narcotic withdrawal
Excess ethanol intake
Anabolic steroids.
Food substances:
Sodium chloride
Licorice
Tyramine-containing foods (with MAO inhibitors).
Chemicals:
Lead poisoning
Mercury
Thallium and other heavy metals
Lithium chloride.
Mechanisms of Primary Hypertension

Hypertension is due to increased CO and/or increased PR.31 (see Table 15.7 and
Fig. 15.14).
Hence, increased CO could be due to increased preload or increased contractility,
while increased PR could be due to functional vascular constriction or structural (vas-
cular) hypertrophy.
Increased preload: It is due to excess Na intake or due to reduced number of
nephrons.
Excess Na intake (10 g) causes fluid volume preload and CO.
Reduced nephron number (congenital or acquired) leads to decreased filtration
surface which causes renal retention of excess dietary Na which in turn leads
to preload and CO.
Low birth weight due to fetal undernutrition, results in increased incidence of high
BP later in life32, and this intra-uterine growth retardation is responsible for decreased
number of nephrons.33
Table 15.7 Pathogenesis of hypertension cardiac output (CO) and/or peripheral

resistance (PR) by the following mechanisms
Mechanism CO or PR
1. Increased preload CO

2. Increased contractility CO
3. Functional vasoconstriction PR and vascular hypertrophy

4. Vascular hypertrophy PR and vasoconstriction
Peripheral
Cardiac output HTN
resistance
Contractility Preload Vasoconstriction Vascular hypertrophy
Sympathetic Cell membrane

Fluid volume
activity alteration
Renal sodium
Hyper
retention
insulinemia
Filtration surface
Stress and Excess Genetic

IUGR Obesity
sleep apnea sodium intake predisposition
Fig. 15.14 | Mechanisms

retardation.
of primary hypertension (HTN)IUGR: intra-uterine growth
Increased contractility: It is due to increased sympathetic activity and endothelin

release.
Stress and sleep apnea lead to increased sympathetic activity which increases
myocardial contractility and CO.
Sleep apnea also causes endothelin release in response to hypoxemia during apnea.
Stress also increases renin-angiotensin through increased sympathetic activity, which
decreases filtration surface and thereby results in renal Na retention, increased fluid
volume and preload.
Functional vasoconstriction: It directly increases PR. It also causes vascular hypertro-
phy, which in turn again elevates PR.
Excess renin-angiotensin due to sympathetic stimulation (stress induced) causes
vasoconstriction that elevates the peripheral resistance.
Genetic alteration causes cell membrane alteration which leads to both vasocon-
striction and vascular hypertrophy that elevate peripheral resistance.
Genetic contributions have been estimated to range between 3060%.34
Structural (vascular) hypertrophy: It directly increases PR and causes functional
vasoconstriction, which again elevates PR.
Hyperinsulinemia due to obesity causes:
(i) Structural hypertrophy
(ii) Sympathetic activity contractility and preload
(iii) Na retention and thereby increase preload.
Endothelial dysfunction due to (a) Lack of endothelial derived relaxing factors

(EDRF), mainly the nitric oxide (NO) synthesis (as in insulin resistance) or due to
impaired NO mediated vasodilation and (b) Increased endothelial derived constrict-
ing factors (EDCF), mainly endothelin-1 leads to vasoconstriction and vascular
hypertrophy
Hence, excess Na intake, stress, obesity, sleep apnea, intrauterine growth retardation
and genetic predisposition alter neurohumoral system, which causes increase in pre-
load, contractility, vasoconstiction or vascular hypertrophy alone or in combination
resulting in hypertension.
Complications of Hypertension
These are broadly classified into two categories.
Hypertensive complications
Accelerated-malignant hypertension
LVF and CHF
Hemorrhagic stroke
Nephrosclerosis leading to renal failure
Aortic dissection
Atherosclerotic complications
Coronary artery disease
Sudden death and other arrhythmias
Athero-thrombotic stroke
Peripheral vascular disease
REFERENCES
1. Chobanian AV, Bakris GL, Black HR et al. The seventh report of the Joint National Committee on
Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: The JNC 7 Report.
JAMA 2003;289:25602572. PR.
2. Hales S. Statistical Essays: Containing Haema-staticks; or, an Account of some Hydraulick and
Hydrostatical Experiments Made on the Blood and Blood Vessels of Animals. London: Innys W,
Manby R; 1733.
3. Booth J. A short history of blood pressure measurement. Proc R Soc Med 1977;70(11):793799.
4. Riva-Rocci S. Un sfigmomanometro nuovo. Gaz Med Torino 1896;47:981996, 10011007.
5. Korotkoff NS. On methods of studying blood pressure: second presentation [in Russian]. Izv Imper
Voen-Med Acad. 1906;12:254257.
6. McCutcheon EP, Rushmer RF. Korotkov sounds: An experimental critique. Cir Res 1967;20:
149161.
7. Neilsen PE, Janniche H. The accuracy of auscultatory measurement of arm blood pressure in very
obese subjects. Acta Med Scand 1974;195(5):403409.
8. Canznello VJ, Jensen PL, Schwartz GL. Are aneroid sphygmomanometers accurate in hospital and
clinic settings? Arch Intern Med 2001;161:729731.
9. Gould BA, Hornung RS, Kieso HA et al. Is the blood pressure the same in both arms? Clin Cardiol
1985;8(8):423426.
10. Wooley CF, Hosier DM, Booth RW, et al. Supravalvular aortic stenosis. Am J Med 1961;31:717725.
11. Park MK, Guntheroth WG. Direct blood pressure measurements in brachial and femoral arteries in
children. Circulation 1970;41(2):231237.
12. Felix WR, Hochbert HM, George MED, et al. Ultrasound measurement of arm and leg blood
pressure. JAMA 1973;226(9):10961099.
13. Sapira JD, Quincke, de Musset, et al. Some aortic regurgitations. South Med J 1981;74:459467.
14. Donald KW, Lind AR, McNicol GW et al. Cardiovascular response to sustained contractions. Circ
Res 1967;20(suppl 1):1530.
15. Masaki KH, Schatz IJ, Burchfiel CM, et al. Orthostatic hypotension predicts mortality in elderly
men: Honolulu Heart Program. Circulation 1998;98(21):22902295.
16. Mukai S, Lipsitz LA. Orthostatic hypotension. Clin Geriatr Med 2002;18(2):253268.
17. Sato T, Nishnaga M, Kawamoto A, et al. Accuracy of a continuous blood pressure monitor based on
arterial tonometry. Hypertension 1993;21(6 pt 1):866874.
18. Asmar R, Benetos A, Topouchian J, et al. Assessment of arterial distensibility by automatic pulse wave
velocity measurement: Validation and clinical application studies. Hypertension 1995;26:485490.
19. Pickering T. Recommendations for the use of home (self) and ambulatory blood pressure monitoring.
American Society of Hypertension Ad Hoc Panel. Am J Hypertens 1996;9(1):111.
20. Kario K, Pickering TG, Umeda Y, et al. Morning surge in blood pressure as a predictor of silent and
clinical cerebrovascular disease in elderly hypertensives: a prospective study. Circulation 2003;107:
14011406.
21. Pickering TG, Coats A, Mallion JM, et al. Blood Pressure Monitoring. Task force V: White-coat
hypertension. Blood Press Monit 1999;4:333341.
22. Franklin SS, Gustin W, Wong ND, et al. Hemodynamic patterns of age-related changes in blood
pressure. The Framingham Heart Study. Circulation 1997;96(1):308315.
23. Clement DL, De Buyzere ML, De Bacquer DA, et al. Prognostic value of ambulatory blood pressure
recordings in patients with treated hypertension. N Eng J Med 2003;348(24):24072415.
24. Wain H. The story behind the word. Springfield, Illinois: Charles C Thomas 1958:159.
25. Anderson GH Jr., Blakemann N, Streeten DHP. The effect of age on prevalence of secondary forms
of hypertension in 4429 consecutively referred patients. J Hypertens 1994;12(5):609615.
26. Rahman M, Dixit A, Donley V, et al. Factors associated with inadequate blood pressure control in
hypertensive hemodialysis patients. Am J Kidney Dis 1999;33(3):498506.
27. MartinezCaselao A, Hueso M, Sanz V, et al. Treatment of hypertension after renal transplantation:
Long term efficacy of verapamil, enalapril and doxazosin. Kidney Int 1998;68(suppl):130134.
28. Rudnick JV, Sackett DL, Hirst S, et al. Hypertension in family practice. Can Med Assoc J 1977;
3; 492.
29. National High Blood Pressure Education Program. Report of the National High Blood Pressure
Education Program Working Group on High Blood Pressure in Pregnancy. Am J Obstet Gynecol
2000;183(1):S1S22.
30. Sinclair AM, Isles CG, Brown I, et al. Secondary hypertension in a blood pressure clinic. Arch
Intern Med 1987;147(7):12891293.
31. Kaplan NM: Clinical Hypertension. 7th ed. Baltimore, Williams & Wilkins, 1998:45.
32. Law CM, Shiell AW. Is blood pressure inversely related to birth weight? The strength of evidence
from a systematic review of the literature. J Hypertens 1996;14(8):935941.
33. Brenner BM, Chertow GM. Congenital oligonephropathy: An inborn cause of adult hypertension
and progressive renal injury? Curr Opin Nephrol Hypertens 1993;2(5):691695.
34. Harrap SB. Hypertension: Genes versus environment. Lancet 1994;344:169171.
JUGULAR VENOUS PULSE
16. Introduction and jugular venous pulse waves 271

17. Estimation of venous pressure and JVP in diseased conditions 283
CHAPTER 16
I NTRODUCTION AND J UGULAR
V ENOUS P ULSE WAVES
INTRODUCTION 271 3) c Wave 276

History 271 4) v Wave 276
EXAMINATION OF JUGULAR 5) y Descent or Diastolic Collapse 277
VENOUS PULSE (JVP) 272 6) h Wave 277
1) Which JVP? 272 ABNORMALITIES OF THE WAVES 277
2) Position of the Patient 274 1) Abnormalities of a Wave 277
ANALYSIS OF THE JUGULAR 2) Abnormalities of x Descent 279
VENOUS PULSATIONS 275 3) Abnormalities of v Wave 279
1) a Wave 275 4) Abnormalities of y Descent 281
2) x Descent (Systolic Collapse) 276 REFERENCES 282
INTRODUCTION
The venous system contains about 7080% of the circulating blood volume which
is non-pulsatile. However, changes in flow and pressure caused by the right atrial
and right ventricular filling produce pulsations in the central veins that are transmit-
ted to the peripheral veins (e.g. jugular veins) and are opposite to the direction of
the blood flow.
The arterial pulse and blood pressure reflects the dynamics of the left side of the
heart, while the jugular veins provide the information about the hemodynamic
events from the right side of the heart-right atrial pressure during systole and right
ventricular filling pressure during diastole.
Hence, an accurate assessment of the venous pulse, the jugular venous pulse (JVP)
reflects the dynamics of the right side of the heart.1
History
Lancis (1728) first described the cervical venous pulse of the external jugular vein in
a patient with tricuspid regurgitation (see Table 16.1).
However, the classic graphic recordings of the JVP were done by Chauvea and
Marey (1863).
But it was Potain (1869) who accurately described the wave pattern in the internal
jugular vein.
272 JUGULAR VENOUS PULSE
Table 16.1 History of jugular venous pulse
Author Year Description
1. Lancis 1728 Venous pulse of external jugular vein

2. Chauvea and Marey 1863 Graphic recordings of JVP
3. Potain 1869 Wave pattern in internal jugular vein
4. James Mackenzie 1902 Nomenclature of JVP
5. Paul Wood 1950s Rekindle the interest in assessment of JVP
Subsequently, James Mackenzie (1902) provided the nomenclature of JVP and

applied this principle of examination at the bedside. The Mackenzies nomenclature
is being used today with little or no significant modifications.
In 1950s Paul Wood rekindled this interest of assessment of JVP.
EXAMINATION OF JUGULAR VENOUS PULSE (JVP)
The bedside examination of the JVP is done:

To estimate the central venous pressure (CVP) and
Assess the waveform.
1) Which JVP?
As the venous pulse is not palpable, the right internal jugular vein is usually assessed
both for waveform and for the estimation of the CVP.
The internal jugular vein is located deep within the neck, covered by sternocleido-
mastoid muscle and hence usually not visible as a discrete structure (except in the
presence of venous hypertension). However, the venous pulsations of the jugular
bulb (a slight dilatation of the internal jugular vein at its junction with the subcla-
vian vein and located between the two heads of the sternocleidomastoid muscle) are
transmitted to the overlying skin and soft tissues.
The Internal Jugular Vein is Preferred to the External

Jugular Vein
Anatomically, the internal jugular veins (IJVs) are closer to the right atrium (see Fig.
16.1) as they take a direct course (straight line) through innominate veins to the
superior vena cava (SVC) and right atrium (RA), while the external jugular veins
(EJVs) follow a more circuitous route, and hence IJVs more accurately reflect the
dynamics of the right heart (see Table 16.2).
The prominent valves at the proximal portion of the EJVs may prevent the trans-
mission of the pulsations from the RA, while there are no or less significant numbers
of valves in the internal jugular veins.
EJV passes through more fascial planes than the IJV so is more likely to be affected
by an extrinsic compression from other structures in the neck and upper thorax.
INTRODUCTION AND JUGULAR VENOUS PULSE WAVES 273
Sternocleidomastoid muscle
Internal jugular vein
External
Clavicle
jugular vein
Fig. 16.1 | Jugular veinsinternal jugular vein is in direct continuity with the right atrium.
Table 16.2 Reasons for preference of internal jugular vein (IJV) over external jugular vein (EJV)
1. Direct continuation of right atrium (RA) With IJV

2. Transmission of RA pulsations prevented by Prominent valves at the proximal EJV
3. Other structures of neck and upper thorax Causes extrinsic compression of EJV
4. Sympathetic activity (as in CHF) Causes vasoconstriction of EJV Pulsations
become barely visible
Due to increased sympathetic activity as in CHF, the EJVs may become small and
pulsations are barely visible as a result of vasoconstriction.
The Right IJV is Preferred to Left IJV

The right IJV and innominate vein extend in an almost straight line from the SVC
and RA, while the left innominate vein into which left IJV drains, does not extend
in a straight line from the SVC and RA.
The left innominate vein may be kinked or compressed by a variety of normal struc-
tures, by a dilated aorta or by an aneurysm.
However, if there is any difficulty in visualization of the JVP on the right side, both
sides of the neck should be carefully examined.
Sometimes, it is difficult to differentiate between carotid and jugular venous pulses
especially when the latter exhibits prominent waves (e.g. prominent v waves in a
patient with TR). Following are the helpful clues (see Table 16.3):
The carotid pulse is deep and medial in the neck, well localized, while jugular pulse
is more superficial and lateral in the neck.
The carotid pulse is felt better than seen, while pulsating jugular vein is readily visi-
ble than felt.
The carotid pulse usually exhibits a single upstroke (single peaked) in patients with
sinus rhythm, while the JVP usually has two peaks (double peaked) and two troughs
per cardiac cycle.
Table 16.3 Differences between jugular venous and carotid pulses
Jugular venous pulsation Carotid pulsation
1. Superficial and lateral in the neck Deeper and medial in the neck
2. Better seen than felt Better felt than seen
3. Has two peaks and two troughs/cardiac cycle Has single upstroke
4. Descents obvious than crests Upstroke brisker and visible than descent
5. x and y prominent during inspiration No effect
6. a and v transiently during expiration No effect
7. Jugular venous pressure falls during inspiration No effect
8. Digital compression at the root of neck abolishes No effect
jugular venous pulse
The carotid upstroke is brisker ( visible) than its descent, whereas the descents are
more obvious than their crests in JVP.
The carotid pulsations do not change when the patient assumes upright posture,
whereas the mean venous pressure falls, unless the venous pressure is greatly elevated.
The carotid pulsations do not change during respiration, whereas x and y descents
become more prominent with increased venous return to the right heart during
inspiration and thereby there is increased RA and RV contraction. During expiration,
a wave diminishes in size and v wave may become transiently dominant.
Abdominal compression elevates the jugular venous pressure transiently, while it has
no effect on the carotid pulsations.
Gentle digital compression at the root of the neck, just above the clavicle does not
affect the carotid pulse but usually abolishes the JVP, except in the presence of
extreme venous hypertension.
2) Position of the Patient

The patient should lie comfortably and in most normal subjects, it is examined when
the trunk is inclined by less than 30. It is often helpful to elevate the chin and slightly
rotate the head to the left, gently stretching the skin of the right lower neck and supra-
clavicular area (see Fig. 16.2).
However, most patients with heart disease are examined most effectively in the 45
position.
But in patients with high venous pressure, a greater (6090) inclination is required
to obtain visible venous pulsations.
Whereas in patients with low jugular venous pressure, a lesser ( 30) inclination is
desirable.
The inclination angle should be subtended between the trunk and the bed and at
the neck, while the neck and trunk should be in the same line.
When the neck muscles are relaxed, shining a beam of light tangentially across the skin
overlying the IJV often exposes its pulsations.
Simultaneous palpation of the left carotid artery and/or cardiac auscultation aids in
the timing of the jugular venous pulsations in the cardiac cycle (see Fig. 16.3).
Fig. 16.2 | Position of the patient for examining jugular

Fig. 16.3 | Simultaneous palpation of left
common carotid artery for timing
venous pulse.
of jugular venous pulsations.
a
x a
c h
v wave
x
y
x trough Ascending limb
S1 S2
Fig. 16.4 | Normal jugular venous wave pattern.
ANALYSIS OF THE JUGULAR VENOUS PULSATIONS
The normal JVP reflects the phasic pressure changes in the RA and consists of two
visible positive waves (a and v) and two negative troughs (x and y) (see Fig. 16.4).
However, two additional positives can be recorded: c wave which interrupts the
x descent and h wave which precedes the next a wave (see Table 16.4).
1) a Wave
The first positive presystolic a wave is:
Due to the right atrial contraction which results in retrograde blood flow into the
SVC and jugular veins during RA systole.
Normally, it is the dominant wave in the JVP especially during inspiration. It is
larger than v wave.
Table 16.4 Normal Jugular venous pulse
Features Crest/trough Causes
1. a wave Crest Right atrial (RA) contraction

2. x descent Trough Atrial relaxation
3. x descent Trough RA floor descent and downward pulling of tricuspid valve (TV)
by contracting right ventricle (RV)
4. c wave Crest Impact of the carotid artery and upward bulging of the closed TV
5. v wave Crest RA filling during RV systole when TV is closed
6. y descent Trough RA emptying during early RV diastole when TV opens
It precedes the upstroke of the carotid pulse, almost synchronous with S1, but
follows the P wave of the ECG.
2) x Descent (Systolic Collapse)

The a wave is followed by the systolic x descent which is due to atrial relaxation during
atrial diastole.
Often, the x descent is the most prominent motion of the normal JVP which begins
during systole and ends just before S2.
It is larger than y descent.
x Descent
More often x descent is interrupted (when recorded) by a second positive venous
wave, the c wave. The x descent below the c wave is the x descent which is due to
Fall in the right atrial pressure during early RV systole
Descent of the floor of the RA and
Downward pulling of the tricuspid valve (TV) by the contracting right ventricle.
3) c Wave
This second positive venous wave interrupts the x descent and is produced by:
The impact of the carotid artery which is adjacent to the IJV and
Upward bulging of the closed TV into the RA during RV isovolumic contraction.2
4) v Wave
It is the third positive wave (but the second major positive wave) which begins in late
systole and ends in early diastole.
It results from the rise in right atrial pressure due to continued right atrial filling
during ventricular systole when the TV is closed.
It is roughly synchronous with carotid upstroke and peaks after S2.
5) y Descent or Diastolic Collapse

It is the down slope of v wave.
It results from the decline in the right atrial pressure due to right atrial emptying
and right ventricular filling when the TV opens in early diastole.
The initial y descent which occurs in early diastole corresponds to the RV rapid filling
phase, while the ascending limb of the y wave is produced by the continued diastolic
inflow of blood into the right side of the heart, i.e. it begins and ends during diastole
well after S2.
6) h Wave
When the diastole is long (as in slow heart rates), ascending limb of the y wave is often
followed by a small, brief, positive wave known as h wave, which occurs prior to the
next a wave during the period of diastasis. It was described by Hirschfelder in 1907
(h from Hirschfelder).
At times, there is a plateau phase rather than a distinct h wave.
With increasing heart rate, the y descent is immediately followed by the next a wave.
h plateau without a prominent a wave and a prominent y descent is common in con-
strictive pericarditis.
With faster heart rates, some of the venous pulse waves may merge together, which
makes the accurate analysis difficult at the bedside.
ABNORMALITIES OF THE WAVES
1) Abnormalities of a Wave
The a wave may be prominent or absent or may occur regularly or irregularly (see
Table 16.5).
Prominent or Large a Waves

These may be due to:
Increased resistance to RA emptying and thereby increased RA contraction as in TS,
RA myxomas, or tricuspid atresia (see Fig. 16.5).
Decreased RV compliance which is usually associated with increased right ventricu-
lar end diastolic pressure leading to right ventricular hypertrophy and is seen in:
PS
PH due to any cause e.g. mitral stenosis
RV cardiomyopathy
Acute pulmonary embolism
RV infarction in association with inferior wall MI.
Bernheims effect: Severe LVH with thickened ventricular septum (symmetrical or
asymmetrical) interferes with RV filling as in severe AS, HCM (with asymmetrical
septal hypertrophy).
Table 16.5 Abnormal a waves
Large a waves Cannon waves Absent a waves
1. TS, RA myxomas, 1. Junctional rhythm VT 1:1 retrograde 1. Atrial fibrillation

tricuspid atresia conduction, isorhythmic AV dissociation
2. PH, PS, acute PE 2. CHB, VT, VPC, classic AV dissociation, 2. Sinus tachycardia
ventricular pacing
3. RV cardiomyopthy,
RV infarction
4. Severe AS, HCM
TS: tricuspid stenosis, RA: right atrial, PH: pulmonary hypertension, PS: pulmonary stenosis, PE: pulmonary embolism,
CHB: complete heart block, VT: ventricular tachycardia, VPC: ventricular premature contraction, AS: aortic stenosis,
HCM: hypertrophic cardiomyopathy, AV: atrioventricular, RV: right ventriclar.
a a
a
a c v
Fig. 16.5 | Prominent a waves in tri-

cuspid stenosis.
Fig. 16.6 | Irregular cannon waves in complete AV block.
Giant a Waves or Cannon Waves
These occur whenever the RA contracts against the closed TV during RV systole.
Paul Wood described the giant a wave as venous Corrigan. Cannon waves may
occur either regularly or irregularly and are most common in the presence of
arrhythmias.
Regular cannon waves occur in
Junctional rhythm
Ventricular tachycardia (VT) 1:1 retrograde conduction
Isorhythmic AV dissociation
Irregular cannon waves occur in
Complete heart block (see Fig. 16.6)
Classic AV dissociation
VT
Ventricular pacing
Ventricular ectopics
Absent a Waves
The a wave is absent when there is no effective atrial contraction as in atrial fibrilla-
tion (see Fig. 16.7).
c v
x
y
Fig. 16.7 | Absent a waves in atrial fibrillation.

a v
Table 16.6 Abnormal x descent
y
x Prominent x descent Absent x descent
1. Constrictive pericarditis 1. Tricuspid regurgitation (TR)

Fig. 16.8 | Prominent x and y
descents in constric-
2. Cardiac tamponade
3. Atrial septal defect
tive pericarditis.
In sinus tachycardia, when a wave may fuse with preceding v wave, especially when
the PR interval is prolonged or a wave may occur during the v or y descent and may
be small or absent.
2) Abnormalities of x Descent
Absent x Descent
The x descent is usually absent due to tricuspid regurgitation.3
Blunting of x descent is the early sign of tricuspid regurgitation.
In patients with moderate tricuspid regurgitation, x descent is replaced by a fairly
large positive s (systolic) or r (regurgitant) wave.
The development of atrial fibrillation does not obliterate the x descent except in the
presence of TR, but its size may be reduced.
Prominent x Descent
The x descent becomes prominent:
when RV contracts vigorously as in cardiac tamponade and constrictive pericarditis
(x descent may be more prominent than y descent, see Fig. 16.8) and
in RV overload as in ASD (see Table 16.6).
3) Abnormalities of v Wave
Prominent v Wave
It results from an increased right atrial blood volume during ventricular systole when
normally TV is closed as in tricuspid regurgitation (see Fig. 16.9). In significant tricuspid
regurgitation, obliteration of x descent and prominent v wave result in a large positive
a
y
Fig. 16.9 | rapid

Prominent v waves with absent x descent but
y descent in severe tricuspid regurgitation.
c
Table 16.7 Abnormal v waves v
Prominent v waves Diminished v waves y

x
1. Tricuspid regurgitation (TR) 1. Hypovolemia
2. Large atrial septal defect 2. Use of nitrates
3. Gerbodes defect Fig. 16.10 | The v waves become
prominent in atrial fib-
4. Severe congestive heart failure
5. Atrial fibrillation rillation due to absence
6. Corpulmonale of a waves.
systolic (s) or regurgitant (r) wave (Lancis sign) which simulate the RV pressure (trac-
ing) and is known as ventricularization of the atrial pressure/jugular venous pressure
(see Table 16.7).
This giant v wave sometimes causes;
A systolic movement of the earlobe,4
A right to left head bobbing (movement) with each ventricular systole
Pistol shots heard over the IJV and
Pulsatile exophthalmos.
Prominent v Wave in Absence of Tricuspid Regurgitation

Large ASD
VSD of LV to RA shunt (Gerbodes defect)
Severe CHF
Atrial fibrillation (see Fig. 16.10)
Cor pulmonale
Prominent a and v Waves

Prominent and equal a and v waves in RA and JVP occur in
Non restricted ASD with normal venous pressure5 (see Fig. 16.11)
Constrictive pericarditis with increased venous pressure (see Fig. 16.12)
RVF with sinus rhythm and increased venous pressure. Sometimes, the tall a and v
waves may alternate with each other, that results in right atrial pulsus alternans.
a v a v
y
x
Fig. 16.12 | Prominent a and v waves with rapid x and

Fig. 16.11 | Prominent a and v waves in non-
restricted ASD.
y descents in constrictive pericarditis.
Table 16.8 Abnormal y descent
Rapid y descent Slow y descent
1. Severe tricuspid regurgitation 1. Tricuspid stenosis

2. Constrictive pericarditis 2. Right atrial myxoma
3. Severe right ventricular failure 3. Pericardial tamponade
4. ASD with mitral regurgitation
v a
y
Fig. 16.14 | Slow y descent with prominent
a in tricuspid stenosis.
Fig. 16.13 | Rapid y descent with prominent v in
tricuspid regurgitation.
Diminished v waves may be seen in conditions of hypovolemia and treatment with

venodilators such as nitrates.
4) Abnormalities of y Descent
Rapid (Diastolic Collapse) y Descent
It occurs in conditions with elevated venous pressure, myocardial dysfunction or
severe ventricular dilatation as in (see Table 16.8):
Severe tricuspid regurgitation (see Fig. 16.13).
Constrictive pericarditis. This diastolic collapse is known as Friedreichs sign which
is usually accompanied by pericardial knock (Friedreich, 1864).
Severe RVF.
ASD with mitral regurgitation.
Slow y Descent
When right atrial emptying and RV filling are impeded, y descent is slow and gradual as in
Tricuspid stenosis6 (see Fig. 16.14)
Right atrial myxoma6 and

Pericardial tamponade (y descent may even be absent).
REFERENCES
1. Swartz MH. Jugular venous pressure pulse: its value in cardiac diagnosis. Prim Cardiol 1982;8:197.
2. Wood P. Diseases pf the Heart and Circulation, 2nd ed. Philadelphia: Lippincott; 1957.
3. Messer AL, Hurst JW, Rappaport MB, Sprague HB. A study of the venous pulse in tricuspid valve
disease. Circulation 1950;1(3):388393.
4. Butman SM, Ewy GA, Standen JR, et al. Bed side cardiovascular examination in patients with severe
chronic heart failure: importance of rest or inducible jugular venous distension. J Am Coll Cardiol
1993;22(4):968974.
5. Dexter L. Atrial septal defect. Br Heart J 1956;18(2):209225.
6. Perloff JK, Harvey WP. Clinical recognition of tricuspid stenosis. Circulation 1960;22:346364.
CHAPTER 17
ESTIMATION OF V ENOUS
P RESSURE AND JVP IN
D ISEASED CONDITIONS
1. ESTIMATION OF VENOUS on the Undersurface of
PRESSURE 283 the Tongue (Mays Sign) 287
a) Measurement of Jugular 2. JVP IN DISEASED CONDITIONS 288
Venous Pressure 283 a) JVP in Arrhythmias 288
b) AbdominalJugular Reflux 286 b) JVP in Conduction Defects 288
c) Measurement of Venous c) JVP in Valvular Lesions 289
Pressure by Examining d) JVP in Acyanotic CHD 291
the Veins of the Hand e) JVP in Cyanotic CHD 292
(Gaertners Method) 287 f) JVP in Cardiomyopathy 294
d) Assessment of Venous g) JVP in Pericardial
Pressure by Examining Diseases 295
the Visible Engorged Veins REFERENCES 295
1. ESTIMATION OF VENOUS PRESSURE
The estimation of venous pressure can be done at bed side by:

Measuring jugular venous pressure1 (usually internal jugular venous pressure)
Hepatojugular reflux
Examining the veins on the dorsum of the hand
Examining the veins of the undersurface of the tongue.
a) Measurement of Jugular Venous Pressure

Jugular veins could be markedly distended with minimal increase in pressure (espe-
cially EJV) or not visibly distended despite a highly elevated pressure.
In adults with normal chest, the sternal angle or angle of Louis (Pierre Charles
Alexander Louis, 17871872) is found to be approximately 5 cm above the center of
the right atrium. As the distance between the sternal angle and center of right atrium
remains relatively constant regardless of the position of the thorax and as the sternal
angle is approachable in all positions of the body, Paul Wood recommended sternal
Normal
Sternal angle =
venous pressure
Right atrium
45 Upright
Fig. 17.1 | The distance between the sternal angle and center of the RA remains relatively
constant regardless of the position of the thorax.
Fig. 17.2 | Measurement of JV pressure by two scale methodA horizontal scale at the
top of the oscillating venous column in IJV cuts the vertical scale at the sternal
angle. The vertical distance from the sternal angle gives the RA pressure in cm.
angle to be taken as reference point for measurement of jugular venous pressure at

bed side2 (see Fig. 17.1).
Use of sternal angle as the zero reference is simple and practical, besides it provides a
reproducible and readily identified standard for bed side appraisal of venous pressure.
With the patient in an optimum position (3090 recline) and relaxed neck mus-
cles, shining a beam of light tangentially across the skin overlying the internal jugu-
lar vein exposes the top of the oscillating venous column (the height of the venous
column at the peak of a and v waves usually taken).
One horizontal is drawn (in relation to the ground by using a scale) at the top level
of the venous column and another at the sternal angle. The vertical distance in cms
(use another scale) between the two horizontals, i.e. from the top of the oscillating
venous column in the IJV to the sternal angle will give the JV pressure which reflects
the mean right atrial pressure (see Fig. 17.2).
In normal, JV pressure does not exceed 4 cm above the sternal angle which cor-
responds to a central venous pressure (RA mean pressure) of 9 cm, since the right
ESTIMATION OF VENOUS PRESSURE AND JVP IN DISEASED CONDITIONS 285
atrium is approximately 5 cm below the sternal angle (4 5 9 cm). By way of

conversion, 1.3 cm column of water is equal to 1 mmHg. Hence, normal right atrial
mean pressure does not exceed 7 mmHg (9 cm of JVP/1.3 6.92).
Elevated venous pressure can also be identified if EJV is distended and prominent.
Empty the EJV digitally and selective release at the inferior site results in prompt
filling of EJV from below in case of high central venous pressure.
Elevated JV pressure: i.e. JV pressure of 4 cm above the sternal angle reflects an
increase in RA pressure (see Fig. 17.3 and Table 17.1) which could be due to:
Increased RV pressure and thereby reduced compliance occurs in patients with:
Pulmonary stenosis
Pulmonary hypertension
RVF secondary to LVF or any cause
RV infarction.
Obstruction/impedance to RV inflow as in:
Tricuspid stenosis
Right atrial myxoma
Constrictive pericarditis.
Raised right
atrial pressure
Venous pressure
Sternal angle
Right atrium
45 Upright
Fig. 17.3 | Measurement of JV pressureraised JVP indicating raised RA pressure.

Table 17.1 Elevated jugular venous pressure
RV compliance RV inflow impedance Circulatory overload Others
1. Pulmonary stenosis 1. Tricuspid stenosis 1. Renal failure 1. SVC obstruction

2. Pulmonary hypertension 2. Right atrial myxoma 2. Excessive fluid 2. COPD
administration
3. RVF (any cause 3. Constrictive
including LVF) pericarditis
4. RV infarct
SVC: superior vena cava, COPD: chronic obstructive pulmonary disorders, RVF: right ventricular failure, LVF: left
ventricular failure.
Hypervolemia/circulatory over load as in:

Renal failure
Excessive fluid administration.
Superior vena caval obstruction: Bilateral jugular veins are distended with little or no
pulsations, and are associated with cyanosis, edema of face and eyes.
COPD: JV pressure may be elevated only during expiration.
Kussmauls sign:3 Normally, JV pulsations (especially a wave) become prominent
during inspiration, while the mean JV pressure decreases as a result of increased fill-
ing of the right side associated with decreased intrathoracic pressure.
But if the venous pressure increases during inspiration, it is known as Kussmauls
sign, which occurs in patients with:
Constrictive pericarditis (first described in constrictive pericarditis)
Sever right heart failure
Right ventricular infarction4
Restrictive cardiomyopathy.
b) AbdominalJugular Reflux (AJR)

Rondot (1898) coined the term hepatojugular reflux.
It is a useful diagnostic maneuver when the JVP is borderline elevated or when the
latent RVF or silent TR is suspected.
Gently apply firm pressure to the periumbilical region for 1030 sec with patient
lying comfortably and breathing quietly (should avoid Valsalva maneuver) while
JVP is observed (see Fig. 17.4). Pressure should not be applied over the liver in right
hypochondrium region, as it be may be painful in presence of hepatic congestion.
Fig. 17.4 | Examination for abdominal jugular reflex-by applying gentle pressure in
periumbilical area.
In normal subjects, JV pressure rises transiently (15 sec.) to 3 cm while abdom-

inal pressure is continued, whereas in positive AJR, JV pressure remains elevated, as
failing RV may not be able to receive the augmented venous return to the right heart
without a rise in mean venous pressure.5
Positive AJR suggests elevated central venous pressure or pulmonary artery wedge
pressure6 and occurs in (see Table 17.2):
1. Incipient or actual right ventricular failure
2. LVF with hypervolemia or fluid overload
3. Tricuspid regurgitation7
4. COPD: In COPD, a sudden disproportionate increase in intrathoracic pressure
impedes venous return, which elevates the venous pressure and results in false
positive AJR.
5. In conditions with increased generalized sympathetic tone, systemic vasocon-
striction (resulting in decreased distensibility of the venous bed) may also show
positive AJR.
c) Measurement of Venous Pressure by Examining the

Veins of the Hand (Gaertners Method)
Prominent antecubital veins or superficial veins on the dorsum of the hand are utilized
for estimation of venous pressure.
With the patient sitting or lying at a 30 elevation, the arm is slowly and passively
raised from a dependent position until the vein collapses.
The height of the limb above the level of sternal angle at which the vein collapses
represents the venous pressure.
When the venous pressure is normal, the veins of the hand collapse at the level of
the sternal angle. However, the local venous obstruction or augmented peripheral
venous constriction diminishes the accuracy of this method.
d) Assessment of Venous Pressure by Examining the Visible

Engorged Veins on the Undersurface of the Tongue (Mays Sign)
In sitting posture, visible engorged veins on the undersurface of the tongue also indi-
cate elevated venous pressure (see Fig. 17.5).
Table 17.2 Conditions with positive abdominaljugular reflux (AJR)
Positive AJR False positive AJR
1. Incipient right ventricular failure (RVF) 1. Chronic obstructive pulmonary

disorders
2. RVF (compensated) 2. Generalized sympathetic tone
3. Left ventricular failure with volume 3. Systemic vasoconstriction
overload
4. Tricuspid regurgitation
Fig. 17.5 | Engorged veins on the undersurface of the tongueMays sign indicating
elevated venous pressure.
2. JVP IN DISEASED CONDITIONS
a) JVP in Arrhythmias
Occasionally, a wave is better seen in JVP than P wave in ECG in some arrhythmias.
In sinus bradycardia, slow normal regular sequence of a and v waves is maintained.
In atrial fibrillation, JVP simulates TR as v wave is prominent due to the absence of
a wave and diminution of x descent. So, the absence of a wave in a patient of irregular
pulse is diagnostic of fibrillation; while in other irregular rhythms such as VPC,
irregular cannon waves are present.
In atrial premature contractions, normal sequence of a wave carotid pulse and v
wave is maintained.
In SVT with heart rates of 160/min, a and v waves merge into a single venous
crest which resembles cannon waves of junctional tachycardia.

In VT and junctional tachycardia, cannon waves are characteristic.
b) JVP in Conduction Defects

PR interval can be estimated from the interval between a wave and carotid pulse (C)
so, increase a-C duration indicates prolonged PR interval.
Hence, 1 AV block can be made out from a-C interval. However, complete LBBB
also prolongs the a-C interval slightly.

In Wenkebach (Mobitz type I), gradual lengthening of sequential a-C intervals,
ending with an a wave that is not followed by a carotid pulse (nonconducted beat),
can be made out.
In Mobitz type II AV block, a-C interval does not vary but is suddenly inter-
rupted by isolated a waves that are not followed by a carotid pulse (nonconducted
beat).
In 2:1 AV block, two a waves for every one carotid pulse are present.
With RVF
JV pressure With ASD
With TS
a waves: Absent a waves:

Mitral stenosis
with PH & TS with Af
or absent x descent:
JV pulse
with Af & TR
Rapid y descent:
with TR & RVF
v waves:
with TR & RVF Slow y descent:
with TS
Fig. 17.6 | JVP in Mitral stenosisRVF: right ventricular failure, PH: pulmonary hyperten-
sion, TS: tricuspid stenosis, TR: tricuspid regurgitation, Af: atrial fibrillation,
ASD: atrial septal defect.
Complete AV block is characterized by intermittent cannon waves in a patient with

bradycardia.
c) JVP in Valvular Lesions

(1) JVP in Mitral Stenosis (MS)
JV pressure is elevated with RVF or when associated with TS or ASD
Prominent a waves with PH or when associated with TR
Absent a waves with atrial fibrillation
Diminished or absent x descent with atrial fibrillation or when associated with TR
Prominent v waves with RVF and when associated with TR
Rapid y descent: with TR or RVF
Slow y descent when associated with TS (see Fig. 17.6).
(2) JVP in Mitral Regurgitation (MR)

Elevated JV pressure:
(i) With RVF
(ii) When associated with ASD or TS
(iii) In secondary MR due to cardiomyopathy or CAD
Prominent a waves with PH or MR due to HOCM
Prominent v waves with RVF or associated with TR or ASD
Rapid y descent: with RVF and TR (see Fig. 17.7).
(3) JVP in Tricuspid Stenosis (TS)

Elevated JV pressure, but may be normal in mild or moderate TS on diuretics
Prominent a waves associated with presystolic hepatic pulsations
Slow y descent.
With RVF With ASD

JV pressure
Secondary MR:
With TS
CM or CAD
Mitral regurgitation
a waves:
with PH due to HOCM
Rapid y descent:
JV pulse
with TR and RVF
v waves:
with TR, RVF or ASD
Fig. 17.7 | JVP in Mitral regurgitationRVF: right ventricular failure, PH: pulmonary
hypertension, TR: tricuspid regurgitation, TS: tricuspid stenosis, Af: atrial
fibrillation, CM: cardiomyopathy, CAD: coronary artery disease, ASD: atrial
septal defect, HOCM: hypertrophic obstructive cardiomyopathy.
With RVF
JV pressure With MS and PH
With TS
Aortic stenosis
a waves: JV pulse a waves:

with MS, PH and TS in HOCM
Fig. 17.8 | JVP in Aortic stenosisRVF: right ventricular failure, MS: mitral stenosis,
PH: pulmonary hypertension, TS: tricuspid stenosis, HOCM: hypertrophic
obstructive cardiomyopathy.
(4) JVP in Tricuspid Regurgitation (TR)

Elevated JV pressure with RVF or PH
Prominent v waves: with obliteration of x descent, forms a prominent s wave, i.e.
Lancis sign and ventricularization of the RA pressure
Rapid y descent, but slow descent when associated with TS.
(5) JVP in Aortic Stenosis (AS)

Elevated JV pressure with RVF or when associated with MS and PH, or TS
Prominent a waves in severe AS, HOCM or when associated with MS and PH or TS
(see Fig. 17.8).
(6) JVP in Aortic Regurgitation (AR)

Elevated JV pressure with RVF; with CRF and fluid overload
Prominent a waves with TS, MS and PH
Prominent v waves and rapid y descent with RVF (see Fig. 17.9).
With RVF JV pressure With MS and PH
Aortic regurgitation
a waves:
with MS, PH and TS
Rapid y descent:
JV pulse
with RVF
v waves:
with RVF
Fig. 17.9 | JVP in aortic regurgitationRVF: right ventricular failure, MS: mitral steno-
sis, PH: pulmonary hypertension, TS: tricuspid stenosis.
With RVF
JV pressure With severe PH
With MS or MR
Atrial septal defect
a waves: Equal a and v waves:

JV pulse
with MS, PH and PS usual
v waves: Rapid y descent:

with TR with TR and RVF
Fig. 17.10 | JVP in Atrial septal defectRVF: right ventricular failure, MS: mitral steno-
sis, MR: mitral regurgitation, PH: pulmonary hypertension, TR: tricuspid
regurgitation, PS: pulmonary stenosis.
(7) JVP in Pulmonary Stenosis (PS)

Elevated JV pressure with RVF
Prominent a waves in severe PS
Prominent v waves and rapid y descent: with RVF or TR.
d) JVP in Acyanotic CHD

(1) JVP in Atrial Septal Defect (ASD)
Elevated JV pressure with RVF; when associated with MS/MR or severe PH
Prominent a waves with PS or MS and PH
Equal a and v waves, but more prominent v waves with TR
Rapid y descent with TR or RVF (see Fig. 17.10).
With CHF
JV pressure In Gerbodes defect
In AV canal defect
Ventricular septal defect
a waves: Absent x descent:

JV pulse
with severe PS with TR and in Gerbodes defect
v waves: Rapid y descent:

with CHF, TR and in Gerbodes defect with CHF, TR and in Gerbodes defect
Fig. 17.11 | JVP in Ventricular septal defectCHF: congestive heart failure, PS: pulmonary
stenosis, TR: tricuspid regurgitation.
Table 17.3 JVP in Eisenmenger complex and syndrome
ASD with R L shunt VSD with R L shunt PDA with R L shunt
1. JV pressure may be elevated Usually normal May be elevated

2. Normal a waves, but absent with Normal a waves a waves may be prominent
atrial fibrillation
3. Prominent v waves with CHF Normal v waves CHF and Prominent v waves with CHF
or TR TR are rare or TR
R L: right to left, CHF: congestive heart failure, TR: tricuspid regurgitation.
(2) JVP in Ventricular Septal Defect (VSD)

Elevated JV pressure with CHF; in AV canal defect (VSD with MR/TR), VSD with
LV to RA shunt (Gerbodes defect)
Prominent a waves with severe PS
Prominent v waves and rapid y descent with CHF, TR, and in Gerbodes defect
Absent x descent with TR and in Gerbodes defect (see Fig. 17.11).
e) JVP in Cyanotic CHD

(1) JVP in Eisenmenger Complex and Syndrome
In Eisenmenger complex (VSD with right to left shunt), the jugular venous pressure is
usually normal with normal a and v waves. In Eisenmenger syndrome with ASD and
PDA, jugular venous pressure may be elevated with prominent v waves (see Table 17.3).
(2) JVP in Tetralogy of Fallot (TOF) or TOF Like Physiology

JV pressure: normal, but may be elevated in TOF when associated with PDA, AR,
after shunt operation, or in adult TOF
Normal a and v waves (see Fig. 17.12).
in Adult TOF,
Usually normal JV pressure
after shunt surgery
Tetralogy of Fallot
a waves: v waves:
JV pulse
normal normal
Fig. 17.12 | JVP in Tetralogy of Fallot (TOF).
JV pressure
TGA with PBF
v waves:
a waves JV pulse
normal
v waves:
with CHF and TR
Fig. 17.13 | JVP in Transposition of great arteries (TGA)PBF: pulmonary blood flow,
CHF: congestive heart failure, TR: tricuspid regurgitation.
(3) JVP in PS with Intact Interventricular Septum and

Right to Left Shunt
Elevated JV pressure
Prominent a waves
Normal v waves, but prominent with TR.
(4) JVP in Tricuspid Atresia

Elevated JV pressure with restrictive ASD
Prominent a waves
Normal v waves, but prominent with MR.
(5) JVP in Transposition of Great Arteries (TGA) or Total

Anomalous Pulmonary Venous Connection (TAPVC) with
Increased Pulmonary Blood Flow
Usually elevated JV pressure
May be prominent a waves
Normal v waves, but prominent with CHF or TR (see Fig. 17.13).
Table 17.4 JVP in cardiomyopathy
JVP Dilated CM Restrictive CM EMF
1. JV pressure May be elevated May be elevated Usually elevated

2. a waves Normal Prominent Prominent
3. v waves May be prominent Normal Prominent due to TR
4. x descent Normal Normal Obliterated with TR
5. y descent May be rapid Normal Rapid descent due
descent to TR
6. Kussmauls sign Negative May be positive Negative
EMF: endomyocardial fibrosis, CM: cardiomyopathy, TR: tricuspid regurgitation.
Table 17.5 JVP in pericardial diseases
JVP Cardiac tamponade Constrictive pericarditis
1. JV pressure Elevated Elevated

2. a waves Never prominent Normal, may be prominent
3. v waves Normal Usually equal to a waves
4. x descent Normal Prominent
5. y descent or absent Rapid
6. Kussmauls sign Negative, may be positive Usually positive
JV pressure
Constrictive pericarditis
Equal a and v waves x descent:

JV pulse
prominent
Kussmauls sign: y descent:

usually positive rapid
Fig. 17.14 | JVP in constrictive pericarditis.

Elevated JV pressure in cyanotic CHD (other than Eisenmengers syndrome) indicates
intact IVS or increased pulmonary blood flow or both.
f) JVP in Cardiomyopathy
Examination of jugular venous pulse helps in the differentiation of various causes of
cardiomyopathy (see Table 17.4).
JV pressure
Cardiac tamponade
a waves: x descent:
JV pulse
normal normal
v waves: Kussmauls sign: y descent:

normal usually ve, may be ve slow or absent
Fig. 17.15 | JVP in cardiac tamponade.

g) JVP in Pericardial Diseases
Examination of jugular venous pulse is essential in the diagnosis of the pericardial
diseases (see Table 17.5). The prominent and rapid x and y descents with positive
Kussmauls sign are diagnostic of constrictive pericarditis (see Figs 17.14 and 17.15).
REFERENCES
1. Ewy GA, Marcus FI. Bedside estimation of the venous pressure. Heart Bull 1968;17:4144.
2. Wood P. Diseases of the Heart and Circulation, 2nd ed. Philadelphia: Lippincott; 1957.
3. Kussmaul A. Uber schwielige Mediastino-Pericarditis und den paradoxen Puls. (3 parts) Berl Klin
Wochenschr 1873;10:433, 445, 461.
4. DellItalia L, Starling MR, ORourke RA. Physical examination for exclusion of hemodynamically
important right ventricular infarction. Ann Intern Med 1983;99(5):608611.
5. Ewy GA. The abdominojugular test: Technique and hemodynamic correlates. Ann Inter Med 1988;
109(6):456460.
6. Ducas J, Magder S, McGregor M. Validity of the hepatojugular reflux as a clinical test for congestive
heart failure. Am J Cardiol 1983;52(10):12991303.
7. Maisel AS, Atwood JE, Goldberger AL. Hepatojugular reflux: Useful in the bedside diagnosis of
tricuspid regurgitation. Ann Intern Med 1984;101(6):781782.
CARDIOVASCULAR SYSTEM
EXAMINATION
18. Inspection of the precordium 299

19. Palpation of the precordium 315
20. Percussion of the precordium and precordial
findings in common heart diseases 333
21. Cardiac auscultation 354
CHAPTER 18
I NSPECTION OF THE P RECORDIUM
1. EXAMINATION OF THE CHEST 299 a) Apical Impulse 306

a) Shape of the Chest 300 b) Pulsations in the (Aortic Area)
b) Cutaneous Lesions 303 Right and Left (Pulmonary Area)
c) Breast Abnormalities 303 2nd Intercostal Spaces 310
d) Distended Vessels Over the c) Pulsations in the
Chest and Back 304 Sternoclavicular Area 310
2. EXAMINATION OF THE d) Left Parasternal Pulsations 311
PRECORDIUM 305 e) Pulsations in the
a) Ossification of the Sternum 305 Epigastrium 312
b) Ossification of the Ribs 306 f) Pulsations in the Ectopic Areas 313
3. CARDIOVASCULAR PULSATIONS 306 REFERENCES 314
Since ancient times, inspection and palpation of the anterior chest and precordium have
been practiced as a part of the cardiovascular examination by the Physicians, the results
of which have been correlated with noninvasive studies, hemodynamic data, surgical and
autopsy studies.1,2 Hence, they are an important part in the evaluation of the cardiovascu-
lar disorders.
Inspection of the anterior chest and precordium includes the following:
Examination of the chest: for its shape, cutaneous lesions, breast abnormalities and
distended vessels over the chest and back
Examination of the precordium for any precordial bulging
Examination of the cardiovascular pulsations, which include:
Apical impulse
Pulsations in the right and left 2nd intercostal spaces (aortic and pulmonary areas)
Pulsations in the right and left sternoclavicular area
Left parasternal pulsations
Pulsations in the epigastrium
Pulsations in ectopic areas.
1. EXAMINATION OF THE CHEST
The patient should lie comfortably in supine position with thorax elevated to 30.
Examine the thorax tangentially, first from the foot end of the bed and then from the
patients right side directing a beam of light across the precordium (see Fig. 18.1).
300 CARDIOVASCULAR SYSTEM EXAMINATION
A B
Fig. 18.1 | Examination of the chest (A) from foot end of the bed, and (B) from patients right side.
a) Shape of the Chest
The normal chest in an adult is bilaterally symmetrical and elliptical in cross section
with the transverse diameter greater than the anteroposterior diameter and has a sub-
costal angle of about 90. However; in a normal infant the cross section of the chest
is almost circular with its anteroposterior and transverse diameters being equal (see
Fig. 18.2). The chest may be distorted by various disorders (see Table 18.1). An abnormal
chest may cause precordial bulging and displace the apex with functional murmurs
mimicking an organic lesion (see Fig. 18.3).
In barrel shaped chest (The chests anteroposterior diameter is more than its trans-
verse diameter and is usually suggestive of emphysema, chronic bronchitis), the normal
cardiovascular pulsations may not be visible/palpable over the chest (see Fig. 18.4).
A muscular thorax in contrast to less developed lower limbs occurs in coarctation
of aorta.
A broad chest with a prominent angle between the manubrium and body of the
sternum is known as shield chest, which is associated with widely separated nipples
and is frequently observed in:
Turner syndrome and
Noonan syndrome.
Pectus carnitum (pigeon chest): marked forward protrusion of the sternum and
adjacent costal cartilages, (see Figs 18.5 and 18.6) is associated with:
Marfan syndrome
Noonan syndrome
Or may be secondary to the chronic nasal or nasopharyngeal obstruction or rickets
in childhood.
Pectus excavatum (funnel chest: exaggerated normal hollow over the lower end of
the sternum, i.e. the sternum is displaced posteriorly, see Figs 18.7 and 18.8) is
observed in:
Marfan syndrome
Homocystinuria
INSPECTION OF THE PRECORDIUM 301
A B
Fig. 18.2 | Cross section of a normal chest in A: adult, B: infant.
Table 18.1 Cardiovascular significance of chest abnormalities
Shape of the chest Causes
1. Barrel shape Chronic obstructive pulmonary

disorders
2. Muscular thorax with thin lower limbs Coarctation of aorta
3. Shield chest (broad chest) Turner and Noonan syndromes
4. Pigeon chest (pectus carinatum) Marfan and Noonan syndromes
5. Funnel chest (pectus excavatum) Marfan, Ehler-Danlos, Hunter-Hurler
syndromes and Homocystinuria
Kyphoscoliosis Straight back

Abnormal chest
Barrel shaped Funnel chest
Murmurs and
Apex displacement Precordial bulging abnormal S2 split
Mimics organic
lesion
Fig. 18.3 | Effects of abnormal chest on cardiovascular examination.

Ehlers-Danlos syndrome
Hunter-Hurler syndrome
Cobblers as an occupational hazard. The cobblers present with the caving-in of
the lower part of the sternum due to the constant pressure of the shoe against it.
However, presently this type of acquired chest deformity is rarely seen with the
mechanized and improved techniques.
Secondary to rickets in childhood.
A E
Fig. 18.4 | Cross sections of normal chest (A) and barrel shaped chest (E).
A D
Fig. 18.5 | Cross sections of normal chest (A) and pigeon

chest (D).
Fig. 18.6 | Pigeon chest.
A F
Fig. 18.7 | Cross sections of normal chest (A) and funnel chest (F).
Depending upon the degree of deformity (hollowness), pectus excavatum is catagorized
as saucer, cup or funnel type. This deformity may compress/displace the heart to the
left, elevate the systemic or pulmonary venous pressures, with prominent pulmonary
artery pulsations. The parasternal mid systolic murmur may falsely suggest the presence
of organic heart disease.
Fig. 18.8 | Pectus excavatum. Fig. 18.9 | Aneurysm of aorta eroding the sternum.
Table 18.2 Cardiovascular significance of breast abnormalities
Abnormality Causes
1. Male gynecomastia Adverse effect of digitalis, Klinefelters syndrome

2. Female hypomastia Mitral-valve prolapse
3. Widely spaced nipples Turner and Noonan syndromes
Straight back syndrome (i.e. loss of normal thoracic kypohsis) is associated with expi-
ratory splitting of S2, parasternal systolic impulse, mid systolic murmur and promi-
nence of pulmonary artery on radiography, mimicking the atrial septal defect.
Aortic aneurysm may present as a bulging to the right of the upper sternum (see
Fig. 18.9).
Harrisons sulci extend transversely as grooves from the sides of the xiphisternum on
either side, giving the thorax an appearance of transverse constriction. These grooves
correspond to the costal attachments of the diaphragm and are due to the pulling of the
softened ribs, which are observed in children with rickets or chronic nasal or nasopha-
ryngeal obstruction.
b) Cutaneous Lesions
Lesions such as spider nevi are seen in:
Hepatic cirrhosis and
Osler-Weber-Rendu syndrome.
c) Breast Abnormalities
These abnormalities should also be noted carefully (see Table 18.2).
Male gynecomastia either unilateral or bilateral is observed in patients on digitalis
(as one of its adverse effects). It also occurs in Klinefelter syndrome (see Fig. 18.10).
Fig. 18.10 | Gynecomastia in Klinefelters syndrome. Fig. 18.11 | Shield chest and widely spaced nipples
in Turners syndrome.
Female hypomastia is a part of the asthenic habitus in the patients with mitral valve
prolapse.
Widely spaced nipples associated with broad shield chest are typical of Turners and
Noonan syndromes (see Fig. 18.11).
d) Distended Vessels Over the Chest and Back

Veins
Distended veins on the anterior chest wall (with caudal flow) suggest obstruction of supe-
rior vena cava, while the distended veins with cranial flow indicate inferior vena caval
obstruction.
Arteries
Collateral vessels may be seen in the interscapular and infrascapular regions or in the pos-
terior intercostal spaces and are palpable in patients with coarctation of aorta, when the
patient stands and bends forward with arms hanging down by the sides (Suzmans sign,
see Figs 18.12 and 18.13).
Fig. 18.12 | Examination of collateral vessels in

the inter-scapular and infra-scapular
regions. Fig. 18.13 | Visible collaterals in a patient of coarc-
tation of aorta (Suzmans sign).
2. EXAMINATION OF THE PRECORDIUM
The precordium is examined for any bulging:

Precordial prominence with bulging of the intercostal spaces without the
involvement of the ribs is suggestive of pericardial effusion.

Precordial prominence involving both intercostal spaces and ribs suggests car-
diac enlargement (usually due to RV dilatation) of long standing duration, which

usually develops before puberty. However, precordial prominence may also be pres-
ent to a lesser extent in patients in whom cardiomegaly has developed in adult life,
after the period of thoracic growth3 (i.e. after ossification of sternum and ribs).
Precordial bulging of non-cardiovascular origin can occur in:
Skeletal deformities such as scoliosis, kyphoscoliosis or rickety deformity of the chest

(see Fig. 18.14)
Diseases of the lungs such as bronchogenic carcinoma
Mediastinal new growths (see Table 18.3).
a) Ossification of the Sternum

The sternum is developed from the fusion of the two cartilaginous plates along the mid-ver-
tical line.
The primary centers of ossification for manubrium and body of the sternum appear in
56th months of foetus.
Manubrium: secondary centers of ossification (13) appear at about puberty and are
completed by about 25th year.
Body of the sternum has four sternal segments, known as sternebrea. The fusion of the
sternebrea starts at about puberty and is completed by about 25th year.
Table 18.3 Causes of precordial bulging
Precordial bulging Causes
1. Cardiac Pericardial effusion, cardiomegaly

2. Non-cardiac Skeletal abnormality: scoliosis,
kyphoscoliosis, rickety chest,
bronchogenic carcinoma,
mediastinal new growth
Fig. 18.14 | Precordial bulging due to

severe khyphoscliosis.
The xiphoid process begins to ossify in the 3rd year and fuses with the body of the sternum
at about 40th year.
The bony fusion of the manubriosternal joint (sternal angle) may take place at about
60th year or after.
b) Ossification of the Ribs

A rib is ossified from primary and secondary centers of ossification. The primary ossification
appears at about 2nd month of intra-uterine life, while secondary centers appear at about
puberty and fuse with the rest of the bone after 20 years.
3. CARDIOVASCULAR PULSATIONS
Besides examining the main areas of precordium (apex, pulmonary, aortic, tricuspid
and left parasternal areas), the cardiovascular pulsations should also be sought over
sternoclavicular, epigastric and other ectopic areas (see Fig. 18.15).
a) Apical Impulse
It is examined for its site, extent and any lateral retraction.
The normal apical impulse is due to (see Table 18.4).
An anterior and counter clock-wise rotation of the LV on its long axis as the isovo-
lumic intraventricular pressure rises, which lifts the cardiac apex (lower part of the
IVS and anteroseptal portion of LV) and makes a contact with the left anterior chest
wall during early systole.
Followed by medial retraction during late systole due to recoil of the heart as it
rotates clock-wise with the completion of the LV ejection.
2 3
4 E
5
6
Fig. 18.15 | Cardiovascular pulsations are examined in the following areas

1: Sternoclavicular area, 2: Right parasternal area, 3: Pulmonary area, 4: Left
parasternal area, 5: Apical area, 6: Epigastric area, E: Ectopic areas.
Table 18.4 Cause for normal apical impulse
Cause Chamber Timing
1. Anterior and counter LV Early systole

clock-wise rotation
2. Medial retraction due LV Late systole
to clock-wise rotation
Table 18.5 Characteristics of normal apical impulse
1. Early systole Outermost and lowermost point of maximum impulse

2. Late systole Medial retraction
3. Location Fifth left ICS at or medial to mid-clavicular line and 10 cm
from the mid sternal line
4. Extent 3 cm in diameter, one intercostal space
5. Duration 50% of systole
Normal apical impulse is defined as:

The outermost and lowermost point of maximum impulse (PMI) in early systole,
which imparts a perpendicular gentle thrust to a palpating finger, followed by a
slight medial retraction in the late systole. The medial retraction is better seen than
felt (see Table 18.5).
It is located in the 4th or 5th left intercostal space at or inside the mid-clavicular line,
10 cm from the mid sternal line.
It is confined to one intercostal space, which is 3 cm in diameter, and lasts for 50%
of systole.
However, the point of maximum impulse or maximum precordial pulsation may be
produced by a hypertrophied RV, a dilated aorta or pulmonary artery or due to the LV
wall motion abnormality instead of a normal cardiac apex.
(i) Absent Apical Impulse

It could be due to (see Table 18.6):
Cardiovascular causes:
CAD with decreased apical motion and reduced ejection fraction (EF)
Dilated cardiomyopathy
Pericardial effusion.
Non-cardiovascular causes:
When it is behind the rib
Muscular chest wall
Obesity
COPD including emphysema with barrel chest
Left pleural effusion.
(ii) Double Apical Impulse

It may be seen in:
HOCM (could be double or triple apical impulse)
LV dyssynergy or LV aneurysm.
(iii) Lateral Retraction of the Apical Impulse (Skodas Sign)

It is due to:
Right ventricular hypertrophy (RVH), when RV occupies the apex, extending from
left sternal edge to cardiac apex with exaggerated lateral apical retraction.
It may be due to adhesive pericarditis.
Broadbents sign: It is a systolic in-drawing or retraction of 10th and 11th left inter-
costal spaces, in the scapular or posterior axillary line. It is typically described in adhe-
sive pericarditis. The apical retraction is equivalent of paradoxical septal motion in
echocardiogram.
(iv) Displacement of Apical Impulse

Lateral displacement is often due to:
Skeletal abnormalities: scoliosis, straight back syndrome, marked pectus excavatum.
Table 18.6 Causes of absent apical impulse
CV causes Non-CV causes
1. Dilated cardiomyopathy 1. Behind the rib

2. Pericardial effusion 2. Muscular chest wall
3. CAD with decreased apical 3. Obesity
motion and ejection fraction 4. COPD
5. Left pleural effusion
Intrathoracic pathology: marked right-sided pleural effusion, right-sided pneumo-

thorax, or left lung collapse.
Eccentric LVH due to mitral regurgitation or aortic regurgitation: apical impulse is
displaced outwards and downwards.
RVH, e.g. due to mitral stenosis apical impulse is displaced laterally.
Downward displacement only: Aortic aneurysm and mediastinal new growth may
push the apical impulse downwards.
Upward displacement
In children apical impulse is usually seen and felt in 4th left intercostal space at or
inside the mid-clavicular line.
Intra-abdominal causes: ascites, massive abdominal tumor, or advanced pregnancy.
Pericardial effusion: it may displace apical impulse usually upwards and to the left,
since fluid, as a rule, first collects in the lower portion of the pericardial sac.
Right-sided apical impulse
Often due to dextrocardia and congenital heart disease.
Sometimes due to intra-thoracic pathology such as left-sided massive pleural effu-
sion or pnuemothorax and right lung collapse.
Skeletal abnormalities such as scoliosis (see Table 18.7).
(v) Extent of Apical Impulse

Diffuse apical impulse of 3 cm in diameter or apical impulse present in more than
one intercostal space may be due to:
Cardiovascular causes:
Eccentric LVH as in aortic regurgitation
LV aneurysm.
Table 18.7 Displacement of apical impulse
Lateral displacement Upward displacement Downward displacement
1. Skeletal abnormalities: scoliosis, 1. Normal children 1. Aortic aneurysm

straight back syndrome,
pectus excavatum
2. Intrathoracic abnormality: 2. Pregnancy 2. Mediastinal new growth
right pleural effusion,
pneumothorax, left lung collapse
3. Eccentric LVH (mitral regurgitation, 3. Ascitis
aortic regurgitationalso
downwards)
4. RVH (mitral stenosis) 4. Abdominal tumor
5. Pericardial effusion
(displaced upward and left)
Table 18.8 Pulsations in aortic and pulmonary areas
Aortic area Pulmonary area
1. Aneurysm of ascending aorta 1. PH of any cause: mitral stenosis, primary pulmonary hypertension
2. Chronic aortic regurgitation 2. Pulmonary artery dilatation: idiopathic or aneurysmal
3. pulmonary blood flow: PDA, ASD
4. Hyperdynamic circulation: fever, pregnancy
PH: pulmonary hypertension, PDA: patent ductus arteriosis, ASD: atrial septal defect.
Non-cardiovascular causes:
Subjects with thin chest wall
Hyperdynamic circulation: fever, thyrotoxicosis
Retraction of the lung due to fibrosis or collapse.
b) Pulsations in the (Aortic Area) Right and Left (Pulmonary Area)

2nd Intercostal Spaces
Ascending aorta lies to the right of the sternum at the level of 2nd right intercostal space
and the pulmonary trunk lies beneath the 2nd left intercostal space, while RV outflow
(infundibulum) lies beneath the 3rd left intercostal space (see Table 18.8).
Presence of abnormal pulsations in the aortic area may be due to the dilatation of
ascending aorta because of:
Aneurysm of ascending aorta or
Chronic aortic regurgitation.
Pulsations in the 2nd or 3rd left intercostal space may be due to dilated pulmonary
artery as a result of:
Pulmonary hypertension of any cause e.g. mitral stenosis, primary pulmonary
hypertension
Idiopathic pulmonary artery dilatation2
Increased pulmonary blood flow as in PDA, ASD
Aneurysmal dilatation of pulmonary artery
Hyperdynamic circulation as in fever, pregnancy and
Rarely due to retraction of the left lung from fibrosis or collapse.
c) Pulsations in the Sternoclavicular Area

The sternoclavicular area includes the right and left sterno-clavicular joints, manubrium
sterni and supra-sternal notch (Table 18.9). No pulsations are normally visible or palpa-
ble in this area.
Abnormal pulsations in this area are usually due to:
Aortic dissection: sternoclavicular joint pulsation in a patient with chest pain may
be an early clue to the diagnosis of aortic dissection.4
Table 18.9 Pulsations in the sternoclavicular area
Sternoclavicular pulsations Suprasternal pulsations
1. Aortic dissection 1. Aneurysm of arch of aorta

2. Aneurysm of aorta 2. Thyroidea ima artery
3. Aortic regurgitation
4. Right aortic arch
5. Blalock-Taussig shunt
Fig. 18.16 | Left parasternal pulsations better appreciated by placing a light object
(paper, pencil) in the parasternal area.
Aneurysm of aorta: atherosclerotic or syphilitic.2

Systolic pulsation of the right sternoclavicular joint or manubrium may be due to
aortic regurgitation.
Pulsation in the right sternoclavicular area may suggest right aortic arch as in patients
with cyanotic congenital heart disease e.g. TOF.5
Blalock-Taussig shunt (classical on the opposite side of aortic arch while the modified
shunt is performed on the same side of aortic arch).
Suprasternal pulsations may be due to:
Aneurysm of aorta (arch of aorta)
Thyroidea ima artery.
Pulsations in the suprasternal notch or supraclavicular area may be due to:
Kinked tortuous right carotid artery2
Dilated and tortuous of brachiocephalic artery2
Anomalous right subclavian artery.
d) Left Parasternal Pulsations

RV inflow portion underlies the mid to lower left sternal edge (4th and 5th intercostal
space) while its outflow portion (infundibulum) lies behind the 3rd left intercostal
space. In normal adults of average build, RV activity is neither visible nor palpable as
it retracts away from the anterior chest wall during systole (see Fig. 18.16).
Table 18.10 Left parasternal pulsations
Due to right ventricular hypertrophy Normal right ventricle
1. Pressure over-load: 1. Mod-severe mitral regurgitation

Pulmonary hypertension (squid effect)
Primary pulmonary hypertension
Pulmonary stenosis
2. Volume over-load: 2. Regional wall motion
Tricupid regurgitation (moderate) Abnormality (RWMA) of left ventricle
ASD, VSD
ASD: atrial septal defect, VSD: ventricular septal defect, RWMA: regional wall motion abnormality.
Left parasternal pulsations may be seen in:

Children and thin adults with a small antero-posterior diameter or in patients with
pectus excavatum.
RVH with pressure over-load conditions (see Table 18.10):
Pulmonary stenosis
PH due to mitral valve disease, LVF, left to right shunt (PDA, VSD and ASD)
Pulmonary embolism
Corpulmonale
Primary pulmonary hypertension.
RVH with volume over-load conditions (see Table 18.10): Mild-moderate tricuspid
regurgitation, ASD, VSD.6
Left parasternal pulsations due to anterior systolic movement of normal RV:
(i) Moderate to severe mitral regurgitation in the absence of PH produces apparent
RV impulse at the left parasternal area. This apparent late anterior systolic move-
ment of RV is due to:
Jet or squid effect as a result of regurgitation of blood into the LA which lies
behind the RV7 and
Subsequent systolic expansion of the enlarged LA causing anterior displacement
of RV.
With a coexisting PH, the left parasternal impulse will be sustained throughout the
systole, and the squid effect and subsequent expansion of LA may not be detectable.
(ii) Regional wall motion abnormalities (RWMA) of LV: Dyskinetic motion of the
ventricular septum during angina pectoris displaces the RV forward and results
in a transient left parasternal impulse that promptly disappears on relief of the
angina.
e) Pulsations in the Epigastrium

The pulsations in the epigastrium may be:
Cardiac, aortic or hepatic in origin (see Table 18.11 and Fig. 18.17).
Table 18.11 Epigastric pulsations
Cardiac Aortic Hepatic
1. Right ventricular 1. Thin built/hyperkinetic 1. Tricuspid regurgitation

hypertrophy individuals 2. Tricuspid stenosis
2. Aneurysm of descending
aorta
3. Aortic regurgitation
Cardiac Epigastric pulsations Hepatic
Right ventricular Tricuspid regurgitation,

Aortic
hypertrophy tricuspid stenosis
Aortic aneurysm,
aortic regurgitation,
thin individuals
Fig. 18.17 | Causes and importance of epigastric pulsations.

Cardiac Pulsations in the Epigastrium
These pulsations are due to marked RV dilatation or RVH of any cause. The inferior
portion of the RV transmits its impulse to the sub-xiphoid or epigastric region, which
is accessible to palpation during held inspiration.
In COPD with RVH, RV impulse is accessible only in this region.
Aortic Pulsations in the Epigastrium

In thin built or hyperkinetic individuals, aortic pulsations may be visible or palpable in
the epigastrium.
However, abnormally large pulsations in the epigastrium may be due to aneurysm of
descending aorta or due to aortic regurgitation.
Hepatic Pulsations in the Epigastrium

These may be due to:
Tricuspid regurgitation (systolic pulsations)
Tricuspid stenosis (presystolic pulsations).
f) Pulsations in the Ectopic Areas

Occasionally, cardiac pulsations are encountered in areas other than in the usual areas
of the precordium.
Ectopic LV impulse is located usually above and medial to the normally expected
cardiac impulse:
Due to dyskinesia of the LV either during the episodes of angina pectoris or after
acute myocardial infarction.
Persistent paradoxical ectopic pulsations due to ventricular aneurysm because of
myocardial infarction or trauma.
Ectopic LA impulse: In a patient of severe MR with giant LA that extends to the right,
an ectopic systolic pulsation may be encountered in the right anterior or lateral chest or
in the left axilla.2
RA impulse: Normally, RA forms the right lower cardiac border, which lies behind
the right lateral border of the sternum in the 4th intercostal space, and RA impulse is
not visible or palpable. However; in enlarged RA as in tricuspid regurgitation, systolic
expansion of the enlarged RA causes late systolic movement of the entire right lower
chest especially in the 4th right intercostal space.
Ectopic impulse beneath the left clavicle is seen in patients with PDA.
REFERENCES
1. Corvisart JN. An Essay on the Organic Diseases and Lesions of the Heart and Great vessels.
Translated from the French, with notes by Jacob Gates. New York: Hafner, 1962.
2. Schlant RC, Hurst JW. Examination of the precordium: Inspection and Palpation. New York:
Am Heart Assoc 1990:128.
3. Davies H. Chest deformities in congenital heart diseases. Br J Dis Chest 1959;53:151157.
4. Logue RB, Sikes C. A new sign in dissecting aneurysm of aorta: Pulsation of a sternoclavicular joint.
JAMA 1952;148(14):12091212.
5. Perloff JK. The movements of the heartobservation, palpation and percussion. In: Physical Examination
of the Heart and Circulation. Philadelphia, Saunders, 1982:130170.
6. Nagle RE, Tamara FA. Left parasternal impulse in pulmonary stenosis and atrial septal defect.
Br Heart J 1967;29:735741.
7. Basta LL, Wolfston P, Eckberg DL, et al. The value of left parasternal impulse recordings in the
assessment of mitral regurgitation. Circulation 1973;48(5):10551065.
CHAPTER 19
PALPATION OF THE PRECORDIUM
1. EXAMINATION OF THE CHEST f) Palpation of Epigastrium 328

FOR THE SHAPE AND g) Palpation in the Ectopic
DISTENDED VESSELS 316 Areas 328
2. PALPATION OF THE PRECORDIUM 4. TRACHEAL TUG
FOR ANY TENDERNESS 316 (OLIVERS SIGN) 329
3. PALPATION OF THE 5. KINETIC CARDIOGRAM 330
CARDIOVASCULAR PULSATIONS, a) The Apical Impulse in
PALPABLE SOUNDS, THRILLS Normal Adults 330
AND RUBS 316 b) Hyperdynamic/Hyperkinetic
a) Palpation of the Cardiac Apex 318 Apex 331
b) Palpation of Left Parasternal c) Sustained/Heaving Apex 331
Area 322 d) Hyperkinetic RV Impulse 331
c) Palpation of Lower Left e) Sustained RV Impulse 331
Sternal Area (Tricuspid Area) 326 f) Systolic Movements are
d) Palpation of Aortic and Inconspicuous in
Pulmonary Areas 326 Cardiomyopathy 331
e) Palpation of Sternoclavicular g) In Constrictive Pericarditis 332
Areas 328 REFERENCES 332
Egyptian physicians and priests employed the technique of palpation, and it was one of
the techniques of examination in the ancient Greece.
Practice of precordial palpation was recorded in the Ebers papurus (1500 BC).
William Harvey (1628) was familiar with the movements of the chest wall and
described, Motion of the heart. In 1857, Chauvea confirmed Harveys contention that
precordial movement seen when the heart strikes against the breast resulted from the ven-
tricular contraction. Jean Nicolas Corvisart, French physician pioneered the art of bedside
inspection and palpation of the precordium.1
Method of examination: Palpation of the precordium includes systematic examination
of the following:
Examination of the chest for the shape and distended vessels
Palpation of the precordium for tenderness
Palpation of the cardiovascular pulsations, palpable sounds, thrills and rubs
Examination for tracheal tug.
1. EXAMINATION OF THE CHEST FOR THE SHAPE AND

DISTENDED VESSELS
i) Confirm the barrel shape chest by measuring the antero-posterior (AP) and trans-
verse diameters, in which AP diameter is transverse diameter.
ii) For associated abnormalities, see inspection of the precordium.
iii) Distended veins over the anterior chest with caudal flow suggest SVC obstruction;
while with the cranial flow indicate IVC obstruction.
iv) Collateral arteries may be seen in the infrascapular and interscapular regions or in the
posterior intercostal spaces in a patient with coarctation of aorta and are palpable
when the patient stands and leans forward with arms hanging down by the sides
(Suzmans sign).
2. PALPATION OF THE PRECORDIUM FOR ANY TENDERNESS
Tenderness of the costochondral junction occurs in Tietze syndrome, which is impor-

tant to rule out myocardial ischemia in a patient with chest pain.
Precordial tenderness may be associated with acute pericarditis and acute myocarditis
(see Table 19.1).
3. PALPATION OF THE CARDIOVASCULAR PULSATIONS,

PALPABLE SOUNDS, THRILLS AND RUBS
Palpation of the precordium is performed from the right side of the supine patient
with the upper trunk elevated to 30 and the chest completely exposed. Palpation of
the apex should also be done in the left lateral position, rotated 4590,2 which
causes the heart to move laterally and increases the palpability of apex (see Fig. 19.1).
Palm of the hand and ventral surface of the proximal metacarpals are used for the initial
localization of palpable cardiac motion such as the cardiac apex and for the detection
of the precordial thrills, while the pads of the fingers are used for precise localization
and assessment of left and right ventricular activity (see Fig. 19.2).
Once the precordial impulse is identified, varying pressure should be applied with the
hand. While high frequency movements such as ejection sounds, valve closure sounds
and mitral opening sounds are more easily detected with the palm and proximal meta-
carpals held firmly against the chest, the low frequency movements such as ventricular
diastolic filling events (S3, S4) are best felt by applying light pressure with the fingertips.
Table 19.1 Precordial tenderness
1. Tietze syndrome
2. Acute pericarditis
3. Acute myocarditis
PALPATION OF THE PRECORDIUM 317
Thrills are most easily palpated with fingertips or by applying firm pressure with
palm and proximal metacarpals. Occasionally, thrills are readily detected with the
right palm firmly placed over the anterior chest and the left hand supporting the
posterior thorax with equal force.3
All precordial movements should be timed with the simultaneous palpation of carotid
pulse with the left hand or auscultation of the heart sounds (see Fig. 19.3).4
Palpation of the cardiovascular pulsations includes:
Cardiac apex
Left parasternal area
Localized
pulsations
Thrills
Heaves or lifts
Fig. 19.2 | Optimal areas on the examiners hand

for precordial palpation.
Fig. 19.1 | Initial palpation of the apex in left lateral

position.
Fig. 19.3 | Localization and determining the character of the apex beat while timing
with the carotid.
Lower left sternal area (tricuspid area)

Aortic and pulmonary areas
Sternoclavicular areas
Epigastrium
Ectopic areas.
a) Palpation of the Cardiac Apex

(i) Size and Extent of the Cardiac Apex
Confirm site and extent of the cardiac apex by palpation in supine position with trunk
elevated to 30. If the apical impulse was not visible, palpate for the cardiac apex and
determine its location and extent.
Normal cardiac apex: See apical impulse
Displaced cardiac apex: See displaced apical impulse
Double or triple cardiac apex: See double apical impulse.
In HOCM, a mid or late systolic secondary bulge may be present that results in a double
or bifid apical impulse. When S4 is palpable, the apex beat may actually be triple or trifid
in nature (triple ripple).
Extent of cardiac apex: See extent of apical impulse.
(ii) Character of the Apex Beat

The apex should be palpated first in supine position with trunk elevated to 30 and
then the character of the cardiac apex is determined in left lateral position rotated to
4590. The outward movement of the apical impulse is normally felt during the first
third of systole, but the systolic inward movement is only visible as medial retraction.
The cardiac apex may be (see Table 19.2 and Fig. 19.4):
Absent or feeble
Tapping
Hyperdynamic
Heaving.
Absent or feeble apex beat: See absent apical impulse.
Table 19.2 Types of apex beat
Tapping Hyperdynamic Heaving
1. Mitral stenosis 1. Aortic regurgitation, mitral 1. Pressure overload: aortic stenosis,

regurgitation HCM, systemic hypertension
2. PDA, VSD 2. Severe LV dysfunction
3. AV fistula 3. LV aneurysm
4. Blalock and Waterston shunts 4. Severe aortic regurgitation
5. Hyperkinetic states: anemia, 5. Severe mitral regurgitation of
pregnancy, thyrotoxicosis ischemic origin
6. Thin chest, pectus excavatum
CAD, DCM, MCW, obesity,

Mitral pericardial COPD,
stenosis effusion behind the rib
Tapping Apex beat Absent or feeble
AS, HCM,
Hyperdynamic Heaving LV aneurysm,
severe LVD
AR, MR, Hyperdynamic

VSD, PDA, circulation,
AV fistula thin chest,
pectus excavatum
Fig. 19.4 | Apex beat and its importanceCAD: coronary artery disease, DCM: dilated
cardiomyopathy, MCW: muscular chest wall, COPD: chronic obstructive pul-
monary disorders, AR: aortic regurgitation, AS: aortic stenosis, MR: mitral
regurgitation, MS: mitral stenosis, VSD: ventricular septal defect, PDA: patent
ductus arteriosus, HCM: hypertrophic cardiomyopathy, LVD: left ventricular
dysfunction, AV: arteriovenous.
Tapping apex beat

Tapping apex beat is characteristic of mitral stenosis in which the apex beat is often
impalpable and is replaced by a short systolic tap, a palpable equivalent of a loud S1.
A shortened outward movement of the apex during early systole due to the reduced
ventricular filling during diastole gives the apex beat its sharp, short and tapping
nature in mitral stenosis.
Hyperdynamic/hyperkinetic/forceful apex beat
There is an increase in amplitude and duration of excursion of the apical impulse,
but is ill sustained i.e. duration of excursion is 50% of systole with partial lifting
of the examining fingers.
This type of cardiac apex is characteristic of volume overload conditions and eccentric
LVH. It is best appreciated by simultaneous auscultation and palpation.
Cardiovascular causes
Valvular regurgitations: Aortic regurgitation, mitral regurgitation
Left to right shunts:
Congenital: VSD, PDA, systemic arteriovenous fistula
Acquired: Systemic to pulmonary artery shunt: Blalock and Waterston shunts,
systemic arteriovenous fistula.
Non-cardiovascular causes
Hyperkinetic circulatory states: Pregnancy, anemia, thyrotoxicosis, Beri-beri
Thin chest wall, pectus excavatum.
Heaving/sustained apex beat

There is a sustained increase in the duration of excursion of apical impulse besides
its amplitude, due to increased duration of the LV ejection i.e. duration of excursion
is 50% of systole with sustained lift of the examining fingers.
This type of cardiac apex is characteristic of pressure overload conditions and concen-
tric LVH. It is also better appreciated by simultaneous auscultation and palpation.
Pressure overload: Aortic stenosis, systemic hypertension, hypertrophic cardiomyopathy
CAD: LV aneurysm, severe LV dysfunction
Severe volume overload conditions such as severe aortic regurgitation and severe mitral
regurgitation secondary to CAD may also present with sustained apex beat.
(iii) Palpable Low Frequency Sounds at the Apex

Normally, the diastolic events such as the ventricular filling during rapid filling phase and
presystole are neither visible nor palpable. Low frequency sounds such as S3, S4 and peri-
cardial knock are best felt by light palpation with fingertips in held expiration, but firm
pressure would dampen them.
Palpable LV S3 (rapid filling wave, see Table 19.3)
Left ventricular failure
Chronic mitral regurgitation
Non-cardiovascular causes
Physiological: Children and pregnancy
Hyperkinetic circulatory states: Anemia, thyrotoxicosis
Palpable pericardial knock: It occurs in constrictive pericarditis with systolic retrac-
tion of whole of the pericardium especially in the left 10th and 11th intercostal spaces
in the posterior axillary/scapular line (Broadbents sign).
Palpable LV S4 (a wave/presystolic impulse, see Table 19.3): Presystolic atrial contrac-
tion, which distends the LV is normally not palpable, but is felt in the non-compliant
LV when the left ventricular end diastolic pressure (LVEDP) is 1518 mmHg (normal
LVEDP is 12 mmHg).
Table 19.3 Palpable S3 and S4
Palpable S3 Palpable S4
1. Children 1. Aortic stenosis

2. Pregnancy 2. Hypertrophic cardiomyopathy
3. Left ventricular failure 3. Acute mitral regurgitation and
acute aortic regurgitation
4. Chronic significant mitral regurgitation 4. Acute or CAD
5. Normal women of 40 years of age
Aortic stenosis
Acute mitral regurgitation, acute aortic regurgitation
CADacute or chronic
It is sometimes palpable in normal women of 40 years of age.
(iv) Palpable High Frequency Sounds at the Apex

Opening snaps, tumor plops and ejection sounds (clicks) are best felt by applying firm
pressure to the chest with palm and proximal metacarpals (see Table 19.4).
Palpable loud S1: It occurs due to mitral stenosis, which imparts a tapping type of
apex beat.
Palpable opening snap: It occurs in early diastole due to mitral stenosis with pliable
mitral valve. It may radiate to the lower left sternal edge when loud.
Palpable tumor plop: It is a rarely palpable early diastolic sound due to abrupt deceler-
ation of a mobile pedunculated LA or RA myxoma as the tumor sits in the mitral or
tricuspid orifice.
Palpable ejection sounds
Ejection sound (click) of congenital aortic stenosis sometimes more readily palpable
over the apex than in the 2nd right intercostal space (ICS).
However, the ejection sounds due to dilated aortic root are better felt at the right base
(2nd right ICS) and
Pulmonary ejection sound is felt in 2nd left ICS during normal expiration.
(v) Palpable MurmursThrills at the Apex

Diastolic or presystolic thrill
Diastolic thrill of mitral stenosis is highly localized to the apex, which generally
indicates mobile and non-calcified mitral valve.
If thrill is equivocal even in the left lateral position, a brisk cough will make it more
pronounced as it transiently increases the heart rate and mitral flow.
Table 19.4 Palpable high frequency sounds at the apex
Sounds Cause
1. Loud S1 Mitral stenosis

2. Opening snap Mitral stenosis (pliable mitral valve)
3. Tumor plop LA myxoma (mobile)
4. Systolic ejection sound Congenital aortic stenosis (bicuspid aortic valve)
Systolic thrills: These are not common at the apex. They may occur due to:
Severe mitral regurgitation especially due to chordal rupture. However, systolic thrills
due to mitral regurgitation are not common.
Aortic stenosis: Thrill may be traced from 2nd right ICS to the apex and may get
conducted to the carotids. However, it may only be felt at the apex in calcified aortic
atenosis in the elderly patients.
VSD: It is better felt in the 3rd4th ICS at the left sternal edge.
Palpable pericardial rub: It occurs in acute pericarditis and is best felt at the left ster-
nal border in sitting and leaning forward positions.
b) Palpation of Left Parasternal Area

A French Physician, Jean Nicolas Corvisart (in the late 18th and early 19th century) pio-
neered the art of inspection and palpation of precordium (especially the left parasternal
area) and correlated the clinical findings with the autopsy findings.1
i) Left Parasternal Lift
For parasternal lift due to RV hypertrophy; heel of the hand with the wrist cocked
upwards, is placed over the lower half of the sternum during the held end expiration
(see Fig. 19.5). The movements of the examining hand and fingers should be carefully
observed as the low amplitude RV activity is better seen than felt.
Alternatively, tips of three fingers (index, middle, ring) are placed in the 3rd, 4th, and
5th intercostal spaces near the left sternal edge during the full held expiration which
not only permits the detection of gentle RV systolic impulses but also localizes the
movements to the inflow portion (4th and 5th ICS) or to the infundibulum/outflow
portion (3rd ICS) (see Fig. 19.6).
The left parasternal area can also be palpated with the ulnar border of the hand and
the pulmonary artery pressure can be judged clinically by applying varying pressure
(see Fig. 19.7).
Fig. 19.5 | Palpation of left parasternal area (LPA) with heel of the hand and wrist
cocked upwards.
Grading of parasternal lift: There is no standard method of grading parasternal lift

(PSL). However, in general, there are two accepted methods: subjective and objective.
The subjective method assesses the amplitude of excursion of PSL while for the objective
assessment; the duration of the PSL (sustained/ill sustained) is noted by simultaneous
auscultation. More clinical information is obtained with the combination of these two
methods (see Table 19.5).
GRADE-1/3 (mild): Mild lift can be made out after careful inspection of the
parasternal area (see Fig. 19.8).
Light objects such as pencil or scale kept along the parasternal region, may make it
more obvious.
It disappears with the application of mild counter pressure. It is short of systole i.e.
ill sustained, 1/3rd of systole.
Fig. 19.6 | Palpation of left parasternal area (LPA) with tips of the three fingers.
Fig. 19.7 | Alternative

of the hand.
method of palpation of left parasternal area (LPA) with ulnar border
Table 19.5 Left parasternal lift
Grade-1/3 Grade-2/3 Grade-3/3
1. Normal children and 1. Mild-moderate pulmonary 1. Moderate-severe

young adults hypertension pulmonary stenosis
2. Thin chest wall 2. RV volume overload: tricuspid 2. Severe pulmonary
regurgitation, ASD, VSD hypertension
3. Pectus excavatum 3. Moderate-severe mitral
regurgitation
Fig. 19.8 | Grade I left parasternal left.

It may be seen
normally in children and young adults
in thin adults with a small AP thoracic diameter or
in subjects with pectus excavatum.
GRADE-2/3 (moderate): An obvious lift that can be easily made out.
It disappears/diminishes with the application of moderate counter pressure.
It is not well sustained i.e. 50% of systole but not throughout the systole.
It is usually seen in:
RV volume overload conditions such as tricuspid regurgitation, ASD, VSD
Mild-moderate pulmonary hypertension of any cause e.g. moderate mitral stenosis,
left ventricular failure, left to right shunts (VSD, PDA)
Moderate-severe mitral regurgitation due to jet/squid effect.5
Characteristics of PSL in mitral regurgitation
Simultaneous palpation of the apex and the parasternal area is mandatory to identify
this type of PSL due to the anterior movement of normal right ventricle.
Fig. 19.9 | Simultaneous palpation of apex (with index finger) and left parasternal area
(with ulnar border of the hand) for parasternal lift in mitral regurgitation
ICS: intercostal space.
Fig. 19.10 | Simultaneous palpation of apex (with index finger) and left parasternal area
(with index finger of other hand) for parasternal lift in mitral regurgitation
ICS: intercostal space.
PSL occurs in the second half of systole following S1 and after the cardiac apex is felt.
It is short in duration (ill sustained) and more diffused and indicates a non compliant
enlarged left atrium.
It can be recognized by placing the index finger of one hand at the cardiac apex and
the index finger or ulnar border of the other hand at the left parasternal region in the
3rd4th ICS (see Figs 19.9 and 19.10). The movement of the latter begins and ends
slightly later than that of the former.
GRADE-3/3(severe): It is a very prominent parasternal lift.
Application of moderate counter pressure does not diminish the PSL.
It is well sustained i.e. PSL is present throughout the systole and beyond A2.
Characteristic of RV pressure overload conditions such as:

Pulmonary stenosis (moderate-severe)
And severe pulmonary hypertension due to severe mitral stenosis, left to right
shunts (PDA, VSD) and left ventricular failure.
No PSL in TOF: There is no PSL in RVH due to TOF2
As it can decompress easily into the overriding of aorta and through VSD and
RV is not excessively dilated.
(ii) Palpable Low Frequency Sounds

RV S3 and S4 may be palpable in this area or occasionally in the epigastrium in held
inspiration which is attenuated or even disappears during expiration.
RV S3 usually indicates RV dysfunction or failure, chronic severe tricuspid regurgitation
and ASD
RV S4 is associated with pulmonary stenosis, decreased RV compliance secondary to
pulmonary hypertension.
c) Palpation of Lower Left Sternal Area (Tricuspid Area)

Patient should be in supine position with right lateral rotation.
Palpable Low Frequency Sounds

RV S3 and RV S4 may only be palpable in this area in supine and right lateral rotation.
Palpable High Frequency Sounds

Opening snap of organic tricuspid stenosis is sometimes palpable with the fingers
firmly applied in this area or in the epigastrium.
Palpable MurmursThrills
Occasionally, diastolic thrill of organic tricuspid stenosis and rarely, systolic thrill of
severe tricuspid regurgitation may be palpable.
d) Palpation of Aortic and Pulmonary Areas

The basal areas of the heart (2nd right ICS and 2nd3rd left ICS) should be palpated in
the sitting and leaning forward positions in held expiration, which increases the palpa-
bility of these areas (see Figs 19.11 and 19.12).
(i) Palpable High Frequency Sounds

In aortic area: Palpable A2 in the aortic area occurs in:
Systemic hypertension, dilated aortic root and moderate aortic stenosis
Cyanotic congenital heart disease: When pulmonary trunk is small as in TOF or
when the aortic root is anterior to the pulmonary trunk as in transposition of great
arteries (TGA).
Fig. 19.11 | Palpation of aortic area.

Fig. 19.12 | Palpation of pulmonary area.
Palpable ejection sound originating in the dilated aortic root. Ejection sound of
congenital aortic stenosis is sometimes more readily palpable over the apex than in the
right 2nd ICS and should be differentiated from a loud S1.
In pulmonary area
Palpable P2 in the pulmonary area occurs in pulmonary hypertension of any cause,
which may be widely transmitted to mid and lower left sternal edge and apex espe-
cially when the RV occupies the apex.
Palpable ejection sound in the pulmonary area occurs in pulmonary stenosis during
normal expiration.
(ii) Palpable MurmursThrills

In aortic area
Systolic thrill in the aortic area (palpable in held expiration with firm application of
fingertips) occurs in aortic stenosis, which may be conducted to the carotids. It may be
occasionally detected at the apex in the older patients with calcified aortic stenosis.
Rarely, a diastolic thrill may be palpable due to dilated aortic root as in Marfan
syndrome.
In pulmonary area
Palpable systolic thrill in the pulmonary area may be felt in pulmonary stenosis in
sitting and leaning forward positions in held expiration, while thrill of infundibular
pulmonary stenosis is best felt in the left 3rd ICS.
Continuous thrill of PDA is felt maximal beneath the left clavicle, which begins
in systole, is reinforced before and after S2 and proceeds into the diastole without
interruption.
Table 19.6 Precordial thrills
Apex Tricuspid area Pulmonary area Aortic area
1. Diastolic: mitral stenosis 1. Diastolic: tricuspid 1. Systolic: pulmonary 1. Systolic: aortic

stenosis stenosis stenosis
2. Systolic: acute severe mitral 2. Systolic: rarely 2. Continous: patent
regurgitation (chordal rupture), severe tricuspid ductus arteriosus
calcified aortic stenosis regurgitation
Rarely, Graham Steel murmur (early diastolic) of high pressure pulmonary regurgita-
tion may be palpable.
It is rare to detect a palpable diastolic thrill of aortic regurgitation along the left sternal
edge in the 3rd ICS (neo aortic area), unless there is perforation or eversion of an aortic
cusp resulting in an extremely loud diastolic murmur.
Presence of thrills in main areas of the precordium (i.e. at the apex, tricuspid, pulmonary
and aortic areas) is helpful in the diagnosis of underlying disorders (see Table 19.6).
e) Palpation of Sternoclavicular Areas

Continuous/systolic thrill is palpable on the left side due to Blalock-Taussig shunt
operation, while it is felt on the same side in the modified shunt operation.
f) Palpation of Epigastrium
The subxiphoid region, which allows the palpation of RV, should be examined with
the tip of the index finger. It should be done during held inspiration and in supine
position (see Figs 19.13 and 19.14).
This technique is particularly useful in patients with an increased AP diameter,
COPD, obesity or muscular chest when the RV enlargement is suspected, but precor-
dial impulse is not felt for evaluation.
However, pulsations in the epigastrium could also due to the aortic pulsations or
hepatic pulsations.
While palpating the epigastrium, the pulsations due to RV hypertrophy are felt by
the fingertip, aortic pulsations by the palmar surface and hepatic pulsations by the
lateral surface of the examining index finger.
g) Palpation in the Ectopic Areas

Occasionally, cardiac pulsations may be palpable in the areas other than in the usual
areas of the precordium.
(i) Ectopic LV Impulse
It is usually palpable above and medial to the normally expected cardiac apex
Due to dyskinesia of CAD, during the episodes of angina pectoris or after acute
myocardial infarction
Fig. 19.14 | Palpation of the epigastrium with the tip of

the index finger.
Fig. 19.13 | Initial palpation.

Ventricular aneurysm: Persistent paradoxical palpable ectopic pulsations due to ventric-
ular aneurysm because of myocardial infarction or trauma.
(ii) Ectopic LA Impulse

In patients with severe mitral regurgitation with giant LA that extends to the right,
ectopic systolic pulsations of the enlarged LA may be felt in the right anterior or lateral
chest or in the left axilla.3
(iii) Ectopic RA Impulse

Normally RA impulse is not visible or palpable. However if RA is enlarged as in tricuspid
regurgitation, systolic expansion of the enlarged RA may be palpable in the entire right
lower chest especially in the 4th right ICS.
(iv) Due to PDA

Palpable ectopic impulse beneath the left clavicle in patients with PDA.
4. TRACHEAL TUG (OLIVERS SIGN)
Raise the chin of the patient and apply firm upward pressure with fingers on the two
sides of the circoid cartilage (see Fig. 19.15).
S4 E P2 S3
S1 A2
RFW
o
Fig. 19.16 | Normal apex cardiogram (ACG).

Fig. 19.15 | Examination for tracheal tug.
A downward tug felt by the fingers with each beat of the heart suggests the possibility
of the presence of an aortic aneurysm.
It is due to the downward pull exerted by the aneurysmal aortic arch on the left
bronchus, later transmitted to the trachea and cricoid.
However, the movement of the cricoid is forward and backward due to transmitted
pulsations from the vessels of the neck to the cricoid, but not a distinct forward pull
as in tracheal tug.
5. KINETIC CARDIOGRAM
It is the graphic representation of the precordial movements.

Kinetic apex cardiogram is the graphic representation of the apical movements,
which consists of systolic and diastolic events (see Fig. 19.16).
a) The Apical Impulse in Normal Adults

The normal apex cardiogram (ACG) is characterized by palpable outward apical
movements in early systole (E point) lasting for a brief period (up to 0.08 sec.), and
later systolic inward movement partly due to recoil of the heart as it rotates clockwise
on its long axis, which is only visible as medial retraction.
Diastolic events which occur with the opening of the mitral valve (O point), consist
of an early diastolic outward movement due to the rapid ventricular filling (Rapid fill-
ing wave, RFW) corresponding to S3 and a late diastolic outward movement due to
the late ventricular filling {because of left atrial contraction (a wave)} corresponding to
S4, are normally not palpable.
Occasionally, RFW may be palpable in normal children and young adults.
A B
S4 E P2 S3
S1 A2
S4 E P2 S3
S1 A2
a
a
RFW RFW
o
o
Fig. 19.17 | ACGNormal apex (B) and Hyperdynamic LV apex (A).

b) Hyperdynamic/Hyperkinetic Apex
It is associated with eccentric LVH and is characterized by the exaggeration of the
normal apex (E point) with rapid upstroke both in amplitude and duration (50%
of systole) followed by marked mid or late systolic retraction (see Fig. 19.17).
RFW may be palpable coinciding with the S3 as in mitral regurgitation.
c) Sustained/Heaving Apex
It is associated with concentric LVH and is characterized by slow LV upstroke but
increase in duration (50% of systole) (see Fig. 19.18).
a wave may be palpable coinciding with S4.
A double outward systolic thrust (which is often palpable) may be recorded in hyper-
trophic cardiomyopathy. (see Fig. 19.19).
d) Hyperkinetic RV Impulse
It is associated with RV volume overload conditions.
It is characterized by outward movement in both amplitude and duration (50% of
systole) of the left sternal edge in 3rd and 4th ICS followed by retraction, which is
augmented during inspiration.
e) Sustained RV Impulse
It is associated with RV pressure overload conditions.
It is characterized by sustained (50% of systole) outward movement of the left
sternal edge in 3rd and 4th ICS, which is augmented during inspiration.
f) Systolic Movements are Inconspicuous in Cardiomyopathy

While diastolic movements of RFW and a wave (corresponding to S3 and S4) may be
prominent and may merge to form a summation gallop in tachycardia.
A B
E E
S4 P2 S3
S1 A2
S4 P2 S3
S1 A2
a a
RFW
o
o RFW
Fig. 19.18 | ACGNormal apex (A) and Sustained LV apex (B).

A B
S4 E P S
S1 A2 2 3
S1 SM
S4 S2
a
a
RFW
o
Fig. 19.19 | ACGNormal apex (A) and Double outward systolic thrust in hypertrophic
cardiomyopathy (B).
g) In Constrictive Pericarditis
There is a conspicuous inward apical movement (retraction) during systole with an
exaggerated RFW (corresponding to the pericardial knock) which is often palpable.
REFERENCES
1. Corvisat JN. An Essay on the Organic Diseases and Lesions of the Heart and Great vessels. Translated
from the French, with notes by Jacob Gates. New York: Hafner, 1962.
2. Stapleton JF, Groves BM. Precordial palpation. Am Heart J 1971;82:409427.
3. Schlant RC, Hurst JW. Examination of the precordium: Inspection and Palpation, New York: Am heart
Assoc 1990:128.
4. ONeill TW, Smith M, Barry M, et al. Diagnostic value of the apex beat. Lancet 1989;1(8635):
410411.
5. Basta LL, Wolfson P, Eckberg DL, et al. The value of left parasternal impulse recordings in the assess-
ment of mitral regurgitation. Circulation 1973;48:10551065.
CHAPTER 20
P ERCUSSION OF THE P RECORDIUM
AND P RECORDIAL F INDINGS IN
COMMON H EART D ISEASES
METHODS OF PERCUSSION 334 PRECORDIAL FINDINGS IN COMMON

Direct Percussion 334 HEART DISEASES 338
Indirect Percussion 334 Acquired Heart Diseases 338
Auscultatory Percussion 334 Acyanotic Congenital Heart
THE SCHEME OF PERCUSSION 334 Diseases 343
Determination of the Cardiac Cyanotic Congenital Heart
Borders 335 Diseases (CCHD) 349
Percussion of the Pulmonary Precordial Findings in
and Aortic Areas 336 Cardiomyopathy 351
Direct Percussion of the Sternum 337 REFERENCES 353
Special Percussions 337
Joseph Leopold Auenbrugger introduced percussion of the thorax, as a new method of

clinical examination in 1761, after witnessing the practice of tapping of the wine bar-
rels in his fathers cellar to determine their contents.1 However, his invention remained
dormant until Corvisart, personal Physician to Napoleon, published Auenbruggers
text in 1821.
Percussion was once employed routinely and was regarded as a valuable and indis-
pensable method of clinical examination of cardiovascular system, but some clinicians
have lately abandoned it. However, it is still a useful and informative method of clini-
cal examination provided its limitations are understood.
It furnishes information about the size and shape of the heart.
It is particularly useful in patients in whom apical thrust is neither visible nor palpa-
ble as in pericardial effusion or dilated cardiomyopathy or marked displacement of
the hypokinetic apex.
It is of undoubted value in the diagnosis of aortic aneurysm.
It is useful in the detection of enlarged right atrium, right ventricle and pulmonary
conus.
It is a useful tool in determining the visceral status i.e. situs solitus or situs inversus.
Percussing finger: Movement

Perpendicular stroke at the wrist
Vertical position of
terminal phalanx
Percussed finger in close

contact with body surface
Fig. 20.1 | Indirect method of percussion.
METHODS OF PERCUSSION
Generally, there are three methods of percussion:
Direct Percussion
In direct percussion, strokes are aimed directly at the chest wall especially over the
bony structures such as clavicle and sternum.
Indirect Percussion
In indirect percussion, strokes are aimed at some intermediate object, e.g. finger
(pleximeter) applied to the surface of the chest wall. Percussing finger is the plexor and
percussed finger is the pleximeter (see Fig. 20.1).
Auscultatory Percussion
It is a special technique of percussion to determine the cardiac borders, in which chest
piece of the stethoscope is placed over the sternum just above the xiphisternum, and
the skin is lightly scratched inwards from the axillae towards the sternum. The point at
which the soft scratching sound becomes suddenly intense corresponds to the cardiac
border on that side2 (see Fig. 20.2).
THE SCHEME OF PERCUSSION
Percussion of the precordium includes the systematic examination of the following:

Determination of the cardiac borders
Percussion of the pulmonary and aortic areas
Direct percussion of the sternum.
PRECORDIAL FINDINGS IN COMMON HEART DISEASES 335
Fig. 20.2 | Auscultatory percussion for determination

of right heart border. Fig. 20.3 | Determination of right
heart border.
Fig. 20.4a | Percussion for right border of the heartupper border of the liver dullness
is dilenated (5 ICS in mid-clavicular line).
th
Determination of the Cardiac Borders

Besides the conventional indirect method of percussion, auscultatory percussion may
be used to determine the cardiac borders. It is customary to percuss from resonant to
dull areas or centripetally from surrounding areas towards the heart when indirect per-
cussion method is used. (See above for auscultatory percussion.)
Right Border of the Heart (see Figs 20.3, 20.4a and 20.4b)
The upper margin of liver dullness on the right side is defined first by percussing
from above downwards in each intercostal space in the mid-clavicular line. Usually,
the upper border of liver dullness is in the 5th intercostal space (ICS).
Percussion is then carried out in the intercostal space above this level (usually 4th ICS)
moving inwards towards the sternum, either parallel or at right angles to the right
cardiac border.
4th ICS parallel

to sternum
Fig. 20.4b | costal

Then, Percussion is carried out in 4 inter-
th Fig. 20.5 | Percussion of the aortic area.
space (ICS) parallel to sternum.
Normally, right cardiac border corresponds to the right sternal margin.

If the percussed border is 1 cm outside the right sternal margin, following should
be entertained:
Cardiac enlargement (often RA/sometimes LA enlargement, rarely both)
Displacement of the heart to the right (often due to intrathoracic pathology) or
Left Border of the Heart

The cardiac apex is palpated and percussion is done in the same ICS from the axilla
towards the left cardiac border. Usually, the left cardiac dullness corresponds to the car-
diac apex. However, it does not correspond to the apex beat in the following conditions:
In a patient with large pericardial effusion, the apex beat may actually be detected
medial to the lateral border of the percussible cardiac silhoutte.
LV aneurysm: Ectopic LV impulse is often above and medial to the left border of
the apex.
Percussion of the Pulmonary and Aortic Areas

Percuss the 2nd ICS to the right of the sternum (aortic area, see Fig. 20.5). Normally,
it is resonant and dullness in this area, if present may be due to:
Aortic aneurysm, dilated ascending aorta
Superior mediastinal tumor or
Percuss the 2nd ICS to the left of the sternum (pulmonary area, see Fig. 20.6). It is
normally resonant. Dullness in this area indicates the presence of:
Dilated pulmonary artery
PDA or
Sometimes, enlarged LA appendage.
Fig. 20.6 | Percussion of the pulmonary area. Fig. 20.7 | Direct percussion of the sternum.
Direct Percussion of the Sternum
Direct percussion of the sternum is done with the patient in supine position,3 and normally
whole of the sternum except for a small area at the xiphisternum is resonant (see Fig. 20.7).
Flat note or dullness of the manubrium sternum (which extends to the 1st or 2nd
ICS) is due to:
Aortic aneurysm
Mediastinal pathology (especially tumor).
Flat note or dullness of the lower part of sternum indicates:
RV hypertrophy or
Special Percussions
Auscultatory Percussion
It is used to determine the cardiac borders.
Rotchs Sign
The upper border of liver dullness and the right border of cardiac dullness along the
right sternal edge form the cardio-hepatic angle. In moderate to large pericardial effu-
sion, the cardio-hepatic angle becomes obtuse (Rotchs sign) which is frequently asso-
ciated with dullness in the 2nd right ICS.
Enlarged LA Appendage
The cardiac dullness (left cardiac border) in the 3rd ICS if extends 3.5 cm from the
mid sternal line, may suggest enlarged LA appendage as in severe MS or MR.
Determination of the Situs

Percuss over the fundus of the stomach (normally resonant) and determine liver
dullness (see Fig. 20.8). In the situs solitus (see Fig. 20.9), fundus of the stomach is on
Absolute
dullness
(cardiac)
Tympany
Relative
(traubes semilunar
dullness
space)
(liver)
Fig. 20.8 | Method of percussion over the fun-

dus of the stomach for determina- Fig. 20.9 | Situs solitus with liver dullness on the
right side and tympany of the fundus on
tion of the situs.
the left side.
AK
AAo
PT
DAo
Apex
S L
Fig. 20.10 | Dextrocardia with situs inversusS: spleen, L: liver, PT: pulmonary trunk,
DAo: descending aorta, AAo: ascending aorta, AK: aoric knuckle.
the left side and liver dullness is on the right while it is reversed in situs inversus (see
Fig. 20.10).
PRECORDIAL FINDINGS IN COMMON HEART DISEASES
Acquired Heart Diseases

1. Mitral Stenosis (MS)
Apex
Apex is formed by hypertrophied RV, which is localized, laterally displaced, and tap-
ping in character (due to palpable S1) in moderate to severe MS (see Table 20.1 and
Fig. 20.11).
Palpable S1 and Opening snap medial to apex indicate a relatively mobile mitral valve.
Table 20.1 Precordium in mitral stenosis (MS)
Features Significance
1. Apex Formed by hypertrophied right ventricle, and tapping in character,

palpable opening snap, and diastolic thrill
2. Left parasternal lift Sustained heave
3. Pulmonary area Palpable P2: with pulmonary hypertension
4. Epigastric pulsations Right ventricular hypertrophy
5. Pulsatile liver Associated tricuspid regurgitation/stenosis
6. Precordial percussion Enlarged right ventricle; /flat note in left 2nd ICS; note over
lower sternum
Diastolic thrill Palpable P2

with PH
Pulmonary
area (PA)
Systolic thrill
Palpable S1, OS with ASD
Tapping Apex Mitral stenosis Left parasternal
Epigastric
Due to RVH
pulsations
Due to PH and TR PSH with PH
RV S3 in RVF
Precordial RAE with
Tricuspid area
percussion TS or TR
Diastolic thrill
with TS
Note over LS Note in PA
due to RVH with RH
Fig. 20.11 | Precordium in mitral stenosisOS: opening snap, RVH: right ventricular hypertrophy, PH:
pulmonary hypertension, RVF: right ventricular failure, TS: tricuspid stenosis, TR: tricuspid
regurgitation, ASD: atrial septal defect, PSH: parasternal heave, RAE: right atrial enlarge-
ment, LS: lower sternum, PA: pulmonary area.
Diastolic thrill in moderate-severe MS indicates a relatively mobile valve. It may be

absent in mild MS, severe calcified MS and in severe RVF.
Sustained parasternal heave (Gr 2-3/3) in moderate to severe MS with PH
Hyperkinetic parasternal lift when MS is associated with ASD (Lutembacher syndrome)
Both sustained and hyperkinetic parasternal lift: moderate-severe MSPH with TR/PR
or both
Normal or Gr 1/3 LPS impulse: mild MS, thick chest wall, or associated TS.
Table 20.2 Precordium in mitral regurgitation (MR)
1. Apex Formed by hypertrophied left ventricle, and hyperkinetic in character; systolic

thrill less common (only in chordal rupture), LV S3: in chronic MR, LV
S4: in acute MR
2. Left parasternal Late, lower and ill sustained (skid effect). Sustained with pulmonary
lift hypertension
Tricuspid area
Palpable RV S3 occurs in RVF that correlates with rapid Y descent in JVP, and rules
out associated TS.
Palpable RV S4 occurs in severe PH with noncompliant RV and associated PS but
rules out TS. It correlates with prominent a wave in JVP.
Palpable diastolic thrill is present in associated moderate-severe TS.
Epigastric pulsations
These indicate RV enlargement.
May occur in MSPH with TR
Pulmonary area
Visible pulsations and palpable P2 indicate PH.
Systolic thrill is felt when associated with ASD.
Precordial percussion
Enlarged RA when associated with TR/TS
Flat note or dullness in pulmonary area in the dilated pulmonary artery due to PH
Dullness over the lower part of the sternum in hypertrophied RV.
2. Mitral Regurgitation (MR)

Apex
Apex is formed by the hypertrophied (eccentric) LV, which is displaced laterally and
downwards, and is hyperdynamic in character in moderate-severe MR (see Table 20.2
and Fig. 20.12).
Sustained/heaving apex is felt in MR when it is associated with hypertrophied
obstructed cardiomyopathy (HOCM).
Palpable systolic thrill is less common. Thrill is felt in severe MR, usually due to the
chordal rupture.
Palpable S3 in chronic moderate MR, and when complicated with congestive heart
failure
Palpable S4 in acute MR, and when associated with CAD or HOCM.
Late ill sustained parasternal lift in severe MR without PH (due to skid effect), and
parasternal heave with significant PH.
Palpable P2 with PH
Systolic thrill: in Pulmonary

severe MR area (PA)
Systolic thrill with ASD
Palpable S3; S4 with
CAD or HOCM
PSH with PH
Hyperdynamic
Apex Left parasternal
Sustained with HOCM

Precordial
PSL in severe MR
percussion
Note in PA with PH LAE (appendage)
Fig. 20.12 | Precordium in mitral regurgitation (MR)PH: pulmonary hypertension,

ASD: atrial septal defect, PSH: parasternal heave, LAE: left atrial enlarge-
ment, PSL: parasternal lift, CAD: coronary artery disease, HOCM: hyper-
trophic obstructive cardiomyopathy.
Table 20.3 Precordium in aortic stenosis (AS)
1. Apex Formed by hypertrophied left ventricle, and heaving in character;

systolic thrill in calcified AS, S4 may be palpable
2. Aortic area Systolic thrill, and conducted to the carotids
3. Percussion /falt note in 2nd right Intercostal space
Pulmonary area
Visble pulsations and palpable P2 with PH
Systolic thrill is felt when associated with ASD.
Left cardiac dullness may be 3.5 cm from the mid-sternal line in the 3rd ICS due
to the enlarged LA appendage.
Flat note or dullness is noted in the pulmonary area with PH.
3. Aortic Stenosis (AS)

Apex
Apex is formed by hypertrophied (concentric) LV, which is normal in position or there
is a little lateral displacement with sustained/heaving apex in moderate-severe AS
(see Table 20.3 and Fig. 20.13).
It is displaced downwards and outwards when associated with dominant AR, PDA,
or is complicated by CHF.
Systolic thrill in Aortic

Systolic thrill
sclerotic AS stenosis (AS)
Palpable S4 Apex Aortic area (AA)
Precordial
Heaving Note in AA
percussion
Fig. 20.13 | Precordium in aortic stenosis.

Table 20.4 Precordium in aortic regurgitation (AR)
1. Apex Formed hypertrophied left ventricle and hyperdynamic in

character; palpable S4: in acute AR
2. Aortic area Diastolic thrill: rare (in root causes due to cusps retroversion)
3. Carotids Systolic thrill due to functional aortic stenosis in severe AR
4. Percussion /flat note in 2nd right ICS: AR of root causes
Sustained/heaving apex is noted in mild AS when it is associated with systemic

hypertension, severe AR, large PDA or myocardial infarction.
Palpable S4: Moderate-severe AS, rules out associated significant MS; HOCM unlikely
in the absence of palpable S4
Palpable S3: AS complicated by LVF; AS associated with MR or PDA.
Aortic area
Systolic thrill at the aortic area and conducting to the carotids: It may also occur in
the functional AS with severe AR.
Systolic thrill only at the carotids favors supravalvular AS. Other conditions associ-
ated with thrill at the carotids are carotid stenosis and Takayasu aortitis.
Systolic thrill at the apex in calcified AS in elderly patients.
Flat note or dullness in the 2nd right ICS may be present.
4. Aortic Regurgitation (AR)

Apex
Apex is formed by the hypertrophied (eccentric) LV, which is displaced outwards and
downwards, and is hyperdynamic in character in moderate-severe AR with medial
systolic retraction (see Table 20.4 and Fig. 20.14).
It is normal in location in mild AR, but also gets displaced laterally and downwards
when associated with MR, PDA, VSD or coarctation of aorta.
Palpable S3 with Aortic

Systolic thrill
LVF or MR regurgitation
Sustained in
Apex Carotids
severe chr AR
Precordial Note in AA in
Hyperdynamic
percussion root causes
Fig. 20.14 | Precordium in aortic regurgitationLVF: left ventricular failure, MR: mitral
regurgitation, chr: chronic, AA: aortic area.
Table 20.5 Precordium in atrial septal defect
1. Apex Formed by enlarged right ventricle which is diffused

systolic retraction: when left to right shunt is 1.5:1
2. Left parasternal lift Hyperkinetic, but sustained with pulmonary hypertension (PH)
3. Tricuspid area RV S3: with right ventricular failure (RVF)
4. Pulmonary area Pulsations; palpable P2: with PH/large shunt
5. Epigastric pulsations Due to right ventricular enlargement
6. Percussion RA enlarged, /flat note over lower sternum due to right ventricular
hypertrophy (RVH)
It is also hyperdynamic in character when mild AR is associated with MR, VSD or PDA.
It may be sustained/ heaving, especially in chronic AR.
Palpable S4 (a wave) is noted in acute AR, and may be associated with systemic
hypertension or acute aortic dissection.
Palpable S3 is noted when complicated with LVF or it is associated with significant MR.
Aortic area
Diastolic thrill is rarely palpable due to the retroversion of the aortic cusps as in aortic
root diseases.
Systolic thrill is palpable only at the carotids in functional AS with severe AR.
Due to the aortic root causes, flat note or dullness is noted in the 2nd right ICS in AR.
Acyanotic Congenital Heart Diseases

1) Atrial Septal Defect (ASD)
Apex
Apex is formed by the enlarged RV (see Table 20.5 and Fig. 20.15).
Apical impulse is diffused and hyperdynamic with systolic lateral retraction. The
systolic retraction often suggests a moderate-large left to right shunt (1.5:1).
Sustained with
PH, MS or PS
Visible pulsations
LP impulse Palpable S3
with RVF
Pulmonary
area (PA)
Hyperkinetic
Tricuspid area
Palpable P2 with
Hyperkinetic LS or PH
Atrial
septal defect Systolic thrill
Diffused
may with LS
Apex Precordial Epigastric

percussion pulsations
Systolic Sustained with Due to RVH

retraction LS or PH
RAE
Note over lower

Note in PA with PH
sternum due to RVH
Fig. 20.15 | Precordium in atrial septal defectMS: mitral stenosis, PH: pulmonary
hypertension, PS: pulmonary stenosis, RVH: right ventricular hypertrophy,
RAE: right atrial enlargement, LS: large shunt, LP: left parasternal.
Apical impulse is localized when associated with MR or ostium primum defect.

It may be sustained with PH or in the presence of a large shunt without elevated
pulmonary artery pressure.
Usually, hyperkinetic left parasternal lift is noted.
Sustained/heaving is noted when complicated with PH, or is associated with PS or MS.
Lower left sternal area
Palpable S3 is noted with RVF.
Palpable diastolic thrill is more likely due to Ebsteins anomaly than with simple ASD.
Pulmonary area
Visible pulsations are more likely with ASD than with PS.
Palpable P2 is noted in a large shunt or with PH.
Systolic thrill is noted in a large left to right shunt in 25% of the cases, however PS
is more likely than ASD.
These pulsations occur due to RV enlargement.
Flat note or dullness is noted in the pulmonary area with moderate-large shunt or
with PH.
Table 20.6 Precordium in ventricular septal defect (VSD)
1. Apex Formed by hypertrophied left ventricle and hyperdynamic in

character; palpable S3: with left ventricular failure/associated
significance mitral regurgitation
2. Left sternal border In 3rd4th intercostal space (ICS): systolic thrill
3. Left parasternal lift Hyperkinetic but sustained with pulmonary hypertension (PH)
4. Pulmonary area Pulsations and palpable P2: with PH systolic thrill: in supracristal/
subpulmonary VSD
5. Percussion /flat note in 2nd left ICS: in large shunt or with PH
Visible pulsations
Sustained with PH with LS or PH
Systolic thrill in
SA VSD
Pulmonary
LP impulse
area (PA)
LSB
Hyperkinetic Palpable P2 with PH
Ventricular
Hyperdynamic septal defect Systolic thrill
in SP VSD
Apex Precordial
RSB
percussion
Localized Sustained with Systolic thrill in

HF or MR Gerbodes defect
RAE in Gerbodes
Note in PA with PH
defect
Fig. 20.16 | Precordium in ventricular septal defect (VSD)PH: pulmonary hypertension,

LS: large shunt, LP: left parasternal, SA: subaortic, SP: sub pulmonary,
MR: mitral regurgitation, HF: heart failure, LSB: left sternal border, RSB:
right sternal border.
Flat note or dullness of lower part of the sternum (direct percussion) occurs due to
the RV enlargement.
Right heart border (RA) may be enlarged.
2) Ventricular Septal Defect (VSD)

Apex
Apex is usually formed by the hypertrophied left ventricle (see Table 20.6 and
Fig. 20.16).
It is localized and hyperdynamic in moderate-large VSD.
It is sustained when associated with coarctation of aorta or AS.
Palpable S3 is noted with heart failure or when associated with significant MR.
Table 20.7 Precordium in patent ductus arteriosus (PDA)
1. Apex Formed by hypertrophied left ventricle and hyperdynamic in

character; palpable S3: with left ventricular failure
2. Left parasternal lift Hyperkinetic; but sustained: with pulmonary hypertension (PH)
3. Pulmonary area and Pulsations and palpable P2: with PH or large PDA; continuous
left infraclavicular region thrill, but only systolic with PH
4. Percussion /flat note in 2nd left intercostal space, left infraclavicular region:
moderate-large shunt/PH

Hyperkinetic left parasternal lift is noted in moderate VSD without PH.
It becomes sustained with PH.
Isolated sustained parasternal lift with the loss of characteristic apical impulse occurs
in VSD associated with PH with little or no left to right shunt.
Pulmonary area
Visible and palpable pulsations occur in moderate-large left to right shunt or with PH.
Palpable P2 suggests PH and rules out PS.
Systolic thrill suggests supracristal/subpulmonary VSD.
Left sternal border
Systolic thrill is consistent with VSD (subaortic) in the 3rd4th ICS.
Right sternal border
Systolic thrill suggests LV to RA communication (Gerbodes defect) in the 4th ICS.
Flat note or dullness in the pulmonary area occurs in moderate-large shunt or with PH.
Enlarged RA may be noted in Gerbodes defect.
3) Patent Ductus Arteriosus (PDA)

Apex
Apex is formed by the hypertrophied left ventricle (see Table 20.7 and Fig. 20.17).
It is localized, hyperdynamic and is displaced downwards & outwards in moderate-
large PDA with left to right shunt.
It becomes sustained when associated with coarctation of aorta or with AS.
Palpable S3 is noted in heart failure.
Hyperkinetic parasternal lift is noted in moderate-large PDA without PH.
It becomes sustained with PH.
Pulmonary area
Visible and palpable pulsations are noted in moderate-large PDA or with PH.
Palpable P2 is noted in moderate-large ductus or with PH.
Sustained with PH
Systolic thrill in Visible pulsations
SA VSD with MLD or PH
LP impulse
Palpable P2 with
LSB
MLD or PH
Hyperkinetic
Patent ductus Pulmonary

Hyperdynamic arteriosus area (PA)
Continuous thrill
Apex Precordial extending to LIC
percussion
Systolic thrill
Localized Sustained with PH
with COA
Palpable S3 Note in PA and
with HF LIC with PH or MLD
Fig. 20.17 | Precordium in patent ductus arteriosusPH: pulmonary hypertension,

MLD: moderate-large ductus, LP: left parasternal, SA VSD: subaortic ven-
tricular septal defect, HF: heart failure, LSB: left sternal border, LIC: left
infraclavicular region, COA: coarctation of aorta.
Continuous thrill extending to the left infra-clavicular region or the supra-sternal

notch is consistent with ductus. (Differtial diagnosis: peripheral pulmonary artery
stenosis in which isolated right ventricular enlargement is present)
Only systolic thrill is noted in PDA with PH.
Left sternal border
Systolic thrill is noted when associated with VSD.
Flat note or dullness in the pulmonary area and the left infraclavicular region is
noted in moderate-large PDA or with PH.
4) Pulmonary Stenosis (PS)

Apex
Apex is formed by the diffuse hypertrophied RV (see Table 20.8 and Fig. 20.18).
Sustained parasternal lift is noted in moderate-severe PS.
Palpable RV S4 is present in the left parasternal/tricuspid area in severe PS and it
favors intact ventricular septum.
Palpable RV S3 is present in the left parasternal/tricuspid area in RV failure.
Pulmonary area
Systolic thrill is noted in valvular PS.
Diastolic thrill occurs in dysplastic pulmonary valve (PSPR) of Noonan syndrome
or it is noted when complicated by infective endocarditis.
Table 20.8 Precordium in pulmonary stenosis (PS)
1. Apex Hypertrophied right ventricle (RV) and diffused

2. Left parasternal lift Sustained
3. Left parasternal area/ Palpable RV S4 in severe PS; palpable RV S3: with right ventriclar failure
tricuspid area
4. Pulmonary area Systolic thrill; diastolic thrill: in dysplastic pulmonary valve
5. Third/fourth left ICS Systolic thrill: in infundibular PS
6. Percussion /flat note in 2nd left intercostal space (ICS): valvular PS; in 3rd4th left
ICS: infundibular PS, in left infraclavicular region: supravalvular PS
Sustained lift
Systolic
thrill in IPS
LP
3rd4th Systolic thrill
Palpable RV S4 LICS in SPS
Palpable RV S3 Pulmonary
LIC
with RVF stenosis
Systolic thrill
Apex Precordial Pulmonary
percussion area (PA)
Diffused Diastolic thrill with
Note in PA Note in LIC in SPS dysplastic PV
By HRV
Note in third to
RAE with TR
fourth LICS in IPS
Fig. 20.18 | Precordium in pulmonary stenosisLP: left parasternal, LIC: left infraclavicular region, LICS:
left intercostal spaces, IPS: infundibular pulmonary stenosis, SPS: supravalvular pulmonary
stenosis, PV: pulmonary valve, RV: right ventricle, HRV: hypertrophied right ventricle, RAE:
right atrial enlargement, TR: tricuspid regurgitation.
Systolic thrill in other regions

It is noted in the 3rd/4th left ICS in the infundibular PS.
It is present in the infraclavicular region/lateral to pulmonary area in the supravalvu-
lar PS.
These occur when associated with TR.
Flat note or dullness is felt in the pulmonary area (valvular PS), 3rd/4th left ICS
(infundibular PS) or in the left infraclavicular region (supravalvular PS).
There is enlarged RA when associated with TR.
Table 20.9 Precordium in cyanotic congenital heart diseases (CCHD) with decreased pulmonary
blood flow
1. Apex Formed by the hypertrophied right ventricle (left ventricle in tricuspid

atresia), unimpressive; no S3
2. Left parasternal lift Unimpressive
3. Pulmonary area Unimpressive; systolic thrill if pulmonary stenosis is present
Cyanotic Congenital Heart Diseases (CCHD)

It is broadly classified depending upon the pulmonary blood flow:
CCHD with decreased pulmonary blood flow:
a) With right ventricular hypertrophy (RVH)
Tetralogy of Fallot (TOF)
VSD PS (TOF like) physiology:
Double outlet right ventricle (DORV) with PS

Transposition of great arteries (TGA) with VSD and PS
Single ventricle with PS.
b) With left ventricular hypertrophy (LVH)
Tricuspid atresia (increased pulmonary blood flow with d TGA)
Pulmonary atresia with intact ventricular septum, ASD and hypoplastic right ventricle.
CCHD with increased pulmonary blood flow

a) With right ventricular hypertrophy
Total anomalous pulmonary venous connection (TAPVC).
b) With biventricular hypertrophy (BVH)

TGA, VSD without PS
DORV without PS
Truncus arteriosus
Pulmonary atresia with bronchial collaterals or PDA
TOF with PDA.
c) With left ventricular hypertrophy

Single ventricle (double inlet left ventricle).
Precordial Findings in CCHD with Decreased Pulmonary Blood Flow

Apex
It is mostly formed by the hypertrophied RV (with no gross cardiac enlargement)
except in the tricuspid atresia in which it is formed by the hypertrophied LV (see

Table 20.9 and Fig. 20.19).
Normal or unimpressive/impalpable apex is present.

Unimpressive or Gr 1/3 left parasternal lift is noted.
Left
Unimpressive No pulsations
parasternal
No palpable P2
Pulmonary
Unimpressive Apex PBF area
Systolic thrill
with PS
Cyanotic
CE CHD
Pulmonary
Palpable S3 Apex PBF Visible pulsation
area
Systolic thrill LSB-3rd4th Palpable P2

due to VSD ICS
Fig. 20.19 | Precordium in cyanotic congenital heart diseases (CCHD)PBF: pulmonary blood flow, CE:
cardiac enlargement, mostly biventricular, PS: pulmonary stenosis, VSD: ventricular septal
defect, LSB: left sternal border, ICS: intercostal space.
Table 20.10 Precordium in cyanotic congenital heart diseases (CCHD) with increased pulmonary
blood flow
1. Apex Mostly due to biventricular hypertrophy; but right ventricular hypertrophy

in total anomalous pulmonary venous connection and left ventricular
hypertrophy in single ventricle; palpable S3
2. 3rd4th left intercostal Systolic thrill due to presence of ventricular sepal defect
space at sternal edge
3. Pulmonary area Pulsations; palpable P2
Pulmonary area
There are no palpable pulmonary pulsations or palpable P2.
Systolic thrill is noted if PS is present.
Other accompanying diagnostic features
There is absence of heart failure.
There is absence of S3.
Jugular venous pressure is normal.
There is absence of flow murmurs (diastolic) across the AV valves.
Precordial Findings in CCHD with Increased Pulmonary Blood Flow

Apex
There occurs cardiac enlargement mostly due to BVH. There is RVH in TAPVC
while LVH is present in single ventricle (double inlet left ventricle, DILV) (see Table
20.10 and Fig. 20.19).
Palpable S3 is often present.
Table 20.11 Precordium in tetralogy of Fallot (TOF)
1. Apex Formed by hypertrophied right ventricle and unimpressive; no S3/S4 are

palpable
2. Left parasternal lift Unimpressive
3. Pulmonary area No pulsations/palpable P2/thrills
Left sternal edge (3rd4th ICS)

Systolic thrill (due to VSD) is palpable.
Pulmonary area
Visible/palpable pulmonary pulsations are present.
Palpable P is noted.
2
Other accompanying diagnostic features

Heart failure is noted with S .
3
Jugular venous pressure is elevated.
Flow murmurs (diastolic) are present across the AV valves.
Precordial Findings in TOF

Apex
Apex is formed by the hypertrophied RV, but there is no gross cardiac enlargement
(see Table 20.11).
Normal or unimpressive/impalpable apex beat is present.
It is hyperdynamic when associated with AR, PDA or sometimes in pink TOF with
left to right shunt.
Insignificant or Gr 1/3 parasternal pulsations are present.
Pulmonary area
There are no pulmonary pulsations. P is not palpable and no systolic thrill is felt.
2
Continuous thrill is present at the pulmonary area/infraclavicular region when asso-
ciated with PDA.

Other features
No S or S are palpable.
3 4
Signs of heart failure are present when associated with AR, systemic hypertension
and in adult type of TOF.
Precordial Findings in Cardiomyopathy

It is broadly classified into the following three categories (see Table 20.12):
Dilated congestive cardiomyopathy
Table 20.12 Precordium in cardiomyopathy
Dilated congestive Hypertrophic Restrictive

Features
cardiomyopathy cardiomyopathy cardiomyopathy
1. Apex Diffused and displaced; Formed by left ventricle Normal; hyperdynamic

never hyperdynamic/ and sustained, may be with significant mitral
sustained triple-ripple regurgitation
2. Palpable S3 Common May in failure May palpable
3. Palpable S4 Not palpable Common Common
4. Thrills No thrills Systolic thrill with left Absent, may be with
ventricular outflow signigicant tricuspid
tract obstruction regurgitation/mitral
regurgitation
Restrictive cardiomyopathy.
The diagnosis of cardiomyopathy is unlikely in the presence of the following features:
Systolic retraction of the apical impulse (more likely constrictive pericarditis which
simulates restrictive cardiomyopathy)
Impalpable S3 or S4
Signs of significant pulmonary hypertension:
Visible or palpable pulmonary artery pulsations in the pulmonary area
Palpable P2 in the pulmonary area
Left parasternal impulse of Gr 2/3
Prominent systolic or diastolic thrill.
1) Dilated Congestive Coardiomyopathy

Apex is diffused and displaced but is never hyperdynamic or sustained.
Palpable S3 is common.
No systolic/diastolic thrills are present.
2) Hypertrophic Cardiomyopathy
Apex is formed by hypertrophied (concentric) LV, which is localized and often
sustained.
Palpable S4 (a wave) is common.
Occasionally, mid or late systolic lift (giving a triple ripple) is present.
Palpable S3 may occur in heart failure.
Systolic thrill is superior and medial to the apical impulse (usually with the LV out-
flow tract obstruction).
3) Restrictive Cardiomyopathy
Apical impulse is often normal unless it is associated with significant AV regurgitation
(when it may be hyperdynamic).
Palpable S4 is common.
S3 may be palpable.
Thrills are usually absent, but may be palpable with significant TR/MR as in endomy-
ocardial fibrosis.
REFERENCES
1. Vakil RJ, Golwalla AF. The Cardiovascular system-Historical note on percussion. In: Clinical
Diagnosis. 2nd ed, Bombay, Asia Publshing House, 1967:200.
2. Vakil RJ, Golwalla AF. The Cardiovascular system-Special techniques of percussion. In: Clinical
Diagnosis. 2nd ed, Bombay, Asia Publshing House, 1967:214.
3. Vakil RJ, Golwalla AF. The Cardiovascular system-Percussion of the sternum. In: Clinical Diagnosis.
2nd ed, Bombay, Asia Publshing House, 1967:213214.
CHAPTER 21
CARDIAC AUSCULTATION
PRINCIPLES AND TECHNIQUES 354 Prosthetic Valve Sounds 400

The Human Acoustic Acuity 354 Extra-Cardiac Sounds 402
Factors Affecting Cardiac Sound THE HEART MURMURS 404
Transmission 355 Definition 404
Characteristics of the Cardiac Mechanism of Production of the
Sounds 355 Murmurs 404
The Stethoscope 356 Factors for the Production of
Examination of the Patient 358 Murmurs 406
Phonocardiography 361 Characteristics of Murmurs 406
THE HEART SOUNDS 361 Systolic Murmurs 422
The First Heart Sound 362 Diastolic Murmurs 431
The Second Heart Sound 369 Continuous Murmurs 441
Diastolic Sounds 383 REFERENCES 451
The Systolic Sounds 396
PRINCIPLES AND TECHNIQUES
Direct or immediate auscultation was practiced by Hippocrates (400 B.C) and was an
established diagnostic technique in the ancient medicine. It is performed by applying
the ear to the chest,1 However, there is no recorded account of precordial auscultation
until William Harvey (1616) referred the heart beat as two clicks of a water bellow.2
The modern era of cardiac auscultation began in 1826 with the invention of the
stethoscope by RTH Laennec, which initiated the Golden Century of Stethoscopy.3
The Human Acoustic Acuity
The human ear is capable of detecting sound vibrations from 20 to 20000 Hz
(cycles per s, CPS). However, it is most sensitive to the auditory vibrations between
1000 and 5000 Hz, while the optimal range of auditory acuity is 1000 to 2000 Hz
(see Table 21.1).
In humans, higher frequency events are better heard at any level of sound intensity
than low frequency sounds, and most of the cardiovascular sounds and murmurs are in
the range of 30 to 1000 Hz. As the normal ears acoustic sensitivity decreases at fre-
quencies below 1000 Hz, and as the low frequency sounds and murmurs are more
commonly missed by the examiner, the clinician has to use an instrument such as the
CARDIAC AUSCULTATION 355
Table 21.1 Human acoustic acuity
1. 2020000 Hz Human ear capability

2. 10005000 Hz Human ear sensitivity
3. 10002000 Hz Optimal human auditory acuity
4. 301000 Hz Most cardiovascular sounds and murmurs
5. 0.02 s interval between two sounds Human ear capable of detecting two sounds
stethoscope for auscultation of the heart which has a bell (for lower frequency
events) and a diaphragm (for higher frequency events).
Human ear is capable of detecting two sounds separated by an interval of as little as
0.02 s when the sounds are relatively high pitched.
Factors Affecting Cardiac Sound Transmission

The sound transmission from the heart is affected by the factors such as chest wall
thickness, obesity, breast size and emphysema that attenuate the cardiac sounds,
while the lean individuals with little excess body tissue tend to have louder heart
sounds and murmurs.
The level of noise in the hospital rooms, clinics, or typical examination rooms is
6070 decibels, which is well above the optimal setting of an ideal soundproof auscul-
tation room (i.e. 35 decibels). This environmental noise in the routine hospital sur-
roundings can prevent the detection of the cardiac murmurs, particularly those of high
frequency.
Excessive noise levels due to auto or air traffic, construction work or human conver-
sation near the examination area, higher frequency cardiac sounds and murmurs
may be inaudible even to the most experienced clinicians.
However, coryza does not interfere with the ability of the physician to hear the car-
diac sounds and murmurs through a stethoscope, but with aging, a selective high
frequency ( 3000 Hz) hearing loss is common.
Characteristics of the Cardiac Sounds

Loudness of sound is a subjective judgement and is closely related to the amplitude or
intensity of sound waves, while the pitch of a heart sound or murmur is related to the
underlying frequency.
The heart sounds and murmurs are classified depending upon their frequency as
follows (see Table 21.2):
Low frequency: (25125 CPS) Low-pitched sounds e.g. S3, S4 and pericardial
knock; low-pitched murmurs are rough and rumbling in character e.g. mid diastolic
murmur (MDM) of mitral and tricuspid stenosis.
Medium frequency: (125300 CPS) Rough flow murmurs e.g. innocent systolic
murmurs, physiological flow murmurs.
Table 21.2 Frequencies of heart sounds and murmurs
Low frequency High frequency Medium frequency Mixed frequency
1. 25125 cycles per 300 CPS 125300 CPS Combination of medium and
second (CPS) high frequencies
2. Low pitched High pitched Rough Harsh
High frequency: (300 CPS) High-pitched sounds e.g. A2, P2, opening snap (OS)
and ejection sound; high pitched murmurs could be soft and blowing in character
e.g. systolic murmur (SM) of mitral regurgitation, early diastolic murmur (EDM) of
aortic regurgitation or musical in nature e.g. cooing murmur of papillary muscle
rupture.
Mixed frequency: Sounds and murmurs result from a combination of medium and
high frequencies. Mixed frequency sound e.g. S1; while the murmurs are harsh in
character e.g. SM of aortic and pulmonary stenosis and pansystolic murmur (PSM)
of VSD.
The Stethoscope
Remembering a well-known acoustic fact that if the ear be applied to one end of a
plank, it is easy to hear a pin scratching at the other end, French physician Rene
Theophile Hyacinthe Laennec (1826) constructed his primitive monoaural stetho-
scope. It had a perforated wooden cylinder with a chest piece at one end and an ear-
piece at the other end. Presently available stethoscope does not represent a major
advance over the wooden cylinder of Laennec.
However, electronic and magnetic stethoscopes are available but clinicians are not
using them on a routine basis.
Although considered as out-dated or primitive by some in the present high tech era
with easy availability of sophisticated equipment for the diagnosis of cardiac ail-
ment, the stethoscope continues to remain a bed side source of vital information
about the heart.
A stethoscope consists of a dual chest piece with a valve that allows switching from
bell to diaphragm, tubing, binaural connectors and earpieces (see Fig. 21.1). It should
be durable without air leaks and should be easy to use. A good stethoscope should not
distort the cardiac sounds and it is useful to examine the acoustic and practical char-
acteristics, such as sound transmission, frequency filtration, masking and interference
of this indispensable instrument.
The Bell of the Stethoscope

It should be trumpet shaped with a diameter of atleast an inch and should have a rubber
lining which allows light skin contact pressure, minimizes air leakage, does not get cold
in winters, and amplifies the sound by increasing the diameter of the bell (see Fig. 21.2).
The bell is used for the detection of low frequency heart sounds and murmurs.
Binaural
Dual chest Tubing connectors
piece
Earpiece
Fig. 21.1 | Stethoscope

earpieces.
with a dual chest piece, tubing, binaural connectors and
Bell
Diaphragm
Fig. 21.2 | Bell of the stethoscope with 1" in

diameter.
Fig. 21.3 | Diaphragm
diameter.
of the stethoscope with 1" in
It should be used with the lightest possible contact pressure. If increased pressure is
applied to the bell, the firm pressure stretches the skin of the chest wall, due to which
the bell acts like the diaphragm of the stethoscope attenuating the low frequencies
but accentuating the higher frequency sounds.
The Diaphragm of the Stethoscope

It should be 1" in diameter (see Fig. 21.3). To prevent air leakages due to incomplete
contact of the stethoscope with the chest wall, an ideal diaphragm should be slightly
bowed outward or may have a small central elevated ridge for firmer stethoscope-chest
wall compression without causing the diaphragm to bulge inwards and interfer with
the sound transmission.
The diaphragm is used for the detection of high frequency heart sounds and murmurs.
It should be used with firm pressure, which filters out the low frequencies and
amplifies the high frequency sounds.
Tubing of the Stethoscope

The optimum tubing length is 1012".
Double tubing or double lumen within a single external tube is ideal, while single
tube or Y tubing attenuates high frequencies.
The tubing should be thick, durable and made of plastic (than rubber) with an ideal
internal diameter of 1/8" (3 mm) to minimize buckling of the tube and external
noise contamination.
Binaurals and Earpiece

These should be comfortable and properly fit, as improper fit of the binaurals and
earpieces can result in decreased acuity in cardiac auscultation.
The binaurals should be adjustable, oriented slightly forwards and upwards without
creating undue pressure on the ear canal and without producing any air leakage.
The earpieces should comfortably fit into the external ear canal. Large rather than
small earpieces are best, since small earpieces can penetrate too far into the external
ear canal and may become occluded.
Examination of the Patient

The examination should be done in a quite, well lighted comfortable room with
the patient properly gowned and adequately exposed to the waist. Usually, examina-
tion is initiated from the right side. Adequate clinical history, general physical exami-
nation, inspection, palpation and percussion of the precordium should precede
auscultation, as auscultatory counterparts will definitely aid for confident clinical
diagnosis e.g.
A history of repeated abortions may be a clue to seek for syphilitic aortic
regurgitation.
A wide pulse pressure, collapsing pulse may be a clue for the diagnosis of aortic
regurgitation.
A tall stature with increased arm-span length should alert the clinician to aortic regur-
gitation murmur.
Prominent a waves in jugular venous pulse, should alert the examiner to a low-
pitched right-sided S4.
Large v waves in jugular venous pulse, which augments with inspiration should seek
for tricuspid regurgitation murmur.
A rapid jerky rise of the carotid pulse may be a clue to seek for the diagnosis of
hypertrophic cardiomyopathy.
The topographical areas of cardiac auscultation are (see Fig. 21.4):
The aortic area: Primary in the 2nd right ICS, secondary (Erbs neo aortic area) in
the 3rd left ICS adjacent to the sternum
The pulmonary area in the 2nd left ICS
The tricuspid area in the 4th and 5th intercostal spaces adjacent to the left sternal
border
The mitral area at the cardiac apex.
In addition, auscultation should regularly be carried out at:
The axillae (for radiation of PSM of MR)
Ao
PA
RV LV
Fig. 21.4 | Classic precordial sites of auscultationAo: aortic area, PA: pulmonary area,
LV: left ventricular (mitral) area, RV: right ventricular (tricuspid) area.
The back: Interscapula (murmurs of coarctation of aorta, aneurysm of descending

thoracic aorta often better heard), infrascapula (brui of collateral circulation) and
over the spine (murmurs of aneurysm of descending thoracic aorta, coarctation
of aorta)
Anterior chest on the opposite side (right side in case of dextrocardia)
Over the carotids (for conduction of systolic murmurs of aortic valve disease)
Above and below the clavicles (for characteristic continuous murmur of PDA)
Epigastrium (for tricuspid regurgitation murmur in emphysematous patient with
PH) and
Over the peripheral arterial sites, especially over the femorals may disclose the
murmurs of great diagnostic significance (e.g. Duroziezs murmur of aortic
regurgitation).
Method of Auscultation
Levine and Harveys inching:4 One should adopt a systematic way of ausculatation,
starting at the apex (mitral area) and left axilla, moving to the lower left sternal area (tri-
cuspid area) and epigastrium, and progressing along the sternal border (neo-aortic area)
to the base of the heart (aortic and pulmonary areas, below and above the clavicles) and
over the carotids.
Identification of systole and diastole: Identify systole and diastole in each area.
S1 identifies the onset of ventricular systole and S2 identifies the onset of ventricular
diastole.
The carotid upstroke and beginning outward thrust of the apex beat immediately
follow S1, while S2 occurs shortly after the carotid pulse and apex beat.
Selective listening: Use both the bell and the diaphragm at each area and divide systole
and diastole into three parts- early, mid, and late, selectively focusing on only one segment
of the cardiac cycle (e.g. assessing S1 in early systole).
Fig. 21.5 | Auscultation at the apex in supine and

left lateral position.
Fig. 21.6 | Auscultation at the apex in supine
position and timing with the carotids.
Aortic Pulmonary
area area
Fig. 21.7 | Ausculatation at the basesaortic area

in sitting and leaning forward position.
Fig. 21.8 | Ausculatation at the basespulmonary
area in sitting and leaning forward
position.
First, the heart sounds (S1, S2, S3, S4 and OS) are assessed, followed by attention to
the murmurs (systolic, diastolic) in each segment of systole and diastole selectively at
each area.
Heart sounds and murmurs are heard and discovered only when they are searched
out carefully with intent listening and concentration, which is a key to competent
cardiac auscultation.
Position of the patient
In general, three positions are routinely employed-left lateral decubitus (for mitral
area), supine (for tricuspid area), and sitting and leaning forward (for basal areas)
(see Figs 21.521.8).
In addition, patient should also be examined in right lateral decubitus (for making
the tricuspid valve murmurs more prominent, see Figs 21.9 and 21.10) standing,
and squatting positions, which alter the circulatory dynamics and may yield the
diagnostic information.
Fig. 21.9 | Auscultation at the tricuspid area in

supine and right lateral position.
Fig. 21.10 | Auscultation for tricuspid events in
supine position with passive legs raising.
Dynamic auscultation
The impact of respiration on the heart sounds and murmurs should be assessed routinely
(besides the postural changes), as it gives clue to their site of origin (right-sided/left-sided).
In selected cases, isometric exercises, the Valsalva maneuver, the Muller maneuver and
pharmacological maneuvers (amyl nitrate inhalation) should be employed, which cause
changes in the pre- and afterloads of the heart affecting the heart sounds and murmurs.
Phonocardiography
It is the graphic recording of the auscultatory events of the precordium, carotid, jugu-
lar venous and apical precordial pulsations simultaneously with the ECG.
In essence, it is the graphic representation of the cardiovascular examination
enhancing its accuracy.
It is an excellent teaching aid even though the high frequency events (such as EDM
of aortic regurgitation) are difficult to record.
THE HEART SOUNDS
The heart sounds are relatively brief discrete auditory vibrations that are character-
ized by intensity (loudness), frequency (pitch), and quality (timber).
Sudden deceleration of the blood within the cardiovascular system produces the heart
sounds. The rapid deceleration of blood initiates vibrations of the cardiac structures
immediately after the coaptation of the valves that produces S1 and S2, while the rapid
deceleration of blood in the ventricular inflow producing the vibrations of the cardiovas-
cular structures appear to be responsible for the production of S3 and S4 (see Fig. 21.11).
Basically, the heart sounds are of two types:
High frequency transients due to closing and opening of the valves
Low frequency sounds that are related to early and late diastolic filling events of
the ventricles.
S1 S2 S3 S4
Fig. 21.11 | Basic heart sounds.

i) High frequency sounds due to opening of the atrioventricular valves are:
Sounds due to opening of the atrioventricular valves: Opening snaps (mitral and
tricuspid), non-ejection sounds

Sounds related to closure of the atrioventricular valves: S (mitral and tricuspid
1
closing soundsM1 and T1) are mixed frequency sounds.
ii) High frequency sounds due to closing and opening of semilunar valves are:
Sounds related to closure of the semilunar valves: S (aortic and pulmonary clo-
2
sure soundsA2 and P2)
Sounds related to opening of the semilunar valves: Early valvular ejection
sounds or clicks.
iii) Low frequency sounds related to diastolic filling of the ventricles are:
Physiological and pathological third heart sound (S ) which is associated with
3
early ventricular filling events
Presystolic atrial gallop (S ) associated with late diastolic filling events
4
Summation gallop due to merging of S and S (synchronous occurrence of S
3 4 3
and S4) as occurs in tachycrdia.
iv) Other heart sounds include
Pericardial knock and rubs
Tumor plops (atrial myxoma)
Prosthetic valvular sounds.
Depending upon the cardiac cycle, the heart sounds are also classified into:
Diastolic sounds
Early diastolic sounds: Opening snaps, (OS), tumor plops, pericardial knock,
opening sounds of prosthetic valves
Mid diastolic sounds: S3
Late diastolic sounds: S4.
Systolic sounds
Early systolic sounds: Aortic and pulmonary ejection sounds, closing sounds of
prosthetic valves
Mid to late systolic sounds: Non-ejection sounds or clicks.
The First Heart Sound (S1)

The first heart sound signals the onset of left ventricular contraction and consists of
two major audible components (M1 and T1) and two inaudible components.
Table 21.3 Characteristics of S1
Characters Value
1. Frequency Medium to high

2. Duration 0.14 s
3. M1T1 interval 2030 ms
4. C point of MV echocardiogram Coincides with M1
5. Down stroke of c wave of LA pressure Coincides with M1
6. Down stroke of c wave of RA pressure Coincides with T1
M1
Apex
phono A2
Aorta
LV
a v
c LA
30 ms
EKG
Fig. 21.12 | Characteristics of S phonocardiogram and LV-LA pressuresM coincides

1
with down stroke c wave of the LA pressure.
1
The first inaudible low frequency vibrations coincide with the beginning of the LV
contraction and are muscular in origin.
It is followed by high frequency audible M1 and T1 components, which are produced
due to the closure of mitral and tricuspid valves (Docks hypothesis5 and Leatham6).
The last inaudible low frequency vibrations coincide with opening of the semilunar
valves with ejection of blood into the aorta and the pulmonary trunk.
Characteristics of S1
S1 is typically medium to high frequency with an average duration of 0.14 s (see
Table 21.3).
M1 is followed by T1 which are separated by 2030 m. Hence, in normal subjects S1 is
appreciated as a single sound, but split S1 can be recorded with a phonocardiogram.
It is auscultated with diaphragm of the stethoscope timed simultaneously with the
palpation of the carotid or cardiac apex.
M1 coinicides with C point of the mitral valve echocardiogram7 and down stroke
of the left atrial c wave of LA pressure tracing, which is delayed from the LV-LA
pressure crossover by 30 ms8 (see Fig. 21.12).
Similar echocardiographic correlates are more difficult to demonstrate for T1 in the
normal subjects, but T1 has shown to coincide with the down stroke of the RA c wave
pressure tracing9 with greater delay between T1 and RV-RA pressure cross-over.
Table 21.4 Determinants of intensity of S1
1. Structural integrity of AV valve Thickness and mobility of the leaflets

2. Velocity of the MV closure Position of AV valve at the time of ventricular systole
3. Status of ventricular contraction Isovolumic systole, myocardial contractility, heart rate
4. Physical characteristics Vibrating structutres
5. Transmission characteristics Thoracic cavity and chest wall
Determinants of the Intensity of S1

The intensity of S1 often gives clues to the diagnosis and degree of abnormality of the
involved structures. The primary factors determining the intensity of S1 are (see Table 21.4):
(1) Structural integrity of the AV valve: Thickness and mobility of the leaflets.
(2) Velocity of the valve closure: Position of the mitral valve at the onset of ventricular
systole.
(3) Status of ventricular contraction: The rate of rise of LV pressure (dP/dt, isovolu-
mic systole), myocardial contractility and heart rate.
(4) Physical characteristics of the vibrating structures.
(5) Transmission characteristics of the thoracic cavity and chest wall.
1) Structural integrity of the mitral valve: The normal mitral valve has thin pliable
leaflets, which are capable of producing a normal S1.
However, there is an inadequate coaptation of the mitral leaflets causing attenuation
of S1 in the setting of severe MR.
Also, the loss of leaflet tissue as in infective endocarditis attenuates the intensity of S1.
A calcified mitral valve as in long standing MS immobilizes the valve leaflets, which
results in diminished or absent M1.
2) Velocity of the valve closure: It is one of the most important factors affecting the
intensity of S1, which is determined by the position of the mitral valve at the onset of
ventricular systole. The position of the mitral valve at the onset of ventricular systole is
altered by (i) relative timing of the atrial and ventricular systole (PR interval) and (ii)
the rate of LV filling during atrial systole.
(i) PR intervals from 140200 ms usually result in a normal S1 (see Fig. 21.13).
At short PR interval (80140 ms) as in Wolff-Parkinson-White and Lown-
Ganong-Levine syndromes, the mitral leaflets are maximally separated by the

LA contraction at end diastole, due to which the MV closes at a high speed
with a large excursion, which results in a loud and late M1.10,11
At longer PR intervals (200500 ms), there is less separation of the mitral
valve leaflets which have already begun to close with atrial relaxation (prema-
ture MV closure due to LV diastolic pressure exceeding LA pressure), and there
is less excursion of the mitral valve with LV contraction (which occurs at lower
LV pressure) which results in softer and early M1.
However; when PR interval is 500 ms, the mitral valve reopens and closes
with rapid velocity producing a loud S1.

S1
S2
Short PR
Increased S1
Normal PR
Normal S1
Long PR
Soft S1
Fig. 21.13 | Relationship of intensity of S and PR interval.

1
(ii) The rate of LV filling during atrial systole:11

When venous return is decreased in noncompliant hypertensive LV, there is more
effective transportation of atrial volume into the relatively underfilled LV resulting
in widely separated mitral leaflets that produce a loud S1 but soft and late S4.
Increased venous return causes more vigorous atrial contraction, which results
in less wide separation of the mitral leaflets (at the onset of ventricular systole)
producing a loud and early S4 but a softer S1. This is the most likely explanation
of a soft S1 in hypertensive patients with normal PR intervals.
3) Status of ventricular contraction: It is also an independent factor affecting the
intensity of S1.11 Ventricular contraction is affected by i) the rate of rise of LV pressure
(dP/dt, isovolumic contraction) and ii) heart rate.
(i) Increased myocardial contractility: Following causes increase myocardial con-
tractility, this increases the rate of rise of LV pressure (dP/dt) and thereby increases the
velocity of the closing mitral leaflets. This further produces a loud S1.12
Exercise
Hypoglycemia
Thyrotoxicosis
Pheochromocytoma
Catecholamine infusion
High output states: Anemia, pregnancy, AV fistula, fever and anxiety
In addition, high output states are associated with tachycardia that causes (i) shortened
PR interval, and (ii) widely open valve due to the high flow through a shortened dias-
tole resulting in a loud S1.
Similarly, a loud T1 in ASD is due to the high flow through the tricuspid valve sec-
ondary to the left-to-right shunt at the atrial level.
(ii) Decreased myocardial contractility results in decreased rate of rise of LV pressure
producing a soft S1, which may be found in:
Acute myocardial infarction
Cardiomyopathy
Myocarditis
Myxedema
Ventricular aneurysm
Drug induced myocardial depression: beta-blockers, Ca blockers, disopyramide.
(iii) Loss of isovolumic contraction (dP/dt) results in decreased velocity of MV closure

producing muffling of S1, as in:
Severe mitral regurgitation
Severe aortic regurgitation
Large ventricular septal defect
Ventricular aneurysm.
(iv) Heart rate: Tachycardia accentuates S1 due to:
The Shortening of PR interval
Wide open valve as diastole is shortened and
Increase in myocardial contractility as a result of Stair-case phenomenon (while
bradycardia has the opposite effect).
4) Physical characteristics of the vibrating structures
Alterations in the physical characteristics of the vibrating structures may also vary
the intensity of S1.
Pacing-induced myocardial infarction and ischemia have been shown to decrease the
intensity of S1 secondary to these alterations.13
5) Transmission characteristics of the thoracic cavity and chest wall
Higher frequency heart sounds are attenuated to a greater extent than the lower fre-
quency sounds.14
Conditions such as obesity, emphysema, large pleural or pericardial effusions will
decrease the intensity of all the auscultatory events.
Whereas a thin body habitus tends to increase the intensity of heart sounds and
murmurs.
Evaluation of S1
(1) Increased intensity of S1: It occurs in (see Fig. 21.14):
(i) Mitral stenosis: Loud S1 is due to:
The thickened but mobile leaflets
The presystolic gradient between LA and LV prevents preclosure of the mitral
leaflets but kept wide open at end diastole. Delayed MV closure at a higher LV
1. MS 1. Severe MR
2. LA myxoma 2. Severe AR
3. MVP 3. Calcified MS
Loud Diminished
1. Hyperkinetic 1. LV aneurysm
states 2. AMI
2. Exercise S1 3. CM
4. LBBB
1. Af
2. Afl with
Wide splitting
varying block Variable Split 1. RBBB
3. AT with
2. LV pacing/ectopics
varying block
1. CHB with AV 3. Ebsteins anomaly
4. VT with AV
dissociation 4. RA myxoma
dissociation
2. Mobitz I with
AV dissociation Reverse splitting
1. RV pacing/ectopics
2. LA myxoma
3. Significant MS
Fig. 21.14 | Evaluation of first heart sound (S )MS: mitral stenosis, MR: mitral regurgi-
1
tation, MVP: mitral valve prolapse, AR: aortic regurgitation, AMI: acute
myocardial infarction, CM: cardiomyopathy, LBBB: left bundle branch block,
RBBB: right bundle branch block, LV: left ventricular, RV: right ventricular,
LA: left atrial, RA: right atrial, Af: atrial fibrillation, Afl: atrial flutter, AT: atrial
tachycardia, VT: ventricular tachycardia.
pressure at a time when there is a more rapid rise of LV pressure (dP/dt)

increases the velocity of valve closure.
(ii) Left atrial myxoma: Similar mechanism for booming S1 as that of MS.
(iii) Exercise: Loud S1 is due to:
Tachycardia induced shortened PR interval, increased myocardial contractility
(due to Treppe phenomenon) and due to the wide open valve (as diastole is
shortened) and
Increased flow across the AV valve.
(iv) Hyperkinetic circulatory states: These accentuate S1 due to:

Increased flow across the AV valve and
Tachycardia.
(v) Holosystolic mitral valve prolapse (non rheumatic MR)15: Loud M1 is due to:
Increased amplitude of leaflet excursion
May be due to the summation of normal M and an early non-ejection click of

1
valvular prolapse.
(vi) Loud T1 occurs in:
TS: similar mechanism as in MS
ASD: due to increased tricuspid flow secondary to the left to right shunt at the
atrial level
Anomalous pulmonary venous connection: due to increased tricuspid flow.
(2) Decreased intensity of S1: It occurs in:

(i) Severe mitral regurgitation: Diminished S1 is due to:
Diminished mobility of the leaflets as a result of fibrosis and shortening
Failure of the leaflets to close and
Loss of isovolumic contraction
Myocardial depression that contributes in secondary MR (due to ischemia).
(ii) Flail mitral leaflet: MVP with middle or late systolic prolapse usually has normal
S1 while MVP patients with flail leaflet have a soft S1.
(iii) Severe aortic regurgitation: Attenuated S1 is due to:
Premature closure of normal mitral valve due to marked increase in the end-
diastolic pressure as a result of volume overload as seen in acute severe AR.

Loss of isovolumic contraction as in chronic severe AR.
(iv) Ventricular aneurysm results in soft S1 due to:

Loss of isovolumic contraction and
Decreased myocardial contractility.
(v) Acute myocardial infarction: S1 is muffled because of:

Diminished ventricular contractility
Ventricular aneurysm and
Left bundle branch block (LBBB).
(vi) Cardiomyopathy: Soft S1 is due to:

Decreased myocardial contractility
MR/TR and
LBBB.
(vii) Myocarditis attenuates S1 because of the diminished myocardial contractility.

(viii) Calcified MS: Attenuated S1 is due to immobility of the mitral valve.
(ix) LBBB:16 M1 is delayed and decreased in intensity due to:
Delay in the onset of LV contraction
Decreased LV contractility
Presence of noncompliant LV facilitates atriogenic preclosure of the mitral
valve
Presence of concomitant first degree heart block.
It is likely that more than one mechanism is operative in most of the patients with
LBBB. At times there could be a reversal of the sequence of S1 (i.e. T1 followed by M1).
(3) Variable intensity of S1: Variation in the intensity of S1 occurs because of variation
in the PR intervals and varying force of ventricular contraction. Loud S1 occurs at
short PR intervals, while a softer S1 occurs at longer intervals when the valve leaflets
have partially closed.17 Variable S1 occurs in (see Table 21.5):
Atrial fibrillation
Complete heart block with AV dissociation
Table 21.5 Intensity of S1
Increased (loud S1) Decreased (diminished S1) Variable S1
1. Mitral stenosis 1. Severe mitral regurgitation 1. Atrial fibrillation

2. LA myxoma 2. Flail mitral leaflet (middle/late 2. Complete heart block
3. Holosystolic mitral valve systolic prolapse) with AV dissociation
prolapse (non rheumatic) 3. Severe aortic regurgitation 3. Mobitz type I heart block
4. Exercise 4. Ventricular aneurysm with AV dissociation
5. Hyperkinetic circulatory 5. Acute myocardial infarction 4. Ventricular tachycardia
states 6. Cardiomyopathy with AV dissociation
6. Loud T1: tricuspid stenosis, 7. Myocarditis 5. Atrial tachycardia with
atrial septal defect, anomalous 8. Calcified mitral stenosis varying block
pulmonary venous connection 9. Left bundle branch block
Mobitz type I heart block with AV dissociation

Ventricular tachycardia with AV dissociation
Atrial flutter with varying block
Atrial tachycardia with varying block.
(4) Abnormal wide split of S1: Split of S1 into M1 and T1 is normally not audible as
two components are synchronous or narrowly split (0.020.03 s) but may be audible
in 40% of the normal individuals when the split is more wide (0.03 s). However, it
is readily recordable with a phonocardiogram. The split of S1 is best detected at the
lower left sternal border with firm pressure on the diaphragm of the stethoscope.
(i) Abnormal wide split with normal sequence (M1, T1) occurs because of delayed
tricuspid component, which is due to:
Electrical delays (delayed contraction of RV): as in complete RBBB (proximal
type), LV ectopics, LV pacing and idioventricular rhythms originating from
LV.18
Mechanical delays as in Ebsteins anomaly19 (sail sound due to delayed activation
and RA pressure), and sometimes in TS and right atrial myxoma (due to RA
pressure).
(ii) Reverse splitting of S1 (T1, M1) because of delayed mitral component, which is
due to:
Electrical delays (delayed contraction of LV): as in RV pacing, RV ectopics and
idiovenricular rhythm originating from the RV.
Mechanical delays (due to increased LA pressure): Reverse splitting may also be
present in significant MS,20 and left atrial myxoma.
The Second Heart Sound (S2)

The second heart sound signals the onset of ventricular diastole and has two com-
ponents: A2 (first component) and P2 (second component).
Characters Findings
1. Frequency High
2. Duration 0.11 s
3. Incisura of aortic pressure coincides With A2
4. Incisura of pulmonary pressure coincides With P2
5. A2P2 interval: during expiration 30 ms
: during inspiration 4050 ms
6. A2 is earlier than P2
7. A2 is louder than P2 even at pulmonary area
8. Well heard at aortic, pulmonary areas and apex A2
9. Well heard only at pulmonary area P2
It is produced by the sudden deceleration of retrograde flow of blood column in

the aorta and the pulmonary artery, which initiates the vibrations of the haemocar-
diac structures coinciding with the closure of aortic and pulmonary leaflets.
Characteristics of S2
The second sound is the key to auscultation of the heart21 (see Table 21.6).
(i) S2 is a high frequency sound with an average duration of 0.11 s.
(ii) A2 and P2 are coincident with the incisura of aorta and pulmonary artery pressure
tracing, which signals the end of LV and RV ejection periods.
(iii) Compared to S1, S2 is higher in pitch and frequency due to:
Low elasticity of semilunar valves and arterial trunks than that of AV valves
and ventricles.
Less blood volume in arteries than ventricles and so low inertia of the vibrating
mass producing higher frequency of vibrations.

S is shorter and snappier than S as the higher frequency vibrations damp out
2 1
earlier and more rapidly.
(iv) A2 is earlier and louder than P2
A is louder due to higher pressure in the aorta than in the pulmonary artery.
2
A occurs earlier than P as:
2 2
RV ejection begins earlier, lasts longer than LV ejection, and ends after LV
ejection resulting in P2 occurring after A2.
Hang out interval on the aortic side (approximately 30 ms) is less than on the
pulmonary side (approximately 80 ms).
(v) Normally, A2 is well heard in aortic and pulmonary areas as well as at the apex,
while P2 is well audible only at the pulmonary area and rarely at the apex.22
(vi) Even at the pulmonary area, P2 is softer than A2.
(vii) Normal physiological split of S2 was first recognized by Potain in 1866.
During expiration, A and P are separated by an interval of 30 ms so, these are
2 2
heard as a single sound (S2); while during inspiration, splitting or separation of the
two components (A2, P2) is distinctly audible23 as the interval widens to 4050 ms.
EKG EKG
P1 A2 P P1 A2 P
2 2
PHONO
PHONO
Aortic pressure
Inspiration
Hang out
Expiration interval 30 ms
Aortic
pressure
MPA
pressure
Hang out (80 ms)

interval (60 ms)
Right ventricular Left ventricular pressure
pressure
Fig. 21.15 | Hang out interval on the right side

Fig. 21.16 | Hang out interval on the left side.
MPA: main pulmonary artery.
However, in recumbent position in some normal subjects expiratory separa-

tion of A2 and P2 may be 30 ms and expiratory split is audible but becomes sin-
gle on assuming upright position24 and hence basal areas should always be
examined in upright position.
Splitting of S2 is usually best heart at the second or the third left intercostal space.
Hang out interval
The semilunar valves are expected to close at the point of cross-over of the pressures,
i.e. the point where the ventricular pressures fall lower than the arterial pressures
(LV pressure falls lower than aortic pressure, RV pressure falls lower than PAP),
however in reality these valves close slightly later (at the incisura of aorta and pul-
monary artery pressure tracing).
This time interval from the crossover of the pressures to the actual closer (occur-
rence of A2 and P2) is called hang out interval.
In general, the duration of hang out interval depends upon the pressures in the
arteries, vascular resistance, distensibility and recoil of the arterial system.
Due to higher pressure and less distensibility (complaint), the hang out interval on
the aortic side is less than that of on the pulmonary side.
The hang out interval is measured between the incisura of aorta and LV pressure at the
same level on the left side and between the incisura of pulmonary artery and RV
pressure at the same level on the right side (see Figs 21.15 and 21.16).
The ventricular mechanical systole is the sum of the isovolumic contraction time
and ejection period minus the hang out interval.
Mechanism of normal split of S2:25 Normal inspiratory split of S2 is due to (see
Fig. 21.17):
Delayed P2 accounting for 73%
Early occurrence of A2 contributing about 27%.
A2 P A2 P
2 2
S1 S2 S1 S2
Expiration Inspiration
Fig. 21.17 | Normal physiological splitting of S . 2
Table 21.7 Abnormal splitting of S2
Wide splitting Reversed splitting
1. Atrial septal defect 1. Left ventricular outflow tract obstruction:

2. Significant mitral regurgitation aortic stenosis
3. Ventricular septal defect 2. Complete left bundle branch block
4. Complete right bundle branch block 3. Right ventricular ectopic beats
5. Premature ventricular contractions 4. Right ventricular pacing
6. Left ventricular pacing 5. Patent ductus arteriosus
7. Mod-severe pulmonary stenosis with 6. Post stenotic dilatation of aorta secondary
intact ventricular septum to aortic stenosis and aortic regurgitation
8. Acute pulmonary embolism 7. Wolff-Parkinson-White syndrome type B
9. Pulmonary hypertension with right heart failure 8. Chronic ischemic heart disease
10. Idiopathic dilatation of pulmonary artery 9. Hypertensive cardiovascular disease
The inspiration results in changes in the systemic and pulmonary venous return.
(i) The inspiratory increase in the systemic venous return due to fall in the intratho-
racic pressure increases the RV stroke volume. This causes a delay in P2 by:
Decreasing the pulmonary vascular impedance (i.e. capacitance of the pul-
monary vascular bed) and thereby increasing pulmonary artery hang out inter-
val (contributing about 45% for delayed P2) and
Prolonging the RV ejection (contributing about 28%).
(ii) The inspiratory decrease in the pulmonary venous return (due to pooling of blood
in the pulmonary vasculature) decreases LV stroke volume which causes an early
occurrence of A2 by
Decreasing the LV ejection, and
Decreasing the hang out interval on the aortic side.
The net result is the wide inspiratory splitting of S2.
Abnormal splitting of S2 is defined as the presence of audible expiratory split (of
30 ms) both in supine and upright positions26 (see Table 21.7). Abnormal splitting
of S2 could be
Persistent physiological splitting of S2
Wide fixed splitting of S2
Reversed or paradoxical splitting of S2
Single S2.
A2 P A2 P2 P2
2 P2 A2 A2
S1 S2 S1 S2
Expiration Inspiration S1 S2 S1 S2
Fig. 21.18 | Wide physiological splitting of S . 2
Fig. 21.19 | Narrow physiological splitting of S .

2
(i) Persistent physiological splitting of S2: It could be wide or narrow.

(a) Wide physiological splitting of S2 (see Fig. 21.18):
(i) Due to delayed pulmonic closure (P2):
27
Delayed electrical activation of the right ventricle :
Complete RBBB (proximal type)

LV ectopic beats (premature ventricular contrations)
LV pacing
Prolonged RV mechanical systole:
Moderate to severe PS with intact ventricular septum18

PH with right heart failure28
Acute pulmonary embolism29
Increased hang out interval (80 ms) (decreased impedence of pulmonary vascu-
lar bed)
Mild PS30
Idiopathic dilatation of pulmonary artery30
Normotensive ASD30
Postoperative ASD (in 70%)8
(ii) Early aortic closure (A2):
Shortened LV mechanical systole (LV ejection time due to the loss of isovolu-
mic contraction)
Significant MR30
VSD31
(iii) Other benign causes which mimic wide splitting of S2
Pectus excavatum
Straight back syndrome
Occasionally, in normal children
(b) Narrow physiological splitting of S2: The splitting of S2 into A2 and P2 during expi-
ration with narrow splitting interval (30 ms) and loud P2, is a common finding in
severe PH (see Fig. 21.19). However, in PH, the split could be wide with loud P232 or
could be a wide fixed split32, which indicates a more severely compromised RV.
The wide split in PH could be due to the prolongation of RV systole.
While the wide fixed split in PH could be due to
Inability of the compromised RV to accept the augmented venous return associ-

ated with inspiration and
Altered pulmonary vasculature.23
(ii) Wide fixed splitting of S2: It is defined when the interval between A2 and P2 is not only
wide and persistent but also remains unchanged during the respiratory cycle (i.e. inspira-
tion and expiration)33 i.e. A2 and P2 are widely separated during expiration and exhibit
little or no change in the degree of splitting with inspiration or Valsalva maneuver.
Wide split is caused by a delay in P2 due to the increased pulmonary vascular capac-
itance prolonging the hang out interval
While fixed split is due to little or no inspiratory delay in P2 because of little or no
change in RV filling and stroke volume during inspiration.
Clinical recognition of wide fixed splitting of S2: Apparent fixed split is occasionally
audible in young normal subjects in supine position but it disappears in upright posi-
tion. Hence for wide fixed split, the patient should always be auscultated both in
supine and upright positions. In doubtful cases auscultation should be done during
the straining phase of Valsalva maneuver.
Wide fixed splitting of S2 occurs:
Due to failure to increase RV stroke volume with inspiration as in RV failure, acute
and chronic pulmonary embolism
Due to simultaneous increase in RV and LV filling as in secundum ASD
Due to obligatory ASD as in total anomalous venous connection (TAPVC).
Wide splitting of S2 in ASD: It is caused by the delay in P2, which is due to increased
systemic venous return and RV filling during inspiration, which in turn results in
Prolong RV systole
Prolong hang out interval (i.e. PV impedence) and
Delayed electrical activation of RV if associated with RBBB.
Fixed splitting of S2 in ASD: Fixed splitting of S2 is an ausculatatory hallmark of
ostium secundum ASD.
The phasic changes in systemic venous return during respiration are associated with
reciprocal changes in the volume of the left-to-right shunt minimizing respiratory
variations in the RV filling34 i.e
Venous return during inspiration is associated with no left-to-right shunt through
interatrial communication and
Venous return during expiration is associated with left-to-right shunt through
interatrial communication minimizing the respiratory variations in RV filling,
resulting in simultaneous increase in RV and LV filling.
Since the impedance of pulmonary vascular (PV) bed is appreciably decreased (i.e. PV
capacitance), there is little or no additional of PV impedance (i.e. PV capaciance)
during inspiration and no or little inspiratory delay in P2.
The net effect is the characteristic wide and fixed splitting of S2 (see Fig. 21.20).
A2 P A2 P
2 2
Normal
S1 S2 S1 S2
A2 P A2
2 P2
ASD
S1 S2 S1 S2
Fig. 21.20 | Wide and fixed split of S 2 in ASD.
Importance of Valsalva maneuver in ASD patients: In patients suspected of having

an ASD, the Valsalva maneuver may be used to assess the splitting of S2.
In normal subjects, S2 fuses during the strain phase as both RV and LV filling decreases,
and on release of the strain, immediate surge in RV filling and stroke volume produces
delay in P2 resulting in a prominent S2 splitting for 68 beats. When augmented blood
volume reaches the left heart (i.e. LV filling and stroke volume), it prolongs the LV
systole resulting in the narrowing of S2 splitting (i.e. narrow split wide split
narrow split).
However, in patients with ASD, S2 splitting widens during the strain phase due to left-
to-right shunt (and thereby RV filling and stroke volume and delay in P2). On release
of the strain, the expected S2 split does not occur due to the altered interatrial shunting.
In patients of ASD with atrial fibrillation: S2 splitting is prominent after the long
cycle due to greater left-to-right shunting with long diastoles in contrast to patients
with Af without ASD.
(iii) Reversed or paradoxical splitting of S2: It is an inaudible split during inspiration

and an audible split during expiration due to the reverse sequence of semilunar valve
closure i.e. P2 preceding A2.33
Types of reversed splitting of S2
Type I or classic reversed splitting of S2: There is no split or single S2 during inspiration
and split during expiration with reverse sequence due to delay in A2 (see Fig. 21.21).
It occurs in delayed LV electromechanical systole i.e. Q-A2 interval. During expi-
ration, prolonged LV systole causes A2 to follow P2 (i.e. audible expiratory split); while
during inspiration, Q-P2 normally increases, but Q-A2 shortens or remains unchanged
(i.e. no split/single S2).
Type II or partial reversed splitting of S2: Normal inspiratory S2 splitting and expira-
tory splitting of S2 with reverse sequence (see Fig. 21.22).
Type III reversed splitting of S2: It is similar to type II but A2 P2 separation is
20 ms with reverse sequence during expiration and S2 is heard as a single sound in
both the phases of respiration.
A2
P2 A2 P2
S1 S2 S1 S2
Fig. 21.21 | Reversed splitting of S 2 (type I).
A2
P2 A2 P2
S1 S2 S1 S2
Fig. 21.22 | Partial reversed splitting of S 2 (type II).
Clinical recognition of reversed splitting of S2

Only type I is recognizable clinically while type II and III are detectable only by a
phonocardiogram. The reversed splitting of S2 may be confused with wide physio-
logical (variable) or wide fixed splitting of S2.
Trace the two components of S2 (i.e. A2 and P2) away from the pulmonary area, since
normally, only first of the two components (A2) is traced to the apex while the second
component (P2) is usually not (or faintly) audible away from the pulmonary area.
When the later (A2) of the two components is traceable to the apex, a reversed split-
ting of S2 is likely.
Valsalva maneuver in patients with reversed S2 split, results in widening of S2 split
during the strain phase, narrowing of S2 split upon release of the strain and subse-
quent widening of the S2 split again (wide split narrow split wide split). In
contrast, a normal S2 narrows during the strain phase, widens upon release and then
narrows again (i.e. narrow split wide split narrow split).
Causes of reversed splitting of S2

a) Due to delayed aortic closure (A2)
Due to delayed electrical activation of the LV
Complete LBBB (proximal type)35
RV pacing18
RV ectopic beats.18
Due to prolonged LV mechanical systole
Complete LBBB (peripheral type)35
Left ventricular outflow tract obstruction (AS)35
Hypertensive cardiovascular disease36
Arteriosclerotic heart disease37: chronic ischemic heart disease, angina pectoris.
1. ASD
1. Significant MR 1. Funnel chest
2. TAPVC
2. PH with RVF 2. Straight back
3. RVF
3. Acute PE syndrome
4. PE
Wide split S2 splitting Wide fixed split
1. CRBBB 1. PS with
2. LV ectopy/ intact IVS
Narrow split Reverse split
LV pacing 2. ASD
3. VSD
Type II: Type I:

Severe PH WPW syndrome 1. CLBBB
type B 2. RV ectopics/
RV pacing
3. PDA
4. Chronic IHD
Fig. 21.23 | Splitting of second heart sound (S )CRBBB: complete right bundle branch block, CLBBB:
2
complete left bundle branch block, MR: mitral regurgitation, PH: pulmonary hypertension,
PE: pulmonary embolism, PS: pulmonary stenosis, RVF: right ventricular failure, ASD: atrial
septal defect, VSD: ventricular septal defect, IVS: inter ventricular septum, PDA: patent duc-
tus arteriosus, TAPVC: total anomalous pulmonary venous connection, IHD: ischemic heart
diease, WPW: Wolff-Parkinson-White.
Due to decreased impedance of systemic vascular bed ( hangout interval)

Post-stenotic dilatation of the aorta secondary to AS or AR35
PDA35
LBBB is the most common cause of reversed splitting of S2.
b) Due to early pulmonic closure (P2)
Due to early electrical activation of RV as in Wolff-Parkinson-White syndrome
(Type B)38, it commonly results in type II reversed splitting of S2.
c) Rarely to shortened RV systole because of decreased RV filling as in right atrial
myxoma and TR (see Fig. 21.23).
(iv) Single S2: Absence of an audible S2 split in either phases of respiration results in
single S2 (see Table 21.8).
A single S2 is heard when the separation of A2 and P2 is narrow (30 ms) often due
to delayed A2 (i.e. type III reverse splitting of S2) or when either of two components
(A2 or P2) is absent or inaudible.
The common causes of single S2 are:
a) When P2 is absent or undetectable:
Aging: upto 50% in subjects of 60 yrs of age due to:
Age related lengthening of LV isovolumic contraction resulting in QA2 interval
and delay of A239
Table 21.8 Single S2
P2 absent/undetectable A2 absent/undetectable
1. 60 yrs of age 1. Severe aortic stenosis

2. Obesity, thick chest wall, emphysema 2. Severe pulmonary stenosis
3. Severe pulmonary stenosis (PS) 3. Severe pulmonary hypertension
4. Severe aortic stenosis 4. Aortic atresia
5. Tetralogy of Fallot 5. Eisenmengers ventricular septal defect
6. Pulmonary atresia 6.Single ventricle
7. Tricuspid atresia 7. All causes of reversed splitting of
8. Double outlet right ventricle with PS S2 due to delayed A2
9. Transposition of great arteries
10. Eisenmengers ventricular septal defect
11. Single ventricle
Age related physiological decrease in pulmonary vascular compliance and a short-

ening of hangout interval resulting in QP2 interval and early P2.40
Age related increase in thoracic A-P diameter resulting in muffling or masking
of P2.
Obesity, thick chest wall or emphysema results in muffling of P2.
Acyanotic CHD:
Deformed pulmonary valve: severe PS in which P2 is late and soft
Concealed or masked by the systolic murmur: severe AS
Masked by a sound: loud A2 in AS or AR and loud opening snap in
significant MS.
Cyanotic CHD:
Deformed pulmonary valve: TOF, pulmonary atresia, tricuspid atresia (due to
associated PS in most cases), DORV with PS
Posterior location of pulmonary valve: TGA
Only one semilunar valve is present, and could be due to synchronous closure of
quadricuspid valve: Truncus arteriosus
P2 is synchronous with A2 due to the equalization of hangout intervals because of
equal RV and LV systoles: Eisenmengers VSD, single ventricle.
b) When A2 is absent or undetected
Deformed aortic valve: severe AS, aortic atresia
A2 is synchronous with P2 due to the equalization of hangout intervals because of
equal RV and LV systoles: Eisenmengers VSD, single ventricle
Concealed or masked by a murmur or sound:
Severe PH: loud P2 may mask A2 by the phenomenon of retrograde masking.
However, both the components are detected at the apex and the lower sternal area.
Severe PS: prolonged SM may mask A2, but both components are audible at the
apex or at the lower sternal area.
Table 21.9 Intensity of A2
A2 A2
1. Hyperkinetic circulatory states 1. Aortic sclerosis

2. Systemic hypertension 2. Valvular aortic stenosis (AS)
3. Dilatation of ascending aorta: aneurysm, 3. Valvular aortic regurgitation
syphilis, ankylosing spondylitis
4. Congenital biscuspid aortic valve with
no significant AS
5. Transposition of greart arteries
6. Pulmonary atresia
Table 21.10 Intensity of P2
Loud P2 Diminished P2
1. Thin chest wall, straight back syndrome 1. Thick chest wall, obesity, COPD
2. Hyperkinetic circulatory states 2. Pulmonary stenosis
3. Pulmonary hypertension of any cause 3. Dysplastic pulmonary valve
4. Atrial septal defect 4. Mild tetralogy of Fallot
c) All conditions that delay A2 and cause reverse splitting of S2: When the split-
ting interval is 30 ms, single S2 is produced.
d) The continuous murmur may mask the split of S2: As in PDA and sometimes
in severe MR.
Intensity of S2
The intensity of the two components should also be assessed. It could be loud A2 or
P2, or diminished or soft A2 or P2 (see Table 21.9 and Table 21.10).
Determinants of the intensity of S2 are:
1. Pressure in the vessel
2. Flow across the valve
3. Size of the vessel beyond the valve: The dilated vessel becomes closer to the anterior
chest wall resulting in loud S2 (A2 or P2)
4. Status of the valve (stenosis or regurgitation)
5. Site of origin of the vessel: The vessel becomes closer to the anterior chest wall if it
arises anteriorly.
Increased size of the vessel, increased pressure in the vessel beyond the valve and
increased flow across the valve results in accentuated S2, while a stenotic or regurgitant
valve usually causes diminished S2.
a) Loud or accentuated A2: It occurs in:
Hyperkinetic states: Due to increased flow across the normal valve
Systemic hypertension: Due to elevated pressure in the vessel beyond the valve, and
dilatation of the ascending aorta
Aneurysm of ascending aorta: Due to dilatation of the ascending aorta

Aortic root related causes of AR e.g. syphilis, ankylosing spondylitis. Loud S2 is due
to the dilatation of the ascending aorta and the increased flow across the valve with
a well preserved leaflet mobility.
Congenital heart disease:
Congenital bicuspid aortic valve when stenosis is not significant: Due to thick-
ened but mobile leaflets
TGA as aorta arises anteriorly34
Pulmonary atresia in which anterior pulmonary trunk is small or absent, which
causes aorta to be more closer to the anterior chest wall.34
b) Diminished or muffled A2: It occurs in:
Elderly individuals with aortic sclerosis: Due to thickened leaflets and diminished
mobility
Valvular AS: Due to distorted valve anatomy and diminished valve mobility
Valvular AR: Due to restricted valve mobility.
A2 is normal in hypertrophic cardiomyopathy and subaortic stenosis, but may be
diminished in supravalvular AS.
c) Loud or accentuated P2: It occurs in:
Thin chest wall ( anteroposterior diameter) or loss of thoracic kyphosis (as in
straight back syndrome) due to more nearness to the anterior chest wall.41
Hyperkinetic states: increased flow across the normal valve.
Pulmonary hypertension (PH) of any cause: increase pressure in pulmonary artery
results in higher closing pressure of the valve and dilated pulmonary trunk. Loud P2
is the sine qua non of PH.
ASD (secundum): due to dilatation of pulmonary trunk and increased flow across
the valve in the absence of PH.
Grading of accentuated or loud P2
1. Mild or grade 1 (): when intensity of P2 is equal to A2: occurs in mild PH (sys-
tolic pressure: 3049 mmHg, mean pressure: 2134 mmHg)
2. Moderate or grade 2 (): when intensity of P2 exceeds A2, i.e. P2 is louder
than A2: occurs in moderate PH (systolic pressure: 5075 mmHg, mean pressure:
3550 mmHg)
3. Severe or grade 3 (): when P2 is loud and banging and is audible beyond the pul-
monary area: occurs in severe PH (systolic pressure: 75 mmHg, mean pressure
50 mmHg)
d) Diminished or decreased P2: It occurs in:
Thick chest wall, obesity and COPD: due to the masking effect
PS: due to thickened leaflet and diminished valve mobility
Dysplastic PV as in Noonans syndrome: due to distorted valve anatomy and dimin-
ished mobility
Mild TOF (Pink TOF): soft and delayed P2 may be heard due to mild PS.
Evaluation of S2 in Common Clinical Conditions

(a) Valvular heart diseases
(i) Mitral stenosis
Mild to moderate MS without PH: normal S and normal intensity of P
2 2
Severe MS with severe PH: S is closely (narrow) split with loud P
2 2
Intensity of P correlates with the severity of PH
2
S OS is often mistaken for a wide split of S in MS. However, it is initial of the two
2 2
components i.e. S2 is loudest in S2OS; while in split S2 it is the last of the two compo-
nents i.e. P2 is loudest.
(ii) Mitral regurgitation

Mild to moderate MR: S2 split is normal and P2 is accentuated when complicated
with PH
Severe MR: S2 split is wide and variable
S2 split becomes wide and fixed when complicated with heart failure, when associated
with ASD, or when MR is a part of the AV canal defect
Reverse splitting of S2: it occurs in MR due to HOCM or CAD (see Fig. 21.24).
1. Age >60 yrs 1. Severe PS 1. Hyperkinetic 1. Bicuspid AoV

2. Obese 2. Severe AS states 2. TGA
3. TC wall 2. Systemic HTN 3. P At
4. Emphysema
Single P2 absent
1. TOF 1. AA aneurysm
or undectable A2 2. Syphilis
2. P At
3. T At 3. Anky spond
4. TGA
5. DORV S2 A2
with PS 1. Valvular AS
6. SV Single A2 absent 2. Valvular AR
7. Eis VSD or undectable 3. Aortic sclerosis
P2
1. Th C wall
1. Severe AS P2 2. SB syndrome
2. Severe PS 3. Hyperkinetic
3. Severe PH 1. PH
states
4. Aortic At 2. ASD
1. TC wall 1. PS
1. Eis VSD 2. Obese 2. Dysplastic PV
2. SV 3. COPD 3. TOF
Fig. 21.24 | Evaluation of second heart sound (S )PH: pulmonary hypertension, PS: pul-
2
monary stenosis, ASD: atrial septal defect, VSD: ventricular septal defect, Eis:
Eisenmenger, SV: single ventricle, P At: pulmonary atresia, T At: tricuspid atre-
sia, At: atresia, TC: thick chest, ThC: thin chest, SB: straight back, Bicuspid
AoV: congenital bicuspid aortic valve with insignificant AS, AS: aortic stenosis,
AR: aortic regurgitation, AA: ascending aorta, TOF: tetralogy of Fallot, TGA:
transposition of great arteries, DORV: double outlet right ventricle, HTN:
hypertension, COPD: chronic obstructive pulmonary diseases, Anky spond:
ankylosing spondylitis.
(iii) Aortic stenosis

Reverse splitting of S2: due to delayed A2
Single S2 due to masking effect of P2 or absence of A2 (deformed valve).
(iv) Aortic regurgitation
Usually, S2 split is normal
A2 is loud in aortic root causes of AR
A2 is soft in valvular causes of AR
A2 may be loud when associated with VSD or TOF.
(b) Congenital heart diseaseAcyanotic
(i) ASD
S2 split is wide and fixed with loud P2 even in the absence of PH
Eisenmengers syndrome: S2 split remains wide and fixed with loud banging P2.
(ii) VSD
Small VSD: normal S2 split with normal intensity of P2
Moderated VSD: normal S2 split with moderate accentuation of P2
Large VSD: narrow S2 split with loud P2
Eisenmenger VSD: single loud P2
VSD with PS physiology (as TOF, TGA, DORV): single loud A2.
(iii) PDA
Small PDA: normal S2 split and normal intensity of P2 however S2 is masked by the
continuous machinery murmur
Large PDA: normal S2 split with accentuated P2
Eisenmenger PDA: closely S2 split with loud P2.
(iv) Pulmonary stenosis
Mild PS: normal S2 split with normal intensity of P2
Moderate-severe PS (with post-stenotic dilatation): wide variable split of S2 with
diminished P2. P2 may be absent in severe cases
Dysplastic pulmonary valve or when associated with TOF: P2 is absent.
(v) Bicuspid aortic valve
In the absence of significant AS or AR: S2 is normal split with accentuated A2.
(vi) Coarctation of aorta
Usually, normal splitting of S2 with accentuated A2 due to hypertension. There may
be reverse splitting of S2.
(c) Congenital heart diseaseCyanotic: Normal S2 is uncommon
(i) Single S2
Single loud A2 in TOF: due to the absence of P2 and anterior and dextroposed aorta
Single loud A2 in TGA, DORV, Single ventricle: inaudible P2 due to the posteriorly
placed pulmonary trunk
Single loud A2 in Tricuspid atresia: due to PS resulting in the absence of P2
Single loud S2 in Truncus arteriosus: due to the presence of single semilunar valve
with a dilated truncal root.
(ii) Wide splitting of S2: It occurs in:
Total anomalous pulmonary venous connection
Eisenmenger ASD
Ebsteins anomaly
Single atrium
PS with intact ventricular septum and right-to-left shunt (through PFO).
Diastolic Sounds
a) The Third Heart Sound (S3)
It is a low frequency mid-diastolic sound, which occurs during the rapid ventricular
filling phase (see Fig. 21.25). When heard in disease states, S3 is called as S3 gallop,
protodiastolic gallop, or ventricular diastolic gallop.
i) Characteristics of S3: S3 is of two types: physiological and pathological (see Table 21.11).
S1 A2 A2
Base
Phono
Apex
Phono S3 S3
S1
ACG
RFW
Fig. 21.25 | Third heart sound occurring during rapid filling wave (RFW) of apex cardio-
gram (ACG).
1. Low frequency sound

2. Physiological S3 occurs: 120200 ms after A2
3. Pathological S3 occurs: 140160 ms after A2
4. Coincides with RFW of apex cardiogram
5. Coincides with y descent of atrial pressure
(i) Physiological S3
It occurs 120200 ms after A2.
It is normally heard in children, adolescents and young adults.42
It is rare in adults after 40 yrs of age (40 yrs in men and 50 yrs in women), but
may be present in thin asthenic individuals.43
It coincides with the rapid filling wave of the apex cardiogram,44 and y descent of the
atrial pressure tracing.
It is best heard with lightly placed bell of the stethoscope at the apex in left lateral
position.
It is differentiated from the pathological S3 primarily by the company it keeps,45 (i.e.
cardiac enlargement in pathological S3, besides it is early and loud).
The genesis of physiological and pathological S3 is same. However, whether the RV
contributes to the physiological S3 is unknown.
(ii) Pathological S3
It occurs in mid-diastole 140160 ms after A2.
When S3 is heard in disease states, it is called as a gallop sound (protodiastolic, ven-
tricular diastolic gallop).
Pathological S3 is generally regarded as an exaggeration of the physiological S3.
Often, it is quite faint and easily overlooked.
Often, S3 is heard only intermittently rather than with each beat.
Presence of S3 or S4 results in triple rhythm (gallop), while presence of both S3 and S4
produces quadruple rhythm, which may simulate a mid diastolic murmur of MS.
Quadruple rhythm is commonly heard in patients with LV aneurysm, cardiomyopa-
thy, or severe LV failure and dilatation of any cause.
S3 may summate (fuse) with S4 producing a single loud summation sound or gallop dur-
ing sinus tachycardia (when ventricular diastole is shortened) or long PR intervals,46
while an incomplete summation may simulate a mid diastolic rumble of MS.
ii) Mechanism of production of S3
(i) Prerequisites for genesis of S3
Non-obstructed AV valve: A non-stenotic AV valve is a prerequisite for the genera-
tion of S3 as the presence of a stenotic AV valve impedes ventricular inflow.
(ii) Theories for production of S3: Three major theories have been proposed for the
genesis of S3: valvular theory, ventricular theory and impact theory.
The valvular theory: Diastolic tensing of the AV valves at the termination of rapid
ventricular filling results in S3. However, recent phonocardiographic studies dis-
proved this explanation.45
The ventricular theory: Sudden deceleration of the onrushing column of blood in the
ventricular inflow during rapid ventricular filling phase sets the entire cardiovascular
system into vibration, producing S3.4749
The impact theory (of Reddy et al)50: The ventricular mechanism could explain for S3
recorded within the ventricular cavity and epicardial surface, but the external S3 recorded
from the chest wall was not due to passive transmission of the sound originating
from the LV through the intervening structures to the chest wall. Hence, S3 heard
with the stethoscope is due to the dynamic impact of the heart with the chest wall.
The force of impact and resultant intensity of S3 are primarily dependent on:
The size of the heart ( space between the enlarged heart and chest wall, thereby
facilitating a more forceful impact)
The motion of the heart within the thorax ( motion more impact)
The chest wall configuration (thick chest wall, COPD, and obesity dampens the S3)
Phase of respiration (inspiration for RV S3)
Position of the patient (e.g. left lateral for LV S3, supine for RV S3).
This theory explains the presence of S3 in hyperdynamic states as well as in condi-
tions with increased end-systolic volume secondary to LV dysfunction.
However, the ventricular mechanism together with dynamic impact of the heart on
the chest wall explains the presence of S3 in most disease states.
iii) Causes of S3 (see Table 21.12 and Fig. 21.26)
(i) Physiological S3
Children and young adults (men 40 yrs, women of 50 yrs)51
High output states (diastolic overload): 3rd trimester pregnancy, after exertion and
anxiety related tachycardia.
(ii) Pathological S3
Excessive rapid ventricular filling (diastolic overload states with atrial pressures):
As RV is more compliant than LV; presence of a RV S3 is relatively uncommon.
1. Hyperkinetic states (high output states):
Anemia
Thyrotoxicosis
Arteriovenous fistula.
Table 21.12 Causes of S3
Physiological Pathological
1. Children 1. Heart failure

2. Young adults (men 40 yrs, 2. Hyperkinetic circulatory states
women 50 yrs of age) 3. Mitral regurgitation
3. Pregnancy 4. Tricuspid regurgitation
5. Ventricular septal defect (VSD)
6. Patent ductus arteriosus
7. Total anomalous pulmonary venous
connection
8. Double outlet right ventricle without
pulmonary stenosis
9. Truncus arteriosus
10. Transposition of great arteries with VSD
11. Ischemic heart disease
12. Dilated congested cardiomyopathy
2. Atrioventricular valve incompetence:

MR (chronic moderate to severe)
TR (RV S3)
3. Left-to-right shunts:
VSD
PDA
ASD (RV S3) (rare)
4. Cyanotic CHD with increased pulmonary blood flow: TAPVC, DORV without
PS, truncus arteriosus, TGA with VSD
Increased end-systolic and end-diastolic volumes and high filling pressures secondary to
ventricular dysfunction (i.e. ejection fraction and ventricular failure):
Ischemic heart disease
Dilated cardiomyopathy
Systemic hypertension
Valvular heart disease
Congenital heart diseases.
Hyperkinetic 1. Heart failure

states: 2. IHD
1. Anemia 3. DCM
Children and 2. Thryotoxicosis 4. Sytemic HTN
young adults 3. AV fistula 5. PH
Physiological S3 Pathological
High output states: VHD: ACHD:

1. 3rd TM 1. MR 1. VSD
2. After exertion 2. TR 2. PDA
3. Anxiety related
tachycardia
CCHD with PBF:
1. TAPVC
2. DORV without PS
3. TGA with VSD
4. Truncus arteriosus
Fig. 21.26 | Evaluation of third heart sound (S )TM: trimester of pregnancy, AV: arterio
3
venous, MR: mitral regurgitation, TR: tricuspid regurgitation, VSD: ventricular
septal defect, PS: pulmonary stenosis, TGA: transposition of great arteries,
DORV: double outlet right ventricle, PDA: patent ductus arteriosus, TAPVC:
total anomalous pulmonary venous connection, IHD: ischemic heart disease,
DCM: dilated cardiomyopathy, HTN: hypertension, PH: pulmonary hyper-
tension, VHD: valvular heart disease, ACHD: acyanotic congenital heart dis-
ease, CCHD: cyanotic congenital heart disease, PBF: increased pulmonary
blood flow.
Conditions in which S3 is expected but rarely heard at the bed side:

ASD and AR inspite of volume overload
A loud S3 in ASD should suggest (i) the possibility of Ebsteins anomaly mistaken
for ASD, (ii) ASD with mitral valve disease, (iii) ostium primum ASD with MR
or TR
In chronic AR, S3 is audible when end-systolic volume increases with the devel-
opment of LV dysfunction.
S3 is sometimes audible in restrictive and hypertrophic cardiomyopathy when con-
gestive heart failure occurs.
Pericardial knock of constrictive pericarditis is a high-pitched early diastolic sound
occurring 100120 ms after A2 exaggerated with inspiration (see Table 21.13).
iv) Clinical Recognition of S3: Pathological S3 may be palpable and often sounds like
a distant thud. It is often heard only with the bell of the stethoscope, as it is a low fre-
quency sound with the lightest possible pressure.
LV S3 is best heard at the (LV impulse) apex in left lateral position during expiration,
and increases its intensity with isometric handgrip exercise.
RV S3 is best heard at the (RV impulse) lower left sternal edge (or occasionally sub-
xiphoid region) in supine position, and is exaggerated during inspiration but no
change occurs with isometric handgrip exercise.
Maneuvers, which increase the venous return increase the intensity of the sound and
thereby improve the audibility of S3. These maneuvers are as follows:
Passive elevation of the legs
Coughing
Isotonic exercises (few sit-ups)
Abdominal exercise
Release phase of Valsalva maneuver.
The maneuvers that decrease the venous return, also decrease the intensity of S3, and
include upright posture, tourniquets around the extremities, and the strain phase of
Valsalva maneuver.
In the presence of sinus tachycardia, it is often difficult to recognize S3 from the gal-
lop rhythms or from the summation gallop. Carotid sinus massage transiently slows
the heart and helps in timing the gallop rhythm.
Table 21.13 Early diastolic intervals
Interval Duration (s)
1. A2P2 during expiration 0.03

2. A2P2 during inspiration 0.040.05
3. A2S3 (physiological S3 in children) 0.120.20
4. A2S3 (pathological S3) 0.140.16
5. A2OS 0.030.15
6. A2pericardial knock 0.100.12
b) Pericardial Knock (PK)

It is an early diastolic rapid filling sound. The term pericardial knock was coined by
Dominic J Corrigan in 1842.52 The diastolic pericardial knock is characteristic of con-
strictive pericarditis occurring 0.100.12 s after A2 [while S3 occurs 0.140.16 s
(pathological) and 0.120.20 s (physiologoical) after A2] (see Fig. 21.27).
It is due to the sudden cessation of ventricular filling.53
It is best heard with the bell of the stethoscope in supine position along the left ster-
nal border in rigid constrictive pericarditis and infrequently in the subacute cases of
fibroelastic variety.
PK is earlier and higher frequency than typical S3 and so may be confused with an
opening snap of MS.
However, other clinical features such as elevated JV pressure with rapid y descent
and Kussmauls sign, systolic retraction of the apex (Broadbents sign) and conges-
tive hepatomegaly with ascites help in its detection.
c) The Fourth Heart Sound (S4)

The fourth heart sound is a low frequency late diastolic or presystolic sound heard dur-
ing atrial contraction (last rapid ventricular filling phase, see Fig. 21.28). It is also called
as a presystolic or an atrial diastolic gallop (even though it is ventricular in origin).
i) Characteristics of S4
S4 follows the onset of P wave of ECG by approximately 70 ms and precedes S1.
Presence of S4 indicates a hard working ventricle (while presence of S3 usually means
ventricular failure).
It may occur in elderly subjects (60 yrs) due to the loss of LV compliance with aging.
Presence of S4 or S3 results in triple rhythm (gallop), while occurrence of both S4 and
S3 produces quadruple rhythm.
During tachycardia (induced by mild exercise or forced coughing) or long PR inter-
vals, S3 may summate (fuse) with S4, producing a loud single summation gallop and
an incomplete summation simulates a diastolic rumble of MS.
A
V
X Y
S4 S3
A2 P S1 S2
S1 2
PK
Fig. 21.28 | Third and fourth heart sounds (S
and S ) with atrial pressure tracing
3
PK 4
S3 coincides with Y descent and S4
Fig. 21.27 | Pericardial
pericarditis.
knock (PK) in constrictive with last rapid filling phase following
atrial contraction (A).
ii) Mechanism of production of S4

(i) Prerequisites for genesis of S4
A healthy contracting atrium
Non-obstructive AV valve
Non-complaint ventricle
As the ventricular compliance decreases, atrial systole becomes responsible for more
than 25% of ventricular filling (which normally accounts for 15%) (rapid ventricular
filling phase: 85%, diastasis: 5%) and this vigorous atrial contraction is necessary to
produce S4. Therefore, it is not present in atrial fibrillation.
(ii) Theories for production of S4: These are similar to genesis of S3, ventricular and
impact theories have been proposed for the production of S4.
The ventricular theory: Rapid deceleration of in-coming blood in the ventricular
inflow during late diastolic filling sets the entire cardiovascular system into vibration
producing S4.49 This theory explains the S4 recorded in the ventricles or on the
epicardial surfaces.
The impact theory:50 S4 auscultated at the chest wall is due to dynamic impact of
the heart with the chest wall.
Similarly, the ventricular mechanism together with a dynamic impact of the heart
on the chest wall explains the presence of S4 in most diseases states.
iii) Causes of S4
a) Physiological S4 occurs in elderly subjects (60 yrs)54: recordable (in 50%) and
rarely audible
b) Pathological S4 occurs in:
(i) Excessive rapid late diastolic filling secondary to:
Hyperkinetic states (often associated with S
3 producing quadruple rhythm):
Anemia, thyrotoxicosis
Arteriovenous fistula
Acute valvular regurgitation: MR, TR, AR.
S4 is characteristic of acute MR,55 while S3 is characteristic of chronic signifi-

cant MR
The acute LA volume overload results in a forceful atrial contraction resulting in S4.
S4 is usually absent in MR of rheumatic etiology due to:
The chronicity of MR in which LV is dilated and complaint
Dilated unhealthy LA: LA is incapable of generating enough force
Often complicated by atrial fibrillation which results in the absence of atrial con-
traction and
Often associated with MS due to which enough atrial contraction cannot be
transmitted to LV.
In acute AR, S4 may be audible due to LA volume overload and decreased LV compliance
and its presence rules out associated MS.
(ii) Decreased ventricular compliance due to:

VENTRICULAR HYPERTROPHY: An echocardiographic finding of an increase in
wall thickness to cavity ratio is common in:
Concentric LVH due to:
Left ventricular outflow tract obstruction (moderatesevere AS)
Systemic hypertension (moderate-severe).
S4 in chronic hypertension: Audible S4 is a common feature in chronic hypertension
suggesting LVH and decreased compliance.
S4 in valvular AS
It indicates a significant LV-aortic gradient (peak systolic gradient of 70 mmHg
and left ventricular end diastolic pressure of 13 mmHg56) and significant AS.
Hence; when associated with MS or complicated with atrial fibrillation, S is masked
4
due to obliteration of the pressure gradient across the aortic valve.
S4 in hypertrophic cardiomyopathy: S4 is characteristic of hypertrophic cardiomyopathy
producing a typical triple apical impulse, and an absence of S4 makes its diagnosis unlikely.
Concentric RVH due to:
Right ventricular outflow tract obstruction (moderatesevere PS)
Pulmonary hypertension (moderatesevere)
S4 in pulmonary stenosis:
RV S correlates with a prominent a wave in the JV pulse and right ventricular end
4
diastolic pressure of 12 mmHg.
Occasionally, S in severe valvular PS may be long enough to be mistaken for presys-
4
tolic murmur of TS and inspiratory prominence of S4 is often accompanied by
decrease or disappearance of ejection click.
S4 in pulmonary embolism: Presence of S4 in a suspected case of pulmonary embolism
suggests a significant RV pressure overload.
ISCHEMIC HEART DISEASES:
Myocardial infarction: both acute and old
Angina pectoris
Ventricular aneurysm often associated with S3 (producing quadruple rhythm).
S4 in ischemic heart disease: S4 is a hallmark of ischemic heart disease.
S4, which is audible during anginal pain, may disappear after the administration of
nitroglycerine or after rest.
Persistence of S4 into the post-infarction period may indicate a higher risk for the
subsequent cardiac events.
Presence of S4 in an apparently healthy adult may be a harbinger of a future coronary
event.
A palpable S4 is common in LV asynergy or aneurysm.
(iii) Arrhythmias: S1 is loud with short PR interval while S4 is easily audible with long
PR interval i.e. in heart blocks.
Table 21.14 Causes of S4
Physiological Pathological
1. Elderly 60 yrs of age 1. Hyperkinetic circulatory states

2. Arteriovenous fistula
3. Acute mitral regurgitation, tricuspid regurgitation,
aortic regurgitation
4. Left ventricular outflow tract obstruction:
modsevere aortic stenosis
5. Modsevere systemic hypertension
6. Right ventricular outflow tract obstruction:
modsevere pulmonary stenosis
7. Modsevere pulmonary hypertension
8. Ischemic heart disease
9. Heart blocks
First-degree AV block as it further separates S4 from S1. S4 may be audible even in

the absence of significant cardiovascular disease.
Second-degree 2:1 AV block: Due to increased diastolic volume, S4 is audible (when
mitral valve is open).
Complete heart block: S4 is randomly heard throughout diastole when mitral valve
is open, and summation gallop may occur when S4 occurs simultaneously with rapid
early ventricular filling (see Table 21.14).
iv) Clinical recognition of S4

(i) LV S4:
LV S is best heard at the apex with bell of the stethoscope gently applied in left
4
lateral position during expiration.
Since its intensity is closely related to the left ventricular end diastolic volume,
any maneuver that increases venous return further separates it from S1 and
increases its intensity. Maneuver that decreases venous return does the opposite.
A loud S masks the audibility of a preceding S . So also, the presence of emphy-
1 4
sema and obesity mask S4.
(ii) S4S1 complex: S4 may be difficult to differentiate from S1.
However, S becomes attenuated or disappears with firm pressure on the stetho-
4
scope and in upright position.
S accentuates with handgrip, following sit-ups or coughing.
4
So also, maneuvers that increase venous return further separate it from S ,
1
enhancing its audibility (besides it is often palpable).
(iii) RV S4:
RV S is best heard with bell of the stethoscope at the lower left sternal border
4
during inspiration.
It is often accompanied by prominent a waves in the JV pulse and is occasion-
ally audible over the right jugular vein57 (see Fig. 21.29).
Elderly 60 yrs Physiological
Hyperkinetic states:
S4 1. Anemia 1. Acute MR
2. Thyrotoxicosis 2. Acute AR
3. AV fistula 3. Acute TR
Pathological
1. Moderatesevere 1. Moderatesevere PS 1. IHD: MI, angina

aortic stenosis 2. Moderatesevere PH 2. Ventricular
2. HCM 3. Pulmonary embolism aneurysm
3. Chronic systemic 3. Heart blocks
hypertension
Fig. 21.29 | Evaluation of fourth heart sound (S )AV: arteriovenous, MR: mitral regur-
4
gitation, TR: tricuspid regurgitation, AR: aortic regurgitation, AS: aortic
stenosis, PS: pulmonary stenosis, PH: pulmonary hypertension, HCM: hyper-
tropic cardiomyopathy.
Table 21.15 Characteristics of OS
Features Findings
1. Frequency High
2. Mobile leaflets and high Pre-requisite
atrial pressure
3. A2OS interval (0.030.15 s) Predicts left atrial pressure and severity of MS
4. Common causes MS, TS
MR, TR
VSD, PDA, ASD
Ebsteins anomaly, tricuspid atresia with ASD
d) Opening Snaps (OS)

The opening of the normal AV valves is noiseless, but with thickening and deformity
of the leaflets, a high frequency clicky sound is generated in early diastole, which is called
as opening snap. This term opening snap was coined by Thayer WS in 1908.58
i) Characteristics of OS:
OS is an early diastolic crisp, sharp sound, which correlates with the mobility of the
AV valve i.e. anterior mitral leaflet (AML) in MS and septal leaflet in TS.
The intensity of OS parallels the intensity of mitral component (M1) of S1. The
mobile valves in MS have a loud OS and an accentuated M1, while immobile valves
have an attenuated M1 and a decreased or absent OS, though OS may be found in
5060% of the calcified MS patients, since mere presence of valvular calcium does
not preclude the mobility of valve leaflets.
OS follows A2 by an interval of 0.03 to 0.15 s and A2OS interval has been used to pre-
dict the level of left atrial pressure (LAP) and the severity of MS59,60 (see Table 21.15).
ii) Mechanism of production of OS

(i) Prerequisites for genesis of OS
Thickened but mobile AV leaflets: immobile valve precludes OS as in severely calci-
fied MS
High atrial pressure ( LAP or RAP): OS may occur early or late depending upon
the atrial pressure
High velocity flow across AV valves causes rapid excursion of leaflets producing OS
in the absence of MS or TS.
(ii) Margolies and Wolferth theory: It is due to sudden stopping of the opening move-
ment of the valve.61 This has been confirmed by hemodynamic and angiographic studies.62,63
(iii) It is precisely phonocardiographically correlated with the maximum opening
motion of anterior mitral leaflet in MS,64 and near the O point of apex cardiogram.
Hemodynamically, OS occurs at the maximal MV opening shortly (2040 ms)
after LV-LA pressure crossover.
iii) Causes of OS
Stenotic OS in stenosed but mobile AV valves: MS, TS65
Non-stenotic OS66: Due to high velocity and increased flow across the AV valves
causing rapid excursion of the leaflets producing OS, which is often recordable than
audible (see Fig. 21.30).
(i) Mitral OS (ii) Tricuspid OS
Thyrotoxicosis66 TR
MR67 ASD (large)68
VSD (large)66 Ebstein anomaly
PDA TOF after shunt operation
Tricuspid atresia with a large ASD66
iv) A2OS interval can clinically predict LAP and thereby the severity of MS.
A2OS is 1/ to LAP i.e. higher the LAP (severe MS), earlier the OS (i.e. shorter
A2OS interval) whereas with lower LAP as in patients with mild MS, OS tends to
occur late (i.e. longer A2OS interval) (see Fig. 21.31). However, there is an imperfect
correlation between A2OS and mitral valve area (MVA).69
In mild MS: A OS interval is 120 ms with LAP of 15 mmHg (mean LAP
2
5 mmHg)
In moderate MS: A OS interval is 6080 ms with LAP of 20 mmHg (mean LAP
2
510 mmHg)
In severe MS: A OS interval is 4060 ms with LAP of 25 mmHg (mean LAP
2
10 mmHg)
Factors affecting A2OS interval: A2OS interval is unreliable in predicting the
severity of MS as many factors affect this relationship and hence the occurrence of a
wide A2OS interval cannot rule out tight MS. These factors include:
1. Heart rate
2. Peak systolic pressure
Opening
snap (OS)
Stenotic Non-stenotic Aortic diastolic

pressure
1. MS Aortic
2. TS Mitral OS Tricuspid OS pressure
LAP in
severe MS 25 mmHg
Thyrotoxicosis
1. ASD LAP in 20 mmHg
1. Large VSD 2. Ebsteins mod MS
2. PDA anomaly LAP in 15 mmHg
1. MR 3. T At with a 3. TOF after mild MS
large ASD TR shunt surgery
2. HCM Left ventricular
pressure
In mild,
Fig. 21.30 | Types and causes of opening snap (OS)
MR: mitral regurgitation, TR: tricuspid
Normal LAP
A2 moderate,
S1
severe
regurgitation, HCM: hypertropic car- OS MS (M1)
diomyopathy, MS: mitral stenosis, TS:
tricuspid stenosis, VSD: ventricular sep-
tal defect, PDA: patent ductus arterio- Fig. 21.31 | severe
A OS interval in mild, mod, and
2
mitral stenosis (MS) has an
sus, T At: tricuspid atresia, ASD: atrial
septal defect, TOF: tetralogy of Fallot. inverse correlation with left atrial
pressures.
3. Rate of decline of LV pressure during isovolumic relaxation (i.e. left ventricular end
diastolic pressure, LVEDP)
4. Factors affecting the velocity of MV opening such as AR, calcified MV, decreased
LV complaince (i.e. left ventricular dysfunction) increases A2OS interval.
Heart rate
(i) Tachycardia: A2OS interval due to the shortening of diastole and
(ii) Bradycardia: A2OS interval due to the prolonged diastole
(iii) In atrial fibrillation, A2OS interval varies with the cycle length. With a short
preceding PR interval, the LAP remains high and OS occurs early (i.e. short
A2OS interval); while with a longer preceding PR interval, the LAP declines
and OS occurs late (i.e. longer A2OS interval).
Hypertension: There is A2OS interval as LV systolic pressure takes longer time to
descend below the LAP and there is an early occurrence of A2.
Increased LVEDP as in LV failure, LV dysfunction (diastolic), CAD, and some cases
of cardiomyopathy: A2OS due to obliteration of the trans-mitral gradient.
Conditions affecting MV opening velocity: A2OS interval occurs in
calcified MV: due to late occurrence of OS
AR: due to the early occurrence of A2
LV compliance (LV diastolic dysfunction) due to obliteration of the trans-mitral
gradient.
Table 21.16 Characteristics of tumor plop
1. High pitched
2. Due to mobile atrial myxoma
3. Occurs earlier than S3
4. Occurs later than OS
5. Often occurs with diastolic rumble
AS: A2OS interval in AS is due to the delayed occurrence of A2

Low CO states as in severe RVF: A2OS interval due to the late occurrence of OS
as a result of lower LAP.
v) Absent OS in MS is noted in:
Severly calcified (immobile) mitral valve
Associated with significant MR
Associated with severe AR
Associated with severe AS
Associated with CAD and LV dysfunction.
vi) Clinical recognition of OS
(i) Mitral OS
As OS is a high frequency sound, it is best heard with diaphragm of the stethoscope
in the midprecordium between the left sternal border and just inside the apex with-
out any significant change with respiration.
It is often well heard at the base of the heart (pulmonary area) and may be confused
with S2 split.
The MDM follows the OS after a short interval.
It becomes more prominent with exercise.
A2OS interval: It sounds like a split S2 with the shortest interval (about 40 ms),
simulates wide fixed split of ASD with moderate A2OS interval and it may be mis-
taken for S3 of MR or severe heart failure with widest A2OS interval (120 ms).
(ii) Tricuspid OS
It is frequently not detected due to prominence of the findings of coexisting MS.
It is best heard with diaphragm of the stethoscope with the maximum intensity
closer to the left sternal border during inspiration.
When audible, it generally follows the mitral OS.
e) Tumor Plop (TP)

It is a high frequency early diastolic sound heard in left or right atrial myxomas70
(see Table 21.16).
The generation of tumor plop requires a mobile myxoma attached to the atrial sep-
tum by a long stalk.
It results from an abrupt diastolic seating of the tumor within the right or left AV
orifice70 i.e. it occurs at the maximal diastolic descent of the myxoma.
Table 21.17 Characteristics of systolic ejection sound (ES)
Aortic valvular ES Pulmonary valvular ES
1. High frequency sound with 1. High frequency sound

S1ES interval of 0.05 s
2. Coincides with anacrotic notch 2. Similar coincidence with pulmonary
of upstroke of aortic pressure artery pressure
3. Indicates mobile aortic leaflets 3. Indicates mobile pulmoanry leaflets
4. Defines left ventricular outflow tract 4. Defines right ventricular outflow
obstruction at valvular level tract at valvular level
5. Heard best at apex and aortic area 5. Heard best at pulmonary area
6. Does not vary with respiration (constant ES) 6. Accentuation with expiration
7. Associated with wide/reverse S2 splitting 7. Associated with wide S2 split and soft P2
8. Common causes: congenital bicuspid aortic 8. Common causes: valvular pulmonary
valve, valvular aortic stenosis, truncus stenosis (PS), tetralogy of Fallot (with
arteriosus valvular PS)
It may be confused with OS or S3 as it occurs later than OS and earlier than S3, but
intensity of TP and diastolic rumble may vary with patients body position.
The clinical features of atrial myxomas mimic those of mitral value disease especially
MS. However, often symptoms are sudden, intermittent and related to the patients
body position.71
The right atrial myxoma may also have a diastolic rumble, holosystolic murmur (of TR),
elevated jugular venous pressure with a prominent a wave and rapid y descent besides TP.
Familial myxomas which constitute 10% of all myxomas occurs more in young
females with an autosomal dominant transmission72 and are often associated with
other tumors, pigmentation, NAME (nevi, atrial myxoma, myxoid neurofibroma,
ephilides)72 or LAMB (lentigines, atrial myxoma, blue nevi)73 which are clubbed
together into a syndrome called Carneys syndrome or syndrome of myxoma.74
The Systolic Sounds

a) Systolic Ejection Sounds
The systolic ejection sounds are high frequency early systolic sounds originating from
the right or left side of the heart75 (see Table 21.17).
The ejection sounds originating from the valves (aortic or pulmonic) are called
valvular ejection sounds (see Fig. 21.32) and
Those originating from the roots of the great vessels are called vascular ejection sounds
(see Fig. 21.33).
i) Mechanism of production of systolic ejection sound
(i) Valvular ejection sounds: The ejection sound (ES) is caused by the abrupt cepha-
lad doming and halting movements of the SL valve at the onset of ejection, coinciding
with fully opened position of the valve.76
Prerequisites: Thickened mobile semilunar valves. In severe calcified valve (as in
severe AS), no excursion or piston-like ascent of the deformed valve is possible and
Fig. 21.32 | Valvular systolic ejection sounds. Fig. 21.33 | Vascular systolic ejection sounds.
therefore no sudden tensing of the valve leaflets or abrupt deceleration of the column
of blood occurs.
(ii) Vascular or root ejection sounds: The origin of this non-valvular ejection sounds is
less certain. It could be due to opening movement of the leaflets that resonate in the arte-
rial trunk or due to reverberations of the proximal arterial wall of the dilated great artery.
ii) Causes of ES
(i) Valvular ES
Aortic valve: Valvular AS, congenital bicuspid aortic valve, truncus arteriosus with
quadricuspid valves
Pulmonary valve: Valvular PS, TOF (with valvular PS)
(ii) Vascular ES
Due to an increased pressure beyond the valve:
Systemic hypertension
Due to an increased flow across the valve:
Hyperkinetic circulatory states e.g. anemia, thyrotoxicosis
Left to right shunt: ASD (pulmonary ES)
Due to dilatation of the vessel beyond the valve:
Dilatation or aneurysm of ascending aorta
Dilatation of pulmonary artery: due to increased flow, pulmonary hypertension,
idiopathic dilatation.
iii) Characteristics and clinical recognition of ES
(i) Aortic valvular ES
ES is a high frequency, sharp, discrete sound, similar to S1 in intensity and follows S1
by 0.05 s.
ES is coincident with the sharp anacrotic notch on the upstroke of the aortic pres-
sure tracing.
It defines the left ventricular outflow tract obstruction (LVOTO) at the valvular
level with mobile leaflets.
The intensity of ES correlates directly with the mobility of the valve, and not with
the severity of the obstruction.
It is best heard at the base (aortic area) and apex with the diaphragm of the stethoscope
in sitting and leaning forward position. It does not vary with respiration, i.e. it is a
constant ES (previously known as constant click). It may be loudest at the apex and
at times may be heard only at the apex especially in elderly patients or with COPD,
and may be mistaken for loud S1 or split S1.
The left ventricular end diastolic pressure (LVEDP) in AS does not vary with respi-
ration and is never higher than the aortic diastolic pressure (unlike valvular PS).
However, variable ES may be heard in large biventricular aorta of Truncus arteriosus
and TOF with PS. The mechanism of this variation is not known.
S2 is often normal or diminished in intensity but splitting is always abnormal i.e.
wide or reverse split.
In general, the presence of ES excludes supra- or subvalvular AS or HCM as a cause
of LVOTO and most often it indicates the diagnosis of bicuspid aortic valve.
Audible ES in a patient of coarctation of aorta implies a coexisting congenital bicus-
pid aortic valve, a common associated anomaly.
(ii) Aortic vascular ES
ES is similarly coincident with the complete opening of the aortic valve and upstroke
of the aortic pressure curve.76
It is poorly transmitted from the aortic area and is not well heard at the apex.
S2 is often loud and may be normal split.
(iii) Pulmonary valvular ES
ES also occurs at the maximal excursion of the stenotic pulmonary valve76 and
similar correlation with the pressure curve.77
It is best heard during expiration at 2nd and 3rd left intercostal spaces (but poorly audible
or inaudible at the apex) in sitting and leaning forward position with the diaphragm
of the stethoscope, unlike most right-sided auscultatory events. This variability of
the pulmonary valvular ES is related to the elevated right ventricular end diastolic
pressure (RVEDP) in moderate-severe PS. During inspiration, the increased venous
return to the RV leads to the elevation of RVEDP beyond the pulmonary diastolic
pressure (PADP) resulting in premature opening of the PV in diastole itself, and this
premature opening of the PV decreases the intensity of the ES during inspiration.
In very mild PS, there may not be respiratory variation in the intensity of ES while
in some severe PS, RVEDP may exceed the PADP throughout the respiratory cycle
and ES not audible.
S2 is usually wide split with P2 often soft or inaudible and usually delayed due to
very low pulmonary artery pressure.
(iv) Pulmonary vascular ES
ES is similarly coincident with the complete opening of the pulmonary valve and
occurs at the upstroke of the pulmonary artery pressure curve.76
ES is best heard at the pulmonary area and may also be heard lower down the ster-
num in sitting and leaning forward position during inspiration. It is often palpable
over the pulmonary artery.
P2 is often loud and S2 is usually narrow split.
b) Non-ejection Sounds or Systolic Clicks

Cuffer B in 1887 first described these sounds as a systolic gallop (bruit gallop).78
However, it was Carl Potain in 1894 who described these sounds as well localized, and
small short clicking sounds.79
i) Characteristics of non-ejection sounds (NES) or systolic clicks (SC)
These mid-to-late systolic sounds have sharp, high frequency and clicking quality
and the term click is appropriate.
The systolic click could be single or multiple and often occurs with late systolic
murmur in AV valve prolapse.
ii) Mechanism of NES: Initially in 1932, it was thought to be extracardiac in
origin.80
However, it occurs due to tensing of the redundant leaflets and elongated chordea
tendinea of the AV valves during systole81 which is confirmed by angiographic,82
intra-cardiac phonocardiographic,83 and echocardiographic studies.84
This systolic click coincides with the maximum systolic excursion of the prolapsed
leaflet into the atrium.
The multiple clicks occur because of asynchronous tensing of the different portions
of the redundant mitral leaflets, especially the triscalloped posterior leaflet.
iii) Causes of NES
SC is characteristic of the prolapse of the AV valves more commonly mitral valve
prolapse (MVP), but also tricuspid valve prolapse (TVP).
It has also been described in:
LV aneurysm
Aneurysm of the membraneous ventricular septum associated with VSD85
Incompetent heterograft valves86
Atrial myxomas87
Adhesive pericarditis and
Left-sided pneumothorax.88
iv) Clinical recognition of SC: Presence of SC is the diagnostic of MVP.
It is often associated with loud S1 and systolic murmur.
The clicks of MVP are better heard at the apex with diaphragm of the stethoscope
but if loud, it may be widely transmitted over the precordium, while the SC of TVP
is usually heard best at the lower sternal border.
The physical and pharmacological maneuvers that decrease the left ventricular end dias-
tolic (LVED) volume and LV size cause earlier and greater degree of prolapse that result
in earlier (closer to S1) and loud click.89 These maneuvers include standing, Valsalva
maneuver (phase II), nitroglycerine and amylnitrate inhalation (see Fig. 21.34).
The maneuvers such as squatting, supine position, vasopressor (phenyl epinephrine),
Valsalva maneuver (phase IV) and sustained handgrip which increase LVED volume
and LV size, reduce the degree of prolapse and the click is delayed or absent.
S1
S2
SC
Supine
S1
S2
SC
Standing
S1
S2
SC
Squatting
Fig. 21.34 | Impact of postural changes on systolic click (SC) in MVPstanding results
in an early occurrence of click, while click is delayed on sqatting.
Prosthetic Valve Sounds

The prosthetic valves normally produce murmurs and both opening and closing sounds
which may be systolic or diastolic depending upon the type of valve and its position of
implantation. The prosthetic valve sounds are of high frequency and clicky in quality,
hence are better heard with diaphragm of the stethoscope (see Table 21.18).
i) Both opening and closing sounds or clicks (OC, CC) are audible in:
Ball-in-cage valves: Starr-Edwards valves in both mitral and aortic position
Bileaflet valve: St Judes valves at aortic position
Porcine valves: However, OC is audible in 50% at mitral position and it is uncom-
mon at aortic position.
ii) Only closing sound (CC) is present in tilting disc valves. Only a soft OC may be
phonocardiographically demonstrable at the mitral position: Bjork Shiley, Lillehikaster,
Sri Chitra are the tilting disc valves.
Ball-in-Cage Valves (Starr-Edwards)

(i) In aortic position (see Fig. 21.35)
OC occurs 0.060.07 s after S1 and is coincident with maximal ball excursion.90
Table 21.18 Prosthetic valve sounds
Type Mitral position Aortic position
1. Ball-in-cage OC and CC with SEM OC CC, with SEM

2. Tilting disc CC, may OC, with SEM, and DM CC, with SEM, occasional DM
3. Bileaflet OC and CC, with SEM, may DM OC and CC, with SEM
4. Bioprosthetic CC, OC in 50% with SEM and DM CC with SEM
CC: closing click, OC: opening click, SEM: systolic ejection murmur, DM: diastolic murmur.
Fig. 21.35 | Starr-Edwards ball in cage valve. Fig. 21.36 | Meditronic Hall tilting disc valve.
Multiple CCs are produced when the freely moving ball bounces against the cage
during an early systolic ejection.91 These clicks are accompanied by 2/6 harsh sys-
tolic ejection murmur, but no diastolic murmur is audible.
OC is more prominent than CC in the ratio of 0.5.
Decrease in the intensity of the clicks or absence of OC indicates malfunctioning of
the valve.90
(ii) In mitral position
OC occurs 0.050.15 s after A2.92 Narrowing of this interval indicates an elevation
of LAP, which may be due to valvular obstruction or regurgitation.
A closing click accompanies the normal S1, which varies with changing RR intervals
of atrial fibrillation. CC is loudest with short RR intervals and soft with long RR
intervals.
These clicks are accompanied by 23/6 systolic ejection murmur, but no diastolic
murmur is audible.
Similarly, decrease in the intensity of the clicks occurs with the malfunctioning valve
or with severe LV dysfunction.93
Tilting Disc Valves (Meditronic Hall)

The malfunctioning valve, LV dysfunction, 1 AV block or other arrhythmias soften
the clicks (see Fig. 21.36).
Fig. 21.37 | St. Judes bileaflet valve. Fig. 21.38 | Porcine bioprosthetic valve.
i) In the aortic position

Only CC is distinct with 2/6 systolic ejection murmur and occasionally diastolic
murmur.
Similarly, CC is prominent with 2/6 systolic and diastolic murmurs.
OC may be demonstrable and occurs 0.050.09 s after A2. Shortening of this
interval (A2OC) is due to the elevation of LAP resulting from valvular obstruction
or regurgitation.
Bileaflet Valves (St. Judes)

Both OC and CC are common with a soft systolic ejection murmur.94
Similarly, malfunctioning of the valve or LV dysfunction result in muffling of the clicks
(see Fig. 21.37).
Bioprosthetic Valves (Porcine Valves)

(i) In aortic position
It is characterized by CC and 2/6 systolic ejection murmur.
OC and diastolic murmur are usually not audible (see Fig. 21.38).
CC is constant with 2/6 apical systolic murmur in 50% and diastolic murmur in
5070%.
OC is audible in 50% of the patients at an interval of 0.070.11 s after A2.
Extra-Cardiac Sounds
These include pacemaker sounds, pericardial rub and mediastinal crunch.
i) Pacemaker Sounds
These sounds are brief and high frequency sounds occasionally produced by transve-
nous pacemakers implanted in RV apex, due to stimulation of the intercostal muscles
(through intercostal nerves) by the endocardial electrodes.95
Pectoral muscles and diaphragmatic stimulation can also occur.
They occur synchronously with pacemaker spike and often associated with twitch-
ing of the muscles.
The audible high frequency pacemaker sounds always suggest myocardial perfora-
tion by the endocardial lead, although it is not always present.
ii) Pericardial Rub

Pericardial rub is the hallmark of pericardial inflammation.
a) Mechanism of production of pericardial rub (PR): It is due to the movement of
the parietal and visceral surfaces of the pericardium moving against each other.
b) Components of PR: The classic rub is triple phased: systolic, mid-diastolic and
late diastolic (or presystolic/atrial systole).
However, it is often biphasic, i.e. to and fro rubs due to ventricular systolic and atrial
systolic components.
The diagnosis is the simplest when all the three phases are present, which occurs
only in 50% of the cases. It is commonly audible in uremic pericarditis especially
when associated with hypertension.
The systolic phase is most consistent followed by the presystolic phase.
In the setting of atrial fibrillation presystolic component disappears.
c) Causes:
Acute pericarditis of any etiology: especially tubercular in origin
Following open heart surgery: post cardiotomy pericarditis
Uremic pericarditis
Rheumatic pancarditis
Acute phase of transmural MI giving rise to post MI pericarditis, which dramatically
responds to steroids
Infective endocarditis due to ring abscess.
d) Clinical recognition:
These friction rubs are high-pitched, leathery and scratchy in nature.
They are best heard over the 2nd and 3rd left intercostal spaces over the bare area of
the heart.
They seem close to the ear and are auscultated best with diaphragm of the stetho-
scope with the patient leaning forward or in knee-chest position and holding the
breath after forced expiration (see Fig. 21.39).
Unlike pleural rub, pericardial rub can be present even with large pericardial effusion
and cardiac tamponade.96
Occasionally, the short scratchy pulmonic ejection systolic murmur heard in hyper-
thyroidism (Means-Lerman sign) is misinterpreted as pericardial rub.97
Fig. 21.39 | Eliciting pericardial rub in knee-chest position.

iii) Mediastinal Crunch
It is a series of high-pitched scratchy sounds heard in mediastinal emphysema, which
is designated as Hammans sign.98
These sounds are common following cardiac surgery.
They occur most frequently during ventricular systole in a random fashion.
They may be prominent during different phases of respiration or different postures.
The mediastinal emphysema is clinically confirmed by noting the crepitations in the
neck secondary to subcutaneous air.
THE HEART MURMURS
Definition
Murmur is a Latin word. A heart murmur is defined as a prolonged series of audible
signals/vibrations of varying intensity (loudness), frequency (pitch), configuration, and
duration detectable with the aid of a sthetoscope.99
Mechanism of Production of the Murmurs

The sudden deceleration of blood results in heart sounds, while most of the murmurs
are produced by turbulent blood flow100 (see Fig. 21.40). Turbulence arises when the
Reynolds number reaches 2000, i.e.
When the blood flow velocity is high
Orifice (vessel/chamber) diameter is small or
Kinetic viscosity is low (as in anemia).
Therefore, turbulence (Reynolds number 2000) Flow/2 (diameter) (kinetic
velocity)
High flow Small orifice Low kinetic

velocity diameter viscosity
Turbulence
Vortex Eddies Periodic

Jet impact Cavitation Flitter
shedding formation wake
Murmur
Fig. 21.40 | Mechanism for production of murmurs.

Table 21.19 Turbulent blood flow
Causes of turbulence Consequences of turbulence
1. High blood flow velocity 1. Vortex shedding

2. Small orifice diameter 2. Jet impact
3. Low kinetic viscosity 3. Cavitations
4. Eddies
5. Periodic wake phenomenon
6. Flitter
Turbulence occurs when there is disproportion between the velocity of blood flow
and the dimensions of the orifice through which it flows.
It is the consequence of turbulence rather than turbulence itself that explains the
genesis of most of the cardiac murmurs. Rushmer RF described six theoretical conse-
quences of turbulence that may produce a heart murmur100 (see Table 21.19).
1. Vortex shedding of the orifices
2. Jet impact
3. Cavitations (micro-bubbles)
4. Eddies around the jet
5. Periodic wake phenomenon and
6. Flitter.
1. Vortex shedding: As the blood flow passes a narrow orifice, vortices produced at
the tip of the orifice are shed laterally to hit the vessel wall producing vibrations
and thereby a high-pitched (musical) murmur.
2. Jet impact: A jet of turbulent blood flow may directly hit the wall of the heart or
blood vessel producing vibrations and thereby a murmur.
3. Cavitations: A high turbulent blood flow can theoretically produce cavitations
(micro-bubbles) that generate a sound of different frequencies, which is often
described as a harsh murmur.
4. Eddies around a jet: A high velocity jet of blood produces eddy currents in the adja-
cent slow moving blood. These eddies cause vibrations in the surrounding soft tissues
that are transmitted to the skin surface, where they are appreciated as a murmur.
5. Periodic wake phenomenon: As blood passes to either side of a structure placed in its
path, a periodic wake phenomenon arises, producing relatively pure musical tones,
i.e. high pitched (musical) murmurs. This mechanism is akin to the Aeolian tones,
which are made by passing the wind through, along and across the cylinders.
6. Flitter: A high-speed jet of blood in a blood vessel may pull the walls of blood vessel
inward by Bernoulli effect. Variations in the speed of the jet, passing a particular point
in the vessel produces a continually varying strength of the Bernoulli effect, which in
turn causes the vessel wall to vibrate and generate a murmur. This is known as flitter.
Factors for the Production of Murmurs

According to Leatham, three main factors are responsible.101 However, most often a
combination of these factors is responsible for the production of murmurs.
High flow rate through normal or abnormal orifices
Forward flow through a constricted or an irregular orifice or into a dilated vessel or
chamber and
Backward or regurgitant flow through an incompetent valve, septal defect or PDA.
Characteristics of Murmurs
Following characteristics of the murmurs should be noted during auscultation:
Timing of the murmur in relation to the heart sounds (i.e. systolic/diastolic/continuous)
Location i.e. site of maximum intensity
Duration or length of the murmur
Intensity or loudness of the murmur i.e. its grade
Frequency or pitch of the murmur
Configuration or shape of the murmur
Transmission of the murmur (i.e. radiation or conduction) (site and direction)
Dynamic auscultation.
Timing of the Murmur

Cardiac murmurs should be timed and are classified into:
Systolic murmurs: Murmur begins with or after S1 and ends at or before S2.
Diastolic murmurs: Murmur begins with or after S2 and ends before the subsequent S1.
Continuous murmurs: Murmur begins in systole and continues without interruption
through S2 into all or a part of diastole. They usually have their peak intensity around S2.
Systolic and diastolic murmurs are sub-classified as early, mid, late or pan (holo).
(i) At normal heart rate, systole is shorter than diastole and identification of the
murmur is seldom difficult.
(ii) But timing of the murmurs may sometimes be difficult in the presence of rapid
heart rates.
In such conditions, the murmur can be timed by simultaneous palpation of the

lower right carotid artery or by identifying the loud S2 at the base.
However, if the murmur in question is at the apex, move the stethoscope from
the base to the apex while fixing the cardiac cycle in mind, using S2 as a refer-
ence point. This method of auscultation is known as inching technique of Harvey
and Levine.4
With sinus tachycardia, carotid sinus pressure may temporarily slow the rate and
make it possible to differentiate systole from diastole.
In the presence of extra systoles, identify the beat that follows a compensatory pause
and the first subsequent sound will be S1.
Location of the Murmur

It must be determined by careful auscultation as it may suggest its site of genesis. The
location of the murmur depends upon its site of origin and intensity and physical char-
acteristics of the chest.102
Murmurs at the apex:
(i) Murmurs heard only at the apex:
Mid diastolic murmur (MDM) of MS, functional MDM of MR
Systolic murmur (SM) of mild MR
Ejection systolic murmur (ESM) of calcified AS in elderly patients with
emphysema as:
Calcified valve results in the loss of jet effect and prevents conduction of the
murmur to the carotids
LV is exposed to the emphysematous chest wall only at the apex.
(ii) Murmurs best heard somewhere else but are also heard at the apex:
Early diastolic murmur (EDM) of AR
ESM of AS
MDM of TS
Pansystolic murmur (PSM) of TR
PSM of VSD.
(iii) Murmurs usually not heard at the apex:

Murmurs of right-sided origin, but can be audible when RV forms the apex
e.g. TS and TR murmurs

ESM of PS
EDM of PR.
Murmurs at the lower sternal area (tricuspid area, TA):

(i) Murmurs heard only at TA: SM of mild TR, MDM of TS (exceptions see above).
(ii) Murmurs best heard somewhere else but also heard at TA:
PSM of MR and VSD
ESM of AS and PS.
(iii) Murmurs usually not heard at TA: MDM of MS.

Murmurs at the left sternal border of 3rd intercostal space:

(i) Murmurs best heard in this area are:
PSM of VSD (commonest)
EDM of AR
ESM of infundibular PS.
(ii) Murmurs best heard somewhere else but also heard in this area are the murmurs
of valvular PS and TR.
(iii) Murmurs usually not heard in this area: MDM of MS.
Murmurs at the pulmonary area (PA) (2nd left intercostal space):
(i) Murmurs best heard at PA:
ESM of PS
Flow murmur of pulmonary origin in ASD
Continuous murmur of PDA
EDM of PR
Murmur of sub-pulmonary VSD.
(ii) Murmurs usually not heard at PA: MDM of MS and TS (see Table 21.20).
Murmurs at the aortic area (AA) (2nd right intercostal space):
(i) Murmurs best heard at the AA:
ESM of AS (valvular, subvalvular), aortic sclerosis
EDM of AR (aortic root origin).
(ii) Murmurs rarely heard at the AA: ESM of PS.

(iii) Murmurs never heard at the AA: MDM of MS.
Duration or Length of the Murmur

It may be short, long or holo (pansystolic/pandiastolic).
It depends on the duration of the event, such as the pressure gradient between the
two sites or cardiac chambers, and reflects the severity of the lesion. This is true in
all stenotic lesions: MS, AS, PS.
Even though the regurgitant murmurs are longer than the stenotic murmurs, the
length of a regurgitant murmur is not related to the severity of the lesion. e.g. MR,
VSD or TR. Long or short murmur may be associated with any degree of severity
and accompanying features are of diagnostic importance.
Table 21.20 Non-audible murmurs
At apex At pulmonary area
1. Systolic murmur of pulmonary stenosis 1. Mid diastolic murmur of mitral stenosis

2. Diastolic murmur of pulmonary regurgitation 2. Mid diastolic murmur of tricuspid stenosis
3. Murmurs of tricuspid stenosis and tricuspid regurgi-
tation (may be heard when RV forms the apex)
In AR: To some extent, length of the murmur correlates with the severity of the
lesion except in a few conditions such as acute AR, when complicated with LVF, and
when associated with systemic hypertension.
Intensity or Loudness of the Murmur

At bed side, the intensity of the murmur is graded from 1 to 6 as described by
Freeman and Levine (1933).103
1. Grade 1/6 murmur: the faintest murmur that can be heard only with special effort
(close concentration) and under optimal conditions (quiet room, relaxed patient
and clinician).
2. Grade 2/6 murmur: a soft or faint murmur that can be readily detected.
3. Grade 3/6 murmur: a moderately loud murmur without associated thrill.
4. Grade 4/6 murmur: a very loud murmur that is palpable (i.e. associated with thrill).
5. Grade 5/6 murmur: an extremely loud murmur that can be heard only if edge of
the stethoscope is in contact with the chest, but cannot be heard if the stethoscope
is removed from the skin. It is accompanied by a thrill.
6. Grade 6/6 murmur: exceptionally loud murmur that can be heard with a stethoscope,
which has just removed contact from the chest wall. It is accompanied by a thrill.
In general, systolic murmurs of grade 3/6 or more in intensity are usually hemodynam-
ically significant i.e. with few exceptions the intensity of the murmur is directly related
to the severity of the underlying condition, while a diastolic murmur of any degree of
intensity is organic in nature.
Factors affecting the intensity of the murmurs: The intensity or loudness of the mur-
murs is directly related to:
Quantity and velocity of blood flow across the sound producing area i.e. degree of
turbulence e.g.
High velocity of blood flow through a small VSD produces a loud murmur, while
a large flow at low velocity through an ASD produces no murmur.
So in high output (hyperdynamic) states, murmurs are accentuated while in
hypodynamic states (due to decreased cardiac output as in CHF) the intensity of
the murmurs is decreased.
Its distance from the stethoscope e.g. murmurs are accentuated in an individual
with thin chest wall.
Transmission qualities of the tissue between the origin of a murmur and a stetho-
scope e.g. obesity, emphysema, significant pericardial or pleural fluid will decrease
the intensity of a murmur.
Functional murmurs with thrill: Grade 4/6 murmurs are usually organic in nature
and are palpable (i.e. associated with thrill). However, there are some functional mur-
murs, which are accompanied by a thrill (see Table 21.21):
Thrill over the neck veins in venous hum
Diastolic thrill (functional MS) in severe MR
Systolic thrill over the carotids (functional AS) in severe AR
Table 21.21 Functional murmurs that are accompanied by thrills
Site Thrill Functional lesion Cause
1. Apex Diastolic Mitral stenosis Severe mitral regurgitation

2. Carotids Systolic Aortic stenosis Severe aortic regurgitation
3. Pulmonary area Diastolic Pulmonary regurgitation Severe pulmonary hypertension
4. Pulmonary area Systolic Pulmonary stenosis Mod-large atrial septal defect
5. Neck veins Continuous Mimicking patent ductus Cervical venous hum
arteriosus/AV fistula
Diastolic thrill (functional PR) in severe PH (especially in primary pulmonary

hypertension)
Systolic thrill in pulmonary area (mimicking PS) in moderate to large ASD.
Character and Frequency (Pitch) of the Murmur

These give a clue to the nature of their origin.
The frequency of a murmur like its intensity has a direct relationship to the velocity
of blood flow.104
(i) High pressure gradient between two sites/chambers results in high velocity flow
producing:
A high-pitched murmur (300 CPS) which could be soft (as in AR), blowing
(as in MR) or musical (as in papillary muscle rupture) in character.

A mixed frequency murmur [combination of high and medium (125300 CPS)
frequencies], which is harsh in character as in AS, PS, VSD.

(ii) Low pressure gradient between two sites/chambers results in low velocity flow
producing a low-pitched murmur (25125 CPS), which could be rough/rumbling
in character as in MS, TS.
In general, all regurgitant murmurs are high pitched and more widely audible, stenotic
murmurs of AV valves are low pitched and confined to the valve area of its origin. But
stenotic murmurs of SL valves are of mixed frequency, with its medium frequency
component best heard at the site of its origin, while high frequency component is more
widely audible and transmitted to other sites, e.g. ESM of AS soft at the apex while it
is harsh at the aortic area.
Configuration or Shape of the Murmurs (Murmur Envelope)

It is also related to the pattern of blood flow velocity and may help in identification of
nature of the lesion.
It is described as:
Crescendo (increasing) e.g. ESM of AS
Decrescendo (decreasing) e.g. EDM of AR
Crescendo-decrescendo (increasing-decreasing or diamond shaped) e.g. SM of
AS and PS
Plateau (even or unchanged) e.g. PSM of MR and
Table 21.22 Dynamic auscultation
Bedside maneuvers Heart sounds Heart murmurs
1. Inspiration RV S3 S4, tricusp OS; Right-sided murmurs

S2 split widens
2. Expiration LV S3 S4, mitral OS, pulmonary Left-sided murmurs except SM
ES; S2 split narrows of MR
3. Valsalva S3 S4; S2 split narrows SM of HOCM
SM of AS, PS, MR, TR
DM of AR, PR, MS, TS
4. Supine from standing RV S3 S4; later LV S3 S4; SM of PS, AS, MR, TR,
or sitting S2 split widens VSD; SM of HOCM
5. Squatting S3 S4 of both sides SM of PS, AS, MR, VSD
SM of HOCM
6. Isometric hand grip LV S3 S4 SM of MR, VSD; DM of MS, AR
SM of AS, HOCM
7. Amylnitrate inhalation S3 OS of both sides, S1; SM of PS, AS, TR; DM of MS,
A2, S3 of MR origin; TS, PR
A2-OS shortened SM of MR, small VSD, TOF; DM
of AR, Austin Flint M, diastolic
component of PDA
Variable (uneven) e.g. classical PSM of MR may have late systolic accentuation or
may taper off in late systole.
However, the true shape of a murmur is usually more difficult to determine clinically,
especially the diastolic murmurs than recording on a phonocardiogram.
Transmission of the Murmurs

A murmur may radiate or conduct to other sites. This is determined by its site of origin,
intensity and direction of blood flow as well as by the physical characteristics of the chest.102
Conduction of the murmur occurs when direct anatomical continuity is present e.g. SM
of AS is conducted to the carotids while PSM of MR is radiated to the left axilla or back.
Loud murmurs transmit widely while soft murmurs are confined to their area of origin.
High frequency sound/murmur transmits best proximal (upstream) to its origin
while low frequency sound/murmur transmits best distal (downstream) to its origin
e.g. harsh component of AS murmur is conducted to base and carotids, while higher
frequency vibrations of the murmur are best heard at the apex.
Low frequency sound/murmur transmits better through the thoracic tissue and is
readily felt as a thrill while a high frequency sound/murmur poorly transmits through
the thoracic tissue and is not accompanied by a thrill.
Dynamic Auscultation
Dynamic auscultation is the technique of altering circulatory dynamics by a variety of
physical and pharmacological maneuvers and determining the effects of these maneu-
vers on heart sounds and murmurs105 (see Table 21.22).
Types of bedside maneuvers

1. Physical: Respiration, postural changes, isometric hand grip, Valsalva and Muller
maneuvers.
2. Non deliberate: Changes in cardiac cycle length non deliberately due to PVC, atrial
fibrillation or heart blocks.
3. Pharmacological: By the use of vasoactive agents such as amyl nitrate, methoxam-
ine and phenylephrine.
1) Normal respiration
Normal physiological changes during respiration:
Inspiration results in changes in the systemic and pulmonary venous return.
(i) The inspiratory increase in systemic venous return due to fall in intra-thoracic
pressure.
Increases RV stroke volume and duration of RV ejection.
Decreases pulmonary vascular impedance thereby increasing the pulmonary
hangout interval (80 ms).
(ii) The inspiratory decrease in pulmonary venous return due to pooling of blood in
the pulmonary vasculature.
Decreases LV stroke volume and LV ejection.
Decreases hangout interval on the aortic side.
During expiration, the events are opposite to that of inspiration.
Effects on heart sound
(i) S2: Potaine in 1866 first noticed normal respiratory variation in the splitting of
S2. During inspiration, normal split of S2 into A2 and P2 occurs, while during expi-
ration S2 is heard as a single sound.
Mechanism of normal S2 split: See second heart sound.
(ii) S3, S4 and OS: RV S3 and S4 and right-sided OS increase in intensity with inspiration
due to increase in the RV stroke volume. So also, LV S3 and S4 and mitral OS are
accentuated with expiration due to an increase in LV stroke volume.
(iii) Aortic ejection sound:
Aortic valvular ejection sound does not vary with respiration i.e. it is a constant
ES (previously known as constant click) as LVEDP does not vary with respira-
tion and it is never higher than the aortic diastolic pressure.
However, ES is variable in a large biventricular Truncus arteriosus and TOF
with pulmonary atesia, but the mechanism of variable ES is not known.
Aortic vascular ES may increase with expiration.
(iv) Pulmonary ejection sound:
Pulmonary valvular ejection sound is best heard during expiration, and its
intensity decreases with inspiration.
Inspiratory increase of venous return and RV stroke volume leads to the eleva-
tion of RVEDP beyond the pulmonary artery diastolic pressure (PADP) causing
premature opening of the pulmonary valve in diastole itself and less upward
motion of the valve leaflets resulting in the decreased intensity of ejection sound.
Pulmonary vascular ES may increase with inspiration.
Effect on heart murmurs
(i) All right-sided murmurs are accentuated during inspiration including the TR
murmur (Carvallo sign) due to the increased RV stroke volume. Conversely, left-
sided murmurs except MR murmur are best heard during expiration when the LV
stroke volume is maximum.
(ii) The inspiratory decrease in LV stroke volume and LV size in patients with MVP
increases the redundancy of mitral valve and thereby increases the degree of valvular
prolapse which results in louder and early occurrence of midsystolic click and
murmur during systole.106
No Change
(i) However, patients complicated with RVF may not demonstrate inspiratory augmen-
tation of right-sided heart sounds and murmurs, as there is a little or no increase in
the systemic venous return due to high RVEDP. But when these patients are auscul-
tated on standing posture (thus reducing the resting right heart filling), expected
respiratory changes may be appreciated.
(ii) Aortic valvular ES: It does not vary with respiration.
(iii) MR murmur does not vary with respiration.
2) The Valsalva maneuver107: It was initially described in 1704 as a method for expelling
pus from the middle ear by straining with mouth and nose closed.34
It consists of a relatively deep inspiration followed by forced expiration against a
closed glottis for 1020 s or
Blowing into a BP manometer to maintain a level of 40 mmHg for 30 s.
It is helpful to demonstrate to the technique of performing this maneuver beforehand.
The normal response to the Valsalva maneuver consists of four phases:
(i) Phase I: As straining commences, intra-thoracic pressure increases which is asso-
ciated with:
A transient rise of LV output and systemic arterial pressure (see Fig. 21.41)
But there occurs a fall in heart rate.
(ii) Phase II (straining phase) is associated with perceptible decrease in systemic venous
return and stroke volume (initially right side followed by left side) which results in:
Decrease of systolic, diastolic and pulse pressures (small pulse) and
Reflex tachycardia.
(iii) Phase III (cessation of straining phase or release of Valsalva maneuver): Cessation of
straining results in:
Sudden increase in systemic venous return
But there is an abrupt, transient decrease in arterial pressure equivalent to the
fall in intra-thoracic pressure.

300
Arterial pressure (mmHg)

4
250
200
1 2
150 3
100
50
0
Fig. 21.41 | Normal systemic arterial pressure response to Valsalva maneuver in a

normal individual 1, 2, 3 and 4 are phases of Valsalva maneuver.
(iv) Phase IV (overshoot phase) consists of return of the events to pre-Valsalva levels
after 68 beats with:
A transient overshoot of systemic arterial pressure, wide pulse pressure and
Reflex bradycardia.
This occurs due to a transient rise in cardiac output as a result of:

Return of pooled blood in the venous system and
Reflex vasoconstriction and tachycardia secondary to low perfusion pressure of
the carotid and baro-receptors during phase III.
Hence; in normal individuals, arterial pressure tracing shows four distinct phases and
the ratio between the longest and shortest RR intervals is 1.6, which is described as the
Valsalva ratio.
Phase I and III are not usually perceptible at bedside.
Since coronary blood flow transiently falls during this maneuver, it should not be
performed in patients with ischemic heart disease.
Effects on heart sounds
(i) During phase II: S3 and S4 are attenuated and S2 split narrows (i.e. A2P2 interval
is narrowed or abolished).
(ii) During phase III: Due to a sudden increase in systemic venous return, right-sided
S3 and S4 augment and S2 split widens.
(iii) During phase IV: Left-sided S3 and S4 return to controlled levels and may tran-
siently be accentuated.
Effects on murmurs
(i) During phase II: As stroke volume and systemic arterial pressure fall, there is an
attenuation of the following murmurs:
Systolic murmurs of AS, PS, MR and TR
Diastolic murmurs of AR, PR, MS and TS.
(ii) During phase II: Reduction in LV volume and size leads to:
Increase in LVOTO with increased pressure gradient resulting in the amplifica-
tion of SM in patients with HOCM.

Increase in the degree of valve prolapse in patients with MVP resulting in loud
and early occurrence of mid systolic click and systolic murmur.

200
Arterial pressure
1 2
150 3
4
(mmHg)
100
50
0
Fig. 21.42 | Square wave arterial pressure response to Valsalva maneuver in a patient
with heart failure with severe LV dysfunction.
(iii) During phase III: Sudden increase in systemic venous return results in the aug-
mentation of right-sided murmurs.
(iv) During phase IV: Left-sided murmurs return to controlled levels and may tran-
siently be accentuated.
(v) Arterial pressure tracing in ASD, MS and heart failure:108 Phases I and III responses
are normal, but as baroreceptor reflexes are not activated, it results in:
The absence of a normal decrease in the arterial pressure during phase II and
No overshoot of arterial pressure during phase IV
1) This gives the arterial pressure tracing a square wave response (instead of
distinct four phases, see Fig. 21.42)
2) Valsalva ratio of 1.0 (instead of normal 1.6) and
3) Pseudo-normalization of transmitral filling velocity pattern on Doppler
echocardiography.
3) The muller maneuver109 is the converse of the Valsalva maneuver.
It consists of forced inspiration against closed glottis i.e. with closed nose and
firmly sealed mouth for about 10 s. This maneuver is less often used, as it is less useful.
Effects on heart sounds and murmurs: As this maneuver exaggerates the inspiratory
effort
S2 split is widened, RV S3 and S4 are accentuated and
All right-sided murmurs are augmented.
4) Postural changes
a) Sudden lying down from standing or sitting posture or sudden passive elevation
of both legs:
It results in an increase of systemic venous return which initially augments the RV
stroke volume followed by
Increased LV stroke volume and LV size after several cardiac cycles.
Widening of S2 split in both phases of respiration
Initially, RV S3 and S4 are accentuated and later after several cardiac cycles, LV S3 and S4
are accentuated.
Effects on the murmurs
(i) Due to increased stroke volume of both RV and LV, following systolic murmurs
are augmented:
SM of PS, AS
Fig. 21.43 | Auscultation in squatting position.
SM of MR, TR

SM of VSD

Functional systolic murmurs.
(ii) Due to increased LVED volume and LV size

SM of HOCM is diminished as the pressure gradient decreases.
Mid systolic click and late SM of MVP are delayed and may be attenuated as
there is little or no prolapse of the mitral leaflets.

b) Sudden standing or sitting up from supine position or sudden standing from squat-
ting position: Physiological changes and effects on heart sounds and murmurs are
opposite to that of sudden lying down position from standing or sitting position. But
no changes occur in patients with true fixed S2 split.
c) Squatting from standing posture: (see Fig. 21.43). It results in:
Increase of systemic venous return and stroke volume
Increase of systemic vascular resistance due to the kinking of iliac arteries and reduc-
tion of distending pressure of gravity on the lower limbs vessels and
Increase of systemic arterial pressure with a transient reflex bradycardia.
Effects on heart sounds: Due to increased venous return and stroke volume, S3 and S4
of both ventricles are accentuated.
(i) Due to increased venous return and stroke volume: Following murmurs become
louder with right-sided events preceding left-sided events.
SM of PS and AS
DM of TS and MS.
(ii) Increased LV size due to increased venous return and elevated arterial pressure
results in:
Decrease of LVOTO in HOCM causing decrease in the intensity of SM
Little or no prolapse in patients with MVP hence, mid systolic click and late SM
are delayed.
(iii) Due to increase in aortic reflex: The inaudible DM of AR becomes audible and
augmented.
(iv) Due to elevated systemic vascular resistance, right to left shunt is decreased with
increased pulmonary blood flow and immediate improvement in arterial oxygen
saturation and thereby alleviates the symptoms and intensity of SM in patients
with TOF.
(v) Due to elevated systemic vascular resistance and systemic pressure,
There is an increased regurgitant volume thereby resulting in the augmentation
of SM of MR.
Left-to-right shunt volume increases through VSD which results in a loud SM.
d) Left lateral recumbent position causes closeness of the heart to the chest wall and a
transient increase in heart rate.
Accentuates S1, LV S3 and S4, and mitral OS.
Accentuates MDM of MS, Austin Flint murmur of AR and SM of MR.
Accentuation and early occurrence of mid systolic click and late SM in MVP as a result
of increased prolapse due to increased heart rate and inotropism.
Occasionally, PVCs can occur and may help in differentiating SM of AS from that
of MR.
e) Sitting up and leaning forward positions causes more closeness of the base of the
heart to the chest wall.
Effects on heart sounds and murmurs:
Loud P2 and split S2 are more clearly audible.
Similarly, DM of AR and PR are more readily audible.
f) Knee-elbow position: This position brings closeness of the heart to the chest wall.
Effects: Pericardial rub becomes more prominent due to increased friction between
parietal and visceral pericardial layers.
5) Isometric exercise
Methods: It is done by sustained handgrip (isometric handgrip exercise, (see Fig. 21.44).
1. Ideally by using calibrated handgrip device simultaneously by both hands
2. By pressing a hand ball simultaneously with both hands or
3. By simply making a hand grip with both hands simultaneously
Sustained the handgrip for 2030 s
It should be simultaneously done by both hands
Fig. 21.44 | Auscultation with sustained handgrip by both hands.
Inadvertently doing Valsalva maneuver during handgrip must be avoided

It should be avoided in patients with ventricular arrhythmias and myocardial
ischemia.
Physiological effects: Isometric handgrip results in transient but significant increase in:
Systemic vascular resistance (SVR)
Arterial pressure
Heart rate
Cardiac output
LV filling pressure and size.
LV S3 and S4 is accentuated.
Effects on the murmurs110
DM of MS becomes louder due to the increased cardiac output.
Accentuation of DM of AR and SM of MR and VSD due to increased systemic vas-
cular resistance.
SM of AS is diminished as a result of reduction of pressure gradient across the aortic
valve due to an increase in arterial pressure and SVR.
As a result of increased LV volume and size,
SM of HOCM diminishes due to decreased pressure gradient
Mid systolic click and late SM of MVP are delayed due to decrease in prolapse.
6) Changes in cardiac cycle length due to arrhythmias (PVC and atrial fibrillation):
During the compensatory pause, that follows a premature ventricular contraction or
following a longer cycle lengths in atrial fibrillation, there is
An increase in the ventricular filling and ventricular size
In addition, there is secondary augmentation of ventricular contractility of the next
beat and transient elevation of the arterial pressure.
S1 SM S2 S1 SM S2 S1 SM S2
Carotid pulse
PVC
Fig. 21.45 | Increase intensity of SM in aortic stenosis after compensatory pause fol-
lowing premature ventricular contraction (PVC).
PSM PSM PSM PSM

S1 S2 S1 S2 S1 S2 S1 S2
PVC
Fig. 21.46 | No change in the intensity of PSM of mitral regurgitation following PVC.
The same observations may be made during transient slowing of the sinus rate by light
carotid sinus pressure.
Effects on heart sounds and murmurs: (see Figs 21.45 and 21.46)
Varying intensity of S1 is observed especially with atrial fibrillation.
SM of AS and PS accentuate due to ventricular filling i.e. prolonging the preceding
diastole and contractility.111
DM of AR becomes louder due to transient elevation in the arterial pressure.
SM of HOCM is augmented due to LVOTO as a result of ventricular contractility,
which is associated with decreased volume in the pulse (Brokenbrough Braunwald
sign).112
Mid systolic click and late SM of MVP are delayed because of decreased prolapse
due to increase in ventricular filling and LV size.
No change
SM of MR and VSD.
7) Pharmacological agents
a) Amyl nitrate inhalation: Place amyl nitrate on a piece of gauze and ask the
patient to take three or four deep breaths over 1015 s.
Physiological changes:105
It induces marked vasodilatation (due to SVR) with the reduction of systemic
arterial pressure in first 30 s.
After 3060 s, it is followed by reflex tachycardia, increase in cardiac output and
velocity of blood flow.
However, the major auscultatory changes occur in the first 30 s after inhalation.
S1 is augmented and A2 is diminished.
Mitral and tricuspid OS become louder and A2OS interval shortens as arterial
pressure falls.
S3 of either ventricle is augmented due to rapid ventricular filling, but S3 of MR origin
diminishes.
(i) Due to increased cardiac output, following murmurs are augmented:
SM of AS and PS
SM of TR
All functional SM
DM of MS and TS
DM of PR.
(ii) Due to SVR, following murmurs are diminished:

SM of MR and small VSD (see Table 21.23)
DM of AR
Austin Flint murmur of AR
Diastolic phase of continuous murmur of PDA
SM in TOF as decreased SVR and arterial pressure increases right-to-left shunt
and decreases the pulmonary blood flow.

(iii) Due to LV volume and size:
LVOTO increases and SM is accentuated in HOCM.
The degree of prolapse increases in MVP, and there is an early onset of mid systolic
click and late SM, but softening of SM due to decreased resistance to LV ejection.
(iv) Though presently amyl nitrate inhalation at the bedside is not routinely practiced, its
response is useful in distinguishing most of the common murmurs (see Table 21.23).
SM of AS (which is augmented) vs SM of MR (which is diminished)
SM of TR (which is accentuated) vs SM of MR (which is diminished)
SM of PS (which is augmented) vs SM of TOF (which is diminished)

Table 21.23 Useful maneuvers to differentiate similar murmurs
Murmurs Maneuvers Maneuvers
1. SM of AS vs HOCM Valsalva Squatting

SM of AS
SM of HOCM
2. SM of AS vs MR Amyl nitrate Post PVC
SM of AS
SM of MR No change
3. SM of MR vs TR Respiration
SM of MR No change
SM of TR Inspiration
4. SM of PS vs TOF Amyl nitrate
SM of PS
SM of TOF
5. SM of PS vs VSD Amyl nitrate
SM of PS
SM of VSD
6. DM of MS vs TS Respiration
DM of MS Expiration
DM of TS Inspiration
7. DM of MS vs AFM of AR Amyl nitrate
DM of MS
Austin Flint murmur
8. Ejection sound (ES) of PS vs AS Respiration
ES of PS Expiration Inspiration
ES of AS No change
DM of MS (which is augmented) vs AFM of AR (which is diminished)

EDM of AR (which is diminished) vs EDM of PR (which is augmented).
b) Methoxamine and phenylephrine: These vasopressor drugs are less commonly
used because of the inconvenience of intravenous administration and greater care
needed in titrating these drugs to achieve the desired effect.
Methods
35 mg of methoxamine IV is administered which elevates arterial pressure by
2040 mmHg for 1020 min.
But 0.30.5 mg of phenylephrine IV is preferred as it elevates the arterial pressure by
30 mmHg for only 35 min.
Physiological response: It is opposite to that of amyl nitrate inhalation.
It increases arterial pressure
It causes reflex bradycardia and decreased contractility and cardiac output
Hence, these drugs should not be used in patients with CHF and hypertension.
Effects on heart sounds and murmurs are opposite to those of amyl nitrate inhalation.
They are especially useful to elicit low intensity DM of AR and to verify AFM of AR,
which are augmented.
Midsystolic
Left sided Right sided
S1 A2 S1 A2 P2
Holosystolic
S1 A2 S1 A2 P2
Early systolic
S1 S2
Late systolic
S1 S2
Fig. 21.47 | Classification of systolic murmurs.

However, there is no change in the intensity of the murmurs with these drugs in the
following conditions:
SM of AS and PS (fixed ventricular outflow tract obstruction)
DM of PR and TS.
Systolic Murmurs
Classification of SM
Systolic murmurs are sub-classified according to their time of onset and termination
as113 (see Fig. 21.47):
Early systolic murmurs (ESM) begin with S1 and confine to early systole.
Mid systolic murmurs (MSM) begin after S1 and end before S2 (left-sided MSM
before A2 and right-sided MSM before P2).
Holosystolic or pansystolic murmurs (HSM/PSM) begin with S1, occupy all of sys-
tole and end with S2 (left-sided PSM end with A2 and right-sided PSM end with P2).
Late systolic murmurs (LSM) begin in mid to late systole and end with S2.
1. Early systolic murmurs (ESM): The early systolic murmurs are high pitch,
decrescendo in configuration, begin with S1 and end well before S2, usually at or before
mid-systole.
Causes: ESM are regurgitant murmurs due to the retrograde flow from a high pres-
sure cardiac chamber to a low pressure chamber and occur in:
Acute severe MR114
Acute TR with normal RV systolic pressure115
Small VSD or nonrestrictive VSD with PH.34
i) Acute severe MR: The regurgitation occurs into a relatively normal sized LA with
limited distensibility and as the LV-LA pressure gradient is abolished during late systole,
termination of retrograde flow and abbreviation of systolic murmur occurs well before
S2. It is often associated with expiratory S2 split, loud S4 with classic radiation of the
murmur and a tall v wave in left atrial pressure tracing. Common conditions that pro-
duce acute MR are:
Spontaneous rupture of chordae tendineae of a myxomatous valve
Subacute bacterial endocarditis of mitral valve
Papillary muscle rupture or dysfunction secondary to acute myocardial infarction
Disruption of mitral apparatus due to chest trauma.
ii) Acute TR: Due to low pressure gradient between RV-RA, the murmur is soft,
medium pitched and abbreviated but as usual augments on inspiration. It is associated
with RV S4 and tall v waves in jugular venous pulse. Acute TR occurs in:
Infective endocarditis in drug abusers
Carcinoid heart disease
RV infarction
Damage of tricuspid valve during open heart surgery or chest trauma.
iii) Small VSD: The murmur is high pitched and abbreviated as ejection continues,
ventricular size decreases, ventricular septum thickens which seals off the small defect
in the septum and ceases the flow. This type of VSD may spontaneously close as the
child grows.
Early SM may also occur in non restrictive VSD with an elevated pulmonary vascu-
lar resistance which decreases or abolishes the late systolic shunting.
2) Mid systolic murmur (MSM): The mid systolic murmurs are high to medium
pitched, crescendo-decrescendo in configuration, are often described as diamond-shaped
or spindle-shaped, and systolic ejection in nature that begin after S1 and end before S2.
The MSM begins after the semilunar valve opens due to the rise in ventricular pres-
sure and is due to flow across the LV or RV outflow tract that reflects the pattern of
phasic flow across the LVOT or RVOT.
As the flow proceeds, the murmur increases in crescendo and as the flow decreases,
the murmur decreases in decrescendo (see Fig. 21.48).
The intensity of the murmurs closely parallels changes in the cardiac output.
Conditions such as exercise, fever, anxiety, pregnancy and thryotoxicosis; which
increase the cardiac output and forward flow or conditions such as PVC, or associ-
ated AR and PDA that increase the stroke volume due to prolonged diastolic filling;
increase the intensity of the MSM.
Any condition such as CHF that decreases the cardiac output, or drugs that cause
negative inotopism such as beta blockers or associated proximal lesions such as MS,
MR and VSD will decrease the intensity of the murmur.
The response of the murmurs to various bedside maneuvers which alter the flow and
loading conditions of the heart (dynamic auscultation) and other auscultatory find-
ings will help in the definitive diagnosis of the MSM.
Aorta
L. atrium
L. ventricle
S1 MSM S1
Fig. 21.48 | Relationship of murmur to hemodynamics in aortic stenosismid systolic

murmur (MSM) is crescendo-decrescendo as the gradient is the greatest
in the middle of the systole.
Causes of mid systolic murmurs (MSM)

Due to the obstruction to ventricular outflow tract:
AS
HOCM
PS.
Functional:
Due to dilatation of aortic root
Due to dilatation of pulmonary trunk
Due to accelerated flow into the aorta or
Due to accelerated flow into the pulmonary artery.
Innocent mid systolic murmurs: Due to flow across the normal ventricular outflow
tracts.
MSM in MR: Due to papillary muscle dysfunction.
1. Aortic stenosis (AS): AS could be acquired or congenital, and congenital could be
valvular, subvalvular or supravalvular.
i) Acquired aortic stensosis
MSM is often harsh, medium pitched, and best heard at the 2
nd
right inter-
costal space and apex.
Depending upon the severity, it may have an early peaking and a short dura-
tion or late peaking and prolonged duration.

Due to high velocity jet within the aortic root, the murmur conducts into the
neck along the carotids.

It is associated with pulsus parvus et tardus, soft or absent S with single S or
2 2
reverse S2 split and S4.
Table 21.24 Systolic murmur of fixed vs dynamic aortic stenosis
Bedside maneuvers Fixed LVOTO Dynamic LVOTO (hypertrophic

(Aortic stenosis) obstructive cardiomyopathy)
1. Respiration No change May increase with expiration

2. Standing Decreases Increases
3. Squatting Increases Decreases
4. Valsalva Decreases Increases
Associated AR is common which increases the intensity of the murmur.

Systemic hypertension or coarctation of aorta if associated, obliterates the gra-

dient and decreases the intensity of the murmur

The elderly patients with aortic sclerosis or stenosis due to fibrocalcific changes
usually have Gallavardin dissociation i.e. two distinct mid systolic murmurs
are audiblethe noisy medium pitch murmur at the right base (due to turbu-
lence caused by the high velocity jet within the aortic root) and high frequency
musical murmur at the apex (due to periodic wake phenomenon caused by
high frequency vibrations of the fibrocalcific aortic cusps).116
ii) Congenital valvular aortic stenosis
MSM is best heard at the 2
nd
right intercostal space.
Associated systolic ejection sound is the hallmark of the congenital bicuspid
AS, the intensity of which correlates well with the mobility of the valve and not
with the severity of the obstruction.
S may be normal or single.
2
S and associated AR are common.
4
iii) Congenital supravalvular stenosis

MSM is prominent in the 1st right intercostal space and over the right carotid.
Characteristic elfin facies is common and right brachial and carotid are more
prominent as compared to the left side.
S2 is normal or single with S4 and associated AR is uncommon.
2. Hypertrophic obstructive cardiomyopathy (HOCM)
MSM is best heard at the apex and lower left sternal edge.
It is associated with brisk arterial pulse (carotids) or pulsus bisferience with double
or triple apex and S4.
A2 is of normal intensity and S2 may be single or reversed split.
Often, a late SM of MR is common due to the distorted mitral apparatus.
Bedside maneuvers i.e. dynamic auscultation help in the definitive diagnosis of
HOCM (see Table 21.24).
3. Pulmonary stenosis (PS): It could be valvular, infundibular or supravalvular.
i) Valvular pulmonary stenosis could be congenital (often) or acquired usually with
an intact ventricular septum.
MSM is best heard at the left 2nd3rd intercostal spaces which accentuates dur-
ing inspiration and may be conducted to the left supraclavicular and left side of
the neck.
It begins with pulmonary systolic ejection sound which accentuates with expi-
ration. But in severe PS, the ejection sound fuses with S1 and S4 appears.
The murmur may have an early peaking with a short duration or a late peaking
with a prolonged duration depending upon the severity of the obstruction (see
Fig. 21.49).
P2 becomes soft and S2 split widens with the increasing severity of stenosis.
However, it is difficult to appreciate the widening split at the bedside as P2
becomes progressively fainter and A2 is lost in the murmur.
Associated with prominent a waves in jugular venous pulse, left parasternal
heave and RV S4 which increases with inspiration.
Associated with PR in dysplastic pulmonary valve (as in Noonans syndrome)
or when complicated with infective endocarditis.
May have hypertelorism and moon face.
ii) Infundibular pulmonary stenosis is often associated with VSD (as in TOF, see
Fig. 21.50).
The MSM is best heard at the 3rd left intercostal space. It becomes shorter with
increased severity of the obstruction and may be accompanied by an ejection
sound due to the dilated aorta.
S1 S2
MSM
S1 S2
MSM
Mild
Mild
A2 P2
A2 P2
PES S1 S2
S1 S2 MSM
MSM
Moderate
Moderate
A2
A2 P2
PES
S1 MSM S2 S1 S2
Shortened
MSM
Severe Severe
S4
A2 P2
PES AES A2
Fig. 21.49 | Mid systolic murmur (MSM) in pul-

monary stenosisPES: pulmonary
Fig. 21.50 | Mid systolic murmur (MSM) in infundibu-
lar pulmonary stenosis as in tetralogy of
ejection sound. FallotAES: aortic ejection sound.
It shortens and decreases in intensity with amyl nitrate inhaltion.

P2 is often absent.

iii) Supra-valvular pulmonary stenosis or branch stenosis of pulmonary artery often

has characteristics facies.
It may be associated with supra-valvular AS.
The murmur is less harsh, high pitched with varying intensity and is best heard
at the upper left sternal border, infraclavicular region and laterally.

In pulmonary artery branch stensosis, the murmur is heard more laterally with
wide transmission to the right chest, back and both axillae.

It may become continuous with severe branch stenosis.
4. Functional MSM: These are short and soft and usually are grade 3/6.
(1) Due to dilatation of aortic root: Short soft MSM is best heard at the apex and
is present in elderly subjects with dilated sclerotic aorta.
(2) Due to dilatation of pulmonary artery
i) Idiopathic pulmonary artery dilatation
MSM is best heard at the pulmonary area and is often confused with ASD due
to the presence of wide expiratory S2 split.

However, X-ray chest PA and lateral views with no evidence of increased pul-
monary blood flow and echocardiogram will help in the definitive diagnosis.
ii) Dilated pulmonary artery secondary to pulmonary hypertension
Functional MSM is identified by the company it keeps i.e. associated promi-
nent parasternal heave, prominent a wave in jugular venous pulse, loud P2 and
RV S4.
A high pitched EDM of PR is often present.
(3) Due to increased flow into the aorta: Functional MSM due to increased cardiac
output and flow into the aorta occurs in:
Pregnancy
Thyrotoxicosis
Anemia
Fever
Exercise and
Peripheral arteriovenous fistula
In significant AR, functional MSM is secondary to a large forward stroke volume
and the murmur may be grade 4/6 associated with a thrill.
(4) Due to increased flow into the pulmonary artery: Functional MSM at the base
occurs due to an increased flow into the dilated pulmonary trunk secondary to signif-
icant left-to-right shunt due to:
ASD: Wide fixed S2 is the hall mark of ASD.
VSD: Holosystolic murmur along the left sternal border is usual.
Straight back syndrome and pectus excavatum117 may be confused with ASD as
expirartory S2 split is often audible. However, physical examination of the spine,
thoracic cage and sternum and X-ray chest will confirm the diagnosis.
5. Innocent MSM occurs without the evidence of physiologic or structural abnormal-

ities in the cardiovascular system. They are always grade 3/6 in intensity and with no
radiation to carotids or axillae. They occur due to flow across the normal LVOT or
RVOT. They are present in 3050% of children.
i) Innocent MSM due to flow across the normal LVOT or Stills murmur118
Stills murmur is common in young children of 38 yrs of age and usually dis-
appears by puberty.
It is related to a small ascending aorta diameter with a concomitant high aortic
blood flow velocity.119

It is a short medium frequency murmur and is croaking or buzzing in character.
rd
The murmur is best heard along the left sternal border at the 3 or 4th inter-
costal space.
ii) Innocent MSM due to flow across the normal RVOT or innocent pulmonary
MSM
It is also common in children, adolescents and young adults.
The MSM is low to medium frequency with a blowing quality.
It is best heard in the pulmonary area with radiation along the left sternal border.
6. MSM in MR:120 The MSM is usually due to the papillary muscle dysfunction as a
result of ischemic heart disease with an early systolic competence of the mitral valve and
midsystolic incompetence, followed by a late systolic decline in the regurgitant flow.
Holosystolic murmurs (HSM) or pansystolic murmurs (PSM): (holos entire) A
holosystolic or pansystolic murmur begins with S1, occupies all of the systole and ends
with S2 on its side of origin.
It is high pitched, blowing in quality and plateau-like in configuration.
HS murmurs are regurgitant murmurs produced by retrograde flow from a chamber
of high pressure to a chamber of lower pressure.101
Causes of HSM
Chronic MR
Chronic TR
Restrictive VSD
Aorto-pulmonary connection: AP window and PDA with PH (see Table 21.25).
(1) HSM in chronic mitral regurgitation (MR)
The murmur in chronic MR is holosystolic as the LV pressure exceeds LA through-
out the systole (see Fig. 21.51).
The classical HSM of chronic MR is high pitched, blowing in quality, plateau-like in
configuration with grade 3/6 in intensity, not accompanied by a thrill and with no or lit-
tle variation in intensity with respiration or changes in cardiac cycle due to arrhythmias.
It is best heard at the apex and radiates to:
The left axilla, angle of the left scapula and occasionally to the vertebral column
with bone conduction from the cervical to the lumbar spine when the regurgitant
jet is directed posterolaterally within the LA due to dominant involvement of
anterior mitral leaflet (as in rheumatic etiology).
Table 21.25 Differential diagnosis of holosystolic murmur
Features Mitral regurgitation Tricuspid regurgitation Ventricular septal defect
1. Best heard Apex Lower left sternal area Left sternal border in 3rd4th
intercostal space
2. Selective Radiation to axilla No selective No selective transmission
transmission and back transmission
3. Thrill Rare (with chordal Does not occur Common
rupture)
4. Character High pitched, soft High pitched, soft and Medium pitched, rough and
and blowing blowing harsh
5. Respiration No change During inspiration During expiration
6. Accompanying Eccentric left Right ventricular Biventricular enlargement and
features ventricular hypertrophy, prominent may have signs of PH
hypertrophy, S1, v in jugular venous pulse,
LV S3 signs of pulmonary
hypertension (PH)
Aorta
LV
LA
HSM
S1 S2
Fig. 21.51 | Relationship of holosystolic murmur (HSM) to hemodynamics in chronic

mitral regurgitationthe murmur is holosystolic as regurgitation persists
to the end of the systole. LV, left ventricular pressure, LA: left atrial pres-
sure, Aorta: aortic pressure.
The left sternal edge, base and may even radiate into the neck when the direction
of the intra-atrial jet is forward and medial against the interatrial septum due to
the dominant involvement of posterior mitral leaflet.
Often associated with muffled S1, a loud LV S3 is produced which is not a manifes-
tation of heart failure, but occurs due to the hemodynamically significant MR.
(2) HSM in high pressure tricuspid regurgitation (TR)

The murmur in TR is holosystolic when there is a substantial elevation of RV systolic
pressure usually secondary to PH or PS. However in organic TR, the murmur is non
pansystolic, lower in frequency and RV systolic pressure is normal (see Fig. 21.52).
PA
RV
RA
HSM
S1 S2
Fig. 21.52 | Relationship of holosystolic murmur (HSM) to hemodynamics in chronic

tricuspid regurgitationthe murmur is holo systolic as regurgitation per-
sists to the end of the systole. RV: right ventricular pressure, RA: right
atrial pressure, PA: pulmonary artery pressure.
Similarly, the murmur is soft, high pitched and blowing in quality with 3/6 in
intensity.
It increases its intensity with inspiration (Carvallos sign), but this augmentation is
absent when associated with organic TR or severe RV failure.
In severe RV failure; the RV fails to take up an additional venous return with
inspiration, fails to increase the cardiac output and thereby no augmentation of
the HSM occurs.
Associated organic TS prevents any further increase in venous return into the RV
and thereby HSM of TR fails to increase during inspiration.
It is best heard at the lower left sternal border (tricuspid area) with no selective radia-
tion. But the HSM may be heard to the right of the sternum and when the RV forms
the apex, it may be heard at the apex in which case it may be mistaken for MR.
It is associated with prominent v wave with a rapid y descent in jugular venous pulse
that augments during inspiration, left parasternal heave and RV S3.
(3) HSM in restrictive ventricular septal defect (VSD)
The murmur is holosystolic as the left ventricular systolic pressure and systemic vas-
cular resistance (SVR) exceed right ventricular systolic pressure and pulmonary vascular
resistance (PVR) from the onset to the end of systole.
The murmur is non pansystolic in large nonrestrictive VSD (0.8 cm2/m2), very
small VSD and multiple VSDs.
VSD murmur is absent in Eisenmengers VSD and only pulmonary ejection sys-
tolic murmur may be present.
Usually, the murmur is medium pitched, harsh in character, 4/6 grade in intensity
and is associated with a thrill.
It is best heard along the left sternal border in 3rd5th intercostal spaces during expi-
ration with no selective transmission.
However, in supracristal VSD, the murmur is best heard at the pulmonary area and
may be conducted to infraclavicular area and left neck. It may be confused for PS.
In Gerbodes defect (VSD of LV to RA), the murmur may be conducted to the
right of the sternum.
VSD of L-TGA may be best heard at the apex and may be mistaken for MR.
Valsalva maneuver and amyl nitrate inhalation decrease the intensity of the murmur.
(4) HSM in AP window and PDA with pulmonary hypertension: Rise in PVR abol-
ishes the diastolic portion of the continuous murmur and HSM may only be audible.34
Late systolic murmurs (LSM) begin in mid to late systole and proceed up to the S2.
Mital valve prolapse is the prototype of LSM which is due to the prolapse of posterior
mitral leaflet.
The murmur is high pitched, sometimes has a musical quality (whoop4 or honk121),
and is best heard at the apex frequently introduced by single or multiple non-ejection
clicks.
Bedside maneuvers which increase or decrease the LV volume and size alter the inten-
sity and length of the murmur (see hemodynamic ausculatation) (see Table 21.26 and
Fig. 21.53).
Diastolic Murmurs
Diastolic murmurs are subclassified according to their time of onset and termination
into:
Early diastolic murmur (EDM): It is confined to early diastole which begins with S2.
Mid diastolic murmur (MDM): It begins at a clear interval after S2 and ends before S1.
Table 21.26 Systolic murmurs
Early systolic Organic mid Functional mid Pan systolic Late systolic
murmur systolic murmur systolic murmur murmur murmur
1. Acute severe mitral 1. Aortic stenosis 1. Severe aortic 1. Mitral 1. MVP

regurgitation regurgitation regurgitation
2. Acute TR 2. HOCM 2. PH 2. Tricuspid
with normal RVSP regurgitation
3. Small ventricular 3. Pulmonary 3. ASD 3. VSD
septal defect (VSD) stenosis
4. Nonrestrictive 4. MR (papillary 4. VSD 4. AP window and
VSD with PH muscle PDA with PH
dysfunction)
5. Idiopathic
PA dilatation
6. Hyperkinetic
circulatory states
7. Stills innocent murmur
Late diastolic murmur (LDM) or presystolic murmur (PSM): It occurs in presystole

immediately before S1.
Pandiastolic murmur (PDM) or holodiastolic murmur (HDM): It begins with S2,
occupy whole diastole and ends with S1.
EDM and PDM are regurgitant murmurs due to the retrograde flow across an incom-
petent semilunar valve, while MDM and LDM are filling murmurs due to an obstruc-
tion to the forward flow across an AV valve.
1) Early Diastolic Murmurs (EDM)

These are SL valve regurgitation murmurs which begin with S2 (see Fig. 21.54).
They are high pitched reflecting the high velocity of the regurgitant blood flow from
the great vessels.
So also the shape and length (decresendo and short) of the EDM reflect the diastolic
pressure gradient between the aorta or pulmonary artery and respective ventricle
(see Fig. 21.55).
1. Small VSD
1. Acute MR 2. Nonrestrictive
2. Acute TR VSD with PH Late SM MVP
Early SM 1. AS MR due to
2. PS PM
Systolic 3. HOCM dysfunction
1. Chronic MR murmur (SM)
2. Chronic TR
Pan SM Mid SM
1. Restrictive VSD
2. PDA with PH
3. AP window Functional Innocent murmur:
with PH 1. Stills murmur
(child 38 yrs)
2. Pulmonary mid
SM (child and
1. ASD 1. Aortic root Significant AR Hyperkinetic young adults)
2. VSD dilatation states:
3. SB syndrome 2. PA dilatation 1. Pregnancy
3. PH 2. Anemia
3. Thyrotoxicosis
4. Exercise
5. AV fistula
Fig. 21.53 | Classification and causes of systolic murmursMR: mitral regurgitation, TR: tricuspid regur-
gitation, HOCM: hypertropic obstructive cardiomyopathy, AS: aortic stenosis, PS: pulmonary
stenosis, VSD: ventricular septal defect, PDA: patent ductus arteriosus, ASD: atrial septal
defect, PH: pulmonary hypertension, PM: papillary muscle dysfunction, PA: pulmonary artery,
SB: straight back, AV: arteriovenous, AR: aortic regurgitation, AP: aorto-pulmonary.
S1 A2 S1 A2P2
Fig. 21.54 | Early diastolic murmurs.
Aorta
L. atrium
L. ventricle
S1 S2 EDM
Fig. 21.55 | Relationship of early diastolic murmur (EDM) to hemodynamics in aortic

regurgitationEDM is due to diastolic pressure gradient.
Causes of EDM
Aortic regurgitation
Functional pulmonary regurgitation (Graham Steell murmur).
i) EDM in aortic regurgitation

The murmur is decrescendo, soft high pitched and blowing in character.
However EDM of acute severe AR is medium-pitched as the velocity of the
regurgitant flow is less rapid and relatively short as aortic diastolic pressure rapidly
equalizes with the steeply rising diastolic pressure of unprepared and nondilated LV.
A cooing dove or musical diastolic murmur occurs due to the rupture or retro-
version of an aortic cusp secondary to bacterial endocarditis or trauma122 and as a
complication of syphilitic AR.123
EDM is best heard in sitting and leaning forward position during a held deep expi-
ration along left sternal border in 3rd and 4th intercostal spaces (Neo aortic area) in
AR of valvular origin, while the AR murmur due to aortic root etiology is usually
best heard at the right 2nd intercostal space and to the right of the sternum.
In AR of valvular origin, A2 is diminished or may even be absent due to an inade-
quate coaptation of the deformed cusps.
Severe AR of valvular etiology is often associated with systolic ejection murmur in

the aortic area without significant associated AS and Austin Flint murmur at the
apex besides the classical peripheral signs.
Prompt squatting and isometric handgrip bring out the faint EDM, while amyl nitrate
inhalation decreases its intensity. So also, EDM of mild AR often disappears during later
stages of pregnancy due to decreased peripheral vascular resistance (SVR) (see Fig. 21.56).
ii) EDM in functional pulmonary regurgitation: The pulmonary annulus cannot
with stand high pressures unlike aortic annulus and the murmur occurs in the setting of
severe PH when the pulmonary artery systolic pressure (PASP) is systemic pressure.
Functional PR is usually secondary to:
Valvular lesions: such as severe MS or combined MS and MR with dominant
MS, usually of rheumatic etiology. It rarely occurs in pure MR and almost never
occurs with aortic valve disease.
Primary pulmonary hypertension.
Congenital heart disease (CHD) with left-to right shunt and severe PH which
often means inoperability.
Eisenmengers syndrome. Rarely, Graham Steell murmur may occur in cyanotic
CHD with increased pulmonary blood flow and severe PH as in TGA, DORV, sin-
gle ventricle or TAPVC.
Sometimes occurs in ASD without PH due to the dilated pulmonary artery and
increased pulmonary blood flow.
Rarely audible in end stage renal failure secondary to fluid overload and reflect
correctible pulmonary hypertension (PH).124
The Graham Steell murmur is a high velocity regurgitant flow murmur which is usually
short, high pitched and blowing in character beginning with loud P2. However, the
murmur may be pandiastolic in severe PH when pulmomary artery diastolic pres-
sure is 50 mmHg, as the length of the murmur reflects the duration of pressure
difference between pulmonary artery and right ventricle in diastole.
Chronic AR Acute AR
SEM EDM ESM EDM
Aortic
area
S1 S2 S1 S1 S2 S1
SEM
S3 S3
AFM ESM
AFM
Apex
Fig. 21.56 | Murmurs in chronic and acute aortic regurgitation (AR) auscultated at aor-
tic area and apexSEM: systolic ejection murmur, EDM: early diastolic
murmur, AFM: austin flint murmur.
The murmur is best heard at the pulmonary area and often during inspiration, but
may also be heard at the apex when the apex is formed by the right ventricle.
However, most often it is helpful from the company the murmur keeps i.e. loud P2,
prominent a waves in jugular venous pulse and left parasternal heave.
2) Pandiastolic or Holodiastolic Murmurs
In severe AR and PR, the murmur becomes pandiastolic, and the length of murmur
reflects the duration of the pressure difference between aorta and LV in AR and PA
and RV in PR during diastole.
3) Mid Diastolic Murmurs (MDM)
MDM are diastolic filling murmurs that begin at a clear interval after S2 in rapid ven-
tricular filling phase (see Fig. 21.57).
They are caused by the forward flow across the AV valves when the atrial pressure
exceeds the declining ventricular pressure (see Fig. 21.58).
They are low pitched and rumbling in character as the velocity of flow is relatively low.
S1 S2 S1
Fig. 21.57 | Mid diastolic murmur.
Aorta
L. atrium
L. ventricle
OS
S1 (loud)
S2
Pre SM MDM
0.07s
Fig. 21.58 | Relationship of murmurs to hemodynamics in mitral stenosismid diastolic

murmur (MDM) and presystolic murmur (Pre SM) are due to diastolic
pressure gradient across the mitral valve.
Causes of MDM (see Table 21.27)

i) Obstruction to the ventricular inflow
Obstruction to the LV inflow: MS, LA myxoma, Cortriatriatum, constriction around
AV groove.
Obstruction to the RV inflow: TS, RA myxoma, Carcinoid syndrome, Ebsteins
anomaly.
ii) Increased flow across the AV valve (diastolic flow murmurs)
Increased flow across the mitral valve i.e. mitral diastolic flow murmurs:
Severe MR
Left-to-right shunts (post-tricuspid shunts): VSD, PDA, AP window, RSOV into RV
Hyperkinetic circulatory states: Anemia, pregnancy, thyrotoxicosis
Complete heart block.
Increased flow across the tricuspid valve i.e. tricuspid diastolic flow murmurs:
Severe TR
Left-to-right shunts (pre-tricuspid shunts): ASD, RSOV into RA, LV to RA com-
munication (Gerbodes shunt), PAPVC, coronary artery to RA communication
Admixture lesions: TAPVC, single atrium.
iii) Mechanisms that interfere with AV opening:
Mechanisms that interfere with mitral opening:
Severe AR (Austin Flint murmur)
Table 21.27 Etiology of mid diastolic murmurs
LV inflow RV inflow Mitral diastolic Tricuspid diastolic MV opening PR with

obstruction obstruction flow murmurs flow murmurs interference no pH
1. Mitral 1. Tricuspid 1. Severe MR 1. Severe TR 1. Severe AR (Austin 1. Organic

stenosis stenosis Flint murmur) PR
2. Left atrial 2. Right atrial 2. VSD 2. ASD 2. Acute rheumatic
myxoma myxoma carditis (Carey
Coombs murmur)
3. Cor 3. Carcinoid 3. PDA 3. RSOV in to
triatriatum syndrome right atrium
4. Constriction 4. Ebsteins 4. AP window 4. PAPVC
around AV anomaly
groove
5. RSOV into 5. Coronary
right ventricle artery to RA
communication
6. Hyperkinetic 6. TAPVC
circulatory
states
7. Single atrium
RSOV: rupture of sinus of Valsalva, PAPVC: partial anomalous pulmonary venous connection, TAPVC: total anom-
alous pulmonary venous connection.
Mitral valvulitis of acute rheumatic carditis: Carey-Coombs murmur.

Mechanisms that interfere with TV opening: Severe PR with normal PA pressure
producing right-sided Austin Flint murmur.
iv) PR with no PH
1) MDM in mitral stenosis is a decrescendo diastolic filling rumble occurring in
the first rapid filling phase (see Fig. 21.59).
i) Pitch:
It is low pitched, rough and rumbling in character and sounds like a bullock
cart slowly moving on a wooden bridge or the sound of a bowling ball racing
down the alley.
It is low pitched as the pressure gradient across the valve is low.
However in a calcified immobile valve, a higher frequency murmur with less
intensity not accompanied by a thrill is often the auscultatory finding.

ii) Intensity:
The intensity of the MDM correlates poorly with the severity of the obstruction,
but the length of the murmur correlates well with the severity of the stenosis.
However, the duration of the murmur is unreliable indicator of the severity in
the following conditions:

Low cardiac output states such as severe RVF, severe PH where the murmur
appears shorter due to lower LA pressure.
Associated hyperkinetic circulatory states such as anemia, pregnancy, thyro-
toxicosis, anxiety where the murmur appears longer due to high cardiac output.
When associated with conditions with high LVEDP such as aortic valve disease,
CAD systemic hypertension where the murmur becomes shorter due to
obliteration of the transmitral gradient.
When associated with arrhythmias: In tachyarrhythmias, the murmur appears
longer due to shortening of the diastole. Gentle carotid sinus massage may
S1 S2 OS S1
PreSM PreSM
MDM
Mild MS
S1 S2 OS S1
PreSM
PreSM MDM
Severe MS
A2 P2
Fig. 21.59 | Murmurs of mitral stenosis (MS)MDM: mid diastolic murmur, PreSM:
presystolic murmur.
temporarily slow the heart rate, and thereby allow uncovering the potential
length of the murmur.
In bradycardia, the murmur appears shorter as diastole is prolonged.
In atrial fibrillation, the duration of the murmur is variable as diastolic cycle
lengths vary. However; if the murmur lasts upto S1 in longer cycles, it indi-
cates the severity of the MS.
iii) Site:
The murmur is well localized and best heard just medial to the apex in left lat-
eral position during expiration with the bell of the stethoscope.

In patients with severe emphysema, the murmur is best heard only at the
xiphisternum.
iv) Introduction:
The murmur is often introduced by a prominent OS (in mobile valve) and is asso-
ciated with a loud S1, presystolic murmur (accentuation) and a diastolic thrill.
However; in severe MS with severely calcified immobile valve, S is soft and no
1
thrill is palpable.
The A OS interval correlates with the level of LA pressure and thereby severity
2
of the stenosis may be clinically determined to some extent.
v) Dynamic auscultation:
The bedside maneuvers such as left lateral position, hand grip exercise and
amyl nitrate inhalation enhance the MDM of MS.

While the Valsalva maneuver diminishes the murmur.
2) MDM in tricuspid stenosis (TS) is often associated with MDM of MS and in

the presence of atrial fibrillation. However, the commonest murmur of TS is presys-
tolic with or without MDM.
The mid diastolic murmur of TS is earlier in onset and crescendo-decrescendo in
configuration as RA systole occurs earlier than that of the left.125
Similarly; it is low pitched, rough and rumbling in character as the pressure gradient
is low. However in RA myxoma, the murmur may be high pitched.
Similarly, the murmur may be introduced by a high pitched OS, which usually follows
mitral OS.
The duration of the murmur also correlates with the severity of the TS. However;
despite the presence of significant TS, the murmur is shorter in the following:
Associated MS with severe PH due to elevated RVEDP and
Ebsteins anomaly due to associated ASD.
The murmur is usually best heard in the tricuspid area during inspiration in right lat-
eral position or with passive leg raising.
TS is often accompanied by puffiness of the face, early edema of the legs, prominent
a waves (in absence of atrial fibrillation) with no history of PND.
3) MDM due to increased flow across the AV valve (functional AV stenosis)
Augmented volume and high velocity flow across the normal or insufficient AV
valves may result in short MDM.
It is often accompanied by S3, especially in the presence of MR or TR but without

presystolic murmur and S1 is usually diminished.
The murmur occurs during rapid closing motion of the AV valve suggesting a func-
tional obstruction during rapid diastolic filling phase.126
The tricuspid diastolic flow murmurs are usually softer in character, relatively
medium pitched and do not increase significantly during inspiration.
The mitral diastolic flow murmurs in left-to-right shunts indicate that the pulmonary
flow is atleast twice the systemic flow and are definite indication for hemodynamic
evaluation and closure of the shunt.
Short mid diastolic flow murmurs occur intermittently in complete heart block
when atrial contraction coincides with the rapid filling phase.
4) Austin Flint murmur (AFM): Original AFM is an apical presystolic murmur
described by A. Flint in1862 in patients with severe AR.127 (see Table 21.28) However,
it could be mid diastolic and/or presystolic murmur best heard at the apex with most
of the qualities of MDM of MS.
It is introduced by S3 rather by an OS and S1 is never accentuated but could be nor-
mal or diminished due to the premature closure of mitral valve.
The bed side maneuvers such as isometric handgrip exercise that accentuate the AR
murmur also increase the intensity of AFM, while amyl nitrate inhalation dimin-
ishes the murmur (MDM of MS is increased).
In acute severe AR, presystolic component of AFM is lost due to the marked eleva-
tion of LVEDP.
Right-sided AFM has been reported in association with severe PR due to PH.128
Pathogenesis of AFM: From the phonoechocardiographic, echo-Doppler and MRI
studies, the AFM in AR is due to the combination of the following:
(i) Regurgitant jet creating vibrations and turbulance in the following way:
Collision of the regurgitant jet with mitral inflow producing the turbulence
Table 21.28 Differential diagnosis of mid diastolic murmur (MDM) of mitral stenosis and Austin Flint
murmur of aortic regurgitation
Features MDM of mitral stenosis Austin Flint murmur
1. Etiology Organic mitral stenosis (rheumatic) Severe aortic regurgitation

(non rheumatic)
2. Diastolic thrill Common Rare
3. Introduce by OS LV S3
4. Presystolic murmur Usually present Absent in severe aortic regurgitation
5. Amyl nitrate inhalation Increases Decreases/disappears
6. Isometric handgrip Variable/increases Increases
7. S1 (with calcified and immobile valve) Normal/diminished
8. Atrial fibrillation Atrial fibrillation is common Usually sinus rhythm
9. Signs of pulmonary Common Unlikely
hypertension
Regurgitant jet impinging on anterior mitral leaflet (AML) producing the

vibrations of AML129
Regurgitant jet impinging on the myocardial wall producing the vibrations
(ii) Increased mitral inflow velocity creating a flow rumble

(iii) Due to rapid closing motion of the mitral valve leaflets during mid diastole and
presystole similar to MR and high output states130
(iv) Due to narrowing of the valve orifice by the regurgitant jet and
(v) Incomplete valve opening during mid diastole and presystole.131
5) MDM in organic pulmonary regurgitation (PR)
MDM is a feature of organic PR without PH as in:
Pulmonary valve endocarditis
Carcinoid syndrome
Dysplastic pulmonary valve
TOF with absent pulmonary valve or
Surgical procedures on pulmonary valve e.g. post balloon dilatation for PS, post
surgical valvotomy, after surgical repair of TOF.
It is a short crescendo-decrescendo murmur which begins well after P2 and ends well
before the subsequent S1. It is heard best at the pulmonary area during inspiration
and is accentuated in supine position or with passive leg raising.34
It is a low velocity retrograde flow and low pitched murmur often associated with a
systolic ejection murmur secondary to large RV stroke volume and a diminished or
absent P2.
The murmur is absent in early diastole (as in AR) as the diastolic gradient is negligible
and regurgitant flow is minimal. But as the RVEDP dips below the PADP in mid
diastole, the regurgitant flow is maximum with maximum intensity of the murmur.
Again, the late diastolic equilibration of pulmonary arterial and RV pressures eliminates
the regurgitant flow and abolishes the murmur (see Fig. 21.60).
4) Late Diastolic or Presystolic Murmurs (LDM/PreSM)

These occur in presystole immediately before S1. The presystolic murmur occurs in
rapid ventricular filling phase which coincides with the atrial systole.
Causes of presystolic murmurs:
AV obstruction: MS, TS
Complete heart block
Austin Flint murmur of moderate AR.
1) PreSM in mitral stenosis:
Presystolic murmur is a typical feature of rheumatic MS with sinus rhythm due to
an increased mitral inflow as a result of LA contraction132 (see Fig. 21.61).
However, presystolic accentuation may also be heard in patients of MS with atrial
fibrillation especially during short cycle lengths.133
It is a crescendo low pitched murmur audible upto S1.
20
PA
RV
0
MDM
S1 P2 S1
Fig. 21.60 | Relationship of mid diastolic murmur (MDM) to hemodynamics in organic

pulmonary regurgitation reflecting diastolic pressure gradient- pulmonary
artery (PA), right ventricular (RV) pressures.
MS TS PreSM
PreSM
S1 S2 S1
S1 S2 S1
Fig. 21.61 | Pre systolic murmur (PreSM)

Fig. 21.62 | Pre systolic murmur (PreSM)
in tricuspid stenosis (TS).
in mitral stenosis (MS).
2) PreSM in tricuspid stenosis:

The commonest murmur of TS is presystolic and typically occurs with sinus rhytm
and even in the absence of MDM.
The PreSM of TS is crescendo-decrescendo and relatively fades before S1.
As usual, the murmur accentuates during inspiration (see Fig. 21.62).
3) PreSM in complete heart block (CHB): Short crescendo-decrescendo presystolic
murmurs are occasionally heard in complete heart block when the atrial contraction
falls in late diastole. However, the murmur in CHB is usually mid diastolic (see Table
21.29 and Fig. 21.63).
Continuous Murmurs
A murmur that begins in systole and continues without interruption through S2 into
all or a part of diastole without change in the character of the murmur is defined as a
continuous murmur.99
Continuous murmurs are usually generated by uninterrupted flow from a high
pressure vascular bed into a low pressure vascular bed without phasic interruption
Table 21.29 Etiology of diastolic murmurs
Early diastolic Mid diastolic murmur Pre systolic murmur Pan diastolic
murmur murmur
1. AR 1. LV inflow obstruction: MS 1. MS 1. Severe AR

2. Functional PR 2. RV inflow obstruction: TS 2. TS 2. Severe PR
(Graham Steell
murmur)
3. Mitral diastolic flow murmurs: 3. AR (Austin Flint
severe MR, left-to-right shunts murmur)
(VSD, PDA)
4. Tricuspid diastolic flow murmurs: 4. Complete heart
severe TR, left-to-right shunts block
(ASD, RSOV into RA, PAPVC)
5. Severe AR (Austin Flint murmur)
6. Acute rheumatic carditis
(Carey Coombs murmur)
7. Organic PR
RSOV: rupture of sinus of Valsalva, PAPVC: partial anomalous pulmonary venous connection.
between systole and diastole. They have to be differentiated from to and fro murmurs
of VSD AR, AS AR, MS MR (see Fig. 21.64).
Causes of Continuous Murmurs:
1. Due to high to low pressure shunts
(i) From systemic artery to pulmonary artery
Aortic run off into pulmonary artery: PDA, AP window, truncus arteriosus
with pulmonary artery stenosis, surgically created aortopulmonary anastomosis

(Blalock, Waterston or Potts shunts).
Bronchial collaterals (bronchial to precapillary pulmonary arterial anastomosis
and resultant aortic pulmonary fistula): Pulmonary atresia, TOF.134

Anomalous left coronary artery from pulmonary artery (ALCAPA).
(ii) From systemic artery to right heart:

Aortic run off into right heart: RSOV into RA or RV.
Coronary cameral fistula: Coronary artery fistula into RA or RV (LA).
(iii) Other shunts:

Left to right atrial shunts with mitral valve obstruction: Lutembachers syn-
drome (MS with ASD), mitral atresia with ASD, Post PTMC.
Arteriovenous fistula.
Venovenous shunts: Anomalous pulmonary venous drainage, porto-systemic
shunt in cirrhosis of liver i.e. Cruveilheir Baumgarten syndrome.

2. Due to rapid blood flow
Cervical venous hum
Mammary souffle
1. AR 1. AR (AFM) 1. MS 1. Severe AR
PreSM
2. Functional PR (GSM) 2. CHB 2. TS 2. Severe PR
Diastolic
Early DM Holo DM
murmur (DM)
Organic PR
MD flow murmur:
Mid DM 1. Severe MR
LV inflow 2. Shunts: VSD, PDA, AP
obstruction: window, RSOV into RV
1. MS 3. Hyperkinetic states:
2. LAM anemia, pregnancy,
3. Cor at thyrotoxicosis
4. Complete heart block
RV inflow
obstruction: TD flow murmur:
1. TS 1. ASD
2. RAM 2. RSOV into RA
3. Carcinoid 3. Gerbodes
syndrome shunt
4. Ebsteins 4. PAPVC,
anomaly TAPVC
5. CA to RA
TV opening 6. SA
MV opening interference:
interference: Severe PR
1. Severe AR (AFM) with normal
2. Acute Rh PA pressure
carditis (CCM) (right-sided AFM)
Fig. 21.63 | Classification and causes of diastolic murmurs-VSD: ventricular septal defect,
PDA: patent ductus arteriosus, ASD: atrial septal defect, PH: pulmonary
hypertension, AR: aortic regurgitation, PR: pulmonary regurgitation, MR:
mitral regurgitation, MS: mitral stenosis, TS: tricuspid stenosis, AP: aorto-
pulmonary, RSOV: rupture of sinus of Valsalva, RV: right ventricle, RA: right
atrium, PAPVC: partial anomalous pulmonary venous connection, TAPVC:
total anomalous pulmonary venous connection, CA: coronary artery to right
atrial communication, SA: single atrium, LAM: left atrial myxoma, RAM:
right atrial myxoma, Cor at: Cor triatriatum, Rh: rheumatic, AFM: Austin
Flint murmur, CCM: Carey Coombs murmur, GSM: Graham Steell murmur,
PA: pulmonary artery, Pre SM: presystolic or late diastolic murmur, MD:
mitral diastolic, TD: tricuspid diastolic.
Hyperthyroidism
Hemiangioma
Hyperemia of neoplasm: Hepatoma, renal cell carcinoma, Pagets disease.
3. Secondary to localized arterial obstruction
Coarctation of aorta
Branch pulmonary artery stenosis
Carotid occlusion
Femoral artery occlusion
Celiac mesenteric artery occlusion
Renal artery occlusion.
S1 S2 S1
Continuous
murmur (PDA)
S1 MSM S2 EDM S1
To-Fro murmur
(AS and AR)
Fig. 21.64 | Continuous murmur in patent ductus

arteriosus (PDA) vs to and fro murmur
i.e. mid systolic murmur (MSM) of aortic
stenosis (AS) and early diastolic murmur Fig. 21.65 | PDA murmur is best heard in infra-
clavicular and pulmonary areas dur-
(EDM) of aortic regurgitation (AR).
ing expiration.
Table 21.30 Continuous murmur of PDA
Features Findings
1. Proper name Gibsons murmur

2. Frequency Combination of high and low
3. Character Rough machinery, crescendo-decrescendo murmur
peaking at S2
4. Best heard In left infraclavicular and pulmonary areas during
expiration
5. Isometric hand grip Augments the murmur
6. Valsalva maneuver Murmur decreases/disappears
7. Amylnitrate inhalation Diastolic component
1. Continuous Murmurs Due to High-to-Low Pressure Shunts

1) Continuous murmur in patent ductus arteriosus (PDA): The classic description of
the PDA murmur was given by George Gibson in 1900 and hence also known as
Gibsons murmur.135
It is classically described as a rough machinery murmur due to the combination of
high and low frequency vibrations and associated thrill is common.
It peaks at S2, after which it gradually wanes until it terminates before S1 (crescendo-
decrescendo murmur).
The murmur is best heard in the left infraclavicular and pulmonary areas during
expiration (see Fig. 21.65).
The systolic component is widely audible, while the diastolic component is
restricted to pulmonary and infraclavicular areas.
Isometric hand grip increases the intensity and duration of the murmur and may bring
out the diastolic component when it is not heard. The murmur decreases or disap-
pears with Valsalva maneuver (see Table 21.30).
Table 21.31 PDA with no continuous murmur
1. Young infants
2. Very small ductus
3. Very large ductus
4. With pulmonary hypertension
5. With Eisenmenger syndrome
6. When associated with:
(i) Preductal coarctation of aorta
(ii) Aortic stenosis
(iii) Large ventricular septal defect
The murmur is not continuous in the following conditions

In young infants (due to high pulmonary vascular resistance), when ductus is too
small (valve-like) or too large (when equalization of pulmonary and systemic pres-
sures occurs) the diastolic component may be very short or absent.
So also in severe PH as the pulmonary vascular resistance increases, PADP approaches
and reaches systemic levels, diminishing and finally abolishing the diastolic flow and
diastolic component of the murmur.
When associated with preductal coarctation of aorta (due to lower aortic pressure),
AS (due to lower aortic pressure and elevated LVEDP), large VSD (due to equalization
of pulmonary and systemic pressures), severe PH secondary to MS, peripheral pul-
monary artery stenosis.
When the equalization of pulmonary and systemic pressures occurs in Eisenmengers
syndrome, the systemic flow across the shunt diminishes and finally ceases leaving
the ductus silent (see Table 21.31).
2) Continuous murmur associated with bronchial collaterals: It is heard in the same
location as that of PDA, but radiates widely especially over the posterior thorax.
3) Continuous murmur in anomalous origin of left coronary artery from pulmonary
artery (ALCAPA): The murmur is continuous when the left-to-right shunt is large
and is usually best heard at left sternal border. The child may have chest pain with
ECG evidence of myocardial infarction.
4) Continuous murmur in RSOV (rupture of sinus of valsalva)
The murmur is usually continuous when RSOV occurs into RA or RV. It may be
continuous when RSOV occurs into LA.
But it is early diastolic when sinus of Valsalva aneurysm ruptures into LV. It also
becomes early diastolic when PH supervenes with high RVSP which shortens or
abolishes systolic flow and systolic component of the murmur.
It is more of a superficial murmur with very prominent diastolic thrill, which is
described as purring of a cat.
It is maximally heard at the lower left sternal border or over the xiphoid correspon-
ding to the fistulous tract.136 It is often well audible to the right of the sternum with
no significant changes with respiration.
5) Continuous murmur in coronary cameral fistula

In general, the murmur is soft, superficial and high pitched.
In 90%, coronary artery (CA) fistula drains into right heart and resultant murmur is
continuous. But in case of CA fistula draining into RV, the murmur softens during
systole (when the systolic flow decreases due to compression of the fistula during RV
contraction).
The murmur is louder in systole as the pressure gradient is more in systole in case of
CA fistula draining into RA or LA.
The murmur is not continuous if it empties into LV. It may be purely diastolic or
systolic and diastolic.
Continuous murmur is also absent and may be silent if multiple coronary artery fis-
tulas empty into pulmonary artery.
Site
The murmur is best heard either left or right of the lower sternal area when CA
drains into RA.
It is maximally heard at left mid to lower sternal border or in subxiphoid region in
CA draining into RV.
In CA draining into LA, it is best heard in upper to mid left sternal border and may
radiate leftward as far as the anterior axillary line.
6) Continuous murmur in left-to-right atrial shunts with MV obstruction
As in Lutembachers Syndrome, mitral atresia with ASD.
Continuous murmur is also heard when a small ASD is produced following
transseptal catheterization or percutenous transmitral commisurotomy (PTMC),
due to high velocity flow across the septal defect especially if the mitral obstruction
is not adequately relieved by the balloon valvuloplasty.
The murmur increases during inspiration and decreases with Valsalva maneuver.
7) Continuous murmur in venovenous shunts
Total anomalous pulmonary venous drainage into a systemic vein (usually superior
vena cava or innominate veins) may produce a continuous murmur (venous hum)
usually heard in pulmonary or left infraclavicular areas.137
Portosystemic shunts: In portal hypertension usually secondary to cirrhosis of liver,
tortuous collateral veins are seen radiating from the umbilicus (Caput medusae). A
continuous murmur (venous hum) may be heard over these collaterals (Cruveilheir-
Baumgarten syndrome) (see Fig. 21.66).
8) Continuous murmur in arteriovenous fistula
Arteriovenous fistulas could be congenital or acquired which give rise to continuous
murmurs.
Congenital AV fistulas include coronary arterial fistula, RSOV, ALCAPA
Acquired AV fistulas include surgically created fistula for hemodialysis, post-
traumatic or after catherization.
Fig. 21.66 | Aascontinuous murmur is heard over the Caput medusae which is described
Cruveilheir Baumgarten syndrome.
Systolic accentuation of the continuous murmur occurs in peripheral arteriovenous

fistulas and is best heard over the site of the fistula.
Local compression may:
(i) Decrease the intensity of the murmur by raising venous pressure and thereby
reducing the AV pressure gradient.
(ii) A baroreceptor-mediated reflex bradycardia may occur (Branhams sign) and
reflex tachycardia occurs on release (see Table 21.32).
2. Continuous Murmurs Due to Rapid Blood Flow

High velocity blood flow through veins and arteries may cause a continuous murmur.
1) The Venous Hum was first recognized by Potain in 1867.
The normal flow of blood across the normal veins in the neck is noiseless. But
increased velocity of blood flow gives rise to a continuous bruit over the neck veins
which is known as cervical venous hum.
It may be rough and noisy and typically louder in diastole.34
The venous hum is best heard in sitting posture with head rotated to the opposite
side and chin upwards, placing the bell of the stethoscope at the base of the neck in
between the two heads of the sternomastoid muscle and may be more prominent on
the right side. Sometimes it may radiate below the clavicles and may be confused
with the continuous murmur of PDA if not evaluated carefully (see Fig. 21.67).
The murmur is abolished by the digital compression of the internal jugular vein
with head in neutral position (see Fig. 21.68).
It is poorly heard in supine position, while
Anemia and thryotoxicosis initiate or reinforce the venous hum (see Table 21.33).
Table 21.32 Continuous murmurs
Due to high-to-low pressure shunts Due to rapid blood flow Due to localized arterial
obstruction
1. PDA 1. Cervical venous hum 1. Coarctation of aorta

2. AP window 2. Mammary souffl 2. Branch pulmonary artery
3. Truncus arterosus with PA stenosis 3. Hemangioma stenosis
4. Pulmonary atresia 4. Hyperthyroidism 3. Carotid occlusion
5. Blalock, Waterston and Potts shunts 5. Hyperemia of neoplasm 4. Femoral artery occlusion
6. ALCAPA (hepatoma, renal cell 5. Renal artery occlusion
7. RSOV into RA, RV carcinoma, Pagets 6. Celiac mesenteric artery
8. Coronay artery fistula into RA, RV disease) occlusion
9. Lutembachers syndrome
10. Mitral atresia with ASD
11. Post PTMC with ASD
12. AV fistula
13. TAPVC into systemic veins
14. Portosytemic shunt
RSOV: rupture of sinus of Valsalva, TAPVC: total anomalous pulmonary venous connection, PTMC: percutaneous
transmitral commisurotomy, ALCAPA: anomalous left coronary artery from pulmonary artery.
Fig. 21.67 | Maneuver to elicit the venous hum-

patients chin is pulled to the left and
Fig. 21.68 | Maneuver to abolish the venous hum by
digital compression of right internal jugu-
upward stretching the neck. lar vein with head in neutral position.
Causes of cervical venous hum include:

i) Physiological causes: Healthy children and young adults, later stages of pregnancy
ii) Pathological causes:
Hyperkinetic circulatory states (due to velocity and viscosity of blood): Anemia,
thyrotoxicosis, beriberi.
Intracranial AV fistula with bruit over the skull.
Compression of the jugular vein by the fascia or bony structures in the neck.
Table 21.33 The venous hum
Features Findings
1. Due to flow into Internal jugular veins

2. Character Rough, noisy, louder in diastole
3. Initiated or by Anemia, thyrotoxicosis
4. Abolished by Digital compression of internal jugular vein
5. Best heard with bell of the In sitting posture with head rotated to opposite
stethoscope side with chin upward at the base of the neck
Fig. 21.69 | Auscultation for mammary souffl.

Probable mechanism of the venous hum: The laminar flow in internal jugular vein
may be disturbed by the deformation of the vein at the level of the transverse process
of the atlas during head rotation designed to elicit the hum.138
2) The mammary souffl: (souffl puff in French) This innocent continuous
arterial murmur occurs in 1015% of pregnant women during 2nd and 3rd trimesters
and in early postpartum period in lactating mothers.139
It is due to increased blood flow to the breast tissue.
This medium to high pitched murmur is best heard over the breast on either side
between 2nd and 6th anterior intercostal spaces with no significant change with respira-
tion and may be confused with the continuous murmur of PDA or AV fistula.140
The mammary souffl usually begins after S1 with a distinct gap and systolic component
is the loudest.
Light pressure with the stethoscope augments the murmur, whereas the firm pressure
with the stethoscope or digital compression abolishes the murmur (see Fig. 21.69).
Valsalva maneuver has no significant effect on the murmur. It disappears after the
termination of lactation (see Table 21.34).
3. Continuous Murmurs Secondary to Localized Arterial Obstruction

Localized stenosis of systemic or pulmonary arteries produce a continuous murmur
or bruit if the obstruction is critical (80%) with no adequate collaterals so that a
Table 21.34 Mammary souffl
Features Findings
1. Type Continuous arterial murmur

2. Cause Blood flow to breast tissue
3. Occurs in 1015% of pregnant women in 2nd3rd
trimester and early post partum period
4. Frequency of the murmur Medium to high pitched
5. Description Begins after S1 with a definite gap, with
loudest systolic component
6. Light pressure over the breast Augments the murmur
7. Firm pressure over the breast Abolishes the murmur
8. Valsalva maneuver No effect on the murmur
9. Termination of lactation Murmur disappears
1. Cervical venous hum 1. COA

2. Mammary souffl 2. Branch PA
3. Hyperthyroidism stenosis
4. Hemiangioma 3. CA occlusion
5. Hepatoma, renal 4. FA occlusion
cell carcinoma 5. RA occlusion
Continuous 6. CMA occlusion
murmur (CM)
Rapid blood Localized arterial

flow obstruction
High to low
pressure shunts
Aortic runoff into PA: Other shunts:
1. PDA 1. Lutembachers
2. AP window syndrome
3. Truncus arteriosus SA to PA: 2. M At with ASD
with PA stenosis 3. Post PTMC
4. After shunt surgery 4. AV fistula
5. Anomalous PVD
6. CM syndrome
SA to right heart:
Bronchial collaterals: 1. RSOV into RA
1. P At or RV
2. TOF 2. Coronary
ALCAPA
cameral fistula
Fig. 21.70 | Classification and causes of continuous murmursPDA: patent ductus arte-
riosus, ASD: atrial septal defect, PA: pulmonary artery, M At: mitral atresia,
P At: pulmonary atresia, TOF: tetralogy of Fallot, AP: aorto-pulmonary, PTMC:
percutaneous transmitral commisurotomy, AV: arteriovenous, PVD: pul-
monary venous drainage, CM syndrome: Cruveilheir-Baumgarten syndrome,
RSOV: rupture of sinus of Valsalva, RA: right atrium, RV: right ventricle, COA:
coarctation of aorta, CA: carotid artery, FA: femoral artery, RA: renal artery,
CMA: celiac mesenteric artery, SA: systemic artery, ALCAPA: anomalous left
coronary artery from pulmonary artery, after shunt surgery e.g. Blalock,
Waterston and Potts shunts.
continuous pressure gradient is produced throughout the cardiac cycle and often
with systolic accentuation.141
With adequate collateral arteries, only systolic gradient persists with no diastolic
gradient across the obstructed artery as the collaterals around the obstructed artery
deliver adequate flow and hence only systolic murmur may be present.142
Continuous murmur in coarctation of aorta (COA) heard over the thorax is pro-
duced by rapid blood flow through tortuous intercostal collaterals. A continuous
murmur may also be produced at the site of coarctation and the murmur is best
heard over the back in the midline between the scapulae.143
Continuous murmurs may also be present in branch pulmonary artery stenosis or par-
tial obstruction of a major pulmonary artery occluded by a massive pulmonary embolus.
Other common causes of continuous murmur are carotid stenosis, femoral artery steno-
sis and renal artery stenosis which have characteristically louder systolic component
(see Fig. 21.70).
REFERENCES
1. Perloff JK. Physical examination of the Heart and Circulation. 2nd ed, Philadelphia. Saunders, 1990.
2. Harvey W. An anatomical disquisition on the motion of the Heart and Blood in animals. London,
1628 (translated from the Latin by Robert Willis, Barnes, Surrey, England, 1847). In Williams FA and
Keys TE (ed): Classics of Cardiology, Vol. 1, Malabar FL, Robert E, Krieger. Publishing Co., 1983.
3. Lennec RTH. Traite de lauscultation mediate, 2d ed. Paris: Brosson et Chaude: 1826.
4. Levine SA, Harvey SP. Clinical Auscultation of the Heart, 2d ed. Philadelphia, Saunders, 1959.
5. Dock W. Mode of production of the first heart sound. Arch Intern Med 1933;51:737746.
6. Leatham A. Splitting of the first and second heart sounds. Lancet 1954;267:607614.
7. Mills P, Craige E. Echophonocardiography. Prog Cardiovasc Dis 1978;20:337.
8. Shaver JA, Salerni R, Reddy PS. Normal and abnormal heart sounds in cardiac diagnosis:Part II.
Systolic sounds. Curr Probl Cardiol 1985;10(4):155.
9. OToole JD, Reddy PS, Cutiss EL et al. The contribution of tricuspid valve closure to the first
heart sound: An intracardiac micromanometer study. Circulation 1976;53(5):752758.
10. Burggraf GW, Craige E. The first heart sound in complete heart block: Phono-echocardiographic
correlations. Circulation 1974;50(1):1724.
11. Stept ME, Heid CE, Shaver JA et al. Effect of altering PR interval on the amplitude of the first
heart sound in the anesthetized dog. Cir Res 1969;25:255263.
12. Thompson ME, Shaver JA, Leon DF et al. Pathodynamics of first heart sound. In: Leon DF,
Shaver JA, eds. Physiologic principles of heart sounds and murmurs. (Monograph 46). New York:
American Heart Association, 1975:818.
13. Clarke WB, Austin SM, Shah PM et al. Spectral energy of the first heart sound in acute myocardial
ischemia. Circulation 1978;57:593598.
14. Ravin A. Auscultation of the Heart. 2d ed. Chicago: Year book, 1967.
15. Tej C, Shah PM, Cherian G et al. The correlates of an abnormal first heart sound in mitral valve
prolapse syndromes. N Eng J Med 1982;307(6):334339.
16. Burggraf GW. The first heart sound in left bundle branch block: An echophonocardiographic
study. Circulation 1981;63:429435.
17. Rytand DA. The variable loudness of the first heart sound in auricular fibrillation. Am Heart J
1949;37:187204.
18. Haber E, Leatham A. Splitting of heart sounds from ventricular asynchrony in bundle branch
block, ventricular ectopic beats, and artificial pacing. Br Heart J 1965;27(5):691696.
19. Milner S, Meyer RA, Venables AW et al. Mitral and tricuspid valve closure in congenital heart
disease. Circulation 1976;53(5):513518.
20. Hultgran HN, Leo TF. The tricuspid component of the first heart sound in mitral stenosis.
Circulation 1958;18(5):10121016.
21. Leatham A. The second heart sound, key to auscultation of the heart. Acta Cardiol 1964;19:395416.
22. Harris A, Sutton G. Second heart sound in normal subjects. Br Heart J 1968;30(6):739742.
23. Leatham A, Towers M. Splitting of second heart sound in health. In:Proceedings of the Thirtieth
Annual General Meeting of the British Cardiac Society, Glasgow, May 10, 1951;13:575.
24. Adolph RJ, Fowler NO. The second heart sound: A screening test for heart disease. Mod
Concepts Cardiovasc Dis 1970;39(4):9196.
25. Curtiss EI, Mathews RG, Shaver JA. Mechanism of normal splitting of second heart sound.
Circulation 1975;51:157164.
26. Shuler RH, Ensor C, Gunning RE et al. The differential effects of respiration on the left and right
ventricles. Am J Physiol 1942;137:620627.
27. Leatham A, Weitzman D. Auscultation and phonocardiographic signs of pulmonary stenosis.
Br Heart J 1957;19:303317.
28. Shapiro S, Clark TJ, Goodwin JF. Delayed closure of the pulmonary valve in obliterative pulmonary
hypertension. Lancet 1965;2:12071211.
29. Susman A, Kefer J, Kumar LV. Abnormal pulmonic sound during acute massive pulmonary
embolism. Chest 1978;74:4549.
30. Shaver JA, OToole JD. The second heart sound: Newer concepts. Part I: Normal and wide phy-
siological splitting. Mod Concepts Cardiovasc Dis 1977;46(2):712.
31. Adolph RJ. Second heart sound: Role of altered electromechanical events. In: Leon DF, Shaver
JA, eds. Physiologic Principles of Heart Sounds and Murmurs. Monograph 46. New York:
American Heart Association 1975:4557.
32. Perloff JK. Auscultation and phonocardiographic manifestations of pulmonary hypertension.
Prog Cardiovasc Dis 1967;9:303338.
33. Leatham A. Auscultation of the heart. Lancet 1958;2:703.
34. Perloff JK. The clinical recognition of congenital heart disease, 4th ed. Philadelphia, WB
Saunders, 1994.
35. Shaver JA, OToole JD. The second heart sound: Newer concepts. Part 2: Paradoxical splitting
and narrow physiological splitting. Mod Concepts Cardiovasc Dis 1977;46(3):1316.
36. Shaver JA, Kroetz FW, Leonard JJ et al. Effect of steady state increases in systemic arterial
pressure on the duration of the left ventricular ejection time. J Clin Invest 1968;47(1):217230.
37. Agnew T, Bucher H, McDonald L et al. Delayed closure of the aortic valve in ischemic heart
disease. Br Heart J 1967;29:775777.
38. Zuberbuhler JR, Bauersfeld SR. Paradoxical splitting of second heart sound in the Wolff-
Parkinson-White syndrome. Am Heart J 1965;70(5):595602.
39. Slodki SJ, Hussain AT, Luisada AA. The Q-II interval: III. A study of the second heart sound in
old age. J Am Geriatr Soc 1969;17:673679.
40. Curtiss EI, Shaver JA, Reddy PS et al. Newer concepts in physiologic splitting of second heart
sound. In: Leon DF, Shaver JA, eds. Physiologic Principles of Heart Sounds and Murmurs.
Monograph 46. New York: American Heart Association;1975:6873.
41. de Leon AC, Perloff JK, Twigg H et al. The straight back syndrome. Circulation 1965;32:193.
42. Sloan AW, Campbell FW, Henderson AS. Incidence of the physiological third heart sound.
Br Heart J 1952;2(4789):853855.
43. Reddy PS, Haider K, Meno F. Relation of intensity of cardiac sounds to age. Am J Cardiol
1985;55(11):13831388.
44. Tavel ME, Campbell RW, Feigenbaum H et al. The apex cardiogram and its relationship to
heamodynamic events with the left heart. Br Heart J 1965;27:829839.
45. Shaver JA, Reddy PS, Alvares FR. Early diastolic events associated with physiologic and patho-
logic S3. J Cardiol 1984;14(suppl V):3046.
46. Perloff JK. Physical examination of the Heart and Circulation. 3rd ed. Philadelphia. WB
Saunders, 2000.
47. Potain C. Du bruit de gallop. Gars d Hosp 1880;53:529.

48. Ozawa Y, Smith D, Craige E. Origin of the third heart sound: II. Studies in human subjects.
49. VandeWerf F, Minten J, Carmeliet P et al. The genesis of third and fourth heart sounds:
A pressure-flow study in dogs. J Clin Invest 1984;73(5):14001407.
50. Reddy PS, Meno F, Curtiss EI et al. The genesis of gallop sounds: Investigation by quantitative
phono- an apexcardiography. Circulation 1981;63(4):922933.
51. Van de Werf F, Geboers J, Math L et al. The mechanism of disappearance of the physiologic third
heart sound with age. Circulation 1986;73:877884.
52. Connolly DC, Mann RF, Dominic J. Corrigan (18021880) and his description of the pericar-
dial knock. Mayo Clin Proc 1980;55(12):771773.
53. Tyberg TI, Goodyer AVN, Langou RA. Genesis of pericardial knock in constrictive pericarditis.
Am J Cardiol 1980;46(4):570575.
54. Spodick DH, Quarry-Pigotti VM. Fourth heart sound as a normal finding in older persons.
New Eng J Med 1973;288(3):140141.
55. Cohen LS, Mason DT, Braunwald E. Signficance of an atrial gallop in mitral regurgitation.
56. Goldbatt A, Aygen MM, Braunwald E. Hemodynamic-phonocardiographic correlations of the
fourth heart sound in aortic stenosis. Circulation 1962;26:9298.
57. Fowler NO, Adolph RJ. Fourth sound gallop or split first sound? Am J Cardiol 1972;30:441444.
58. Thayer WS. The diastolic heart sounds. Trans Assoc Am Phys 1908;13:326357.
59. Bayer O, Loogen F, Wolter HH. The mitral opening snap in the quantitative diagnosis of mitral
stenosis. Am Heart J 1956;51(2):234245.
60. Oriol A, Palmer WH, Nakhjavan F et al. Prediction of left atrial pressure from the second-opening
snap interval. Am J Cardiol 1965;16:184188.
61. Margolies A, Wolferth CC. The opening snap (claguement douverture de la mitrale) in mitral steno-
sis: Its characteristics, mechanism of production and diagnotic importance. Am Heart J
1932;7:443470.
62. McCall BW, Price JL. Movement of the mitral cusps in relation to the first sound and opening
snap in patients with mitral stenosis. Br Heart J 1967;29(3):417421.
63. Thompson ME, Shaver JA, Heidenreich FP et al. Sound pressure and motion correlates in mitral
stenosis. Am J Med 1970;49(4):436450.
64. Salerni R, Reddy PS, Sherman ME et al. Pressure and sound correlates of mitral valve echocardio-
gram in mitral stenosis. Circulation 1978;58:119125.
65. Luisada AA, Slodke SJ, Krol B. Double (mitral and tricupid) opening snap in patients with valvular
lesions. Am J Cardiol 1965;16:800806.
66. Millward DK, McLaurin LP, Craige E. Echocardiographic studies to explain opening snap in
presence of nonstenotic mitral valves. Am J Cardiol 1973;31:6470.
67. Perloff JK, Harvey WP. Auscultation and phonocardiographic manifestations of pure mitral
regurgitation. Prog Cardivasc Dis 1962;5:172194.
68. Leatham A, Gray I. Auscultatory and phonocardiographic signs of atrial septal defect. Br Heart J
1956;18(2):193208.
69. Rahko PS, Shaver JA, Salerni R et al. Echophonocardiographic estimates of pulmonary artery
wedge pressure in mitral stenosis. Am J Cardiol 1985;55(4):462469.
70. Bass NM, Sharratt GP. Left atrial myxoma diagnosed by echocardiography with observations on
tumor movement. Br Heart J 1973;35(12):13321335.
71. Salcedo EF, Cohen GL, White RD et al. Cardiac tumors: Diagnosis and treatment. Curr Probl
Cardiol 1992;17:73.
72. Koopman RJ, Happle R. Autosomal dominant transmission of the NAME syndrome (nevi, atrial
myxoma, mucinosis of the skin and endocrine overactivity). Hum Genet 1991;86:300304.
73. Rhodes AR, Silverman RA, Harrist TJ et al. Mucocutaneous lentigines, cardiomucocutaneous myx-
oma and multiple blue nevi: The LAMB syndrome. Am Acad Dermatol 1984;10(1):7282.
74. Carney JA, Gordon J, Carpenter PC et al. The complex of myxoma, spotty pigmentation and
endocrine overactivity. Medicine 1985;64(4):270283.
75. Waider W, Craige E. The first heart sound and ejection sounds: echophonocardiographic correla-
tion with valvular stenosis. Am J Cardiol 1975;35:346.
76. Mills PG, Brodie B, McLaurin L et al. Echocardiographic and hemodynamic relationships of
ejection sounds. Circulation 1977;56:430436.
77. Martin CE, Shaver JA, OToole JD et al. Ejection sounds of right-sided origin. In: Leon DF,
Shaver JA, eds. Physiological Principles of Heart Sounds and Murmurs. Monograph 46. New
York: American Heart Association, 1975:3544.
78. Cuffer B. Nouvelle recherches sur le bruit gallop. Arch Gen Med 1887;1:131, 301.
79. Potain PC. Clinique medicale de la Charite. Paris, Masson, 1894. In McKusick VA: Cardiovascular
Sound in Health and Disease. Baltomore: Williams and Wilkins Co., 1958.
80. Gallavardin L. Nouvelle observation avec autopsie dun pseudodevoublement mitral. Prat Med
Fra 1932;13:19.
81. Reid JVO. Mid-systolic clicks. S Afr Med J 1961;35:353355.
82. Criley JM, Lewis KB, Humphries JO et al. Prolapse of the mitral valve: Clinical and cine-
angiocardiographic findings. Br Heart J 1966;28(4):488496.
83. Leon DF, Leonard JJ, Kroetz FW et al. Late systolic murmurs, clicks and whoops arising from the
mitral valve. Am Heart J 1966;72(3):325336.
84. Kerber RE, Isaeff DM, Hancock EW. Echocardiographic patterns in patients with syndrome of
systolic click and late systolic murmur. N Eng J Med 1971;284(13):691693.
85. Pickering D, Keith JD. Systolic clicks with ventricular septal defects: A sign of aneurysm of ven-
tricular septum? Br Heart J 1971;33(4):538539.
86. Killebrew E, Cohn K. Observations on murmurs originating from incompetent heterograft
mitral valves. Am Heart J 1971;81(4):490493.
87. Martin CE, Hufnagel CA, deLeon AC Jr. Calcified atrial myxoma: Diagnostic significance of the
systolic tumor sound in a case presenting as tricuspid insufficiency. Am Heart J 1969;78:245250.
88. Roelandt J, Willems J, van der Hauwaert LG et al. Clicks and sounds (whoops) in left-sided
pneumothorax: Clinical and phonocardiographic study. Dis Chest 1969;56(1):3136.
89. Bank AJ, Shaekey SW, Goldsmith SR, et al. Atypical systolic clicks produced by prolapsing mitral
valve masses. Am J Cardiol 1992;69:14911494.
90. Kotler MN, Mintz GS, Panidis I et al. Non invasive evaluation of normal and abnormal pros-
thetic valve function. J Am Coll Cardiol 1983;2(1):151173.
91. Simon EB, Kotler MN, Segal BL et al. Clinical significance of multiple systolic clicks from Star-
Edwards prosthetic aortic valves. Br Heart J 1977;39(6):645650.
92. Hultgren HN, Hubis H. A phonocardiographic study of patients with the Star-Edwards mitral
valve prosthesis. Am Heart J 1965;69:306319.
93. Kotler MN, Segal BL, Parry W. Echocardiographic and phonocardiographic evaluation of pros-
thetic heart valves. Cardiovasc Clin 1978;9(2):187207.
94. DePace NL, Kotler MN, Mintz GS et al. Echocardiographic and phonocardiographic assessment
of the St. Jude cardiac valve prosthesis. Chest 1981;80(3):272277.
95. Harris A. Pacemaker heart sound. Br Heart J 1967;29(4):608615.
96. Shaver JA, Leonard JJ, Leon DF. Examination of the Heart: Part 4, Auscultation of the Heart.
Dallas: American Heart Association; 1990.
97. Lerman J, Means. Cardiovascular symptomatology in exophthalmic goiter. Am Heart J 1932;8:
5565.
98. Hamman L. Spontaneous mediastinal emphysema. Bull Johns Hopkins Hosp 1939;64:121.
99. Soffer A, Feinstein A, Luisada AA et al. Glossary of cardiologic terms related to physical diagnosis
and history. Am J Cardiol 1967;20:285286.
100. Rushmer RF. Cardiovascular Dynamics, 3rd ed. Philadelphia: Saunders; 1970:305.
101. Leatham A. Systolic murmurs. Circulation 1958;17(4 Pt 1):601611.
102. Rushmer RF, Morgan CL. Meaning of murmurs. Am J Cardiol 1968;21(5):722730.
103. Freeman AR, Levine SA. Clinical significance of systolic murmurs: Study of 1000 consective
non-cardiac cases. Ann Intern Med 1933;6:13711385.
104. McKusick VA. Cardiovascular Sound in health and Disease. Baltomore: Williams and Wilkins, 1958.
105. Grewe K, Crawford MH, ORourke RA. Differentiation of cardiac murmurs by dynamic auscul-
tation. Curr Probl Cardiol 1988;13(10):671.
106. Barlow JB. Perspectives on the mitral valve. Phildelphia, FA Davis, 1987.
107. Nishimura RA, Tajik AJ. The Valsalva maneuver and response revsited. Mayo Clin Proc
1986;61(3):211217.
108. Schmidt DE, Shah PK. Accurate detection of elevated left ventricular filling pressure by a simpli-
fied bedside application of the Valsalva maneuver. Am J Cardiol 1993;71(5):462465.
109. Rotham A, Goldberger AL. Aids to cardiac auscultation. Ann Intern Med 1983;99:346.
110. McCraw DB, Siegel W, Stonecipher HK et al. Response of the heart murmur intensity to isomet-
ric (hand grip) exercise. Br Heart J 1972;34(6):605610.
111. Henke RP, March HW, Huktgren HN. An aid to identification of the murmur of aortic stenosis.
Am Heart J 1960;60:354363.
112. Brokenbrough EC, Braunwald E, Morrow AG. A hemodynamic technique for the detection of
hypertrophic subaortic stenosis. Circulation 1961;23:189194.
113. Lembo NJ, DellItalia LJ, Crawford MH, et al. Bedside diagnosis of systolic murmurs. N Eng J
Med 1988;318(24):15721578.
114. Sutton GC, Craige E. Clinical signs of acute severe mitral regurgitation. Am J Cardiol 1967;20(1):
141144.
115. Rios JC, Massumi RA, Breesman WT et al. Auscultatory features of acute tricuspid regurgitation.
Am J Cardiol 1969;23(1):411.
116. Gallavardin L, Pauper-Ravault. Le souffl du retre cissement aortique peut changer de timbre et
devenir musical dans se propagation apexienne. Lyon Med 1925:523.
117. deLeon AC Jr. Straight back syndrome. In: Leon DF, Shaver JA, eds. Physiologic Principles of Heart
Sounds and Murmurs. Monograph 46. New York: American Heart Association;1975:197208.
118. Still GF. Common Disorders and Diseases of Childhood. London: Frowde;1909.
119. Van Oort A, Hopman J, De Boo T et al. The vibratory innocent heart murmur in school children:
A case-control Doppler echocardiographic study. Pediatr Cardiol 1994;15(6):275281.
120. Perloff JK, Harvey WP. Auscultatory and phonocardiographic manifestations of pure mitral
regurgitation. Prog Cardiovasc Dis 1962;5:172194.
121. Rackley CE, Whalen RE, Floyd W et al. The precordial honk. Am J Cardiol 1966;17:509515.
122. Gelfand D, Bellet S. The musical murmur of aortic insufficiency: Clinical manifestations; Based
on a study of 18 cases. Am J Med Sci 1951;221(6):644654.
123. Stembridge VA, Hejtmancik MR, Herrmann GR. Unusual musical murmurs of anerior cusp aortic
regurgitation: Report of 10 cases. Am Heart J 1954;48(2):163172.
124. Perez JE, Smith CA, Meltzer VN. Pulmonic valve insufficiency: A common cause of transient
diastolic murmurs in renal failure. Ann Intern Med 1985;103(4):497502.
125. Wooley CF, Fontana ME, Kilman JW et al. Tricuspid sounds: Atrial systolic murmur, tircupid
opening snap, and right atrial pressure pulse. Am J Med 1985;78(3):375384.
126. Fortuin NJ, Craige E. Echocardiographic studies of genesis of mitral diastolic murmurs. Br Heart
J 1973;35(1):7581.
127. Flint A. On cardiac murmurs. Am J Med Sci 1862;44:2954.
128. Green EW, Agruss NS, Adolph RJ. Right-sided Austin Flint murmur. Documentation by intracardiac
phonocardiography, echocardiography and postmortem findings. Am J Cardiol 1973;32(3):370374.
129. Rahko PS. Doppler and echocardiographic characteristics of patients having an Austin Flint murmur.
Circulation 1991;83:19401950.
130. Fortuin NJ, Craige E. On the mechanism of the Austin Flint murmur. Circulation 1972;45(3):
558570.
131. Reddy PS, Curtiss EI, Salerni R et al. Sound pressure correlates of the Austin Flint murmur: An
intracardiac sound study. Circulation 1976;53(2):210217.
132. Wood P. An appreciation of mitral stenosis: I. Clinical features. BMJ 1954;1(4870):10511063:
contd.
133. Criley JM, Hermer HA. Crescendo pre-systolic murmur of mitral stenosis with atrial fibrillation.
N Eng J Med 1971;285(23):12841287.
134. Ongley PA, Rahimtoola SH, Kincaid OW et al. Continuous murmurs in tetrology of Fallot and
pulmonary atresia with ventricular septal defect. Am J Cardiol 1966;18:821826.
135. Gibson GA. Persistence of the arterial duct and its diagnosis. Edin Med J 1900;1:110.
136. Craige E, Millward DK. Diastolic and continuous murmurs. Prog Cardiovasc Dis 1971;14:
3856.
137. Keith JD, Rowe RD, Vlad P et al. Complete anomalous pulmonary venous drainage. Am J Med
1954;16(1):2338.
138. Cutforth R, Wiseman J, Sutherland RD. The genesis of the cervical venous hum. Am Heart J
1970;80(4):488492.
139. Tabatznik B, Randall TW, Hersch C. The mammary souffl of pregnancy and lactation.
Circulation 1960;22:10691073.
140. Hurst JW, Staton J, Hubbard D. Precordial murmurs during pregnancy and lactation. N Eng J
Med 1958;259(11):515517.
141. Myers JD, Murdaugh HV Jr, McIntosh HD et al. Observations on continuous murmurs over
partially obstructed arteries. Arch Intern Med 1951;10:361367.
142. Edholm OG, Howarth S, Sharpey-Schafer EP. Resting blood flow and blood pressure in limbs
with arterial obstruction. Clin Sci 1951;10:361367.
143. Spencer MP, Johnston FR, Meredith JH. Origin and interpretation of murmurs in coarctation of
aorta. Am Heart J 1958;56:722736.
BASIC INVESTIGATIONS
6A. CLINICAL ELECTROCARDIOGRAPHY

22. Introduction and basic concepts 459
23. The normal electrocardiogram 474
24. Abnormal P, T and U waves 490
25. Ventricular hypertrophy 500
26. Intraventricular conduction defects 516
27. Myocardial infarction and ischemia 533
28. Pericarditis and myocarditis 560
29. Drug effects and electrolyte abnormalities 568
30. Arrhythmias 580
CHAPTER 22
INTRODUCTION AND BASIC CONCEPTS
INTRODUCTION 459 c) Precautions to be Taken for

BASIC CONCEPTS 461 Recording an ECG 472
a) Electrophysiology of the Heart 461 REFERENCES 473
b) Electrocardiographic Instrument,
Recording Electrodes and Lead 466
INTRODUCTION
The electrocardiogram (ECG) is a graphic record of the electrical potentials produced

during heart beat. ECG of today is the product of a series of technological and physi-
ological advances occurred over the past two centuries.
The existence of electricity in the animal (animal electricity) was first suggested by
Edward Bancroft (1769, in torpedo fish)1 and substantiated by John Walsh (1773 in
eel)2 and Luigi Galvani (1780 in dissected frog) (see Table 22.1).
However; it was in 1842, when Carlo Matteucci, Professor of Physics at the University
of Pisa first showed that an electric current accompanies each heart beat in a dissected
frog,3 which was later confirmed by Rudolph von Koelliker and Heinrich Muller
in 1856.4
First successful attempt to record an ECG in humans was made by Alexander Muirhead,
a Telegraph engineer in 1869 at St. Bartholomews hospital, London, using Thomson
Siphon recorder.
Table 22.1 History of development of ECG
Discovery/invention Scientist
1. Animal electricity Bancroft (1769), Walsh (1773)

and Galvani (1780)
2. Electric current accompanies each Matteucci (1842), Koelliker and
heart beat (frog) Muller (1856)
3. Capillary electrometer Gabriel Lippmann (1872)
4. String galvanometer Willem Einthoven (1901)
5. Attempt to record ECG in humans Alexander Muirhead (1869)
6. Recorded first human ECG Augustus D Waller (1887)
7. Naming of deflections in ECG as PQRST Willem Einthoven (1895)
460 BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY
French Physicist Gabriel Lippmann invented (1872) capillary electrometer, a glass tube
with a column of mercury beneath the sulphuric acid, for which he was awarded
a Nobel Prize in 1908.
British Physiologists John Burden Sanderson and Frederick Page in 1878 first recorded
the hearts electric current with a capillary electrometer which consisted of two phases
from the ventricle of a frog.5
But it was in 1887 when Augutus D Waller, British Physiologist, at St. Marys Medical
school, London, recorded the first human ECG with a Lippmanns capillary elec-
trometer and labeled the deflections as V1, V2 and the third wave which was later
discovered as A.6
After witnessing the Wallers demonstration in 1889, the Dutch Physiologist
Willem Einthoven recorded ECG with an improved Lippmanns electrometer
in 1895 and named the deflections as ABCD and with a correction formula
as PQRST7 as per the mathematical convention derived from the French
Philosopher Descartes points on the curves (1662).8 His invention of string gal-
vanometer later in 1901 provided a reliable and direct method for recording ECG,
and by 1910 the string galvanometer emerged from the research laboratory in the
clinic.9
Subsequent improvement of the instrument and better understanding of the ECG
resulted in the wide use of ECG and has become an invaluable clinical tool for the
detection and diagnosis of a broad range of cardiac conditions.
Though at present not a sine qua non for the diagnosis of the heart diseases, it con-
tinues even 100 yrs after its inception to be the most commonly used cardiologic
test
For the diagnosis of the cause of chest pain
As a reliable tool for the diagnosis of acute myocardial infarction and dictates the
timely administration of life saving thrombolytic therapy
For the diagnosis and the management of cardiac arrhythmias
Can help with the diagnosis of the cause of breathlessness
For the diagnosis of pericarditis and
For assessing the electrolyte disorders, drug effects and toxicity (see Table 22.2).
A patient with an organic heart disorder may have a normal ECG and a perfectly
normal individual may show non-specific ECG abnormalities. Hence, a patient
should not be given an unwarranted assurance of the absence of heart disease solely on
the basis of a normal ECG.
Table 22.2 Utility of ECG in the current era
Diagnosis Management Assessment
1. Chest pain 1. Acute myocardial infarction 1. Electrolyte disorders

2. Acute myocardial infarction 2. Cardiac arrhythmias 2. Drug effects and toxicity
3. Pericarditis
4. Cardiac arrhythmias
INTRODUCTION AND BASIC CONCEPTS 461
BASIC CONCEPTS
The basic concepts are described as follows:

Electrophysiology of the heart
Electrocardiographic instruments, recording electrodes and leads
Precautions to be taken for recording an ECG.
a) Electrophysiology of the Heart

1) The Conduction System of the Heart
See Part-1: Basic anatomy and physiology: chapter 6.
2) The Contractile or Working Myocardial Cell

See Part-1: Basic anatomy and physiology, chapter 7:
a) Sarcolemmasee p57
b) Intercalated discssee p58
c) Sarcotubular systemsee p59
d) Diadic cleftsee p60
e) Contractile proteinssee p61
3) Electrical Activity of the Heart

a) Properties of the transmembrane potentials: see Part-1: Basic anatomy and physi-
ology, chapter 8
b) Recording of the electrical potentials (electrogram) produced by the normal
cardiac cell:
(i) Resting cell: In a resting cardiac muscle cell, molecules dissociate into positively
charged ions on the outer surface and negatively charged ions on the inner surface of
the cell membrane, and the cell is in an electrically balanced or polarized resting state.
If an electrode is placed on the surface of the resting cell, no deflection is recorded by
the galvanometer as entire cell surface has zero potential due to high impedance of the
cell membrane (see Fig. 22.1).
(ii) Depolarization: When the cell is stimulated (S) by an excitatory electrical wave,
the negative ions migrate to the outer surface of the cell and positively charged ions
pass into the cell, this reversal of polarity is called depolarization.
If an electrode is placed so that the depolarization wave flows toward the electrode,
a galvanometer will record a positive or an upward deflection.
When a depolarization current is directed away from an electrode, a negative or
downward deflection is recorded.
If an electrode (E) overlies the mid portion of the cell (muscle strip), the deflection
will be diphasic. The initial deflection is upward due to an advancing positive charge,
while the second deflection is downward due to the effect of passing negative charge
(see Fig. 22.2).

Electrical activity
Polarized resting state

no deflection

Depolarization
positive redeflection

Fig. 22.1 | Electrical activity in resting cell and effect of depolarization.

E E
Upward deflection Downward deflection

S S
Current flow towards the electrode Current flow away from the electrode
E

Diphasic deflection
S
Electrode overlying the mid portion of a cell
Fig. 22.2 | Depolarization wave in a single cell. E: electrode, S: stimulation.

E E
S
Two muscle strips of equal size
Fig. 22.3 | Depolarization wave in two cells of equal size. E: electrode, S: stimulation.
If two cells (muscle strips) of approximately equal size are stimulated at a central point,
a positive of equal magnitude is recorded at either end (see Fig. 22.3).
If two cells (muscle strips) of different sizes (e.g. RV and LV) are stimulated at a central
point, a large positive deflection is recorded over the large cell (muscle mass) and a small
positive deflection followed by a deep negative deflection or entirely negative deflection
is recorded over the smaller cell surface (muscle mass) (see Fig. 22.4).

OR E
S
Two muscle strips of different sizes
Fig. 22.4 | Depolarization wave in two cells of unequal size. E: electrode, S: stimulation.

E E E E
S
Depolarization towards the electrode Repolarization in the opposite direction
Fig. 22.5 | Repolarization in the opposite direction of depolarization. E: electrode, S: stimulation.

E E E E
S
Depolarization towards the electrode Repolarization in the same direction
Fig. 22.6 | Repolarization in the same direction of depolarization. E: electrode, S: stimulation.
(iii) Repolarization: During recovery period, positively charged ions return to the
outer surface and negatively charged ions move into the cell. The electrical balance of the
cell is restored; this process of return of the stimulated cell to the resting state is known
as repolarization.
If the repolarization occurs in a direction opposite to that of depolarization, the deflec-
tion will be in the same direction as that produced by depolarization (see Fig. 22.5).
If the repolarization occurs in the same direction as that of depolarization, the
deflection will be opposite to that of depolarization (see Fig. 22.6).
c) Intracellular and extracellular ion concentrations: see Part-1: Basic anatomy
and physiology, chapter 8.
The transfer of the Na and K ions across the cell membrane plays an important
role in generating cardiac electrical activity.
Intracellular concentration of K is 30 times greater than extracellular K. Na
concentration is 30 times less inside the cell as compared to outside.
Because of this ionic composition, membrane of the resting cardiac fiber is in an
electrically balanced or polarized state.
d) Origin and sequence of cardiac activation: see Part-1: Basic anatomy and
physiology, chapter 8.
e) Phases of cardiac action potential: see Part-1: Basic anatomy and physiology,
chapter 8.
f) The modifying transmission factors: These factors affect transmission of electrical
activity of the heart throughout the body and are broadly grouped into four categories:
(i) Cellular factors determine the intensity of the current flow. They include:
Intracellular and extracellular resistance
Intracellular and extracellular ions: Lower ion concentrations reduce the intensity
of the current flow by reducing the movement of the ions and by lowering the extra-
cellular potentials.
(ii) Cardiac factors affect the transmission of current from one cardiac cell to another.
These include:
Anisotropy: It is the property of the cardiac tissue to propagate more rapidly along the
length of the fiber than transversely. Hence, the recording electrodes oriented along
the long axis of a cardiac fiber register larger potentials than the electrodes oriented
perpendicular to the long axis.
Connective tissue between the cardiac fibers: It disrupts the effective electrical cou-
pling between adjacent fibers. The waveforms recorded from fibers with little or no
intervening connective tissue are narrow and smooth in contour, whereas those re-
corded from the fibers with abundant connective tissue (fibrosis) are prolonged and
fractionated.10
(iii) Extracardiac factors include all tissues and structures that lie between the region
of cardiac electrical activity and the body surface. These tissues alter the electrical activ-
ity due to differences in electrical resistances of the adjacent tissues i.e. electrical inho-
mogeneities within the torso. e.g. intracardiac blood has lower resistance of 162 -cm
than the lungs (2150 -cm)
Ventricular walls
Intracardiac and intrathoracic blood volume
Pericardium
Lungs
Skeletal muscles
Subcutaneous fat and
Skin.
Table 22.3 Factors modifying transmission of action potential
Modifying factors
1. Intracellular and extracellular resistance

2. Intracellular and extracellular ions
3. Anisotrophy
4. Connective tissue between the cardiac fibers
5. Electrical in-homogeneities within the torso
6. Distance between the heart and recording electrode
7. Eccentric location of the heart
Intracellular and Connective tissue

Intracellular and Eccentric location
extracellular between heart and
extracellular ions of the heart
resistance recording electrode
Cardiac action
Cellular factors Physical factors
potential
Cardiac factors Extacardiac factors
Intracardiac and
Anisotrophy 1. Ventricular walls
intrathoracic
2. Pericardium
blood volume
Connective
tissue between 1. Subcutaneous fat 1. Lungs
cardiac fibers 2. Skin 2. Skeletal muscles
Fig. 22.7 | Factors modifying cardiac action potential.

(iv) Physical factors which affect the electrical activity are:
The distance between the heart and recording electrode is governed by inverse square
law i.e. amplitude of the electrical potential decreases in proportion to the square of
the distance. All electrodes placed at a distance 15 cm from the heart may be con-
sidered to be equidistant from the heart in electrical sense as the amplitude of the
electrical potentials recorded will be the same in all electrodes.
Eccentric location of the heart i.e. the heart is located eccentrically more anteriorly
so that the RV and anteroseptal portion of the LV are located closer to the anterior
of the chest than other parts of the LV and atria. Hence, the ECG potentials and
wave forms generated by the anterior regions of the heart are higher and greater than
those generated by the posterior ventricular regions and atria.
As a result of all these factors, body surface potentials have amplitude of only 1% of the
amplitude of transmembrane potentials (see Table 22.3 and Fig. 22.7).
Table 22.4 Methods of ECG recording
Methods
1. Standard method
2. ECG monitoring
3. Ambulatory ECG
4. Telemetry
b) Electrocardiographic Instrument, Recording Electrodes and Lead

1) Electrocardiographic Instrument
The two main types of apparatus used are:

String galvanometer
Radio amplifier
String galvanometer records on the photographic paper which has to be developed.
It requires experience to operate so as not to damage the valuable string.
Radio amplifier is compact, light, easy to operate and has a direct writer. Many mod-
ern machines record multiple leads simultaneously. Other methods utilized clinically
are (see Table 22.4):
Oscilloscopic viewing of the ECG i.e. ECG monitoring in coronary and intensive care
units. This produces a constant ECG on a fluorescent screen with a facility to obtain
the ECG tracing.
Ambulatory ECG recording: A small ECG tape recorder is attached to the patient
for continuous recordings for 24 hrs while the patient is ambulatory which can be
reviewed later by the attending physician for arrhythmias or myocardial ischemia.
Telemetry ECG: ECGs can be transmitted via telephone lines, for constant or tem-
porary monitoring and interpretation by a physician many miles away from the patient.
Computer facilities are available not only for ECG interpretation but also for the
recognition and quantitation of arrhythmias.
2) Recording Electrodes and Leads

These are as follows:
Bipolar standard or limb leads
Bipolar chest leads
Unipolar augmented limb leads
Unipolar precordial or chest leads
Monitor leads
Unipolar esophageal leads
The Mason-Liker modified standard leads
Unipolar intracardiac leads.
The standard clinical ECG consists of 12 leads: 3 bipolar limb leads (I, II, III), 3 augmen-
ted limb leads (aVR, aVL, aVF) and 6 unipolar precordial leads (V1V6). The bipolar
Connected to ECG
I
RA lead LA lead
II III
RA lead LA lead

Connected to ECG II III Connected to ECG

LL lead LL lead
Fig. 22.8 | Bipolar standard leads (I, II, III).

and augmented limb leads are oriented in the frontal or coronal plane of the body,
while the precordial leads are oriented in horizontal or transverse plane of the body.
(1) Bipolar standard or limb leads: These were introduced by Einthoven.11 These
leads record the potential difference between the two limbs and consists of three leads:
I, II and III with four electrodes: LA (left arm electrode), RA (right arm electrode), LL
(left leg electrode), and RL (right leg electrode) which serves as a ground connection.
The electrodes are usually placed just above the wrists and ankles or to the stump in the
amputated limb.
Lead I represents the potential difference between LA (positive electrode) and RA
(negative electrode) (LA-RA). This lead with aVL is oriented to the left lateral wall.
Lead II represents the potential difference between LL (positive electrode) and RA
(negative electrode) (LL-RA).
Lead III represents the potential difference between LL (positive electrode) and LA
(negative electrode) (LL-LA). Leads II and III with aVF are oriented to the inferior
surface of the heart (see Fig. 22.8).
The relation between these three leads is expressed algebraically by Einthovens equation
or equilateral traiangle:11
Lead II Lead I Lead III i.e. electrical potential recorded in Lead II equals the
sum of electrical potentials recorded in Leads I and III.
This equation is based on Kirchhoff s Law i.e. the algebraic sum of all potential
differences in a closed circuit equals zero. Hence III III 0 or II I III.
(2) Bipolar chest leads: Presently, a special bipolar chest lead (Lewis lead) is some-
times used to amplify the atrial activity and thereby to clarify the mechanism of an
atrial arrhythmia.
The RA electrode is placed in the 2nd intercostal (IC) space to right of the sternum,
the LA electrode is placed in the 4th IC space to right of the sternum, and tracing is
recorded on lead I.
(3) Unipolar augmented limb leads: The unipolar leads (limb leads: VR, VL, VF;
multiple chest leads: V and esophageal leads E) were introduced by Wilson.12
The unipolar leads represent the potentials in a given lead and not the differences in
potentials as in bipolar leads.

The unipolar lead system consists of a Wilsons central terminal or indifferent lead and
an exploring lead. The central terminal is formed by joining electrodes (RA, LA, and
LL) together to 5000 resistor which is attached to negative terminal of the machine.
In unipolar limb leads, the central terminal is connected to the RA electrode of the
machine (which acts as negative terminal) and exploring lead (positive terminal) is
connected to the LA electrode of the machine and the tracing is recorded on lead I.
Although technically this system has two electrodes i.e. bipolar leads, it represents a
unipolar lead since one of the potentials is zero (central terminal has zero potential).
At present, only augmented limb leads (aVR, aVL and aVF, introduced by Emanuel
Goldberger in 1942) are in vogue as the amplitude of the deflections is 50% more
than the non-augmented leads (VR, VL and VF).
To record aVR (a augmented, VR vector of right arm), the LA electrode (exploring
lead) of the machine is placed on the right arm, while RA electrode of the machine
(indifferent lead/central terminal through 5000 resistor) is placed on the left arm
and left leg. This lead is oriented to the cavity of the heart and hence all deflections
(P, QRS, and T) are normally negative.
To record aVL (a augmented, VL vector of left arm), the LA electrode of the
machine is placed on the left arm, while RA electrode of the machine (indifferent
lead through 5000 resistor) is placed on the right arm and left leg. This lead is ori-
ented to the anterolateral or superior surface of LV.
To record aVF (a augmented, VF vector for left leg), the LA electrode of the
machine is placed on the left leg, while the RA electrode (indifferent lead through
5000 resistor) of the machine is placed on the right arm and left arms. This lead
is oriented to inferior surface of the heart (see Fig. 22.9).
The unipolar limb leads bear a definite mathematical relationship to the standard bipolar
leads. This relationship is derived from Einthovens formula: VR VL VF 0.
I 2/3 (aVLaVR) aVR I II/2
II 2/3 (aVFaVR) aVL I III/2
III 2/3 (aVFaVL) aVF II III/2
Bipolar and unipolar leads are not of equal lead strength. An augmented lead is 87%
of the lead strength of a bipolar lead. Therefore, the above equations must be corrected.
When the strength (voltage) of an augmented unipolar lead is determined from the
bipolar lead values, it is corrected by multiplying by 0.87, and when the strength (volt-
age) of a bipolar lead is determined from an augmented lead values, it is corrected by
multiplying by 1.15 (100/87) (see Fig. 22.10).
Hence, I 2/3 (aVLaVR) (1.15) aVR III/2 (0.87)
II 2/3 (aVFaVR) (1.15) aVL IIII/2 (0.87)
III 2/3 (aVFaVL) (1.15) aVF IIIII/2 (0.87)
To determine voltage of R waves in augmented leads from the actual measurements of
R waves from standard leads from illustration Fig. 22.10.
LA lead
LA lead
RA lead ECG aVL
T ead ECG
aVR RA l
Recording on T Recording on
lead l lead l
LL lead
Unattached LL lead
Unattached
RA lead
T ECG
aVF LA lead
Recording on
lead l
LL lead
Unattached
Fig. 22.9 | Augmented limb leadsaVR, aVL, aVF.

111 I = 2/3 (aVL aVR) I III
aVR = aVL =
2 10 2
1.3 3.5
1.7
1 3 0 0.5
11.3 I
aVL
aVR

16
6
5
1 2
2
11 III
II = 2/3 (aVF aVR) III = 2/3 (aVF aVL)

+9.6
+1.3 +3
aVF
II III
aVF =
2
Fig. 22.10 | Relationship between unipolar and bipolar limb leads.

aVR [10 16/2] (0.87) 11.3
aVL [10 6/2] (0.87) 1.7
aVF [16 6/2] (0.87) 9.6
Similar method is to used to determine voltages of P and T waves.
To determine voltage of R waves in standard leads from the actual measurements of
R waves from augmented leads from illustration Fig. 22.10.
I 2/3(1.7 11.3) (1.15) 10

II 2/3(9.6 11.3) (1.15) 16
III 2/3(9.6 1.7) (1.15) 6
Similarly, same equation is used for P and T waves.
(4) Unipolar precordial (chest) leads also consist of a Wilsons central terminal or
indifferent lead, the negative terminal of which is attached to RA lead of the machine,
while one end of the exploring electrode is attached to LA lead of the machine, and
the other end is applied to the desired chest positions, producing multiple unipolar
chest leads i.e. V lead (V1 to V6 in standard lead system and from V1 to V9, V3R9R in
extended lead system). The common precordial positions of the chest leads as per AHA
recommendations 193813 and 1992,14 are as follows:
V : 4
th
1 intercostal space (ICS) at the right of the sternal border
V : 4
th
2 ICS at the left of the sternal border
V : Equidistant between V and V
3 2 4
V : 5
th
4 ICS in left mid-clavicular line. All subsequent leads (V5V9) are taken in the
same horizontal plane as V4 i.e. in the 5th ICS
V : Anterior axillary line
5
V : Mid-axillary line
6
V : Posterior axillary line
7
V : Posterior scapular line
8
V : Left border of the spine
9
V
3R-9R: Taken on the right side of the chest in the same location as the left sided leads
V3V9 (see Fig. 22.11).
However, the usual routine ECG consists of only 12 leads: I, II, III, aVR, aVL, aVF,
and V1V6. The precordial leads are arbitrarily subdivided into: anterior leads: V1, V2,
anteroseptal leads: V3V4, lateral or apical leads: V5 and V6. Leads V1 and V2 tend to
be oriented to RV, while leads V4V6 tend to be oriented to LV.
(5) Monitor leads: In coronary care unit, modified bipolar chest leads are used.
For rhythm evaluation the positive electrode is placed in usual V1 position (modified
CL1), the negative electrode is placed near the left shoulder, and a third electrode which
serves as a ground electrode is placed at a more remote area of the chest (see Fig. 22.12).
For monitoring ST-T changes (due to ischemia), the positive electrode is placed in
V4 or V5 position.
(6) Unipolar esophageal leads are useful in recording atrial complexes, which are greatly
magnified at this location for exploring the posterior surface of the LV (see Fig. 22.13).
Esophageal lead (E) is passed into the esophagus through the nares and is attached to
V (chest) lead of the machine. The nomenclature of the lead is derived from the distance
in cm from the tip of the nares to the electrode in the esophagus. e.g. E50: represents
the esophageal lead at a distance of 50 cm from the nares. For more accurate localization
of the position of the esophageal leads, fluoroscopy may be used.
Leads E1525: These reflect the atria.
Leads E2535: These reflect the region of AV groove.
Leads E4050: These reflect the posterior surface of LV.
Midclavicular line
Anterior axillary
line
Midaxillary line
Horizontal
plane of V46
V1 V2 V3V4 V5V6 V7 V8 V9 V9R V8R V7R

V6RV5RV4RV3R V2R V1R
Fig. 22.11 | Location of unipolar precordial leads.
E20
E30
E50
3 1 2
Fig. 22.12 | Monitoring leads. Fig. 22.13 | Unipolar esophageal leads.

(7) Unipolar intracardiac leads: An electrode contained in a cardiac catheter is
attached to the V (chest) lead. Care must be taken as currents as low as 10 A can
induce ventricular fibrillation. They are used for:
Clarification of an arrhythmia by amplifications of the waves of the atrial activity.
Localization of the catheter tip when a floating pacemaker is inserted without fluo-
roscopic guidance at bed side in intensive care units. The nature of P waves and
QRS complexes will identify the location of the catheter tip.
Pericardiocentesis without fluoroscopic guidance, by attaching V lead to a pericar-
diocentesis needle under sterile conditions. When the needle strikes the epicardium,
ST elevation will be recorded, which is an indication for withdrawal of the needle.
1 small square represents 1 large square represents

0.04 s (40 ms) 0.2 s (200 ms)
RR interval:
5 large squares represent 1 s
Fig. 22.14 | Relationship between the squares on the ECG paper and time.
Recording bundle of His potentials with special catheter electrodes in cardiac laboratory.
Multiple intracardiac recordings with programmed stimulation in specialized elec-
trophysiological laboratories which are of value in determining the site of ectopic
activity, efficacy of the drug therapy and for identification of the accessory pathways.
Orientatation of leads in routine ECG:
Leads I and aVL are oriented to left lateral wall
Leads II, III and aVF are oriented to inferior surface of the heart
Leads V1 and V2 are oriented to RV
Leads V4V6 are oriented to LV
Leads V1V4 are considered to be anteroseptal leads
Leads V5 and V6 are considered to be apical or lateral leads
There is no lead which is oriented directly to the posterior wall of the heart.
3) The Electrocardiographic Grid

The electrocardiographic paper on which ECG is recorded is a graph paper with hori-
zontal and vertical lines present at 1 mm intervals. A heavier line is present at every
5 mm (large square).
Time is measured along the horizontal lines: 1 mm 0.04 s, 5 mm 0.20 s, every
15th large square (a 3 s period) is marked by a vertical line on the upper border for
quick assessment of heart rate (see Fig. 22.14).
Voltage is measured along the vertical lines: 10 mm 1 mV.
For routine ECG, the recording speed is 25 mm/s with usual standardization producing
1 cm or 10 mm deflection with 1 mV signal.
c) Precautions to be Taken for Recording an ECG

For good ECG record, following precautions should be taken:
The procedure should be explained to the patient before hand in order to allay any fears
or anxieties and ECG should be recorded in a comfortable bed/couch and patient must
be completely relaxed as any muscular motions or twitchings can alter the record.
There should be good contact between the skin and the electrode.
Table 22.5 Precautions to be observed for recording ECG
1. Prior procedural explanation

2. Good skin and electrode contact
3. Proper grounding of the patient and equipment
4. Proper standardization of the equipment
5. All electronic equipment should be away from the equipment
The patient and the machine must be properly grounded to avoid alternating current
interference.
The machine must be properly standardized so that 1 mV will produce a deflection
of 1 cm. Incorrect standardization will produce inaccurate voltage of the ECG complexes
which leads to faulty interpretation.
Any electronic equipment such as electrically regulated infusion pump can produce
artifacts in the ECG; hence they should not come in contact with the patient
(see Table 22.5).
REFERENCES
1. Bancroft E. An essay on the natural history of Guiana, London: T Becket and PA de Hondt, 1769.
2. Walsh J. On the electric property of Torpedo: in a letter to Ben Franklin. Phil Trans Royal Soc 1773;
63:478489.
3. Matteucci C. Sur un phenomena physiologique produit par les muscles en contraction. Ann Chim
Phys 1842;6:339341.
4. von Koelhker A, Muller H. Nachwels der negation Schwankung des Murkelstroms am naturlich sich
Kontrahierenden Herzen, Verhand lungen der Physikalisch-Medizinischen Gesellschaft in Wurzberg
1856:528533.
5. Burdon Sanderson J. Experimental results relating to the rhythmical and excitatory motions of the
ventricle of the frog. Proc R Soc Lond 1878;27:410411.
6. Waller AD. A demonstration on man of electromotive changes accompanying the hearts beat.
J Physiol (Lond) 1887;8:229234.
7. Einthoven W. Ueber die Form des menschlichen Electrocardiograms. Arch fd Ges Physiol 1895;60:
102123.
8. Descartes R. De Homine (Treatise of Man). 1662: Moyardum & Leffen, Leiden.
9. Einthoven W. Un nouveau Galvanometre. Arch Necri Sc Ex Nat 1901;6:625633.
10. Spach MS, Dolber PC. Relating extracellular potentials and their derivatives to anisotrophic propa-
gation at a microsopic level in human cardiac muscle. Circ Res 1986;58:356371.
11. Einthoven W. The different forms of the human electrocardiogram and their significance. Lancet
1912(1):853861.
12. Wilson NF, Johnston FE, Macleod AG et al. Electrocardiograms that represent the potential variation
of a simple electrode. Am Heart J 1934;9:447458.
13. Barnes AR, Pardee HEB, White PD et al. Standardization of precordial lead. Am Heart J 1938;15:
235239.
14. Schlant RC, Adolph RJ, DiMarco JP et al. Guidelines for electrocardiography. A report of the
American Collage of Cardiology/American Heart Association Task Force on Assessment of Diagnostic
and Therapeutic Cardiovascular Procedures (Committee on Electrcardiography). J Am Coll Cardiol
1992;19:473481.
CHAPTER 23
T HE N ORMAL E LECTROCARDIOGRAM
WAVES 474 EFFECT OF HEART POSITION ON ECG 484

1. P Wave 474 1. Electrical Rotation of the Heart
2. Q(q) Wave 476 in Frontal Plane on
3. R(r) Wave 476 Anteroposterior Axis 484
4. S(s) Wave 477 2. Electrical Rotation of the Heart
5. R(r) Wave 477 in Horizontal Plane on Long Axis 485
6. T Wave 477 NORMAL ECG VARIANTS 486
7. U Wave 478 1. Normal ECG in Infants and
8. Ta Wave 478 Children 486
INTERVALS 479 2. Juvenile Pattern 487
SEGMENTS 480 3. Early Repolarization 487
THE ELECTRICAL AXIS 481 4. Anxiety and Hyperventilation 489
1. The Hexaxial Reference System 481 5. Postprandial Response 489
2. Methods of Determination of 6. Effect of Deep Respiration 489
Electrical Axis 482 REFERENCES 489
The normal ECG consists of waves, intervals and segments (see Table 23.1). Capital
letters (Q, R, S) are used for large waves of 5 mm, and small letters (q, r, s) refer to
smaller waves of 5 mm in size (see Figs 23.1 and 23.2).
WAVES
1. P Wave
It is the first deflection of the ECG which is small, smooth and rounded.
i) The initial portion is due to RA depolarization and the late portion is due to LA
depolarization. The duration of RA depolarization is 0.020.04 s and that of LA
is 0.050.06 s.
ii) The normal duration of P wave is 0.12 s (120 ms) and its amplitude is not
2.5 mm or 25% of the normal R wave in normal individuals, especially in limb
leads.
iii) It is best seen in lead II, but usually studied in lead V1 as initial and terminal com-
ponents are clearly identifiable, in which it is normally diphasic. The terminal
THE NORMAL ELECTROCARDIOGRAM 475
Isoelectric line: horizontal

PR ST segment level between cardiac cycles
T wave
P
P
QRS
V = Vulnerable
1 period
2
Phase 0 3
Phase 4
QT
Fig. 23.1 | Phases of action potential and normal ECG.

I aVL V1 V4
II aVI V2 V5
III aVF V3 V6
Fig. 23.2 | Normal ECG.

Table 23.1 Composition of normal ECG
Waves Intervals Segments
1. P RR PR
2. Q (q) PP ST
3. R (r) PR J junction
4. S (s) QRS
5. R(r) QT
6. T VAT
7. U
negative deflection should not exceed 0.03 s in duration and 1 mm in depth (see
Table 23.2).
iv) As the normal P wave is oriented to the left, inferiorly in frontal planes (I, II, III,
aVR, aVL and aVF), left and slightly anteriorly in horizontal planes (V1V6).
Table 23.2 Characteristics of normal P waves
Features Findings
1. Duration 0.12 s (RA: 0.020.04 s, LA: 0.050.06 s)

2. Amplitude 2.5 mm
3. Terminal ve deflection in V1 0.03 mm-s
4. Frontal plane axis 0 to 90
5. Best seen II and V1 leads
Table 23.3 Characteristics of normal q waves
Features Findings
1. Duration 0.04 s
2. Depth 3 mm, 25 % of the R wave amplitude
in the same QRS complex
3. QS in V1 Normal
It is upright in leads I, II, aVF, and V3V6 with P axis in frontal plane between
0 and 90.
Inverted in a VR and frequently in V1 and sometimes in V2.
Upright, diphasic or inverted in leads III and aVL.
P wave is upright in lead III if P axis is 30, and inverted if 30.
P wave is upright in lead aVL if P axis is 60, and inverted if 60.
2. Q(q) Wave
All the three waves of the QRS complex are due to ventricular depolarization.
i) This wave is the initial negative deflection which is due to the initial depolariza-
tion of mid portion of left side of the interventricular septum from left to right
and hence it is oriented rightwards and anteriorly.
ii) It is a small wave of 0.04 s in duration and 3 mm deep i.e. 25% of the height
of R wave in the same QRS complex in leads I, II, aVF and V4V6 (see Table 23.3).
A larger Q wave (0.04 s in duration or 25% of the R wave) may normally
be seen alone in lead III (for diagnostic significance, abnormal Q must also be
present in lead aVF) or aVL (for diagnostic significance, abnormal Q must also
be present in lead I or in precordial leads).
iii) A QS complex (entirely negative) is often a normal finding in V1 and occasionally
in V2.
3. R(r) Wave
It is the first positive deflection during ventricular depolarization.
i) After activation of the mid portion of the septum, anteroseptal region of the RV
is depolarized which is oriented rightwards, anteriorly and either superiorly or
inferiorly which results in r wave in V1V2 (right precordial leads) and q wave in
I, V5 and V6, with a duration of 0.03 s.
ii) Then the major activation of both ventricles (major muscle mass) which is oriented
to the left, inferiorly and posteriorly results in a large dominant R wave in leads I,
II, and V4V6 with a duration of 0.030.05 s.
The upper limit of R wave amplitude is 1.5 mV in lead I, 1.0 mV in lead aVL, 1.9 mV
in leads II, III and aVF, and 0.6 mV in V1. Among the precordial leads, the tallest R wave
is commonly seen in V4.
Lead aVF will record R wave when frontal mean axis is 0 to 90, RS or rs complex if
mean axis is 0 and a negative deflection (S) if the mean axis is between 0 and 30.
Lead aVL will record R wave when frontal mean axis is between 30 and 60, and
a negative deflection (S) if the mean axis is 60 to 90.

Lead III will record R wave when frontal mean axis is between 30 and 90, and
a negative deflection (S) if the mean axis is between 30 and 30.
4. S(s) Wave
It is the negative deflection of ventricular depolarization that follows the first positive
deflection (R), with duration of 0.010.02 s.
i) It is due to the activation of last portion of the ventricular mass (posterior basal
portion of LV, pulmonary conus and uppermost portion of the interventricular
septum). In leads I and V5V6 , s is small as it is oriented rightwards.
ii) S wave may be due to major activation of ventricles and may be due to a domi-
nant wave in leads.
aVR: S is most prominent and always dominant, and a maximum amplitude
upto 1.6 mV may be seen. It is deepest in V2 lead among the precordial leads.
aVF when the frontal mean axis is between 0 and 30.
aVL when the frontal mean axis is 60 to 90.
III when the frontal mean axis is between 30 and 30.
5. R(r) Wave
It is the second positive deflection that may occur during ventricular depolarization
following S wave.
If the activation of the last portion of the ventricular mass is oriented anteriorly,
a small positive deflection r is recorded in leads V1V2.
The negative deflection which may occur following r is termed as the s wave.
6. T Wave
It is the deflection produced by ventricular repolarization and coincides with the closure
of the semilunar valves.
The T wave is usually asymmetrical.
Its orientation is to the left and inferiorly with a mean frontal axis between 0 and
90. However, it may normally be oriented slightly superiorly with mean axis
between 0 and 30, with similar QRS orientation.
It should be at least one tenth or 10% of the R wave amplitude in the same complex.
Normally, its amplitude is 6 mm in limb leads with tallest T wave in lead II, and
10 mm in precordial leads with tallest T wave in leads V2 and V3.
It is upright in leads I, II, aVF, and V2V6 and inverted in aVR.
It may be upright, diphasic or inverted in leads III, aVL (analogous to P wave) and V1
(occasionally in V2). It is inverted in V1 in approximately 50% of women and in
33% of men (see Table 23.4).
7. U Wave
It follows T wave preceding the next P wave.
It is normally smaller than T wave, and usually 0.2 mV or approximately 10%
of T wave in amplitude and 0.08 s in duration, with same polarity as the preceding
T wave (see Table 23.5).
The interval from the end of the T wave to the apex of the U wave is 90110 ms,
and the interval from the end of the T wave to the end of the U wave is 160200 ms.
Sometimes, a notch in the T wave may be mistaken for U wave. However, the interval
between the apices of a notched T wave is usually 0.15 s, while the interval between
the apices of the T and U waves is usually 0.15 s.1
It is best seen in leads V2V4 and II as a hump on a camels back ( prominent in
precordial leads).
It is due to slow repolarization of the Purkinje fibers.2 More recently, U wave is
thought to be due to M cells in deep subepicardium (also for J or Osborne wave of
hypothermia).3
8. Ta Wave
It is usually a small negative deflection following P wave due to atrial repolarization
which is not usually seen in a standard 12-lead ECG.
Table 23.4 Characteristics of normal T waves
Features Findings
1. Amplitude 1/10th of R wave in the same QRS complex, 6 mm

in limb leads and 10 mm in precordial leads
2. Upright/diphasic/inverted III, aVF, V1
3. Frontal axis 0 to 90
Table 23.5 Characteristics of U waves
Features Findings
1. Amplitude 10% of T wave of the same complex (0.2 mV)

2. Duration 0.08 s
3. Mean frontal axis 60
4. Best seen V2V4 and II leads
1 small square represents 1 large square represents

0.04 s (40 ms) 0.2 s (200 ms)
QT 0.40 s PR 0.20 s QRS 0.10 s
RR interval:
5 large squares represent 1 s
Fig. 23.3 | ECG intervals (PR and QRS).
INTERVALS
1. RR interval is the distance between the two consecutive R waves.

In regular sinus rhythm, the RR interval in seconds divided by 60 will give the
heart rate/min.
In irregular rhythm, the number of R waves in a given period of time (e.g. 10 s)
converted into the number per minute will give the ventricular rate/min.
2. PP interval is the distance between the two consecutive P waves. The heart rate can be
calculated in regular sinus rhythm similar to RR interval. However, in irregular
rhythm atrial rate per minute is computed similar to the ventricular rate.
3. PR interval is measured from the onset of P wave to the beginning of QRS complex.
It measures the AV conduction time from the onset of atrial depolarization to the
onset of ventricular depolarization which includes:
Depolarization of both atria,
AV node conduction including normal conduction delay in AV node (about 0.07 s),
And passage of impulse through the bundle of His and bundle branches.
The normal PR interval is 0.120.20 s.4 However, it must be correlated with heart rate
as slower the heart rate, longer the PR interval.
4. QRS interval (duration of QRS complex) is measured from the onset of Q (q) wave or
R (r) wave (if Q/q wave is not seen) to the termination of S wave (see Fig. 23.3).
It measures the total ventricular depolarization time.
The normal duration of QRS complex is 0.12 s, which is slightly longer in
males and large and tall subjects than in females and small and short subjects.5
5. QT interval is measured from the onset of Q wave to the end of T wave. It measures
the total duration of ventricular depolarization and repolarization which corresponds
to the duration of ventricular action potential.
Table 23.6 ECG intervals
Features Findings
1. PR interval 0.120.20 s
2. QRS duration 0.12 s
3. QTc interval 0.42 s in men, 0.43 s in women
4. VAT 0.03 s in V1V2
0.05 s in V5V6
Intrinsic deflection
(VAT)
+
E
Fig. 23.4 | Ventricular activation time (VAT).

i) Corrected QT interval (QTc ): As the QT interval varies with the heart rate i.e.
QT interval decreases as the heart rate increases, it should always be corrected by
Bazett (1920) formula6:
QTc QT/(RR)
where QTc is corrected QT interval, QT is the measured QT interval, RR is the
measured RR interval.
The QT is 0.42 s in men and 0.43 s in women.
c
The QT interval is slightly longer in the evening and at night during sleep due
to influence of the autonomic nervous system.7

ii) QU interval: When the end of T wave overlaps the beginning of U wave espe-
cially in metabolic abnormalities, QT is designated as QT (U) or QU interval.
iii) QT interval dispersion: The QT interval also varies from lead to lead, maximum
in mid precordial leads (V2V3) and normally the difference between the longest
and shortest intervals in the leads should not be more than 0.05 s. This variation
in QT interval duration from lead to lead is known as QT interval dispersion and
increased QT interval dispersion indicates electrical instability and risk of occur-
rence of ventricular arrhythmias8 (see Table 23.6).
6. Ventricular activation time (VAT) is the time that the impulse takes to traverse the
myocardium from endocardium to epicardial surface (see Fig. 23.4). It reflects the int-
rinsicoid deflection and is measured from the beginning of the Q wave to the peak of
R wave. Normally, it should not exceed 0.03 s in V1V2 leads and 0.05 s in V5V6 leads.
SEGMENTS
1. PR segment is the portion of the ECG tracing from the end of the P wave to the
onset of QRS complex and normally it is isoelectric.
2. ST segment is the portion of the ECG tracing that lies between the end of the QRS
complex and the beginning of the T wave.
It represents the period when all parts of the ventricles are in depolarized state.
But early repolarization may encroach on the ST segment to a variable degree.

The point at which QRS complex ends and ST segment begins is the J or junction
point. The ST segment from J point to the beginning of T wave is usually isoelec-
tric, but may vary from 0.5 (depression) to 1 mm (elevation) in precordial leads.
THE ELECTRICAL AXIS
The electrical axis may be defined as a vector or an electromotive force originating in the
center of Einthovens equilateral triangle which has magnitude, direction and polarity.9,10
The mathematical symbol expressed is an arrow pointing in the direction of the net
potential (positive or negative), while its length indicates the magnitude of the electrical
force. The electrical axis is usually determined in the frontal plane from the limb leads by
using the hexaxial reference system, derived from Einthovens equilateral triangle.
1. The Hexaxial Reference System

It is composed of lead axis of six frontal plane limb leads. The lead axis of these leads
is rearranged so that their centers overlay one another and these axes divide the plane
into 12 segments, each subtending 30 (see Fig. 23.5).
The postive pole of lead I is designated as 0, and the negative pole as 180
The positive pole of aVF is designated as 90, and the negative pole as 90
The positive pole of lead II is designated as 60, and negative pole as 120
The positive pole of lead III is designated as 120 and negative pole as 60
The positive pole of aVR is designated as 150 and negative pole as 30
The positive pole of aVL is designated as 30 and negative pole as 150
Superior
90o
120o 60o
150o 30o
aV L
R aV
I
180o 0o
+150o +30o
III
II
aVF
Right Left
+120o +60o
+90o
Inferior
Fig. 23.5 | The hexaxial reference system.

Determination of electrical axis is useful in minority of cardiac conditions as in

Fascicular blocks
Ventricular hypertrophy especially RVH and biventricular hypertrophy
Some forms of ventricular tachycardia and
Some forms of congenital heart diseases.
2. Methods of Determination of Electrical Axis

Axis of QRS complex, P wave and T wave can be determined by the following methods:
1. Equiphasic Method
Identify a lead in which the net QRS amplitude is zero i.e. smallest or equiphasic QRS
deflection from the six frontal leads, the mean QRS axis (vector) will be perpendicular
to this lead axis, in which the net QRS deflection will be highest of all frontal leads.
e.g. in Fig. 23.6, the net QRS amplitude is zero in lead I, therefore the lead aVF is per-
pendicular to this lead, and the mean QRS axis will be 90 if the net QRS complex
in aVF is positive or 90 if the net QRS complex is negative as per the hexaxial ref-
erence system (see Fig. 23.5).
I aVF
0o
+90o
aVF
Fig. 23.6 | Determination of axis by equiphasic method.

2. Classical Method9,11
i) The net amplitude of the QRS complex in any 2 (usually I and III) of the 3 stan-
dard limb leads are plotted along the axis of the 2 standard limb leads on the
hexaxial reference system. The net amplitude of the QRS complex represents the
net area of the QRS complex of the corresponding lead. The results are coun-
terchecked by using Eithovens equation (II I III).
ii) Then perpendicular lines are drawn at these locations, and a line drawn from the
center of the hexaxial reference system to the intersection of the perpendicular
represents the approximate mean QRS vector and its angle is the mean QRS axis
in frontal plane. e.g. in Fig. 23.7, the net amplitude of QRS complex in leads I
and III is as follows:
Lead I: R 6 mm, S 2 mm; 6 2 4 mm
Lead III: R 2 mm, S 5 mm; 25 3 mm
Therefore, the net QRS amplitude of 4 mm in lead I and the net QRS amplitude of
3 mm in lead III are plotted along the axis of leads I and III respectively as in Fig. 23.8.
An angle of 15 is obtained with a line drawn from the center of the hexaxial reference sys-
tem to the intersection of the perpendiculars, which is the mean QRS axis in frontal plane.
I: R 6 mm, III: R 2 mm,

S 2 mm S 5 mm
Fig. 23.7 | Determination of axis by classical method.

90o
ABNORM
AL LE
FT
AX
IS
DE
o VI
90 AT
120o 60o IO
30o
N
3
15o
180o 180o 0o I
4
ABNO
RM
ON
AL
TI
IA
RI
EV
60o
G
T 120o D
H
AX
IS III 90o II X IS
DE FA
V IA EO
T IO NG
N L RA
NO RMA
110o
Fig. 23.8 | Determination of axis by classical method.

3. Simplified Method12
Examine QRS complexes in leads I and aVF.
i) If QRS complexes are upright (positive) in both leads axis in frontal plane is
normal (0 to 110 in 40 years of age, 30 to 90 in 40 years of age).
ii) If QRS complex is positive in lead I and negative in lead aVF left axis (30 to
90) in frontal plane.
iii) If QRS complex is negative in lead I and positive in lead aVF right axis (110
to 180) in frontal plane.
Similarly, the axis of P and T waves in frontal plane can be determined by above methods.
Normal Electrical Axes in Frontal Plane.
i) Mean QRS axis: For all age groups is 30 to 110, 40 years of age is 30 to
90, 40 years of age is 0 to 110.
ii) Mean P wave axis: 0 to 90. P wave is inverted in lead III if P axis is 30.
Also, it is inverted in lead aVL if P axis is 60.
iii) Mean T wave axis: 0 to 90.
iv) Mean U wave axis is 60.
v) Left axis deviation (LAD): When the mean QRS axis in frontal plane lies between
30 and 90. Common causes of LAD are:
LBBB
Left anterior fascicular block (hemiblock)
LVH
Some forms of VT
AV canal defect, tricuspid atresia
Mechanical shifts causing a horizontal heart: Pregnancy, ascites.
vi) Right axis deviation (RAD): When the mean QRS axis in frontal plane lies between
110 and 180. Common causes of RAD are:
RVH
Left posterior fascicular block
Pulmonary embolism
Lateral myocardial infarction
Dextrocardia
Mechanical shifts causing a vertical heart: Emphysema.
EFFECT OF HEART POSITION ON ECG
The electrical rotation of the heart may occur in frontal plane on anteroposterior axis
or in horizontal plane on long axis. It is doubtful whether true anatomical rotation of
the heart occurs, and if it occurs it is very minimal.
1. Electrical Rotation of the Heart in Frontal Plane on

Anteroposterior Axis
Besides determining the QRS axis in frontal plane, the resemblance of QRS complex
in precordial leads (V1 and V6) is sought in unipolar limb leads to determine the heart
Table 23.7 Positions of the heart
Features Vertical Horizontal Intermediate
1. Mean QRS axis 75 to 110 30 to 0 15 to 30

2. QRS complex in aVF Resemble V6 Resemble V1 Resemble V6
3. QRS complex in aVL Resemble V1 Resemble V6 Resemble V6
Table 23.8 Electrical rotation of the heart
Clockwise rotation Counterclockwise rotation
1. LV complex in V7V9 1. LV complex in V2

2. S waves of RV complex in V5V6 2. ST elevation in V2V4
position in frontal plane. There are three main electrical rotations of the heart in
frontal plane.
Vertical heart
Horizontal heart
Intermediate heart.
Vertical heart is merely a manifestation of an inferiorly directed mean QRS axis.
Mean QRS axis is 75 to 110.
aVR records RV cavity complex (i.e. all inverted complexes, P, QRS, and T).
aVF records LV epicardial complex (i.e. upright P and T, qR) resembling V6.
aVL may record RV epicardial complexes (i.e. downward major QRS deflection)
resembling V1 or sometimes RV cavity complex resembling aVR.
Horizontal heart is merely a manifestation of left QRS axis deviation.
Mean QRS axis is 30 to 0.
aVR records RV cavity complex.
aVF records RV epicardial complex resembling V1.
aVL records LV epicardial complex resembling V6.
Intermediate heart is merely a manifestation of QRS axis midway between vertical
and horizontal heart.
Mean QRS axis is between 15 and 30.
aVR records usually RV cavity complex.
aVF and aVL record LV epicardial complex resembling V6 (see Table 23.7).
2. Electrical Rotation of the Heart in Horizontal Plane on

Long Axis
The rotation of the heart on long axis may be clockwise or counterclockwise depend-
ing on the appearance of the precordial leads, especially the transitional zone (see
Table 23.8). In an average case, the transitional zone is in the V4 lead.
I II III aVR aVL aVF
V1 V2 V3 V4 V5 V6
Fig. 23.9 | Clockwise rotation with persistence of S waves till V . 6
V1 V2 V3 V4 V5 V6
Fig. 23.10 | Counterclockwise rotationLV complexes from V 3 onwards.
Clockwise rotation: The transitional zone is shifted to the left, so that the typical
LV epicardial complexes do not appear until V7V9, i.e. S waves (typical of RV epicar-
dial complex) persist in V5 and V6 (see Fig. 23.9). If rotation is rightward, S waves will
also be seen in lead I.
If rotation is leftward or superiorly, S waves are also seen in leads II, III, and aVF.
If rotation is posteriorly, all frontal plane leads record normal QRS complexes.
Counter clockwise rotation: The transitional zone is shifted to the right, so that the
typical LV epicardial complexes are seen early in V2 (see Fig. 23.10). ST elevation in
V2V4 is a common accompaniment.
NORMAL ECG VARIANTS
1. Normal ECG in Infants and Children

a) Normal ECG in Infants
RVH pattern: In fetus, RV performs more work than LV and therefore, at birth or in
infancy there is a relative hypertrophy of the RV resulting in electrocardiographic

pattern simulating RVH i.e. tall R waves in V1 or V2 with RAD (see Fig. 23.11).
However, there is no initial q wave and VAT in V1 is not prolonged.
V4
V1
I aVR
II aVL V2 V5
V3 V6
III aVF
Fig. 23.11 | ECG in a child with sinus tachycardia and tall R in V . 1
Table 23.9 Normal ECG variants in infants and children
Features Findings
1. R wave in V1 Tall mimics RVH, normalizes after 5 yrs of age

2. VAT in V1 Normal
3. T wave in V1V4 Inverted after 4 days of birth
May persist into 2nd decade of life
If persist into 3nd decade of life: Juvenile pattern
4. Frontal QRS axis Shifts to left in children
T waves are upright or inverted in V1, upright in V2V6 within first 24 days.
T waves are normally inverted in V1V4 after 4 days.
b) Normal ECG in Children
Tall R waves in V V usually disappears after 5 yrs of age.
1 2
Inverted T waves in right precordial leads may persist into second decade of life.
Frontal plane QRS axis gradually shifts to the left (see Table 23.9).
2. Juvenile Pattern
Inverted T waves in V1V4 may persist into third decade of life which is more com-
mon in Negroes, and more common in women than in men.13
3. Early Repolarization
It is characterized by:
ST segment elevation (usually 2 mm) in mid precordial leads with an upward con-
cavity and relatively tall symmetrical upright T waves (see Fig. 23.12). J point may
be prominent.
Common in young adults especially athletes (see Table 23.10).
V4
I aVR V1
II aVL V2 V5
III aVF V3 V6
Fig. 23.12 | Early repolarization in V V ST elevation with concavity upwards and tall
symmetrical upright T waves.
2 4
Table 23.10 Normal ECG variants-early repolarization
Features Findings
1. ST segment in precordial leads Elevation of 2 mm with concavity upwards

2. Heart rate More in slower heart rates
3. Age of the individual Common in young adults, especially athletes
4. Sex More in men
1. T RVH pattern
RVH 2. QRS disappears
T
pattern axis left >5 years of age
In infants In children
Normal
>In Juvenile Post ST / T
ECG
females pattern prandial or both
variants
Anxiety & Early

hyperventilation repolarization
1. Prolong PR Sinus >In young At slower

2. ST and T tachycardia males heart rates
Fig. 23.13 | Normal ECG variantsST: ST segment depression, T: inverted T waves.
More common at slower heart rates than rapid heart rates, in men than in women,
and often in black men.14
This phenomenon is due to beginning of repolarization of a portion of the myocar-
dium before depolarization is completed in other areas of the myocardium. Following
moderate exercise or hyperventilation, the ST segment may return to the isoelectric line.
4. Anxiety and Hyperventilation

ECG changes are:
Sinus tachycardia,
Prolonged PR interval,
ST depression and T wave inversion in left precordial leads.
5. Postprandial Response
Following a heavy meal especially high carbohydrate meal, ST depression or T wave
inversion or both may occur.
It is due in part to an intracellular shift of potassium in association with intracellular
glucose metabolism.
6. Effect of Deep Respiration

With deep inspiration, the heart becomes more vertical and rotates clockwise.
With deep expiration, the heart becomes more horizontal and rotates counter clock-
wise (see Fig. 23.13).
REFERENCES
1. Lepeschkin E. The U wave of the electrocardiogram. Mod Concepts Cardiovasc Dis 1969;38:3945.
2. Surawicz B. U wave: Facts, hypotheses, misconceptions, and misnomers. J Cardiovasc Electrophysiol
1998;9(10):11171128.
3. Antzelevitch C, Sicouri S. Clinical relevance of cardiac arrhythmias generated by after-depolarization:
Role of M cells in the generation of U waves, triggered activity and torasade de pointes L J Am Coll
Cardiol 1994;23:239.
4. Chou TC. When is the vectorcardiogram superior to the scalar electrocardiogram? J Am Coll Cardiol
1986;8(4):791799.
5. Surawicz B. Stretching the limits of the electrocardiograms diagnostic utility. J Am Coll Cardiol 1998;
32:483485.
6. Bazett HC. An analysis of the time relations of electrocardiograms. Heart 1920;7:35370.
7. Molnar J, Zhang F, Weiss JS, et al. Diurnal pattern of QTc interval: how long is prolonged? J Am Coll
Cardiol 1996;27(1):7683.
8. Franz MR, Zabel M. Electrophysiological basis of QT dispersion measurements. Prog Cardiovasc
Dis 2000;42(5):311324.
9. Einthovan W, Fahr G, de Waart A. Uber die Richtung und die manifeste Grosse der Poten-
tialschwankungen in menchlichen Herzen und uber den Einfluss der Herzlage auf die From des
Elecktrocardiograms. Arch Physiol 1913;150:275315.
10. Barker JM. The Unipolar Electrocardiogram: A Clinical Interpretation. New York: Appleton-Century-
Crotts:1976.
11. Sodi-Palares D, Medrano GA, Bisteni A, et al. Deductive and Polyparametric Electrocardiography.
Mexico: Instituto Nacional Cardiologia Mexico; 1970;36:136.
12. Castellanos A Jr, Lemberg L. A Programmed Introduction to the Electrical Axis and Action Potential.
Oldsmart, FL: Tampa Tracings; 1974;34:114.
13. Vitelli LL, Crow RS, Shahar E, et al. Electrocardiographic findings in a health biracial population.
Am J Cardiol 1998;81(4):453459.
14. Haydar ZR, Brantley DA, Gittings NS, et al. Early repolarization: An electrocardiographic predictor
of enhanced aerobic fitness. Am J Cardiol 2000;85(2):264266.
CHAPTER 24
A BNORMAL P, T AND U WAVES
ABNORMAL P WAVES 490 ABNORMAL T WAVES 495

1. Abnormal Sites of Atrial 1. Tall T Waves 495
Activation 490 2. Flat T Waves 496
2. Dextrocardia 491 3. T Wave Inversion 496
3. Left Atrial Enlargement or ABNORMAL U WAVES 497
LA Abnormality 491 1. Large Prominent
4. Right Atrial Enlargement or U Waves 497
RA Abnormality 493 2. Inverted U Waves (in Leads I,
5. Biatrial Enlargement or II, V5 and V6) 497
Abnormality 494 REFERENCES 499
ABNORMAL P WAVES
Abnormal P waves occur due to alteration in morphology, amplitude, duration or

their absence. Abnormal P waves may be due to:
Abnormal sites of atrial activation
Dextrocardia
LA enlargement or LA abnormality
RA enlargement or RA abnormality.
1. Abnormal Sites of Atrial Activation

Shifts in the site of initial activation away from the SA node to other ectopic sites results
in major changes in the pattern of atrial activation and therefore changes in the mor-
phology of P waves.1 These shifts from the usual initial activation can occur:
As escape rhythms if the normal SA node pacemaker fails or
As AV junctional or ectopic atrial rhythms if automaticity of ectopic site is enhanced.
The resulting P waves abnormalities includes:
Negative P waves in leads II, aVF, V4V6 (in which P waves are normally upright)
with upright P waves in aVR.
Absent P waves in regular rhythm: in SA block and AV junctional rhythm; and
absent P waves in irregular rhythm: consider atrial fibrillation.
ABNORMAL P, T AND U WAVES 491
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 24.1 | Dextrocardiaall complexes in I are inverted and all complexes in aVR are
upright with RV epicardial complexes in V . 6
Polymorphic P waves: 3 different P wave morphologies in the same lead, consider

multifocal atrial tachycardia.
2. Dextrocardia
In true dextrocardia, there is reversal of the polarity of I axis and all deflections
including P wave are inverted in leads I and aVL as P is oriented to the right, inferiorly
and anteriorly, and all deflections including P wave are upright in aVR. The precor-
dial leads V1V6 reflect right ventricular epicardial complexes (i.e. loss of R waves in
V4V6). However, right precordial leads (V4R, V5R) record left ventricular epicardial
pattern (see Fig. 24.1).
In technical dextrocardia, the ECG in limb leads (I, aVL, aVR) mimics true dextro-
cardia due to interchange of RA and LA electrodes but depicts normal ECG pattern
in the precordial leads.
3. Left Atrial Enlargement or LA Abnormality

Anatomical or functional abnormality of LA alters the morphology, duration and
amplitude of P waves in ECG, which is best seen in leads II and V1. Since the ECG
changes of P waves could be due to increased atrial size (LAE), intra-atrial conduction
defects or LV dysfunction, it is preferable to refer these changes as LA abnormality
(LAA) than LA enlargement (LAE) (see Fig. 24.2). ECG criteria of LAA have low sen-
sitivity but high specificity when correlated with echocardiographic findings. Follow-
ing is the diagnostic criteria for LA abnormality (see Table 24.1).
i) Duration
Duration of P wave of 0.12 s (2.5 mm) in lead II.2 Prolonged duration of
P wave was present in 2/3rd of the patients with documented LAE.2
Ratio between the duration of P wave and duration of PR interval in lead II of 1.6
(Macruz index).
Relative shortening of PR interval.
Normal RAA LAA
RA
RA LA LA RA LA
II
RA
RA RA
V1
LA LA
LA
Fig. 24.2 | Pabnormality

wave abnormalities
(LAA).
in right atrial abnormality (RAA) and left atrial
Table 24.1 ECG suggestive of atrial enlargement
Left atrial enlargement Right atrial enlargement
1. P wave duration 0.12 s 1. P wave amplitude in II: 2.5 mm

2. Macruz index: 1.6 2. P initial force in V1: 0.06 mm-s
3. P mitrale 3. P pulmonale
4. Morris index: 0.04 mm-s 4. Frontal P axis: 75
5. Frontal P axis: 30 to 45 5. Right ventricular hypertrophy
6. f waves 1 mm in atrial fibrillation
ii) Morphology
Normal P wave is bullet shaped. If it is notched or is double-peaked like bent staple
or camel humped appearance with a distance of 0.04 s between the notches in
lead II, it is known as P mitrale pattern and indicates LAE.3
However, it was observed in only 1/3rd of the patients with isolated MS proved at
surgery.2
iii) P Terminal Force

Increased P terminal force or Morris index:4 It is derived by multiplying the depth
(in mm) by duration (in seconds) of terminal negative portion of diphasic P wave in
V1 and expressed in mm-s.
If P terminal force is 0.04 mm-s (i.e. depth 1 mm and duration 0.04 s), it
indicates LAE.
The ECG diagnosis of LAE by Morris criterion was confirmed in 68% of cases at
surgery.2 The combined P terminal force and P wave duration are correlated with
echocardiographic LAE in 82%.5
The Morris index may also be positive in COPD with or without corpulmonale, and
in patients with pectus excavatum and straight back syndrome.
Morris index: P duration P initial force in Tall P >2.5 mm-

>0.04 mm-s >0.12 s-P mitrale V1: >0.06 mm-s P pulmonale
Macruz P axis:
index: >1.6 >75
Left atrial Right atrial
enlargement enlargement
P axis: 30 to
45 Abnormal RVH
P waves
f >1 mm in atrial
fibrillation Tall peaked P in Tall and
Biatrial
V1 notched P wide P in
enlargement
in V5 or V6 or II limb leads
Diphasic P
in V1
Fig. 24.3 | Abnormal P wavesdiagnostic criteria of left, right and bi-atrial enlargement.
iv) Frontal P Axis
LAE is usually associated with leftward shift of mean P axis6 between 30 and 45.
However, it lacks specificity and sensitivity, and it occurs only in 10% of the cases
with LAE.
v) In Atrial Fibrillation
If the size of the fibrillatory f waves is 1 mm (coarse atrial fibrillation), is suggestive
of LAE, which is correlated with roentgenographic and anatomic evidence of LAE.7
Fine f waves if they are 0.5 mm in size.7
4. Right Atrial Enlargement or RA Abnormality

As in LAA, the P wave abnormality may be due to increase in RA size or may reflect
a more vertical heart position within the chest due to pulmonary hyperinflation (as in
COPD), hence the term RA abnormality (RAA) is preferred to RA enlargement (RAE).
(see Fig. 24.3) Similarly, the criteria for RAA have low sensitivity but high specificity
when correlated to echocardiographic findings. Following is the criteria for RAA.
i) Amplitude
Tall peaked P waves in lead II of 2.5 mm (250 V) (P pulmonale or church
steeple appearance). P pulmonale was present in about 20% of patients with chronic
corpulmonale.8
ii) Initial Positive Portion of Diphasic P Wave in Lead V1
The amplitude of the initial positive deflection of P wave taller than 1.5 mm
Duration of the initial positive deflection is greater than 0.04 s9
P initial force: 0.06 mm-s. This is derived by multiplying amplitude (in mm) by
duration (in seconds) of initial positive deflection of the diphasic P wave.
iii) Frontal P Axis

Rightward shift of mean P axis of greater than 75.
iv) QRS Complex Abnormalities

These may also suggest RAA
qR pattern followed by a tall R wave in V1 (suggestive of RVH) without the evidence
of myocardial infarction.10 The qR pattern occurs due to an anatomical shift of the
hypertrophied RV by an enlarged and dilated RA.
Low amplitude QRS complexes (6 mm or 600 V) in lead V1 with a three fold
or greater increase in lead V2. This has been attributed to a large volume of blood in
RA that lies between the ventricles and precordial leads.
v) With Echocardiographic Correlation

The best ECG predictors of RAE in the absence of complete RBBB11 were:
A P wave amplitude of 2.5 mm in V1,
A QRS axis of 90, and
An R/S ratio of 1 in V1.
The combined sensitivity of these criteria was 48% with 100% specificity.11
5. Biatrial Enlargement or Abnormality

(i) Notched P wave in lead II: It is seen with initial component increased in ampli-
tude and taller than the second component (P tricuspidale). It is frequently seen
in tricuspid valve disease, and mitral valve disease with PH.
(ii) Diphasic P wave in lead V1: Initial positive deflection is 1.5 mm in amplitude
and second negative portion is wide (1 mm or 0.04 s) and deep (1 mm
depth).12
(iii) A tall peaked P wave (1.5 mm): It is seen in V1 and a wide, notched P wave in
limb leads (II) or in (precordial leads (V5 and V6).12
(iv) Increase in both amplitude (2.5 mm) and duration (0.12 s) of P wave: It
occurs in limb leads12 (see Fig. 24.4 and Table 24.2).
II
V1
V5
Fig. 24.4 | Biatrial enlargement with diphasic P in V , notched P in V , and tall and
wide P in II.
1 5
Table 24.2 Biatrial enlargement
Precordial leads Limb leads
1. Diphasic P in V1 1. Notched P in II with tall peaked P in V1

2. Tall peaked P in V1 with notched 2. Tall and wide P in limb leads
P in V5 or V6
Table 24.3 Abnormal T waves
Tall T Inverted T
1. Hyperkalemia 1. Myocardial ischemia or infarction

2. True posterior wall myocardial infarction 2. Ventricular hypertrophy
3. Cerebrovascular accidents (CVA) 3. Drug effects
4. Pulmonary embolism
5. Bundle branch block
6. Wolff-Parkinson-White syndrome
7. Ventricular ectopics or paced beats
8. CVA
V1 V2 V3 V4 V5 V6
Fig. 24.5 | Tall peaked T waves in precordial leads in hyperkalemia.
ABNORMAL T WAVES
It could be due to the alteration in morphology (tall or flat T waves) or polarity

(inverted T waves) (see Table 24.3).
1. Tall T Waves
The criteria for tall T waves: When amplitude of T waves is 6 mm in limb leads or
10 mm in precordial leads. Following are the common causes:
Tall peaked narrow based tented T waves occur in most of the leads, but are
more prominent in precordial leads and occur in hyperkalemia (serum level of
5.76.5 mEq/L) (see Fig. 24.5).
Tall symmetrical T waves in V1V2 with tall R waves occur in true posterior wall
myocardial infarction.
Tall symmetrical T waves in precordial leads can occur in hyperacute phase of anterior
wall myocardial infarction.
Tall T waves occasionally occur in patients with cerebrovascular accidents.
2. Flat T Waves
These are usually not diagnostic unless associated with ST depression and have the
same significance as that of ST depression.
3. T Wave Inversion
T wave changes may be primary or secondary which may occur alone or may be asso-
ciated with ST changes (elevation or depression).
There is abnormality in shape and duration of action potentials in primary T wave
changes, while there is an alteration of sequence of depolarization in secondary T wave
changes.
Abnormal sequence of repolarization can occur both in primary and secondary
T inversions.
The ventricular gradient (QRS-T angle) may help in differentiating primary T wave
inversions from obligatory secondary T wave inversions.13
QRS-T angle (ventricular gradient):13 The QRS-T angle is calculated by determining
the mean QRS axis and T axis in frontal plane.
QRS-T angle mean QRS axis-mean T axis, which is normally 60.
In primary T wave inversion, QRS-T angle is wide (60) as T wave axis is directed
away from the site of pathology.
a) T Wave Inversion with ST Changes

i) Primary T wave inversions are due to alterations in the duration or morphology
of ventricular action potentials without changes in the activation sequence. Common
causes are as follows:
Myocardial ischemia or infarction
Drug effects: Digitalis effect (associated with shortening of QT interval)
Ventricular hypertrophy
Pulmonary embolism (V V ).
1 3
ii) Secondary T wave inversions are due to the alteration of ventricular activation
(depolarization) without changes in action potentials. Common causes are:
Bundle branch blocks
Wolff-Parkinson-White syndrome
Ventricular ectopics or paced beats.
T wave vector deviates opposite to that of main QRS vector in LBBB, opposite to the
slow terminal QRS component in RBBB and opposite to the delta wave in pre-excitation
syndromes.
b) T Wave Inversion without Significant ST Changes

(Mostly Primary T Wave Inversion)
i) Deep T wave inversion of 5 mm: It is characteristics of
Ischemia or post MI (localized to precordial or limb leads)
Cardiomyopathy (in most of the leads)
Apical cardiomyopathy (inverted giant T waves in V V )

2 4
Cerebrovascular accidents especially in subarachnoid hemorrhage (diffuse CVA
T wave pattern associated with prolonged QT interval)

Post Stokes-Adams syncope
Myocarditis
Pericarditis
Cocaine and alcohol abuse
Pancreatitis and gall bladder disease
Pheochromocytoma
Idiopathic global T wave inversion in women without an apparent cause.

14
ii) Minor T wave inversion of 5 mm: It may be found in all aforementioned

conditions as well as in the following:
Mitral valve prolapse
Hyperventilation
Postprandial (after a meal or cold drink)
Pneumothorax
Normal variant.
ABNORMAL U WAVES
These could be:

Large prominent U waves taller than T wave or 1.5 mm in the same lead or
Inverted U waves.
1. Large Prominent U Waves

These are commonly seen in (see Table 24.4):
Hypokalemia (in mid precordial leads V2V4, see Fig. 24.6)
Digitalis use
Quinidine use
Hypercalcemia
Intracranial hemorrhage
Thyrotoxicosis.
2. Inverted U Waves (in Leads I, II, V5 and V6)

These are commonly observed in:
Severe hypertensionwith systolic or diastolic overload (see Fig. 24.7).
Table 24.4 Abnormal U waves
Prominent U Inverted U
1. Hypokalemia 1. CAD
2. Digitalis use 2. Severe hypertension
3. Intracranial hemorrhage
4. Hypercalcemia
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 24.6 | Prominent U waves in precordial leads (V V ) in hypokalemia.

2 3
U
V1 V4
U
V2 V5
U
V3 V6
Fig. 24.7 | Inverted U waves in V V 4 6 in severe hypertension.
CAD
Acute ischemia (may be the only ECG finding).
Rarely, earliest sign of acute coronary syndrome.15
Exercise-induced transient U wave inversion has been correlated with severe
stenosis of LAD coronary artery.16
Acute anterior wall MI: It usually has less ST elevation, better collateral circula-
tion and a larger amount of stunned but viable myocardium.17
REFERENCES
1. Fitzgerald DM, Hawthorne HR, Crosseley GH, et al. P wave morphology during atrial pacing along
the atrioventricular ring. J Electrocardiol 1996;29(1):110.
2. Saunders JL, Calatayud JB, Schulz KJ. Evaluation of ECG criteria for P wave abnormalities. Am
Heart J 1967;74(6):757765.
3. Thomas P, DeJong D. The P wave in the ECG in the diagnosis of heart disease. Br Heart J
1954;16(3):241254.
4. Morris JJ Jr, Estes EH Jr, Whalen RE, et al. P wave analysis in valvular heart disease. Circulation
1964;29:242252.
5. Velury V, Spodick DH. Axial correlates of PV1 in left atrial enlargement and relation to intraatrial
block. Am J Cardiol 1994;73:998999.
6. Gooch AS, Calatayud JB, Goran PA. Left hand shift of the terminal P forces in the ECG associated
with LAE. Am Heart J 1966;71:727.
7. Thurmann M, Janney JG Jr. The diagnostic importance of fibrillatory wave size. Circulation
1962;25:991994.
8. Fowler NO, Daniels C, Scott RC, et al. The electrocardiogram in cor pulmonale with and without
emphysema. Am J Cardiol 1965;16:500506.
9. Dines DE, Parker TW. Some observations on P wave morphology in precordial lead V1 in patients
with elevated LA pressure and LA enlargement. Proc Staff Meet Mayo Clin 1959;34:401.
10. Sodi-Pallares D, Bisteni A, Herrmann GR. Some views on the significance of qR and QR type com-
plexes in the right precordial leads in absence of MI. Am Heart J 1952;43:716734.
11. Walder LA, Spodick DH. Global T wave inversion: long term follow up. J Am Coll Cardiol
1993;21(7):16521656.
12. Kaplan JD, Evans GT, Foster E, et al. Evaluation of electrocardiographic criteria for right atrial
enlargement by quantitative two-dimensional echocardiograph. J Am Coll Cardiol 1994;23:747.
13. Surawicz B, Knilanu TR. Biatrial enlargement: Diagnostic criteria. In: Chous Electrocardiogrphy in
Clinical Practice. 5th ed, WB Sanders Company, Philadelphia, Pennsylvania. 2001:39.
14. Wilson FN, Macleod AG, Barker PS, et al. The determination and significance of the areas of the
ventricular deflections of the electricardiogram. Am Heart J 1934;10:4661.
15. Jaffe ND, Boden WE. Spontaneous transient, inverted U waves as initial electrocardiographic manifes-
tations of unstable angina. Am Heart J 1995;129(5):10281030.
16. Chikamori T, Kitaoka H, Matsumura Y, et al. Clinical and electrocardiographic profiles producing
exercise-induced U waves inversion in patients with severe narrowing of the left anterior descending
coronary artery. Am J Cardiol 1997;80(5):628632.
17. Tamura A, Watanbe T, Nagase K, et al. Significance of negative U waves in the precordial leads
during anterior wall acute myocardial infarction. Am J Cardiol 1997;79(7):897900.
CHAPTER 25
V ENTRICULAR H YPERTROPHY
1. LEFT VENTRICULAR ECG Changes 508

HYPERTROPHY (LVH) 500 Diagnostic ECG Criteria for RVH 510
ECG Changes 500 Types of RVH 511
Systolic and Diastolic Overload Systolic and Diastolic Overload
of the Left Ventricle 501 of the Right Ventricle 512
Diagnostic ECG Criteria for LVH 502 3. BIVENTRICULAR
2. RIGHT VENTRICULAR HYPERTROPHY (BiVH) 513
HYPERTROPHY (RVH) 507 REFERENCES 514
1. LEFT VENTRICULAR HYPERTROPHY (LVH)
ECG Changes
LVH produces the following ECG changes:
(i) Changes in QRS complex
(ii) Changes in ST segment and T waves
(iii) Changes in axis in frontal plane, and
(iv) Other changes
(i) Changes in QRS Complex

Increased amplitude of R waves in leads facing the hypertrophied LV (I, aVL, V5
and V6) and deeper S waves in leads overlying RV (V1 and V2). High QRS voltages
and prolongation of QRS duration may be due to the increase in LV mass and the
delay in conduction system.1 Besides transmission factors may also contribute i.e.
lateral free wall lies closer to the chest wall due to LVH which causes increase in
body surface potentials in accordance with the inverse square law. LVH may then be
defined when LV mass index is 118 g/m2 in men and 104 g/m2 in women.
There may be widening of QRS complex with an increase in QRS duration of 0.11 s.
Notching of QRS complex may also be observed due to the fractionation of activation
wave fronts as a result of ventricular hypertrophy.
Deep (0.2 mV or 2 mm) and narrow (25 milliseconds) Q waves in leads facing
the left side of the septum (V4V6) in LV diastolic overload.
An increase in VAT of 0.05 s in V5V6. The VAT is usually prolonged with LV sys-
tolic overload than with LV diastolic overload.
VENTRICULAR HYPERTROPHY 501
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 25.1 | LVH with tall R waves, ST segment depression and T waves inversion in V
waves in V and V .
5 and V6, deeper S
1 2
(ii) Changes in ST Segment and T Waves

ST segment depression and asymmetrical inverted T waves in leads with tall R waves
in LV systolic overload (see Fig. 25.1).
Minimal ST segment elevation (usually 1 mm) with concavity upwards with tall
symmetrical T waves and tall R waves in leads V5V6 in LV diastolic overload with
or without initial deep narrow Q waves.
These repolarization changes reflect primary defect of repolarization that accompa-
nies the cellular process of ventricular hypertrophy.
(iii) Changes in Axis in Frontal Plane

LAD may be present but usually it is 30.
QRS-T angle is widened (60) especially in LV systolic overload.
(iv) Other Changes
Inverted U waves in left precordial leads, which is more common in LV diastolic
overload2 (see Fig. 25.2).
Presence of left atrial abnormality or LAE.
Systolic and Diastolic Overload of the Left Ventricle

The concept of systolic and diastolic overload of the ventricle was introduced by
Cabrera and Monroy in 1952.3
The ECG pattern of systolic overload includes high voltage of R wave and secondary
ST and T wave changes in precordial leads, which usually occurs in aortic stenosis,
coarctation of aorta and systemic hypertension. (see Fig. 25.3)
The ECG pattern of diastolic overload includes high voltage of R wave with prominent
Q waves in precordial leads and ST segment is usually elevated (concavity upwards) with
an upright peaked T wave, which usually occurs in AR, MR and PDA. (see Fig. 25.4)
However, the clinical application of this concept is better correlated in young patients
especially with congenital heart disease than in patients with advanced acquired heart
disease.
I II III aVR aVL aVP
V1 V2 V3 V4 V5 V6
U U U
X 1/2 X 1/2 X 1/2
Fig. 25.2 | LVH (voltage criteria and STT changes) with inverted U waves in precordial leads in severe
hypertension.
T T
T
V1 V2 V3 V4 V5 V6
Fig. 25.3 | Systolic overload of LVLVH with ST depression (arrow) and T inversion in precordial leads.
Diagnostic ECG Criteria for LVH
Based on the ECG changes, several diagnostic criteria for LVH have been developed.
However, echocardiography is taken as gold standard for diagnosis of ventricular
hypertrophy as several necropsy studies have demonstrated the superiority of echocardio-
graphy over ECG to detect LVH4 (see Fig. 25.5A and 25.5B). Besides echocardiogra-
phy is also a better noninvasive method for serial follow-up of changes during progression
or regression of LVH.
T T
q
q
V1 V2 V3 V4 V5 V6
Fig. 25.4 | Diastolic overload of LVLVH with prominent Q and upright T in V 5 and V6.
LV
RV
LVH
LA
RA
|
Fig. 25.5A Apical 4 chamber echocardiographic view
Echocardiagraphy is superior to ECG for detecting left
Fig. 25.5B | Diagrammtic representation of
LVH.
ventricular hypertrophy (LVH)RV: right ventricle, LV:
left ventricle, RA: right atrium, LA: left atrium.
(i) Sokolow-Lyon Voltage Criteria5

S in V1 R in V5 or V6 35 mm (3.5 mV): sensitivity 55.6%, specificity 89.5%
R in I S in III 25 mm (2.5 mV): sensitivity 10.6%, specificity 100%
R in aVL 11 mm (1.1 mV): sensitivity 10.6%, specificity 100%
R in V5 or V6 26 mm (2.6 mV): sensitivity 25%, specificity 98%

Largest R largest S in precordial leads 45 mm is more sensitive with less specificity
as compared to S in V1 R in V5 or V6.6
The voltage criteria may overdiagnose LVH in young adults (under 40 years),7 thinly
built and obese individuals.8
Sokolow-Lyon grading system: Depending upon the associated repolarization changes,
it is classified into four grades. The diagnostic sensitivity and specificity increase with
higher grades:
Grade I: only have voltage criteria (as above)
Grade II: voltage criteria low amplitude T waves (10% of R wave in the same
lead)
Grade III: voltage criteria biphasic T waves
Grade IV: voltage criteria inverted T waves
(ii) Romhilt-Estes Point Score System9

Any of the following increased amplitude or depth criteria: 3 points
R or S waves in limb leads 20 mm (2.0 mV)
S wave in V1 or V2 30 mm (3.0 mV)
R wave in V5 or V6 30 mm (3.0 mV)
STT segment changes (typical LV strain pattern)
Without digitalis therapy: 3 points
With digitalis therapy: 1 point
LAE: 3 points
P terminal force in V1 of 4 mV-msec (1 mm depth with a duration of 0.04 s)
LAD: 30: 2 points
QRS duration of 0.09 s: 1 point
Intrinsicoid deflection (VAT) in V5 or V6 0.05 s: 1 point
5 points are diagnostic of LVH, while 4 points suggest probable LVH. Sensitivity is
54% and specificity is 97%.
(iii) Glassglow Scoring System

It is modified Romhilt-Estes point score system which is as follows:
Any of the increased amplitude (R) or depth (S) criteria: 2 points
STT segment changes: 14 points
LAE: P terminal force of 4 mV-msec: 2 points
LAD: 2 points
QRS duration of 0.09 s: 1 point
Intinisicoid deflection of 0.05 s: 1 point.
Definite diagnostic of LVH: 6 points, probable LVH: 5 points and possibility of
LVH: 4 points.
(iv) Cornell Voltage Criteria10

R in aVL S in V3 28 mm (2.8 mV) in men and 20 mm (2.0 mV) in women.
Sensitivity is 36% and specificity is 95%.
(v) Cornell Product (voltageduration measurement)11

Cornell voltage QRS duration 2,436
Sum of voltages in all 12 leads QRS duration 17,472
Sensitivity is 51% and specificity is 95%.
(vi) Cornell Regression Equation10

To further increase the sensitivity, regression equation is devised which is as follows:
1/(1 eexp)
where
exp 4.558 0.093 (R in aVLS in V3)0.306 T in V1 0.211 QRS duration0.278
P terminal force in V1 0.859 (sex)
where
R, S, and T in mV; QRS duration in msec; P terminal force in mm-sec and sex 1 for
men, 2 for women.
LVH is present if exp is less than 1.55.
(vii) Novacode Criteria12

LV mass index (LVMI) can be calculated with the equation of the Novacode criteria
which also enhances its sensitivity in the diagnosis of LVH.
LVMI (g/m2) 36.4 0.010 R in V5 0.20 S in V1 0.28 S* in III 0.182
T(neg) in V6 0.148 T(pos) in aVR 1.049 QRS duration
where
S*: amplitude of S, Q, or QS whichever is larger, neg and pos: amplitudes of negative
and positive portions of T waves respectively.
(viii) Seigels Total QRS Voltage Criteria

Sum of QRS voltages in all 12 leads 179 mm
QRS voltageduration product: voltage criteria QRS duration 17,472.
(ix) The Hernandez Padial Voltage Criterion12

Sum of QRS voltages in all 12 leads 120 mm
It has high specificity and sensitivity for the diagnosis of LVH in systemic hypertension.
(x) Natural History Series-2 (1993)13

QRS duration 120 ms 1 of the following
R or S in the limb leads 20 mm
S in V1 30 mm or R in V6 30 mm.
Table 25.1 ECG diagnostic criteria of LVH
Criteria Sensitivity (%) Specificity (%)
1. Sokolow-Lyon voltage criteria 10.655.6 90100

2. Romhilt-Estes point score system 54 97
3. Cornell voltage criteria 36 95
4. Cornell product 51 95
5. Koito and Spodick criterion 50 100
6. Talbot criterion Low sensitivity 90
S V1R V5 35 mm QRS 102 ms 1 of

1. R aVLS V3 28 mm in
R L1S L3 25 mm 1. R or S in limb lead
men 20 mm in women 20 mm
R aVL 11 mm
2. Voltage QRS 2,436 2. S V1 or R V6 30 mm
R V5 or R V6 26 mm
Natural history Total QRS

Cornell
series-2 120 mm
Sokolow-Lyon
Hernandez-
Padial
R aVL 16 mm Talbot LVH criteria
Seigels
Romhilt-Estes: 5p
Glassglow: 6p Kaito and Spodick Total QRS
179 mm
1. amplitude or 1. amplitude or R V6 R V5
depth criteria: 3p depth criteria: 2p
2. ST-T changes: 3 2. ST-T changes: 14p
or 1p (with digitalis) 3. LAE: 2p
3. LAE: 3p 4. LAD: 2p
4. LAD: 2p 5. QRS 0.09 s: 1p
5. QRS 0.09 s: 1p 6. VAT: 1p
6. VAT: 1p
Fig. 25.6 | Summary of the various diagnostic ECG criteria for left ventricular hypertrophy (LVH)LAE:
left atrial enlargement, LAD: left axis deviation, VAT: ventricular activation time, p: point.
(xi) The Talbot Criterion14

R in aVL 16 mm. It has high specificity (90%) even in the presence of myocardial
infarction and ventricular block but has low sensitivity.
(xii) The Koito and Spodick Criterion15

R in V6 R in V5. This criterion claims 100% specificity with a sensitivity of 50%
(see Table 25.1 and Fig. 25.6).
(xiii) Diagnosis of LVH in Left Bundle Branch Block (LBBB)

The diagnosis of LVH in the presence of LBBB is difficult because LBBB can alter the
amplitude of QRS complex in either direction.
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 25.7 | LVH with complete LBBB with S in V R in V

2 6 is 45 mm.
(i) Kafka et al. criteria based on echocardiogram:16

R in aVL 11 mm (sensitivity: 24%, specificity: 100%)
S in V R in V or V 40 mm (sensitivity: 58%, specificity: 97%)

1 5 6
S in V 30 mm and S in V 25 mm (sensitivity: 75%, specificity: 90%)
2 3
Frontal QRS axis 40 (or S R ) (sensitivity: 39%, specificity: 100%)
2 1
(ii) Klein et al. criteria also based on echocardiogram:17

S wave amplitude in V R wave amplitude in V 4.5 mV (sensitivity: 86%,
2 6
specificity: 100%) (see Fig. 25.7)
Presence of LAE and QRS duration of 160 ms supports the diagnosis.
(xiv) Diagnosis of LVH in the Presence of Left Anterior

Fascicular Block (LAFB)
LAFB can cause a false positive diagnosis of LVH based on voltage criteria without
associated secondary ST-T changes.
R in aVL 13 mm (sensitivity: 35%, specificity: 92%).
S in II maximum sum of R S in any single precordial lead 3.0 mV (sensitivity:
96%, specificity: 87%).18
(xv) Diagnosis of LVH in Presence of Right Bundle

Branch Block (RBBB)
Usual criteria for LVH has to be applied even though the presence of RBBB lowers
the sensitivity and increases the specificity of the voltage criteria for the diagnosis
of LVH.
The combination of LAE or LAD with RBBB also suggests underlying LVH19
(see Fig. 25.8).
2. RIGHT VENTRICULAR HYPERTROPHY (RVH)
The hypertrophy of the RV may occur in one or more of the regions of the RV:
The free wall of the RV
Kafka:
1. R aVL 11 mm
2. S V1 R V5 or
V6 40 mm
3. S V2 30 mm and
S V3 25 mm 1. Usual criteria
4. S L2 R L1 or 2. LAE or LAD
axis 40 with RBBB
LVH in
LBBB RBBB
presence of
Klein: Left anterior R aVL 13 mm

1. S V2 R V6 fascicular block SL2Sum of R and
45 mm S in a precordial
2. LAE and QRS lead 30 mm
160 ms
Fig. 25.8 | Summary of the diagnostic ECG criteria of left ventricular hypertrophy (LVH)
in presence of other conditionsLAE: left atrial enlargement, LAD: left axis
deviation, LBBB: left bundle branch block, RBBB: right bundle branch block.
The right paraseptal portion

The basal portion especially the right ventricular outflow tract.
ECG Changes
The ECG changes in RVH are mainly due to increased mass (hypertrophied cell) and
prolongation of the electrical action time of the RV. The ECG changes could be due to sys-
tolic (pressure) or diastolic (volume) overloads. Following are the ECG changes that
occur in RVH:
(i) Changes in QRS complex
(ii) Changes in ST segment and T wave
(iii) Changes in frontal QRS axis and
(iv) Other changes.
(i) Changes in QRS Complex

There is a progressive increase in the amplitude of R or R waves and progressive
diminution of S waves in right oriented leads (V1 and V2) which is expressed as an
R:S or R:S ratio of 1 with R or R waves 5 mm in amplitude. These changes
indicate RV systolic overload and are often due to hypertrophy of RV free wall or
combination of RV free wall and right paraseptal portion.
Presence of small q in V1 resulting in qR pattern due to anatomical shift of the
hypertrophied RV by an enlarged and dilated RA.20
Partial or complete RBBB pattern (rSr or rsR) in V1 due to RV diastolic overload
as in ASD.
Deep S waves and abnormally small r waves in left oriented leads (I, aVL, V5V6)
with an r:S or R:S ratio of 1 in V5 or V6.
VAT in V1 is 0.03 s.
Evidence of RVH in COPD include:
Deep S waves in lateral precordial leads,
S1Q3T3 pattern, i.e. deep S in lead I (RS or rS), abnormal Q in lead III and
inverted T wave in inferior leads including lead III and
RAD
Evidence of RVH in pulmonary embolism which causes acute RV pressure overload,
includes qR in V1 or V2, S1Q3T3 pattern (occurs in only 10%), ST segment and T
changes in V1V3, incomplete or complete RBBB and sinus tachycardia.
Dominant hypertrophy of right basal portions of RV is uncommon and is character-
ized by deep S in V5V6, tall R or qR in aVR, S1S2S3 syndrome (deep S waves in
Leads I, II, III) and RAD.
(ii) Changes in ST Segment and T Waves

Minimal ST segment depression with T wave inversion in right oriented leads (V1V3)
especially in the presence of RV pressure overload.
(iii) Frontal QRS Axis

There is a dominant RAD and widened QRS-T angle.
(iv) Other Changes

Amplitude of U wave may be diminished or it may be inverted in right precordial
and/or inferior leads in both RV systolic and diastolic overloads.
Associated RAE (see Fig. 25.9) or RA abnormality is common.
I V1 V4
aVR
V2
aVL V5
II
V3 V6
III aVF
Fig. 25.9 | RVH and RAE with peaked P, tall R, and inverted T waves in V and V .
1 2
Diagnostic ECG Criteria for RVH

(i) Natural History Series (1993)13
QRS complex duration 120 ms 1 of the following
R in V1 7 mm
Frontal QRS axis: RAD of 110
rSR in V1 where R is 10 mm (in 1 year of age) or 15 mm (in 1 year of age)
(ii) Milnor Modified Sokolow and Lyon Criteria21

QRS duration 0.12 s and frontal QRS axis of 110 to 180
R/S or R/S ratio in V11 with R or R amplitude 0.5 mV
(iii) Butler-Legger Criteria22

The sensitivity of this criteria varies from 66% to 79% with 97% in pulmonary arterial
disease.
P wave amplitude of 0.25 mV in any of the leads: II, III, aVF, V1 or V2
R wave amplitude in lead I 0.2 mV
A R PL 0.7 mV,
where
A (Anteriorly directed deflection): Derived from R wave amplitude in lead V1 or V2.
R (Rightward deflection): Derived from S amplitude in lead I or V6.
PL (Posterolateral deflection): Derived from S amplitude in lead V1.
(iv) Other Criteria

(a) QRS changes:
qR (has 10% sensitivity but highly specific23) or rsR (with R 10 mm) pattern
in V1
R in V1 7 mm (0.7 mV) has sensitivity of 10%24
R/S in V1 1 with R 5 mm (0.5 mV) has sensitivity: 25% and specificity: 89%24
S in V5 or V6 7 mm (0.7 mV) has sensitivity: 17% and specificity: 93%24
(b) Frontal QRS axis:
RAD has sensitivity: 14% and specificity: 99%24
(c) S1Q3T3 pattern has sensitivity: 11% and specificity: 93%24
(d) S1S2S3 pattern has sensitivity of 10%24 (see Fig. 25.10 and Table 25.2)
(e) Diagnosis of RVH in the presence of RBBB: Even though the mere presence
of RBBB is suggestive of RVH, the presence of RBBB lowers the specificity and
sensitivity of criteria for the diagnosis of RVH.
Barker and Valencia criteria: RVH is suggested with a specificity of 60% by the
presence of R of 1.5 mV in V1 in complete RBBB and 1.0 mV in incom-
plete RBBB.25
QRS 120 ms1 of 1. QRS 120 ms, axis: 1. P 0.25 mV in L2,

1. R V1 7 mm 110 to 180 L3, aVF, V1 or V2
2. RAD 110 2. R/S or R/S in V1 1 2. RL1 0.2 mV
3. rSR in V1R R or R 5 mm 3. RV1 or V2SL1 or
10 mm(1 year of age) V6SV1 0.7 mV
15 mm(1 year of age)
Milnor modified
Sokolow-Lyon
Natural history
RVH criteria Butler-Legger
series
1. S V5 or V6 7 mm
2. S1Q3T3 Others
3. S1S2S3
Fig. 25.10 | Summary of the various diagnostic ECG criteria of right ventricular hyper-
trophy (RVH)RAD: right axis deviation.
Table 25.2 ECG criteria of RVH
Criteria Sensitivity (%) Specificity (%)
1. QRS changes 10 8993

2. Frontal QRS axis (RAD) 14 99
3. S1Q3T3 pattern 11 93
4. S1S2S3 pattern 10
Milnor criteria: Frontal QRS axis of 110 to 270 or R/S or R/S ratio in
V1 1, provided R or R amplitude in V1 is 0.5 mV, with a specificity of
60%.21
However, the likelihood of RVH is increased if both RAD and R of 1.5 mV
in V1 are present.
(f) Diagnosis of RVH in the presence of LBBB: It is difficult to diagnose RVH in pres-
ence of LBBB. However, it can be suspected when RAD is present in LBBB.
Types of RVH
RVH has been described in three types:
Type A RVH: Typical RVH pattern with tall R wave, small S wave, increased R/S ratio
in V1, which is typically present in pulmonary hypertension, congenital PS, TOF.
Type B RVH: Incomplete RBBB pattern, i.e. rSR pattern, characteristic of volume
overload conditions, such as ASD, TR, PAPVC.
V1 V2 V3 V4 V5 V6
Fig. 25.11 | Systolic overload of RV (qR pattern in V ).

1
V1 V2 V3 V4 V5 V6
Fig. 25.12 | Diastolic overload of RV (rSR pattern in V ).1
Type C RVH: Deep S wave, small r wave, and R/S ratio 1 in leads V5 or V6,
typically present in patients with chronic lung disease.
Systolic and Diastolic Overload of the Right Ventricle

The concept of systolic and diastolic overload of the ventricle was introduced by Cabrera
and Monroy in 1952.3
The ECG pattern of systolic (pressure) overload includes tall monophasic R wave or
diphasic RS, Rs, or qR complex in lead V1 with T wave usually inverted, which
typically occurs in PS, PH or TOF. (see Fig. 25.11)
The ECG pattern of diastolic (volume) overload includes rSR pattern in V1, which
is characteristic of ASD, PAPVC and TR. (see Figs 25.12 and 25.13)
However, the hemodynamic correlation of the ECG overload pattern is more satis-
factory in congenital than acquired heart diseases.
AS, COA,
AR, MR, PDA
systemic HTN
LVH (voltage LVH (voltage criteria)
criteria) with tall R Tall R, prominent Q,
and ST and T in T, ST (slight) in
precordial leads precordial leads
LV systolic LV diastolic
overload overload
RV systolic RV diastolic
overload overload
Tall R, RS, Rs, or qR

PS, PH, TOF rSR in V1 ASD, PAPVC, TR
with T in V1
Fig. 25.13 | Systolic and diastolic overloads of left and right ventriclesLVH: left ventricular hypertrophy,
LV: left ventricular, RV: right ventricular, AS: aortic stenosis, AR: aortic regurgitation, MR: mitral
regurgitation, COA: coarctation of aorta, HTN: hypertension, PDA: patent ductus arteriosus,
PS: pulmonary stenosis, PH: pulmonary hypertension, TOF: tetralogy of Fallot, ASD: atrial sep-
tal defect, PAPVC: partial anomalous pulmonary venous connection, TR: tricuspid regurgita-
tion, : upright or elevation, : inverted or depression.
3. BIVENTRICULAR HYPERTROPHY (BiVH)
Hypertrophy of one ventricle may result in an apparent diminution of electrical activ-

ity of the other ventricle and hence there are no specific ECG diagnostic criteria
for BiVH.
i) Features of LVH with one of the following:
RAD (greater than 90) in presence LVH criteria (especially in precordial leads).26
Tall R waves in both right and left precordial leads especially when R/S in V1 is 1.23
Deep S waves in left precordial leads in the presence of LVH criteria.
Large equiphasic QRS complexes (tall R and deep S) in mid precordial leads (V3V4)
which is known as Katz-Wachtel pattern or phenomenon, which is commonly present
in congential heart diseases such as VSD or PDA with PH.27 R S V3 or V4 should
be 60 mm in children and 50 mm in others (see Fig. 25.14).
R wave greater than Q wave in lead aVR, and S wave R wave in lead V5, with
T wave inversion in lead V1 in conjunction with signs of LVH.28
Small s wave in V1 with criteria for RVH or LVH which is known as shallow s
syndrome.
ii) Left atrial abnormality (LAE) with one of the following:24
R/S in V5 or V6 is 1
S wave in V5 or V6 7 mm (0.7 mV)
RAD of greater than 90
V1 V2 V3 V3 V5 V6
Fig. 25.14 | deep

Biventricular hypertrophy with equiphasic QRS complexes in V V , tall R waves in V
S waves in V .
3 4 1 and
5
All the above criteria suggested for BiVH have low sensitivity with moderate speci-
ficity. Jain et al found that 25% had ECG findings compatible with BiVH, 36% had
an LVH pattern and 20% had an RVH pattern in 69 patients of BiVH identified by
echocardiography with sensitivity of 24.6% and specificity of 86.4%.29
REFERENCES
1. Xiao HB, Brecker SJ, Gibson DG. Relative effects of left ventricular mass and conduction disturbance
on activation in patients with pathological left ventricular hypertrophy. Br Heart J 1994;71:548553.
2. Kishida H, Cole JS, Surawicz B. U wave: a highly specific but poorly understood sign of heart disease.
Am J Cardiol 1982;49(8):20302036.
3. Cabrera CE, Monroy JR. Systolic and diastolic loading of the heart. II Electrocardiographic data.
Am Heart J 1952;43(5):669686.
4. Surawicz B. Electrocardiographic diagnosis of chamber enlargement. J Am Coll Cardiol 1986;8(3):
711724.
5. Sokolow M, Lyon TP. The ventricular complex in LVH as obtained by unipolar precordial and limb
leads. Am Heart J 1949;37:161186.
6. Romhilt DW, Bove KE, Norris RJ et al. A critical appraisal of the electrocardiographic criteria of left
ventricular hypertrophy. Circulation 1969;40(2):185195.
7. Manning GW, Smiley JR. QRS-voltage criteria for LVH in a normal male population. Circulation
1964;29:224230.
8. Kitty SE, Lepeschkin E. Effect of body build on the QRS voltage of the electrocardiogram in normal
men: its significance in the diagnosis of left ventricular hypertrophy. Circulation 1965;31:77.
9. Romhilt D, Estes EH Jr. A point score system for the ECG diagnosis of left ventricular hypertrophy.
Am Heart J 1968;75(6):752758.
10. Casale PN, Devereux RB, Kligfield P, et al. Electrocardiographic detection of left ventricular hyper-
trophy: Development and prospective validation of improved criteria. J Am Coll Cardiol 1985;6(3):
572580.
11. Molloy TJ, Okin PM, Devereux RB, et al. Electrocardiographic detection of left ventricular hyper-
trophy by the simple QRS voltage-duration product. J Am Coll Cardiol 1992;20(5):11801186.
12. Rodriguez Padial L. Usefulness of total 12-lead QRS voltage for determining the presence of left
ventricular hypertrophy in systemic hypertension. Am J Cardiol 1991;68(2):261262.
13. Micheal OFallon, Cynthia S Crowson, Linda J Rings, et al. Report from the second joint study on
the natural history of congenital heart defects (NHS-2). Circulation 1993;87:415.
14. Talbot S, Kilpatrick D. Diagnostic criteria for left ventricular hypertrophy. In McFarlane PW, ed.
Progress in Electrocardiology. London: Pittman Medical, 1979:534541.
15. Koito H, Spodick D. Electrocardiographic RV6/RV1 voltage ratio for diagnosis of left ventricular
hypertrophy. Am J Cardiol 1989;63:352361.
16. Kafka H, Burggraf GW, Milliken JA. Electrocardiographic diagnosis of left ventricular hypertrophy
in presence of left bundle branch block: An echocardiographic study. Am J Cardiol 1985;55(1):
103106.
17. Levy D, Labib SB, Anderson KM, et al. Determination of sensitivity and specificity of electrocardio-
graphic criteria for left ventricular hypertrophy. Circulation 1990;81:815.
18. Gertsch M, Theler A, Foglia E. Electrocardiographic detection of left ventricular hypertrophy in
presence of left anterior fascicular block. Am J Cardiol 1988;61(13):10891101.
19. De Leonardis V, Golstein SA, Lindsay J Jr. Electrocardiographic diagnosis of right ventricular hyper-
trophy in presence of complete left bundle branch block. Am J Cardiol 1988;62:590593.
20. Sodi-Pallares D, Bisteni A, Hermann GR. Some views as the significance of qR and QR type
complexes in right precordial leads in absence of myocardial infarction. Am Heart J 1952;43(5):
716734.
21. Milnor WR. Electrocardiogram and vectorcardiogram in right ventricular hypertrophy and right
bundle branch block. Circulation 1957;16(3):348367.
22. Behar JV, Howe CM, Wagner NB, et al. Performance of new criteria for RVH and MI in patients
with pulmonary hypertension due to cor pulmonale and mitral stenosis. J Electrocardiol 1991;24:231.
23. Loperfido F, Digaetano A, Santarelli P, et al. The evaluation of left and right ventricular hypertrophy
in combined ventricular over load by electrocardiography: relationship with echocardiography data.
J Electrocardiol 1982;15(4):327334.
24. Murphy MI, Thenabadu PN, de Soyza N, et al. Reevaluation of electrocardiographic criteria for left,
right and combined cardiac ventricular hypertrophy. Am J Cardiol 1984;53(8):11401147.
25. Barker JM, Valencia F. The precordial electrocardiogram in incomplete RBBB. Am Heart J 1949;
38:376.
26. Soulie P, Laham JP, Papanicolis I, et al. Les principaux types electrocardiographiques de surcharge
ventriculaire combinee. Arch Mal Coeur 1949;42:791.
27. Katz LN, Watchtel H. The diphasic QRS type of electrocardiogram in congenital heart disease. Am
Heart J 1937;13:202.
28. Pagnoni A, Goodwin JF. The cardiographic diagnosis of combined ventricular hypertrophy. Br
Heart J 1952;14(4):451461.
29. Jain A, Chandna H, Siber EN et al. Electrocardiographic patterns of patients with echocardiograph-
ically determined biventricular hypertrophy. J Electrocardiol 1999;32(3):269273.
CHAPTER 26
I NTRAVENTRICULAR
CONDUCTION D EFECTS
1. RIGHT BUNDLE BRANCH WHO/ISFC Task Force Criteria 523
BLOCK (RBBB) 516 3. FASCICULAR BLOCKS 523
WHO/International Society and Left Anterior (Hemiblock)
Federation for Cardiology (ISFC) Fascicular Block 524
Task Force Criteria for RBBB (1985) 517 Left Posterior (Hemiblock)
Variants RBBB 518 Fascicular Block 526
2. LEFT BUNDLE BRANCH BLOCK 520 Multifascicular Blocks 527
WHO/International Society and REFERENCES 531
Federation for Cardiology (ISFC)
Task Force Criteria 522
An intraventricular conduction defect occurs as a result of an abnormality of conduction

through one or more of the divisions of the intraventricular conduction system (RBB,
LBB, left fascicular branches) distal to the bundle of His.
1. RIGHT BUNDLE BRANCH BLOCK (RBBB)
Following are the ECG changes:

QRS duration 120 ms (0.12 s).
Broad notched R waves (rsr, rsR, or rSR patterns) in right precordial leads (V1, V2,
V3R). The wide R is 0.04 s. Sometimes, s is very small or even absent resulting in
an rR complex (see Table 26.1).
The spread of excitation from the SA node down to the AV node and through the
bundle of His occurs normally. Also, the septal activation occurs normally from left to
right producing a small initial r wave. As the RBB is blocked, the excitation next
spreads down the LBB and LV myocardium producing an S or s wave. The impulses
then pass around the blocked RBB into the RV myocardium (after the activation of LV
has been completed) producing a wide R wave (0.4 s), resulting in a typical pattern
of rsR, rSR, or rsr in right precordial leads. In addition, as the LV activation remains
relatively intact, the initial portions of the QRS complex are normal, while delayed acti-
vation of the RV causes prolongation of QRS duration.
INTRAVENTRICULAR CONDUCTION DEFECTS 517
Table 26.1 ECG criteria for intraventricular conduction defects
Right bundle branch block Left bundle branch block
1. QRS duration 120 ms 1. QRS duration 120 ms

2. Broad notched R waves rsr, rsR, or rSR 2. Broad notched R waves or rsR in V5, V6, I, aVL
in V1, V2, V3, R and wide R 0.04 s
3. Wide and deep S 40 ms or 3. q waves absent in left sided leads except aVL
longer than R in V6 and I Small initial r (may be absent) and deep
S waves in right precordial leads
4. VAT in V1 50 ms, but normal in V5, V6 4. VAT in V5, V6 0.06 s, but normal in V1, V2
5. Mean QRS axis is not altered 5. Mean QRS axis is not altered.
6. Minimum secondary STT changes in V1, V2 6. Secondary STT changes in V5, V6, I, aVL
Wide and deep S waves in left precordial leads (V5 and V6), I, and aVL. As the septal
and LV activation are normal, the normal initial small q followed by R waves in left
oriented leads will occur. The wide and deep S waves in left oriented leads are due to
delayed activation of the RV.
There may be minimal depression of ST segment and secondary T wave inversion
in right precordial leads as a result of abnormalities in conduction. T wave is usually
opposite to the terminal deflection of the QRS complex, hence it is upright in Leads I,
V5 and V6, and inverted in right precordial leads. In transitional precordial leads (V3
or V4), the T wave may be diphasic.
The mean QRS axis in frontal plane is not altered by RBBB, and axis shifts occur
when associated with fascicular blocks.
WHO/International Society and Federation for Cardiology (ISFC)

Task Force Criteria for RBBB (1985)
It includes:1
QRS duration 120 ms.
An rsr, rsR, or rSR pattern in Lead V1 or V2 (see Fig. 26.1) and occasionally a wide
notched R wave.
Wide S wave 40 ms or more than duration of R wave in leads I and V6.
Normal R peak time in Leads V5 and V6, but 50 ms in V1.
There is a good correlation between the ECG findings of RBBB and the histopatho-
logical changes of the bundle branch.2 Many subjects with RBBB have no evidence of
underlying heart disease, the incidence increasing with age, the incidence being
1.3/1,000 below 30 years of age, and the incidence being 2.02.9/1,000 between
3044 years of age.3 The long and slender structure of the bundle makes it vulnerable
to the processes associated with aging.
RVH alone can cause an RBBB pattern (complete or incomplete) due to slow con-
duction in the hypertrophied or dilated RV.4 Besides, there is an increased incidence of
RBBB among the populations at high altitude.4
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 26.1 | RBBBrsR in V and V

1 2 with wide S in V5 and V6.
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 26.2 | Incomplete RBBBrsR in V and QRS duration is 120 ms.

1
Variants RBBB
a) Incomplete RBBB
The conduction through right bundle branch and its ramification is still possible, but
is delayed.
Duration of QRS complex is 120 ms (0.12 s) (see Fig. 26.2).
With progressive delay in the conduction of RBB due to progressively increasing
incomplete RBBB, there is a progressive diminution of s waves5 followed by slurring
of the upstroke of the small s waves in V1, which may be only early sign of incom-
plete RBBB.6 Hence, a serial tracing become necessary.
With progressively increasing block, the activation of the free wall of the RV occurs
after the activation of the free wall of the LV producing a small r in V1 and V2,
producing rsr or rSr pattern. As the delay increases, r becomes increasingly taller
(producing rsR pattern) as a larger part of free wall of RV activation will occur after
free wall of LV activation. However, R is not widened beyond 0.04 s. In complete
RBBB, R is widened 0.04 s as conduction occurs through myocardium.
The WHO/ISFC task force criteria for incomplete RBBB are the same as for complete
RBBB, except the QRS duration is 120 ms.1 Even though incomplete RBBB often
occurs in normal subjects, the likelihood of an abnormality increases with increased
QRS duration. Following criteria suggest no abnormality in the presence of incomplete
RBBB7:
Amplitude of initial R 0.8 mV.
Amplitude of r 0.6 mV.
R/S ratio of 1.0.
The likelihood of developing a complete RBBB in 11 yrs follow up of male subjects
with incomplete RBBB was 5.1% as compared to 0.7% of subjects without incom-
plete RBBB pattern; even though there was no demonstrable increase in cardiac deaths
in a follow up of 20 years.8 Besides normal subjects, the pathological incomplete
RBBB can also be present in the following conditions:
During atrial fibrillation, atrial flutter, supraventricular tachycardia (SVT) or atrial
premature contractions (APC); incomplete (sometimes complete) RBBB is the most
common pattern of aberrant intraventricular conduction as the RBB has the longest
action potential and the longest refractory period.
It can occur in massive pulmonary embolism or other forms of acute corpulmonale
due to acute RV distension and conduction delay in the stretched myocardium or in
the peripheral conducting system.
It can occur in RVH (of any cause: corpulmonale, MS, congenital heart disease) due
to slow conduction in the hypertrophied or dilated RV.
Commonly occurs in ASD, Ebsteins anomaly, arrhythmogenic RV dysplasia due to
conduction delay in the myocardium or in the peripheral conducting system.
Complete or incomplete RBBB frequently appears after CABG, heart transplanta-
tion and during right ventriculotomy.
An rSr pattern is often present in patients with pectus excavatum and straight back
syndrome, due to change in the position of the heart as a result of decrease in antero-
posterior diameter of the chest.9,10
b) Brugada Syndrome
It is a special form of incomplete or complete RBBB with persistent ST segment ele-
vation in right precordial leads (V1 and V2) (see Fig. 26.3). It is a characteristic of young
adults of Asian origin and the commonest cause of idiopathic ventricular fibrillation
and sudden death.11
c) Arrhythmogenic Right Ventricular Dysplasia

It is a type of RV cardiomyopathy involving inflow, outflow and apex of the RV, charac-
terized by sudden death in young individuals. ECG characteristics are:
Incomplete or complete RBBB with epsilon wave (terminal notch in QRS) in V1 and V2
as a result of slowed intraventricular conduction (see Fig. 26.4).
T waves inversion in V1V3 (see Fig. 26.5).
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 26.3 | Brugada syndromeRBBB pattern with ST elevation in V and V .

1 2
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 26.4 | Arrhythmogenic right ventricular dysplasiaepsilon wave (arrow head point-
ing to the notch) with T wave inversion in V and V .
1 2
2. LEFT BUNDLE BRANCH BLOCK
Following are the ECG changes:

QRS duration 120 ms (0.12 s) due to delayed and anomalous activation of left
septal mass and free wall of LV.
Absent septal q waves in left oriented leads (V5, V6, I and aVL), instead a small
initial r waves may be present due to septal activation in reverse fashion.
Broad notched R waves or rsR (M-shaped QRS complex) in lateral precordial leads
(V5, V6), I and aVL.
Small initial r waves (may be absent) and deep wide S waves in right precordial leads
(V1, V2) (see Table 26.1 and Fig. 26.6).
The activation from SA node to AV node and bundle of His occurs in a normal
fashion. Due to block in the LBB, the impulse cannot enter the left bundle system but
enters the RBB and activates the septum from right to left in reverse fashion produc-
ing a small initial r wave (instead of the usual q waves) in left oriented leads and a
WHO/ISFC: RBBB complete or

1. QRS 120 ms incomplete with
2. rsr, rsR, ST in V1 and V2
or rSR in V1
3. Wide S 40 ms in
I and V6 or S R
in I and V6 WHO/ISFC:
Brugada 1. QRS 120 ms
4. VAT in V1 50 ms
syndrome 2. Rest similar to
complete RBBB
Complete RBBB Incomplete
RBBB complete
or incomplete
Arrhythmogenic
with epsilon
RV dysplasia
wave and T in
V1 and V2
Fig. 26.5 | Diagnostic criteria for right bundle branch block (RBBB) and its variants
VAT: ventricular activation time, RV: right ventricular.
V1 V6
Normal
R
R
r
RBBB
T q
S S
R
T
LBBB
S T
Fig. 26.6 | (RBBB)

QRS complexes in V and V leadsin normal, right bundle branch block
1 6
and left bundle branch block (LBBB).
small initial q wave in right precordial leads (V1, V2). These initial very small waves
(r in left oriented leads and q in right precordial leads) may not be seen in all con-
ventional ECGs.
As left bundle is blocked, the impulse next spreads down the right bundle branch
activating RV in the normal fashion producing a small s wave in left oriented leads
and small normal r waves in right precordial leads. Since the RV is relatively thin,
the small s waves in left oriented leads may not go down the isoelectric line but
may merely produce a notch in the subsequent R waves. Then the impulse passes
around the blocked left bundle activating LV producing a wide R in left oriented
leads and deep wide S wave in right precordial leads. This results in notched or
slurred widened R or rsR pattern in V5, V6 and I and qrS or rS or QS pattern in
V1 and V2.
VAT in V5, V6 of 0.06 s.
Secondary STT changes due to abnormal intraventricular conduction are dis-
cordant with QRS complexes i.e. ST segment depression and T wave inversion in
leads with positive QRS complexes (i.e. in V5, V6, I and aVL) and ST segment ele-
vation and upright asymmetrical T wave in leads with negative QRS complexes (i.e.
in V1 V2).
Usually, there is no QRS axis shift in frontal plane, and the superior axis shift occurs
often in patients with preexisting left anterior fascicular block.
WHO/International Society and Federation for Cardiology (ISFC)

Task Force Criteria
It includes:1
QRS duration of 120 ms.
Broad and notched or slurred R waves in leads V5, V6 and aVL (see Fig. 26.7).
Absent Q waves in left precordial leads with possible exception of lead aVL.
The R peak time (VAT) in V5 and V6 is 60 ms and normal in V1 and V2.
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 26.7 | LBBBbroad notched R (M-shaped) and absent q waves in V V

with rS pattern in V V .
5 6 and aVL
1 3
Complete LBBB Incomplete
WHO/ISFC: WHO/ISFC:
1. QRS 120 ms 1. QRS 100 ms but
2. Broad and notched 120 ms
R in V5, V6 and aVL 2. Rest similar to
3. Absent q in left complete LBBB
precordial and I leads
4. VAT in V5 or
V6 60 ms
Fig. 26.8 | Diagnostic criteria of LBBBVAT: ventricular action time.
Clinical Significance
The LBBB usually occurs in patients with structural heart disease associated with
hypertrophy, dilatation or fibrosis of the LV myocardium, ischemic heart disease,
cardiomyopathy and advanced valvular heart disease.
It can occur as a result of toxic and inflammatory changes,12 hyperkalemia,13 or
digitalis toxicity.14
Primary degenerative disease of the conducting system, the Lenegre disease15 and
calcification of the cardiac skeleton, the Lev disease16 can also cause LBBB.
The prevalence of LBBB in a general male population at 50 years of age was 0.4%
and 80 years of age was 6.7%.17
Incomplete left bundle branch block is due to conduction delay in the left bundle
branch system. It is suspected when ECG shows LVH with slight QRS widening and
absent Q waves in left precordial leads and lead I. It has similar ECG features except
QRS duration being 120 ms (0.12 s) and VAT 0.06 s.
WHO/ISFC Task Force Criteria

QRS duration 100 ms but 120 ms.1
Prolongation of R peak time (VAT) 60 ms in left precordial leads.
Absence of Q waves in leads V5, V6 and I (see Fig. 26.8).
3. FASCICULAR BLOCKS
Immediately after its origin, the left bundle branch divides into two major divisions or
fascicles (see Fig. 26.9):
The posterior fascicle which arises proximally spreads as a broad band of fibers over
the inferior and posterior endocardium of the LV.
The anterior fascicle which arises more distally spreads as a narrow band of fibers
over the anterior and superior endocardium of LV.
Left posterior fascicle

Bundle of His
Left anterior fascicle
Left septal fibers
Right
bundle branch
Purkinje fibers
Fig. 26.9 | Divisions of left bundle branch.

Normally, the conduction spreads simultaneously through both the fascicles. However,
in a fascicular block which is due to delay or interruption of conduction in one of the
two major fascicles, the conduction will first proceed through the undamaged divi-
sion, altering the normal direction of the mean QRS axis. Left anterior fascicular
block is more common than left posterior fascicular block.
Left Anterior (Hemiblock) Fascicular Block

Due to block in the anterior fascicle, the conduction initially spreads through the poste-
rior fascicle which directs the QRS vector:
Inferiorly producing r wave in inferior leads (II, III, aVF) (see Fig. 26.10) and
To the right producing q waves in I and aVL reflecting normal left to right activation
of the septum.
The anterior fascicle will then be activated via interconnecting Purkinje fibers distal to
the site of the block orienting the QRS vector to:
The left producing R waves in I, aVL, resulting in a qR pattern in the same leads and
Superiorly producing deep S waves in inferior leads resulting in an rS pattern in II,
III and aVF, with deeper S in lead III than in lead II (see Fig. 26.11). Deep S waves
are also present in V5, V6 resulting in an RS (from usual qRs) pattern.18
As there is an alteration in the sequence of LV activation only, the overall duration of
QRS complex is not prolonged and is usually 120 ms (0.12 s) (see Table 26.2).
The most characteristic ECG finding is the marked LAD usually of 45 to 90 due
to the delayed activation of anterosuperior LV wall. The chronic obstructive pulmonary
diseases, CAD and WPW syndrome are other common causes of LAD (see Table 26.3)
Block in Late left

left anterior ventricular
fascicle activation
aVR aVL
Activation of
left anterior 2
fascicle distal 3
to block via
Purkinje fibers
1
I
Initial left ventricular activation via posterior fascicle III aVF II
Fig. 26.10 | Left anterior fascicle blockrS in II, III, aVF and qR in aVL with T inversion and a mean
frontal QRS axis of 60.
I aVR
II aVL
III aVF
Fig. 26.11 | Left anterior fascicular blockQRS complex 120 ms, rS in II, III, aVF and
prominent R in AVL with a mean frontal QRS axis of 60.
Table 26.2 Diagnostic criteria for left anterior fascicular block
Features Findings
1. QRS duration 120 ms

2. QRS morphology rS pattern in II, III, aVF and qR pattern in aVL
3. Frontal QRS axis 45 to 90
Table 26.3 Causes of superior (left) axis deviation in frontal plane
1. Normal individuals20 20 yrs of age in 5%

2. Congenital heart diseases22 AV canal defect, common atrium, tricuspid atresia, common
ventricle with TGA, cTGA with left sided apex
3. CAD: 4% of acute myocardial Anteroseptal or anterolateral myocardial infarction (MI) due to
infarction21 LAD occlusion. Can occur in inferior MI
4. COPD Especially with S1S2S3 ECG pattern
5. WPW syndrome22
6. Degenerative disease of the Lenegre disease15, Lev disease16
conducting system
CAD: coronary artery disease, COPD: chronic obstructive pulmonary disease, WPW: Wolff-Parkinson-White, TGA:
transposition of great arteries, LAD: left anterior descending artery.
Initial left ventricular

activation via
anterior fascicle
Activation of aVR aVL

posterior fascicle 1
Block in distal to block via
posterior Purkinje fibers
fascicle
2
I
Late left ventricular activation III aVF II
Fig. 26.12 | Left posterior fascicular blockrS in I and aVL and qR in III, II and aVF with a mean frontal
QRS axis of 110.
There may be secondary T wave changes due to intraventricular conduction distur-

bances i.e. T wave inversion in I and aVL.
Warner et al improved ECG criteria (1983)19 include:
Prominent R waves in aVL and aVR leads
Peaking of R later in aVR than peaking of R in aVL.
Left Posterior (Hemiblock) Fascicular Block

Due to block in the posterior fascicle, the conduction initially spreads through the
anterior fascicle resulting in the QRS axis oriented to:
the left producing a small r waves (usually 4 mm) in I and aVL and
superiorly producing q waves in inferior leads (II, III and aVF) (see Fig. 26.12).
Table 26.4 Diagnostic criteria for posterior fascicular block Table 26.5 Causes of right axis
deviation (RAD) in frontal plane
Features Findings
1. Right ventricular hypertrophy
1. QRS duration 120 s (RVH)
2. QRS morphology rS pattern in I, aVL and qR pattern 2. Emphysema
in inferior leads 3. Vertical heart
3. Frontal QRS axis 120, exclusion of other factors 4. Extensive lateral wall
causing RAD such as RVH myocardial infarction
The posterior fascicle will then be activated via interconnecting Purkinje fibers distal
to the site of the block resulting in QRS vector oriented to:
the right producing deep S waves in I, aVL resulting in rS pattern in the same leads,
inferiorly producing tall R waves in inferior leads, resulting in a qR pattern in II, III
and aVF, and
posteriorly producing deep S waves in V1 V2.
As there is only an alteration in the sequence of the LV activation, the overall duration of
QRS is not prolonged and is usually 120 ms (0.12 s). The prominent feature is right axis
deviation (RAD); QRS axis in frontal plane is 120 (see Table 26.4). The extensive lat-
eral wall infarct, right ventricular hypertrophy and emphysema can also give rise to RAD
(see Table 26.5). Similarly, there may be secondary T wave changes due to intraventricular
conduction disturbances i.e. T wave inversion in inferior leads but upright T waves in I.
WHO/ISFC Task Force Criteria

Frontal QRS axis 90 to 180.1
QRS duration 120 ms.
A Q waves should always be present in lead III; it may be small or absent in leads II
and aVF (see Fig. 26.20).
Left posterior fascicular block occurs in 0.20.4% of myocardial infarction (anterior
and posterior)23 and is seldom recognized as an isolated finding in the absence of
RBBB because:
It is short and thick
It has a dual blood supply from LAD and PDA coronary arteries, and
It is situated in the less turbulent LV inflow tract.
Multifascicular Blocks
Conduction delay in more than one structural components of the specialized conduc-
tion system can occur. Conduction delay in any two fascicles is known as bifascicular
block and delay in all three fascicles (RBB, LAF, LPF) is called trifascicular block.
However, if block is present in all fascicles, conduction would fail and complete heart
block would result. The multifascicular block:
Indicates advanced conduction system disease.
Is a marker of advanced myocardial disease.
Identifies the patients at risk for complete heart block.
Bifascicular Blocks
Following are the various types of bifascicular blocks:
RBBB with left anterior fascicular block (LAFB)
RBBB with with left posterior fascicular block (LPFB)
RBBB or LBBB with prolonged AV conduction (PR interval 0.2 s)
(i) RBBB with LAFB: It is common and is characterized by ECG pattern of RBBB
and LAD i.e. QRS axis of 45 (see Figs 26.13 and 26.14). This type of bifascicular
block occurs in:
4.87.0% of MI (anterior).21
Primary degenerative disease of the conducting system (Lenegres15 and Lev disease16).
Aortic stenosis, when both fascicles may be involved due to extension of the fibro-
calcific process of the aortic valve.24
It can also occur in congenital heart disease with endocardial cushion defects.
Block in left
anterior fascicle
Block
in right
bundle
branch
Fig. 26.13 | Bifascicular blockRBBB and LAFB.

I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 26.14 | Bifascicular block (RBBB LAFB)RBBB with LAD.

The patients of MI with bifascicular block may progress to complete AV block in

2443%.21
(ii) RBBB with LPFB: It is rare and is characterized by ECG pattern of RBBB
and RAD i.e. QRS axis of 120 (see Figs 26.15 and 26.16).
The causes of this type of bifascicular block are similar to RBBB with LAFB with
CAD being the most commonest cause.
Block in left
posterior fascicle
Block
in right
bundle
branch
Fig. 26.15 | Bifascicular blockRBBB and LPFB.
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 26.16 | Bifascicular block (RBBB and LPFB)RBBB with RAD.

It occurs in 0.8% of acute myocardial infarction,21 which may also progress to

complete AV block (in 2 of 21 patients over a mean period of 2 years follow up).25
Trifascicular Block
It usually involves conduction delay in the right bundle branch plus
Conduction delay either in the main left bundle branch or
Both left anterior and left posterior fascicles (see Fig. 26.17).
The ECG findings are characterized by bifascicular block (most commonly RBBB
LAFB) and prolonged PR interval, which indicates the first degree AV block (see
Figs 26.18, 26.19 and 26.20), but more likely represents an incomplete block in the
third fascicle in this situation.
A complete trifascicular block results in a complete AV block. Hence, His bundle
recording is usually required for definitive diagnosis and for the site of the block.
Block in left
posterior fascicle
Block
in right Block in left
bundle anterior fascicle
branch
Fig. 26.17 | Trifascicular block.
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 26.18 | Trifascicular blockRBBB and LPFB (QRS axis 120) with 1 AV block
(prolonged PR interval).
I aVR V1 V4
II aVL V2 V5
aVF
III V3 V6
Fig. 26.19 | Trifascicular blockRBBB and LAFB (QRS axis 60) with 1 AV block (prolong PR interval).
1. QRS 120 ms RBBB LAFB/ 1. QRS 120 ms
2. rS in II, III and aVF LPFB PR 2. rS in I and aVL
3. qR in aVL 3. qR in II, III and aVF
4. LAD 45 4. RAD 90
to 90 Trifascicular block to 180
Left anterior Left posterior

Fascicular blocks
fascicular block (LAFB) fascicular block (LPFB)
RBBB LAFB: RBBB LPFB:

RBBB with Bifascicular block RBBB with
LAD 45 RAD 120
Fig. 26.20 | Diagnostic criteria of fascicular blocksRBBB: right bundle branch block,
LAD: left axis deviation, RAD: right axis deviation.
REFERENCES
1. Willems JL, Robles de Medina EO, Bernard R, et al. Criteria for intraventricular conduction distur-
bances and pre-excitation. World Health Organizational/International Society and Federation for
Cardiology Task Force Ad Hoc. J Am Coll Cardiol 1985;5(6):12611275.
2. Lev M, Unger PN, Lesser ME, et al. Pathology of the conduction system in acquired heart disease.
Complete right bundle branch block. Am Heart J 1961;61:593614.
3. Hiss RG, Lamb LE. Electrocardiographic findings in 122,043 individuals. Circulation 1962;25:
947961.
4. Horowitz LN, Alexander JA, Edmunds LH. Postoperative RBBB: identification of three levels of
block. Circulation 1980;62:319328.
5. Schamroth L, Myburg DP, Schamroth CL. The early signs of RBBB. Chest 1985;57:180.
6. Sodi-Pallares D, Medrano GA, Bisteni A, et al. Deductive and Polyparametric Electrocardiography.
Mexico: Instituto National Cardiologia Mexico, 1970;36:136.
7. Tapia FA, Proudfit WL. Secondary R waves in right precordial leads in normal persons and in
patients with cardiac disease. Circulation 1960;21:2837.
8. Liao Y, Emidy LA, Dyer A, et al. Characteristics and prognosis of incomplete RBBB, an epidemio-
logical study. J Am Coll Cardiol 1986;7:492499.
9. DeLeon AC Jr, Perloff JK, Twigg H, et al. The straight back syndrome: clinical cardiovascular man-
ifestations. Circulation 1965;32:193203.
10. De Oliveira JM, Sambhi MP, Zimmerman HA. The electrocardiogram in pectus excavatum.
Br Heart J 1958;20(4):495501.
11. Brugada P, Brugada J. Right bundle branch block, presenting ST segment elevation and sudden
death: A distinct clinical and electrocardiographic syndrome. A multicenter report. J Am Coll Cardiol
1992;20:13911396.
12. Brake CM. Complete LBBB in asymptomatic airmen. Aerospace Med 1969;40:781.
13. Cohen HC, Rose KN, Pick A. Disorders of impulse conduction and impulse formation caused by
hyperkalemia in man. Am Heart J 1975;89(4):501509.
14. Singh RB, Agraval BV, Somani PN. LBBB: a rare manifestation of digitalis intoxication. Acta
Cardiol 1976;31:175.
15. Lenegre J. Etiology and pathology of bilateral BBB in relation to heart block. Prog Cardiovasc Dis
1964;6:409444.
16. Lev M. Anatomic basis for atrioventricular block. Am J Med 1964;37:742748.
17. Eriksen P, Hansson PO, Eriksson H, et al. BBB in a general male population: the study of men born
1913. Circulation 1998;98:24942500.
18. Rosenbaum MB, Elizari MV, Lazzari JO. The Hemiblocks. Oldsmar, FL: Tampa Tracings, 1970.
19. Warner RA, Hill NE, Mookherji S, et al. Improved electrocardiographic criteria for the diagnosis of
left anterior hemiblock. Am J Cardiol 1983;51(5):723726.
20. Ostrander LD. Left axis deviation: prevalence, associated conditions and prognosis. Ann Intern Med
1971;75(1):2328.
21. Atkins JM, Leshin SJ, Blomqvist G, et al. Ventricular conduction blocks and sudden death in AMI:
potential indications for pacing. N Eng J Med 1973;288(6):281284.
22. Pryor R, Blount SG. The clinical significance of true left axis deviation: left intraventricular blocks.
Am Heart J 1966;72(3):391413.
23. Rizzon P, Rossi L, Baissus C, et al. Left posterior hemiblock in AMI. Br Heart J 1975;37(7):
711720.
24. Thompson R, Mitchell A, Ahmed M, et al. Conduction defects in aortic valve disease. Am Heart J
1979;98(1):310.
25. Dhingra RC, Denes P, Wu D, et al. Chronic RBBB and left posterior hemiblock: clinical electro-
physiologic and prognostic observations. Am J Cardiol 1975;36:867879.
CHAPTER 27
M YOCARDIAL I NFARCTION
AND I SCHEMIA
1. MYOCARDIAL INFARCTION (MI) 533 ii. Coronary Artery Occlusion and

i. Depolarization Abnormalities 534 ECG Correlation 546
ii. Repolarization Abnormalities 535 6. ECG DIAGNOSIS OF MI IN BUNDLE
iii. Other Changes 540 BRANCH BLOCKS AND DURING
Evolution of ECG Changes 540 RV PACING 552
2. MYOCARDIAL ISCHEMIA 541 i. MI in RBBB 552
3. NONSPECIFIC ST-T CHANGES 542 ii. MI in LBBB 553
4. LOCALIZATION OF ISCHEMIA OR ECG Diagnosis of MI During RV
INFARCTION 542 Pacing 554
i. Right Ventricular Infarction 543 7. SENSITIVITY, SPECIFICITY, AND
ii. Atrial Infarction 543 PROGNOSTIC VALUE OF THE ECG 555
5. PREDICTION OF THE SITE OF i. The Sensitivity of the ECG 555
CORONARY ARTERY OCCLUSION 545 ii. Prognostic Value of ECG for MI 555
i. Occlusion of Coronary Artery 546 REFERENCES 556
The ECG remains a key investigation in the diagnosis of myocardial infarction and coro-
nary syndrome. However, ECG findings vary depending upon the following factors:
Duration of the ischemic process (acute vs chronic)
Extent of ischemia (transmural vs subendocardial)
Its topography i.e. site of ischemia (anterior vs inferiorposterior or right ventricular)
Presence of other underlying abnormalities (e.g. LBBB, WPW syndrome or pacemaker
patterns) which can mask or alter the classic pattern.
1. MYOCARDIAL INFARCTION (MI)
Histopathologically, an infarcted region consists of a central core of necrotic tissue,

surrounded by a zone of injured tissue which in turn is surrounded by a zone of ischemic
tissue, and as a result the ECG changes are as follows:
The myocardial necrosis results in depolarization abnormalities (QRS changes).
The myocardial injury and ischemia cause repolarization abnormalities (injury is ref-
lected by ST segment elevation and ischemia is represented by an inverted symmetrical
T wave).
Other changes: Ischemic U waves, increased QT dispersion.
As the electrode is situated some distance away from the heart, it subtends a relatively
large area which includes all the zones of necrosis, injury and ischemia and conse-
quently, it records all the ECG changes.
i. Depolarization Abnormalities
These often accompany the earliest repolarization abnormalities, which include:
Abnormalities of Q waves
Abnormalities of R wave
Abnormalities of Q Waves
i) Small q waves are normally recorded in leads I, aVF, and V4V6 which are 0.02 s
in duration and q: R ratio is 25%.
ii) However; in myocardial infarction with necrosis of sufficient quantity, the forces
of depolarization are lost in that area and mean electrical forces are directed away
from the area of infarction resulting in:
An abnormal Q wave (0.04 s in duration Q:R ratio of 25%) or
QS complex in the leads overlying the infarct zone.
iii) Often, abnormal Q wave is followed by a small positive terminal r wave due to the
late activation of the overlying viable myocardial tissue resulting in a Qr complex,
while a totally negative QS complex indicates the absence of any viable myocar-
dial tissue.
iv) In the past, abnormal Q waves were considered as markers of transmural myocar-
dial infarction. However, abnormal Q waves occur as early as 2 hours and as late
as 24 hours (mean of 9 hours) after the onset of symptoms of myocardial infarc-
tion, besides experimental and clinicopathological studies have shown that trans-
mural infarcts can occur without abnormal Q waves and subendocardial infarcts
can be associated with abnormal Q waves1 and hence myocardial infarction is bet-
ter classified electrocardiographically as Q or non-Q wave infarction.
v) Q wave infarctions tend to be larger than non-Q wave infarctions.2 Thrombolytic
therapy is indicated in Q wave myocardial infarction, while it is of no benefit in
non-Q wave myocardial infarction.
Abnormalities of R Waves
There is a progressive loss of R wave amplitude in myocardial infarction. The diminu-
tion of R wave amplitude is recorded:
When the infarct is small and necrosis is insufficient to result in an abnormal Q
wave.
In the leads overlying periphery of the infarction.
MYOCARDIAL INFARCTION AND ISCHEMIA 535
ii. Repolarization Abnormalities

These are the earliest and consistent ECG changes that occur during acute ischemia or
infarction. Following are the repolarization abnormalities:
ST segment changes due to myocardial injury and
T wave changes due to myocardial ischemia
ST Segment Changes
The following changes occur in the electrical properties of the myocardial cells of the
ischemic area.
Reduction of resting membrane potential.
Shortening of duration of action potential resulting in early repolarization.
Decrease in rate of rise (upstroke velocity) of the action potential (phase 0) and
Decrease in the amplitude of action potential (phase 0).
The presence of one or more of these changes will establish a voltage gradient between
normal and ischemic zones so that these currents of injury are directed towards the
ischemic region resulting in primary ST segment elevation with convexity upwards in
the surface ECG.
In dominant epicardial injury as in transmural infarction, the overall ST vector is
directed to the outer (epicardial) layers resulting in ST segment elevation (and some-
times tall positive T waves-hyper-acute T waves) over the injury zone, and reciprocal
ST segment depression in leads reflecting contralateral surface of the heart.
In dominant subendocardial injury as in subendocardial infarction, the overall ST
vector is directed towards the inner ventricular layer and the ventricular cavity result-
ing in ST segment depression in the overlying leads and ST elevation in aVR.
However, currently MI is categorized depending upon the ST segment abnormalities
into ST elevation MI (STEMI) and non-ST elevation MI (non-STEMI) as patholog-
ical Q waves most often develop after the onset of symptoms. An abnormal ST eleva-
tion of 1 mm in two or more contiguous leads is diagnosed as STEMI, an indication
for thrombolytic therapy. However, there are many non-cardiac causes in which ST ele-
vation can occur (see Table 27.1). ST elevation in myocardial infarction is usually asso-
ciated with reciprocal ST depression in one or more of the standard 12 leads.
i) In anterior MI, ST elevation is present in precordial leads.
Absence of ST elevation in V may occur and has been attributed to protection
1
by the conal artery arising from right coronary artery (RCA).3
Reciprocal ST depression is nearly always present in leads III and aVF, and
absence of reciprocal changes in aVF indicates occlusion of left anterior

descending artery (LAD) distally4 (see Figs 27.1 and 27.2).
In anteroseptal MI, ST elevation occurs in V V
1 4 (see Figs 27.3 and 27.4),
while in anterolateral MI, ST elevation mainly occurs in I, aVL, V5 and V6 (see
Figs 27.5 and 27.6).
ST elevation mainly in leads I and aVL and fewer changes in precordial leads
occur in the occlusion of first diagonal branch of LAD, while ST elevation

RV LV
Anterior wall infarct
Fig. 27.1 | Cross section through anterior wall infarct.
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 27.2 | Anterior wall MI with ST segment elevation in V V .

1 3
RV LV
Anteroseptal infarct
Fig. 27.3 | Cross section through anteroseptal infarct.

mainly in leads V1 and V2 with reciprocal depression in leads II, III, aVF, V5 and
V6 occurs when main septal branch of LAD is occluded.
ii) In apical or lateral MI, ST elevation occurs in leads V5 and V6 with reciprocal ST
depression in leads III, aVF and occasionally in V1.
iii) In inferior MI, ST elevation is present in II, III and aVF with reciprocal ST depression
in leads I, aVL and one or more of precordial leads (V2V3, see Figs 27.7 and 27.8,).
Absence of reciprocal ST depression, but presence of ST elevation in V , RV MI
1
should be suspected.5
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 27.4 | VAnteroseptal MI with Q waves, ST elevation in V V 1 4 and inverted T in I, aVL,

V .
1 6
RV LV
Anterolateral infarct
Fig. 27.5 | Cross section through anterolateral infarct.
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 27.6 | inversion

Anterolateral Q MI with Q waves in aVL, V V
in I, aVL and V V .
2 3 and ST elevation and T wave
3 5
Fig. 27.7 | Sagittal view through inferior wall infarct.

I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 27.8 | Inferior wall MI with q in III, ST elevation in II, III, aVF and inverted T in aVL.
Presence of additional ST elevation in lateral precordial leads (V5, V6) or in leads
I and aVL (Inferolateral MI) indicates the occlusion of left circumflex (LCx)
coronary artery.6
iv) True posterior MI7 is characterized by:
Tall R waves, ST depression and upright T waves in V and V , (see Figs 27.9
1 2
and 27.10) and
Q waves and ST elevation in leads V V .
7 9
However, posterior MI is often associated with inferior MI (see Fig. 27.11).
v) LV MI involving papillary muscles (PM): Besides ST-T changes in LV leads, ST

depression in inferior leads is associated with anterolateral PM infarction, while
ST depression in lead I or aVL is seen in posteromedial PM infarction.8
T Wave Changes
Leads overlying the ischemic region record inverted symmetrical and pointed T waves,
with frequently increased magnitude as T vector is directed away from the region of
Fig. 27.9 | Sagittal view through posteroinferior wall infarct.
V1 V2 V3 V4 V5 V6
Fig. 27.10 | isPosterior MI with tall R and upright T waves in V V . Tall R waves are not due to RVH, as there
no RAD, no inverted T waves, and no evidence of RAE.
1 2
V1 V2 V3 V4 V5 V6
Fig. 27.11 | inverted

Postero-inferior MI-tall R waves and upright and tall T waves in V with abnormal Q waves and
T waves in inferior leads.
1
I V1 V4
aVR
V2 V5
aVL
II
aVF V3 V6
III
Fig. 27.12 | Anterolateral non-Q MI-symmetrical inverted T waves in aVL and V V .1 6
myocardial ischemia. They are sometimes known as coronary T waves, which are
usually associated with lengthening of QT interval. Inverted T waves occur in:
Leads I, aVL, V5 and V6 in anterolateral infarction (see Fig. 27.12).
Leads V1V3 in anteroseptal infarction.
Leads II, III and aVF in inferior infarction.
Upright T waves occur in right precordial leads in posterior infarction.
iii. Other Changes

Ischemic U Wave Changes
Alterations in polarity or amplitude of U waves can occur in acute ischemia or infarction.
Negative U waves in anterior precordial leads in anterior MI.
Negative U waves in leads III and aVF in inferior infarction.
In severe LAD stenosis, transient inverted U waves in precordial leads appear on
stress test.9
Inverted U waves may be the earliest ECG finding of acute coronary syndromes.10
Increased QT Interval Dispersion

The difference of QT interval in various leads is known as QT interval dispersion. The
increased QT interval dispersion i.e. the greater difference between maximum and
minimum QT intervals (0.05 s) reflects:
A marker of arrhythmia risk after myocardial infarction11 and
A marker of acute ischemia after atrial pacing.12
Evolution of ECG Changes

ST elevation and hyperacute T waves occur as the earliest sign of acute MI, typically
followed by evolving T wave inversion from hours to days and sometimes by abnormal
Q wave in the same leads from 224 hours.
Table 27.1 Other causes of ST elevation
1. Early repolarization
2. Acute pericarditis
3. Pulmonary embolism
4. Myocarditis
5. Acute aortic dissection17
6. Acute cor pulmonale
7. Hyperkalemia
8. Cardiac tumor
9. After mitral valvuloplasty18
10. Pancreatitis and gallbladder disease19
11. Anaphylactic shock20
12. Septic shock
13. Spinal cord injury at C5C6 levels (i.e. lesions that
completely disrupt cardiac sympathetic influences)21
ST segment returns to the isoelectric line after a period of hours to days (most often
2 weeks). In most cases, the initial ST elevation decreases markedly during the first
712 hours after the onset of chest pain.13 It resolved within 2 weeks in 90% of
patients with inferior infarction and in 40% in patients with anterior infarction.14
However, the resolution of ST elevation is complete and much earlier with the
thrombolytic therapy.
The T wave inversion can resolve after days or weeks or may persist indefinitely with
Q waves especially in large transmural infarction with fibrosis. During its evolution,
Pardee T or coronary T may be observed i.e. inverted T wave with ST segment
is isoelectric but shows an upward convexity. In leads showing ST segment depres-
sion, T waves become tall and symmetrical.
Q waves may regress within 2 years. However in the present era of thrombolytic
therapy, regression occurs earlier and more frequently, within 660 months in one
or more leads in 77% of the patients.15
Complete normalization of ECG following Q wave infarction is uncommon but can
occur with smaller infarcts with improved left ventricular ejection fraction (LVEF).
Persistent ST segment elevation together with Q waves for several weeks occurs with
severe LV wall motion abnormalities (akinesia or dyskinesia) or with the develop-
ment of ventricular aneurysm. The el-Sherif sign i.e. rSR in mid precordial leads or
I is another marker of ventricular aneurysm (see Table 27.1).
2. MYOCARDIAL ISCHEMIA
Myocardial ischemia, which is expressed clinically as angina, is associated with the

ECG changes consisting mainly of primary ST-T changes i.e.
ST segment depression of 1 mm in one or more leads. ST segment depression
must be horizontal or downward sloping with duration of atleast 0.08 s, in order to
differentiate it from the normal J point depression.
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 27.13 | Non-STEMIST depression of 1 mm in I, aVL and V V .

1 6
However in Prinzmetal variant angina due to coronary vasospam, there is transient

ST segment elevation which resolves within minutes or is followed by T wave inversion
which may persist for hours or days.
ST segment depression of 1 mm in two or more leads in a patient with chest dis-
comfort and abnormal cardiac enzymes (troponin or CK-MB) is diagnostic of non-
STEMI (see Fig. 27.13).
T wave inversion in one or more leads: Due to a high grade stenosis of proximal
LAD, severe ischemia may be associated with deep coronary T wave inversion in
multiple precordial leads (V1V4), which is described as LAD-T wave pattern.16
Other ECG changes include ischemic U waves and increased QT interval dispersion.
3. NONSPECIFIC ST-T CHANGES
ST segment depression of 1 mm is found in many conditions, such as:

Myocarditis
Pericarditis, constrictive pericarditis
Cardiomyopathy
Pulmonary embolism
Subarachnoid or cerebral hemorrhage
Drugs: Digoxin effect, ethanol abuse
Hyperventilation
After a drink of cold water
Electrolyte imbalance.
4. LOCALIZATION OF ISCHEMIA OR INFARCTION
ECG leads are helpful in localization of ischemia or infarction.

ECG changes in one or more of precordial leads (V1V6): anterior.
Table 27.2 Incidence of RV infarction
Criteria Incidence
1. Autopsy studies 543% with a mean of 19%

2. Hemodynamic studies 1520%
3. Radionuclide studies About 40%
However, ECG changes in V1V2 are usually designated as anterior ischemia or

infarction while ECG changes in V1V6 are designated as extensive anterior.
ECG changes in one or more of precordial leads from V1 to V6 and leads I and aVL:
anterolateral.
ECG changes in V1V4: anteroseptal.
ECG changes in V5V6: apical or lateral.
ECG changes in II, III and aVF: inferior wall.
ECG changes in II, III, aVF and V5V6: inferolateral.
ECG changes of ST segment depression and tall R and T waves in V1V2 are diag-
nostic of true posterior wall infarction. However, ST segment elevation is recorded in
leads V7V9.
i. Right Ventricular Infarction
RV infarction occurs in the presence of inferior wall infarction of LV and as such,
ECG diagnosis of RV infarction offers special challenges.
Most pathological studies show the presence of RV infarct in 1436%.22,23
The clinical diagnosis of RV infarction is only 20%, while with echocardiogram and
nuclear studies it is about 40% (see Table 27.2).
RV infarction usually causes loss of R wave in leads V3R and V4R. Elevation of ST
segment in right precordial leads is the most important diagnostic sign. Hence, ST
segment elevation in right chest leads, V1 and V3RV6R (V3R and V4R are more
sensitive) must be sought in the presence of inferior wall infarction.
Following are the Diagnostic Criteria for RV Infarction in presence of
inferior wall infarction
ST segment elevation in V3R or V4R (Erhadt et al, 1976) with a sensitivity of 100%
and specificity of 68%24 (see Figs 27.14 and 27.15).
ST segment elevation in V6R and V7R (Anderson et al) with 100% sensitivity.22
ST segment elevation in V1V3 (Geft et al25).
ST segment elevation in V1 and ST segment depression in V2 (Mak et al26).
ST segment depression in V2: 50% ST elevation in aVF (Lew et al27).
ST segment elevation in lead III ST elevation in lead II (Anderson et al22).
ii. Atrial Infarction

The atrial infarction has been related to extensive ventricular myocardial infarction,28
and it is suspected when an atrial arrhythmia develops in a patient with a large ventric-
ular infarction.
Aorta
PA
LA
RA
LV
RV
Right ventricular
infarct
Fig. 27.14 | Right ventricular infarct.

I aVR V 1R V4R
II aVL V2R V5R
III aVF V3R V6R
Fig. 27.15 | RV infarction with inferior wall MIST elevation in II, III, aVF and right pre-
cordial leads (V RV R).
3 6
Table 27.3 Characteristics of atrial infarction
1. Atrial infarction occurs in 717%.

2. Mostly associated with ventricular infarction.
3. Right atrium and appendages are more involved.
4. Aluminium phosphate poisoning mimics atrial infarction.
5. Atrial arrhythmias, atrial rupture and thrombus formation
are complications of atrial infarction.
It occurs in 717%. The right atrial infarction is more common and the atrial append-
age is commonly affected (see Table 27.3).
Isolated atrial infarction, which is rare, usually presents with CHF.
The ECG changes of atrial infarct are found in poisoning with aluminium phosphate.
P P
Ta
Fig. 27.16 | Ta: small negative deflection following P wave due to atrial repolarization.
II
P P
aVF
P P P
V2
P P
V6
P P P
Fig. 27.17 | Elevation of PTa (arrow ) is diagnostic of atrial infarction with changes in
morphology of P waves (a minor diagnostic criterion).
Following is the ECG diagnostic criteria proposed by Chi Kong Liu et al (1961)29
i) Major criteria:
Elevation of PTa of 0.5 mm in V5V6 with a reciprocal depression in V1V2.
Elevation of PTa of 1.5 mm in any precordial lead or 1.2 mm in IIII with atrial
arrhythmias.
Elevation of PTa in I with reciprocal depression in II and III.
(Ta: is a small negative deflection following P wave due to atrial repolarization (see
Fig. 27.16), which is not usually seen in standard 12 leads ECG)
ii) Minor Criteria: Minor Criteria alone is not regarded as an evidence of atrial infarction.
Abnormal P morphology: Irregular or notched (M or W) (see Fig. 27.17).
PTa depression with reciprocal changes (see Fig. 27.18).
5. PREDICTION OF THE SITE OF CORONARY ARTERY OCCLUSION
The ECG provides information about the site of occlusion of coronary arteries in
patients with myocardial ischemia or infarction.
ST T in I, ST T in II, 1. PTa 0.5 mm in V5V6

aVL, V5V6 III and aVF with in V1V2
2. PTa 1.5 mm in any
precordial lead or
1.2 mm in IIII with
1. Tall R, ST and Lateral with Inferior with atrial arrhythmia
upright T in or without Q or without Q 3. PTa in I with in IIIII
V1V2 4. Irregular or notched
2. ST in V7V9 P (M or W shape)
Posterior Infarction Atrial
Inferior MI with
1. ST T in 1. ST T in right
precordial leads Anterior with Right precordial leads-
2. U waves in or without Q ventricular V3R, V4R
precordial leads 2. ST in III II
3. ST in V1 and ST in V2
Fig. 27.18 | Types and diagnostic criteria of myocardial infarction: inverted or depression, : elevation
or upright.
i. Occlusion of Coronary Artery

Occlusion of right coronary artery (RCA) causes inferior, posterior, inferoposterior,
inferolateral, and RV MI.
Occlusion of left circumference (LCx) causes posterior and lateral infarctions (poste-
roapical, posterolateral, posterobasal, posteroinferior, inferolateral or high lateral MI).
Occlusion of the dominant LCx causes inferoposterior and posterolateral infarctions.
Occlusion of left anterior descending (LAD) causes anteroseptal and anterior MI.
Proximal LAD occlusion can also result in bundle branch block (BBB) and left ante-
rior fascicular block.
ii. Coronary Artery Occlusion and ECG Correlation

Presence of abnormal Q waves in leads I, aVL, and V1V4 associated with LAD occlu-
sion, and in leads II, III and aVF associated with LCx or RCA occlusion.30
In anterior MI, ST elevation is less frequent in lead V1 than in leads V2 and V3.
Absence of ST elevation in V1 in anterior MI suggests the presence of a large conal
branch of RCA protecting the septum, conversely ST elevation in V1 suggests either
absent or small conal branch of RCA.31
i) Predicting RCA or LCx Occlusion in Inferior Wall MI
ST segment elevation in III II: RCA occlusion with a sensitivity of 99% and a
specificity of 100%, while ST segment elevation in II III: LCx occlusion with a
sensitivity of 93% and a specificity of 100%.
In inferior infarction, ST elevation in lead III II, especially when combined with ST
elevation in V1 is a powerful predictor of RCA occlusion proximal to acute marginal
branch32 (see Fig. 27.19).
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 27.19 | Inferior wall MI with ST elevation in III II and ST elevation also in V V1 2
due to proximal right coronary artery occlusion.
I aVR V1
V4
aVL V2 V5
II
III aVF V3 V6
Fig. 27.20 | Inferolateral MI with ST elevation in II, III, aVF and V V

artery occlusion.
5 6 in left circumflex
In inferior MI with ST elevation in lateral leads V5 and V6 or I and aVL is a sensitive

and specific marker for LCx lesion33 (see Fig. 27.20).
Inferior MI with ST depression in V1V3 is more often associated with LCx occlu-
sion (71%) than of RCA occlusion (40%).34
Similarly, reciprocal changes (i.e. ST segment depression) in aVL predict LCx
occlusion, while reciprocal changes in V4V6 predict multivessel occlusion35 (see
Figs 27.21 and 27.22).
Ratio of ST segment depression in V3 to ST segment elevation in III has 91% sensi-
tivity and specificity.34
0.5 predicts proximal RCA occlusion (see Fig. 27.23)
0.5 1.2 predicts distal RCA occlusion
1.2 predicts LCx occlusion (see Fig. 27.24)
Abnormal R in V1 consistent with posterior infarction is highly specific for LCx
occlusion.33
ii) Predicting LAD Occlusion Site in Anterior Wall Infarction
The ECG criteria for localization of site of LAD occlusion are less sensitive
(5085%) but are more specific (90100%).36,37
I aVR V1 V4
II aVL V5
V2
III aVF V3 V6
Fig. 27.21 | circumflex

Inferior wall MI with reciprocal ST depression in aVL and V V
artery occlusion.
1 3 due to left
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 27.22 | Inferior wall MI with reciprocal ST depression in I and aVL due to left circum-
flex artery occlusion.
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 27.23 | due

Inferior wall MIratio of ST depression in V to ST elevation in III is 0.5
to proximal right coronary artery occlusion.
3
LAD lesions proximal to the first septal branch (S1) have sensitivity of about 50%
and specificity of 90100%, while LAD lesions proximal to first diagonal branch
(D1) have sensitivity of about 60% and specificity of 90%.
LAD lesions distal to S1 have sensitivity of about 25% and specificity of 88%, while LAD
lesions distal to D1 have low (about 1020%) sensitivity but are highly specific (100%).
In anterior MI, presence of reciprocal ST depression in inferior leads suggests a proxi-
mal LAD lesion. Similarly, ST elevation (also in leads I and aVL) is predictive of
proximal (proximal to D1) LAD lesion.38
Type III LAD occlusion is recognized by the presence of ST depression with upright
T waves in lead III.39
a) ST segment depression of 1 mm in inferior leads predicts proximal LAD
occlusion (proximal to septal (S1) or diagonal (D1) branch).
(i) Following are the ECG predictors of LAD occlusion proximal to S1 branch (see
Fig. 27.25)
V1 V4
I aVR
II aVL V2 V5
III aVF V3 V6
Fig. 27.24 | Inferior wall MIratio of ST depression in V

to left circumflex artery occlusion.
3 to ST elevation in III is 1.2due
I V1
II V2
V3
III
V4
aVR
V5
aVL
V6
aVF
Fig. 27.25 | Anterior wall infarction with reciprocal ST depression in inferior leads and V
in V (2.5 mm) and aVRdue to LAD lesion proximal to S .
5 and ST elevation
1 1
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 27.26 | Anterior wall MI with reciprocal ST depression in inferior leads and ST ele-
vation in I and aVLdue to LAD lesion proximal to D .1
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 27.27 | ST
Anterior wall MI with Q waves and ST elevation in V V but no reciprocal
2 5
depression in inferior leadsdue to LAD lesion distal to S .
1
ST segment elevation in V1 of 2.5 mm

ST segment elevation in aVR

Associated with complete RBBB
ST segment depression in V .
5
(ii) Following is the ECG predictor of LAD occlusion proximal to D1 branch (see
Fig. 27.26)
Abnormal Q waves in aVL
ST segment elevation in I and aVL.
(b) Absence of ST depression in inferior leads predicts mid to distal LAD occlusion
(distal to S1 or D1 branch).
(i) Following is the ECG predictor of LAD occlusion distal to S1 branch (see Fig. 27.27)
Presence of abnormal Q waves in V V
4 6
(ii) Following is the predictor of LAD occlusion distal to D1 branch (see Fig. 27.28)
ST segment depression in aVL (see Fig. 27.29)
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 27.28 | reciprocal

Anterior wall MI with ST elevation in V V and ST depression in aVL but no
1 5
ST depression in inferior leadsdue to LAD lesion distal to D . 1
Proximal to S1:
1. ST in V1 2.5mm
2. ST in aVR Proximal to D1:
3. ST in V5 1. Abnormal Q in aVL Distal to D1: Distal to S1:
4. MI RBBB 2. ST in I and aVL ST in aVL Abnormal Q in V4V6
Ant. MI with Ant. MI with

Proximal to D1 and S1 ST of 1 in no ST in II, Distal to D1 and S1
II, III and aVF III and aVF
Proximal occlusion RCA occlusion LAD occlusion LCx occlusion
1. ST in V1 Inf. MI with
CAO
2. V3 ST: III ST 0.5 ST in III II
Inf. MI with
ST in II III
V3 ST: III ST 0.5
Distal occlusion MV occlusion
to 1.2 Inf. MI with
ST in aVL
Inf. MI with
Inf. MI with
V3 ST: III Inf. MI with
ST in V4V6
ST 1.2 ST in I, aVL
or V5V6
Inf. MI with
ST in V1V3
Posterior
MI-tall R in V1
Fig. 27.29 | Predicting coronary artery occlusion (CAO) from ECGMV: multi-vessel, Ant.: anterior, Inf.:
inferior, RCA: right coronary artery, LAD: left anterior descending artery, LCx: left circumflex
artery, : depression, : elevation, RBBB: right bundle branch block.
6. ECG DIAGNOSIS OF MI IN BUNDLE BRANCH BLOCKS AND

DURING RV PACING
The diagnosis of myocardial infarction is often difficult in patients with baseline ECG
showing BBB pattern or a BBB develops as a complication of the infarction.
i. MI in RBBB
The RBBB primarily affects the terminal phase of ventricular depolarization, and hence
diagnosis of MI is usually not impeded by its presence. The criteria for the diagnosis
of MI (Q wave infarct) in the presence of RBBB are the same as in patients with
normal conduction (see Figs 27.30 and 27.31).
V1 V4
V2 V5
V3 V6
Fig. 27.30 | Anterior MI and RBBBST elevation in V V 1

precordial leads with RBBB pattern in V V .
4 and inverted T waves in all
1 3
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 27.31 | Inferior MI and RBBBST elevation and inverted T waves in III and aVF
with RBBB pattern in V .
1
RBBB occurs in 329% of patients with AMI,40 often accompanied by left anterior
fascicular block41 and LAD is usually involved.42
The mortality rate is higher in patients with new onset RBBB than in those with old
RBBB, in contrast to AMI patients with an old LBBB have higher mortality than in
those with recent onset LBBB.42
ii. MI in LBBB
The LBBB:
Affects both early and late phases of ventricular depolarization,
Alters the sequence of repolarization, with ST segment and T wave vectors directed
opposite to QRS complex, producing secondary ST-T changes.
These changes may mask and mimic the ECG findings of MI. Hence, the ECG diagno-
sis of MI in the presence of LBBB is more difficult and sometimes confusing. Following
is the ECG diagnostic criteria of MI in presence of LBBB
i) Based on GUSTO-1 trial (Global Utilization of Streptokinase and Tissue plasmi-
nogen activator for occluded coronary arteries) (Sgarbossa et al criteria, 1996)43
ST segment elevation of 1 mm with concordant (positive) QRS complex: 5 scores
ST segment elevation of 5 mm with discordant (negative) QRS complex: 2 scores
(see Fig. 27.32)

ST segment depression of 1 mm in V , V , or V : 3 scores (Fig. 27.33)
1 2 3
For diagnosis, a total score of 3 is a must, which yields a sensitivity of 78% and
specificity of 90%.
ii) Other diagnostic ECG criteria which are less sensitive and specific are as follows:
R wave regression from V1 to V444
QS pattern in V V
1 4
Presence of Q waves in two contiguous precordial or limb leads. Abnormal Q wave
should be 20 ms in V4 or 30 ms in V5, V6, II and III.
V1 V4
V2 V5
V3 V6
Fig. 27.32 | Anterior wall MI with LBBBDiscordant ST elevation in V V .

1 3
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 27.33 | Inferior wall MI and LBBB with Q waves and concordant ST segment eleva-
tion in lead III and ST segment depression in V and V leads.
2 3
Table 27.4 Other ECG changes in patients of MI with LBBB
1. Presence of abnormal Q waves

2. Notching of S waves (Cabrera sign)
3. Regression of R waves in precordial leads (V1V6)
4. Notching of R waves (Chapman sign)
5. Left axis deviation (LAD)
Positive T wave in V5 or V6
Notching of 0.05 s in the ascending limb of S wave in V3 or V4V5 (Cabrera
sign)
Notching of 0.05 s in the ascending limb of R wave in I, aVL, V5 or V6 (Chapman
sign)45
Terminal prominent S wave in V5 or V6
LAD (see Table 27.4).
ECG Diagnosis of MI During RV Pacing

Similar principles apply for the diagnosis of MI in the presence of RV pacing.
i. Anterior wall MI during RV pacing: Similar to MI in presence of LBBB.
ii. Inferior wall MI during RV pacing: RV pacing masks the inferior wall MI.
Following are ECG criteria for diagnosis of inferior wall MI during RV pacing:
GUSTO-1 criteria46
QR or Qr pattern in inferior leads with a specificity of 100% but with low sensi-
tivity (15%)
Normally, RV pacing results in QS, R, or qR pattern in aVR, hence rS pattern in
aVR is diagnostic with a specificity of 52% and sensitivity of 15%.
Cabrera sign in III, aVF leads is insensitive (see Fig. 27.34).
1. ST 1 mm in
concordant QRS: 5p
2. ST 5 mm in Similar to
GUSTO-1
LBBB
discordant QRS: 2p criteria: 3p
3. ST 1 mm in V1, V2
or V3: 3p
Other less Ant. MI

MI in LBBB
specific criteria
MI in RBBB RV pacing in
1. R regression
QS in V1V4 Same criteria Inf. MI
2. Ab Q in 2 leads without RBBB
20 ms in V4 or
30 ms in V5V6,
II, III Others:
3. Upright T in V5 or V6 1. QR or Qr in
4. Prominent S in II, III, aVF
V5 or V6 2. rS in aVR
5. Cabrera sign 3. Cabrera sign in
6. Chapman sign III, aVF GUSTO-1 criteria
Fig. 27.34 | Diagnosis of myocardial infarction (MI) in bundle branch blocks (LBBB and RBBB) and
during right ventricular pacingAnt.: anterior, Inf.: inferior, GUSTO: Global Utilization of
Streptokinase and Tissue plasminogen activator for Occluded coronary arteries, p: point,
Ab: abnormal.
7. SENSITIVITY, SPECIFICITY AND PROGNOSTIC VALUE OF THE ECG
i. The Sensitivity of the ECG

The sensitivity of the ECG for recognizing autopsy proven MI was 5561%47, while
incidence of the ECG missing the diagnosis of acute infarction is 625%.48,49 The over-
all incidence of false positive diagnosis of MI was 31%.50
ii. Prognostic Value of ECG for MI

i) Q Wave Infarction
It is associated with more serious prognosis.
Q wave infarcts are often larger than non-Q wave infarcts.51
During early stage, mortality is higher among the patients with Q wave MI.52
The patients with Q wave infarct if not revascularized, tend to recur which is associated
with increased mortality rate.53
Deeper and wider Q waves in more leads together decrease the R wave amplitude which
is associated with greater decrease in the left ventricular ejection fraction (LVEF).54
ii) Site of Infarction

Anterior MI is associated with higher early and late mortality rates than inferior MI.55
Inferior MI has more serious prognosis in presence of:
Reciprocal ST depression in leads V1V456
Complete AV block is associated with more serious prognosis56
Extensive RV infarction due to large infarct size47
There is an increased incidence of cardiogenic shock, ventricular fibrillation and
complete AV block in patients with RV infarction.
iii) Abnormal T Waves

Higher T wave amplitude is associated with better prognosis (lower 30 days mortality)
in patients receiving thrombolytic therapy for acute MI.57
Patients with acute Q MI with ST elevation of 2 mm and positive T waves are
associated with large infarct and low incidence of recurrent ischemia, while patients
with ST elevation 2 mm and inverted T waves have smaller infarcts and higher
incidence of recurrent ischemia.58
Persistence of inverted T waves in Q MI indicates the presence of transmural infarct
with a thin fibrotic layer, while positive T waves indicate a non-transmural infarct
containing viable myocardium.59
iv) Associated BBB

It has adverse prognosis.
Presence of LBBB was associated with a 34% increase in the risk of in-hospital
mortality rate.60
Presence of BBB was associated with 53% higher risk for a 30-day mortality in
GUSTO-I trial.61
In TAMI trial, AV block was associated with 20% mortality compared to 4% without
AV block.42
v) QT Dispersion
Increased QT dispersion is an indication of arrhythmia risk in patients with MI and
thereby affecting the prognosis.62
REFERENCES
1. Mirvis DM, Ingram LA, Ramanathan KB, et al. R and S wave changes produced by experimental
nontransmural and transmural myocardial infarction. J Am Coll Cardiol 1986;8(3):675681.
2. Baer FM, Theissen P, Voth E, et al. Morphologic correlate of pathologic Q waves as assessed by
gradient-echomagnetic resonance imaging. Am J Cardiol 1994;74(5):430434.
3. Ben-Gal T, Sclarovsky S, Herz I, et al. Importance of the conal branch of the right coronary artery
in patients with anterior wall myocardial infarction: electocardiographic and angiographic correla-
tion. J Am Coll Cardiol 1997;29(3):506511.
4. Engelen DJM, Gorgels APM, Cheriex EC, et al. ECG criteria differentiating between proximal
versus distal occlusion of the left anterior descending coronary artery [abstracts]. J Am Coll Cardiol
1997;29:430A.
5. Wong CK, Freedman B, Bautovich G, et al. Mechanism and significance of precordial AT-segement
depression during inferior wall AMI associated with narrowing of the dominant right coronary
artery. Am J Cardiol 1993;71(12):10251030.
6. Bairey CN, Shah PK, Lew AS, et al. Electrocardiographic differentiation of occlusion of the left
circumflex versus right coronary artery as a cause of inferior AMI. Am J Cardiol 1987;60(7):456459.
7. Casas RE, Marriott HJL, Glancy DL. Value of leads V7V9 in diagnosing posterior wall AMI and
other causes of tall R waves in V1V2. Am J Cardiol 1997;80:508.
8. Dabrowska B, Walczak E, Prejs R, et al. Acute infarction of the left ventricular papillary muscle:
electrocardiographic pattern and recognition of its location. Clin Cardiol 1996;19(5):404407.
9. Chikamori T, Kitaoka H, Matsumura Y, et al. Clinical and electrocardiographic profiles producing
exercise-induced U waves inversion in patients with severe narrowing of the left anterior descending
coronary artery. Am J Cardiol 1997;80(5):628632.
10. Jaffe ND, Boden WE. Spontaneous transient, inverted U waves as initial electrocardiographic mani-
festations of unstable angina. Am Heart J 1995;129(5):10281030.
11. Schneider CA, Voth E, Baer FM, et al. QT dispersion is determined by the extent of viable
myocardium in patients with chronic Q-wave myocardial infarction. Circulation 1997;96(11):
39133920.
12. Sporton SC, Taggart P, Sutton PM, et al. Acute ischemia: A dynamic influence on QT dispersion.
Lancet 1997;349:306.
13. Zmyslinski RW, Akiyama T, Biddle TL, et al. Natural course of ST segment and QRS complex in
patients with acute anterior MI. Am J Cardiol 1979;43(1):2934.
14. Mills RM, Young E, Gorlin R, et al. Natural history of ST segment elevation after AMI. Am
J Cardiol 1975;35(5):609614.
15. Iwaski K, Kusachi S, Hina K, et al. Q wave regression unrelated to patency of infarct-related artery or
left ventricular ejection fraction or volume after anterior wall AMI treated with or without reperfusion
therapy. Am J Cardiol 1995;76:14.
16. de Zwaan C, Bar FW, Janssen JH, et al. Angiographic and clinical characteristics of patients with
unstable angina, showing an ECG pattern indicating narrowing of left anterior descending coronary
artery. Am Heart J 1989;117(3):657665.
17. Hirata K, Kyushima M, Asato H. Electrocardiographic abnormalities in patients with acute aortic
dissection. Am J Cardiol 1995;76(16):12071212.
18. Ludman PF, Hildick-Smith D, Harcombe A, et al. Transient ST segment changes associated with
mitral valvuloplasty using Inoue balloon. Am J Cardiol 1997;79(12):17041705.
19. Patel J, Movahed A, Reeves WC. Electrocardiographic and segmental wall motion abnormalities in
pancreatitis mimicking myocardial infarction. Clin Cardiol 1994;17(9):505509.
20. Rich MW. Myocardial injury caused by an anaphylactic reaction to ampicillin/sulbactam in a patient
with normal coronary arteries. Tex Heart Inst J 1998;25(3):194197.
21. Lehmann KG, Shanding AH, Yusi AU, et al. Altered ventricular repolarization in central sympathetic
dysfunction associated with spinal cord injury. Am J Cardiol 1989;63(20):14981504.
22. Anderson HR, Falk E, Nielsen D. Right ventricular infarction frequency, size and topography in
coronary heart disease: a prospective study comprising 107 consecutive autopsies from a coronary
care unit. J Am Coll Cardiol 1987;10:1223.
23. Wartman WB, Hellerstein HK. The incidence of heart disease in 2000 consecutive autopsies. Ann
Intern Med 1948;28:41.
24. Erhardt LR, Sjogren A, Wahlberg I. Single right sided precordial lead in the diagnosis of right ventricle
involvement in inferior myocardial infarction. Am Heart J 1976;91(5):571576.
25. Geft HL, Shah PK, Rodriguez L, et al. ST elevation in leads V1 to V3 may be caused by right coronary
artery occlusion and acute right ventricular infarction. Am J Cardiol 1984;53(8):991996.
26. Mak KH, Chia BL, Tan ATH, et al. Simultaneous ST segment elevation in lead V1 and depression
in lead V2: A discordant ECG pattern indicating right ventricular infarction. J Electrocardiol 1994;
27(3):203207.
27. Lew AS, Laramee P, Shah PK, et al. Ratio of ST segment depression in leads V2 to ST segment elevation
in lead aVF in evolving inferior acute myocardial infarction: an aid to the early recognition of right
ventricular ischemia. Am J Cardiol 1986;57(13):10471051.
28. Medrano GA, de Micheli A, Osornio A. Interatrial conduction and STa in experimental atrial damage.
29. Liu CK, Greenspan G, Piccirillo RT. Atrial infarction of the heart. Circulation 1961;23;331338.
30. Fuchs RM, Achuff SC, Grunwald L, et al. Electrocardiorphic localizations coronary artery narrowings:
studies during myocardial ischemia and infarction in patients with one-vessel disease. Circulation
1984;60:1209.
31. Ben-Gal T, Herz I, Solodky A, et al. Acute anterior wall MI entailing ST segment elevation in lead
V1: electrocardiographic and angiographic correlations. Clin Cardiol 1998;21:399.
32. Zimetbaum PJ, Krishnan S, Gold A, et al. Usefulness of ST segment elevation in lead III exceeding
that of lead II for identifying the location of the totally occluded coronary artery in inferior wall
myocardial infarction. Am J Cardiol 1998;81(7):918919.
33. Herz I, Assali AR, Adler Y, et al. New electrocardiogrphic criteria for predicting either right coronary
artery or left circumflex artery as the culprit coronary artery in inferior wall AMI. Am J Cardiol
1997;8:1343.
34. Kosuge M, Kimura K, Ishikawa T, et al. New electrocardiographic criteria for predicting the site of coro-
nary artery occlusion in inferior wall acute myocardial infarction. Am J Cardiol 1998;82:13181322.
35. Birnbaum Y, Wagner GS, Barbash GI, et al. Correlation of angiographic findings and right (V1V3)
versus left (V4V6) precordial ST segment depression in inferior wall acute myocardial infarction.
Am J Cardiol 1999;83:143.
36. Engelen DJ, Gorgels AP, Cheriex EC, et al. Value of electrocardiogram in localizing the occlusion
site in the left anterior descending coronary artery in acute anterior myocardial infraction. J Am Coll
Cardiol 1999;34:389395.
37. Karthik V, Manjunath CN, Srinivas KH, et al. Electrocardiographic localization of the occlusion site
in left anterior descending coronary artery in acute anterior myocardial infraction. IHJ 2004;56(4):
315319.
38. Birnbaum Y, Sclarovsky S, Solodky A, et al. Prediction of the level of left anterior descending coro-
nary artery obstruction during anterior wall AMI by admission electrocardiogram. Am J Cardiol
1993;72(11):823826.
39. Porter A, Sclarovsky S, Ben-Gal T, et al. Value of T wave direction with lead III ST segment depression
in acute anterior wall MI: electrocardiographic prediction of a wrapped left anterior descending
artery. Clin Cardiol 1998;21(8):562566.
40. Moreno AM, Alberola AG, Thomas JG, et al. Incidence and prognostic significance of RBBB in
patients with AMI receiving thrombolytic therapy. Int J Cardiol 1997;61(2):135141.
41. Nimetz AA, Shubrooks SJ, Hutter AM, et al. The significance of BBB during AMI. Am Heart J
1998;21:2651.
42. Simons GR, Sgarbossa W, Wagner G, et al. Atrioventricular and intraventricular conduction disorders
in AMI: a reappraisal in the thrombolytic era. PACE 1998;21:2651.
43. Sgarbossa EB, Pinski SL, Barbagelata A, et al. Electrocardiographic diagnosis of evolving acute
myocardial infarction in the presence of LBBB. GUSTO-1 (Global Utilization of Streptokinase and
Tissue plasminogen activator for Occluded coronary arteries). N Engl J Med 1996;334:481487.
44. Barold SS, Falkoff MD, Ong LS, et al. Electrocardiographic diagnosis of myocardial infarction during
ventricular pacing. Cardiol Clin 1987;5:403417.
45. Chapman MG, Pearce ML. Electrocardiographic diagnosis of myocardial infarction in the presence
of LBBB. Circulation 1957;16:558.
46. Sgarbossa EB, Pinski SL, Gates KB, et al. Early electrocardiographic diagnosis of myocardial infarc-
tion in the presence of ventricular paced rhythm. GUSTO-1 investigators: Am J Cardiol
1996;77(5):423424.
47. Chou TC. Electrocardiography. In: Clinical Practice, 4th ed. Philadelphia: WB Saunders, 1996.
48. Levine HD, Philips E. An appraisal of the newer electrocardiography: correlations in one hundred
and fifty consecutive autopsied cases. N Engl J Med 1951;245(22):833842.
49. Woods JD, Laurie W, Smith WG. The reliability of the electrocardiogram in myocardial infarction.
Lancet 1963;2:265269.
50. Gunnar RM, Pietras RJ, Blackaller J, et al. Correlation of vector cardiographic criteria for myocardial
infarction with autopsy findings. Circulation 1967;35(1):158171.
51. Krone RJ, Greenberg H, Dwyer EM, et al. Long term prognostic significance of ST segment depression
during AMI. J Am Coll Cardiol 1993;22(2):361367.
52. Klein LW, Helfant RH. The Q wave and non Q wave myocardial infarction: differences and similarities.
Prog Cardiovasc Dis 1986;29(3):205220.
53. Birnbaum Y, Chetrit A, Sclarovsky S, et al. Abnormal Q waves on admission electrocardiogram of
patients with first myocardial infarction: prognostic implications. Clin Cardiol 1997;20(5):477481.
54. Sevilla DC, Wagner NB, Pegues R, et al. Correlation of the complete version of the Selvester QRS
scoring system quantitative anatomic findings for multiple left ventricular myocardial infarcts. Am J
Cardiol 1992;69(5):465469.
55. Stone PH, Raabe DS, Jaffe AS, et al. Prognostic significance of location and type on myocardial
infarction: independent adverse outcome associated with anterior location. J Am Coll Cardiol 1988;
11(3):453463.
56. ORourke RA. Treatment of RV infarction: thrombolytic therapy, coronary angioplasty, or neither?
J Am Coll Cardiol 1998;37:882884.
57. Hochrein J, Sun F, Pieper KS, et al. Higher T wave amplitude associated with better prognosis in
patients receiving thrombolytic therapy for AMI (a GUSTO-1 substudy). Am J Cardiol 1998;81(9):
10781084.
58. Sclarovsky-Benjaminov F, Sclarovsky S, Birnbaum Y. The predictive value of the electrocardio-
graphic pattern of acute Q-wave myocardial infarction for recurrent ischemia. Clin Cardiol 1995;
18(12):710715.
59. Maeda S, Imai T, Kuboki K, et al. Pathologic implications of restored positive T waves and persistent
negative T waves after Q wave myocardial infarction. J Am Coll Cardiol 1996;28(6):15141518.
60. Go AS, Barron HV, Rundle AC, et al. Bundle branch block and in-hospital mortality in AMI. Ann
Intern Med 1998;129(9):690697.
61. Sgarbossa EB, Pinski SI, Topol EJ, et al. Acute myocardial infarction and complete bundle branch
block at hospital admission: characteristics and outcome in the thrombolytic era. J Am Coll Cardiol
1998;31(1):105110.
62. Dnyaneshwar V Mulay, Syed M Quadri. QT dispersion and early arrhythmic risk in acute myocar-
dial infarction. IHJ 2004;56(6):636641.
CHAPTER 28
PERICARDITIS AND MYOCARDITIS
PERICARDITIS 560 ii. ECG Changes Due to

i. ECG Changes Due to Superficial Myocarditis 560
Pressure Effects 560 MYOCARDITIS 565
REFERENCES 566
PERICARDITIS
The ECG changes in acute pericarditis mimic early repolarization and acute antero-
inferior infarction, which are believed to be related to an actual current of injury
caused by:
The pressure of fluid or fibrin and
Superficial myocardial inflammation (myocarditis).
The ECG changes in later stages are due to the progression to effusion, tamponade, or
constriction.
i. ECG Changes Due to Pressure Effects

Pressure on the myocardium produces a current of injury manifested by deviation of
the ST segment from the baseline. The ST elevation is due to current flowing from the
epicardial surface to the thorax and back into the heart through atria and great vessels.1
The ST elecation is more common with less pronounced reciprocal ST depression. ST
elevation occurs in 70% in leads I, II, V5 and V6, in 3255% in leads III, aVL, aVF, V3,
and V4, and reciprocal ST depression in 64%, usually in leads aVR and V1.2
The PR segment depression occurs in all leads except in aVR and occasionally in V1, in
which PR segment is elevated. The depression of PR segment occurs in 80% and reflects
abnormal atrial repolarization due to atrial inflammation. However, any PR segment
depression 0.8 mV or elevation 0.5 mV suggests the presence of atrial injury.3
ii. ECG Changes Due to Superficial Myocarditis

Manifested by T wave inversion in all leads except aVR and V1.
However in typical cases of pericarditis, the T wave inversion is incomplete and
amplitude of the inverted T waves is relatively low, which gives rise to a diphasic
PERICARDITIS AND MYOCARDITIS 561
Table 28.1 ECG evolution of acute pericarditis
Epicardial leads: I, II, aVF, aVL and V3V6 Endocardial leads: aVR and V1
Stage ST segment T waves PR segment ST segment T waves PR segment
1. I Elevated Upright Depressed or Depressed Inverted Elevated or

isoelectric isoelectric
2. Early II Isoelectric Upright Depressed or Isoelectric Inverted Elevated or
isoelectric isoelectric
3. Late II Isoelectric Flat or Isoelectric Isoelectric Flat or Isoelectric
inverted upright
4. III Isoelectric Inverted Isoelectric Isoelectric Upright Isoelectric
5. IV Isoelectric Upright Isoelectric Isoelectric Upright Isoelectric
(positivenegative) wave or a notched T wave, a characteristic ECG feature of acute

pericarditis.4
Evolution of ECG Changes
Four stages have been described in the evolution of acute pericarditis, which occurs in
few hours to days, after the onset of pericardial pain5 (see Table 28.1).
Stage I accompanies the onset of chest pain and comprises of:
ST segment (JST) elevation with concavity upwards and upright T waves, PR seg-
ment depressed or isoelectric usually in I, II, aVL, aVF, and V3V6 (see Fig. 28.1).
ST segment depression with inverted T waves and elevated or isoelectric PR segment
occurs in aVR and V1, and sometimes in V2 lead.
QTc is usually normal, but may be prolonged in postoperative pericarditis.
ST elevation in acute pericarditis should be differentiated from acute myocardial
infarction (AMI) and early repolarization
The ST elevation is less pronounced, elevation 0.5 mV is uncommon in pericarditis
as compared to early stages of MI, indicating that injury current is probably smaller
with pericarditis than with AMI.
In MI, ST segment elevation has convexity upwards with frontal QRS axis usually
100 to 120, while in acute pericarditis, ST segment elevation has concavity
upwards and frontal QRS axis is 30 to 60.6
The reciprocal ST depression is less pronounced and in fewer leads than in AMI.
In early repolarization which is often seen in young males (40 years of age), ST
segment changes are accompanied by tall and peaked T waves, RS slurring, ST
segment/T wave ratio in V6 0.25, and no ST evolution. Tallest T wave is noticed in
V4. Acute pericarditis is characterized by ST evolution, tallest T in V5 and ST segment
elevation/T wave amplitude ratio in V6 0.25.7
The PR segment changes in acute pericarditis should be differentiated from atrial injury
Any PR segment depression 0.8 mV or elevation 0.5 mV suggests the presence
of atrial injury.3
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 28.1 | Acute pericarditisdiffuse ST segment elevation (concavity upwards) and PR

segment depression.
Stage II occurs several days later and ECG changes consist of:
In leads I, II, aVL, aVF, and V3V6: Return of the ST segment to the baseline, i.e.
becomes isoelectric. PR segment may become isoelectric or remains depressed.
In late stage II, T waves become progressively flattened to inverted. Such transient
normalized ECG is observed in 20% of the patients for a period of 1 to 5 days
(average of 2.3 days).2
In leads aVR and V1: ST segment also becomes isoelectric. PR segment may also return
to baseline or may remain elevated. In late stage II, T waves become progressively
flattened to upright.
The change in the ST segment usually occurs prior to the appearance of T wave
inversion in the main leads, while in AMI; T waves become inverted before ST segment
returns to the baseline.
Stage III is characterized by T wave inversion in I, II, aVL, aVF and V3V6.
T wave inversion occurs in more leads, but less deep or less completely inverted than
in AMI.
This is not associated with loss of R wave voltage or appearance of Q waves, character-
istic of evolution of myocardial infarction.
The stage III has become less frequent due to effective early treatment with anti-
inflammatory agents.
Stage IV represents the reversion of T wave changes to normal, which may take weeks
to months.
However, T wave inversion may occasionally persist indefinitely in patients with
chronic inflammation due to tuberculosis, uremia or neoplastic pericardial disease.
ECG Variants in Pericarditis

Abnormal ECG changes appear in 90% of cases.
However, all four stages are detected only in about 50%.
Sinus tachycardia is common and may be present in the absence of other contributing
factors such as fever or hemodynamic compromise.8
Other atrial arrhythmias are infrequent. VT, AV block and BBB are not the features
of acute pericarditis.
The variations of the ECG pattern are present in 50% of the cases and includes
typical and atypical variants.
i) Typical ECG variants:
Absence of one or more stages of the ST segment and T wave changes.
There may be rapid evolution of stage I directly to stage IV.
There may be persistence of stage III (T wave inversion) indefinitely or for long
periods due to chronic pericardial inflammation or presaging constrictive evolution.
In stage I, ST segment may be isoelectric or depressed in III, aVL, and isoelectric in I.
ii) Atypical ECG variants:
Absence of any serial ECG changes due to rapid evolution or delayed recording or
accompanying superficial myocarditis is of low grade or absent.
There may be isolated PR segment depression without STT changes.
There is appearance of ST segment changes in only a few leads which may be mistaken
for myocardial ischemia. However in pericarditis, reciprocal ST changes are absent.
Appearance of T wave inversion before the ST segment returned to the baseline is
characteristic of MI.
In stage III, there may be T wave inversion only in some leads, usually V3 or V4V6.
ECG Changes During Progression of Pericarditis

i) Pericardial effusion
Low amplitude ECG (QRS amplitude 0.5 mV in limb leads and 1.0 mV in pre-
cordial leads) is seen in most of the cases (see Fig. 28.2).

Low P wave voltage indicates massive effusion.
There may be STT wave changes due to superficial myocarditis, which may persist or
disappear after paracentesis.
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 28.2 | Pericardial

and V V .
effusionlow voltage ECG with T with inversion in I, II, III, aVF,
5 6
Electrical alternans can occur in pericardial effusion due to the changes in cardiac
position that result from rotational and pendular motion of the heart, which is nor-
mally restrained by the lungs and mediastinum.9 This motion of the heart has been
termed as cardiac nystagmus.10 However, electrical alternans is characteristic of car-
diac tamponade.
Other causes of low voltage ECG include:
Cardiac causes:
Hypothyroidism (myxedematous myocardial involvement)
Chronic constrictive pericarditis
Diffus myocardial diseases: amyloidosis, scleroderma, cardiac neoplasm, myocardial
fibrosis (due to chronic ischemic heart disease).
Non-cardiac causes:
Pleural effusion
Emphysema
Pneumothorax, and
Excess epicardial or subcutaneous fat overlying the heart.
ii) Cardiac tamponade
Electrical alternans is pathognomonic of acute cardiac tamponade in 1/3rd of the cases.
Alternans is usually limited to QRS complex (2:1 or 3:1 pattern), while T and P waves
alternans are rare (see Fig. 28.3). It is critically related to heart rate and beta-blockers
which slow the heart rate and make alternans disappear.
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 28.3 | Cardiac tamponadesinus tachycardia with QRS electrical alternans.

P
I IAB aVR V1 V4
II aVL V2 V5
P
III aVF V3 V6
Fig. 28.4 | Constrictive pericarditislow voltage ECG with flat to inverted T waves and
wide P waves (due to interatrial block: IAB, upright in I, inverted in III, and
biphasic in V1V2).
ECG changes of acute pericarditis of any stage can be found, but most ST segment
deviations are absent and T waves are low to inverted.
QRS-T voltage tends to decrease (usually due to reduced heart size), but the degree
of changes is unrelated to the severity of tamponade.
Acute hemorrhagic tamponade provokes bradycardia often of the AV junctional origin.
iii) Constrictive pericarditis (CP): ECG changes include:
Low QRS voltage seen in 5590%.11
Generalized T wave inversion, flattening or notching is most common ECG finding,
which is seen in 90100% of the cases11,12 (see Fig. 28.4).
P waves may be wide and bifid (interatrial block) and sometimes resembling P mitral
with P wave axis between 90 and 10.
Atrial arrhythmias occur in CP, usually atrial fibrillation (2336%) and occasionally
atrial flutter (610%).11,12 The arrhythmias increase with chronicity and are related
to long standing elevation of atrial pressures and atrial enlargement.
MYOCARDITIS
Myocarditis is said to be present when the heart is involved in an inflammatory process

often caused by any infectious agent. However, it is usually described during and after
a wide variety of viral, rickettsial, bacterial and metazoal diseases. ECG abnormalities
occur more frequently than clinical myocardial involvement, but are usually transient.
ST segment depression or T wave inversion or both in LV epicardial leads: commonest
ECG findings in acute myocarditis13 (see Fig. 28.5).
Prolongation of AV or intraventricular conduction: complete AV block is usually tran-
sient and resolves usually without any sequelae. Intraventricular conduction abnor-
malities are associated with more severe myocardial damage and worst prognosis.14
Lengthening of QTc interval.
V1 V2 V3 V4 V5 V6
Fig. 28.5 | Acute myocarditisT wave inversion in precordial leads.
1. Diffuse ST5 mm
and concavity upwards 1. QRS electrical
2. Diffuse depressed PR Cardiac tamponade alternans
segment and T 2. Flat or T
Pericarditis
1. Less reciprocal ST Pericardial disease Myocarditis

2. Axis: 30o to 60o
3. ST/T amplitude in
V6: 0.25 Pericardial effusion
Constrictive 1. ST T
pericarditis 2. QTc
3. Atrial and ventricular
1. Low voltage ECG arrhythmias
2. STT changes may
persist 1. Low QRS voltage
2. Flat or T
3. Af or Afl
Fig. 28.6 | ECG diagnosis of pericardial diseases and myocarditisAf: atrial fibrillation, Afl: atrial flutter,
vent.: ventricular, QTc: increased corrected QT interval, ST: ST elevation, ST: ST depression,
T: inverted T waves.
Various atrial and ventricular arrhythmias.

QRS abnormalities that may mimic MI may also occur (see Fig. 28.6).
REFERENCES
1. Teh BS, Walsh J, Bell AJ, et al. Electrical current paths in acute pericarditis. J Electrocardiol 1993;26(4):
291300.
2. Surawicz B, Lassiter KC. Electrocardiogram in pericarditis. Am J Cardiol 1970;26(5):471474.
3. Charles MA, Bensinger TA, Glasser SP. Atrial injury current in pericarditis. Arch Intern Med 1973;
131(5):657662.
4. Noth PM, Barnes HR. Electrocardiographic changes associated with pericarditis. Arch Intern Med
1940;55:291.
5. Spodick DH. ECG changes in acute pericarditis. Am J Cardiol 1974;33(4):470474.
6. Kouvaras G, Soufras G, Chronopoulos G, et al. The ST segment as a different diagnostic feature
between acute pericarditis and acute inferior myocardial infarction. Angiology 1990;41:207.
7. Spodick DH. Electrocardiographic abnormalities in pericardial disease. In: Spodick DH: the
Pericardium: a comprehensive Text book, New York, Marcel Dekker, 1997:4064.
8. Dressler N. Sinus tachycardia complicating and outlasting pericarditis. Am Heart J 1966;72(3):
422423.
9. McGregor M, Baskind E. Electrical alternans in pericardial effusion. Circulation 1955;11(6):837843.
10. Littman D. Alternation of the heart. Circulation 1963;27:280291.
11. Dalton JC, Pearson RJ, White PD. Constrictive pericarditis: a review and long term follow up of 78
cases. Ann Intern Med 1956;45(3):445458.
12. Wood P. Chronic constrictive pericarditis. Am J Cardiol 1961;7:48.
13. Chida K, Ohkawa S, Esaki Y. Clinicopathological characteristics of elderly patients with persistent ST
segment elevation and inverted T waves: evidence of insidious or healed myocarditis? J Am Coll Cardiol
1995;25:1641.
14. Matsuura H, Palacios IF, Dec GW, et al. Intraventricular conduction abnormalities in patients
with clinically suspected myocarditis are associated with myocardial necrosis. Am Heart J 1994;
127(5):12901277.
CHAPTER 29
D RUG E FFECTS AND E LECTROLYTE
A BNORMALITIES
DIGITALIS 568 HYPOKALEMIA 574
Digitalis Effects 568 Modification of Hypokalemic Effects
Mechanism of Digitalis Induced by Other Electrolytes 575
Arrhythmias 572 HYPERCALCEMIA 576
ELECTROLYTE ABNORMALITIES AND HYPOCALCEMIA 577
ECG CHANGES: HYPERKALEMIA 572 HYPERMAGNESEMIA 578
Modification of Hyperkalemic HYPOMAGNESEMIA 578
Effects by Other Electrolytes 573 REFERENCES 579
DIGITALIS
It is an inotropic agent discovered by William Withering in 1785. It has a steroid

nucleus with an
, -unsaturated lactone ring attached to C-17 position.
Its positive ionotropic effect is by inhibition of the Na pump (Na, KATPase)
which results in an increase in the cytolic Ca2 concentration through Ca channels
and Calcium pump (NaCa Exchanger) of the sarcolemma.
On oral administration, it is mainly absorbed in small and large intestines, and in
general serum therapeutic level ranges 0.51.5 mg/L.1
Therapeutically, it is mainly used in CHF, and four types of supraventricular tachy-
cardia (SVT)paroxysmal SVT, atrial fibrillation, atrial flutter and Wolff-Parkinson-
White (WPW) syndrome.
Digitalis Effects
The effects of digitalis therapy are mainly classified into three groupstherapeutic,
excessive and/or toxic, unequivocal toxic effects.
Therapeutic Effects
These are acceptable effects of digitalis which include:
ST segment is shortened and depressed with characteristic rounded, concave (scooped)
configuration. With ST depression, T wave is dragged downwards giving the appear-
ance of T wave inversion and inverted right mark appearance (see Fig. 29.1). The
dragged T wave may become diphasic, with initial portion being negative and ter-
minal portion being positive. However, decreased amplitude of T wave and shortened
DRUG EFFECTS AND ELECTROLYTE ABNORMALITIES 569
QT interval are the earliest ECG changes. These STT changes are usually more
pronounced in leads with tall R waves or in inferior and left precordial leads, while
it is less marked in right precordial leads.
Shortening of QT interval with occasional appearance of prominent U waves.
Prolongation of PR interval may also occur.
Slowing of the ventricular response is used in atrial fibrillation or flutter, and con-
version of atrial arrhythmias to sinus rhythm directly or indirectly may also occur.
Excessive or Toxic Effects
Digitalis is known to induce every known arrhythmias but rarely atrial flutter and
BBB. Suspect digitalis toxicity when both increased automaticity and impaired con-
duction are present at the same time.
Non-paroxysmal junctional tachycardia: It is highly specific for digitalis excess or
toxicity.
Atrial tachycardia with block (careful attention to lead V1 distinguishes it from atrial
flutter) (see Figs 29.2 and 29.3). Paroxysmal atrial tachycardia (PAT) with block
occurs in about 73%.2
Second degree AV block usually of the Wenkebach type, while Mobitz type II 2nd
degree AV block is rare (see Fig. 29.4). Complete AV block in digitalis toxicity is
uncommon (see Fig. 29.5) and as a rule is associated with narrow QRS complexes,
since the level of block is proximal to the His bundle bifurcation.
SA block can also occur.
Atrial fibrillation accounts for 10% of the arrhythmias induced by digitalis (see
Fig. 29.6).
V1 V2 V3 V4 V5 V6
Fig. 29.1 | Digitalis effectST depression with dragging of T waves resulting in charac-
teristic inverted right mark and shortened QT interval.
V1
P R P R
Fig. 29.2 | Digitalis toxicityatrial tachycardia with 1:1 conduction.

V1 P P P P
P
R R
aVF
Fig. 29.3 | Digitalis toxicityatrial tachycardia with 2:1 AV block.
V1
P P P P P
V4
Fig. 29.4 | Second degree 2:1 AV block with regular atrial rate of 86/min, ventricular
rate of 43/min and ST depression in V due to digitalis toxicity which is not
4
common.
P P
Fig. 29.5 | Complete AV block with normal QRS complex and blocked premature atrial
contractions (arrow) due to digitalis toxicity which is also not common.
V1
Fig. 29.6 | Atrial fibrillation occurs in 10% of digitalis toxicity.

V1
V6
Fig. 29.7 | Ventricular bigeminydefinite evidence of digitalis toxicity.
Fig. 29.8 | Bidirectional ventricular tachycardia with slight irregularitystrong evidence

of digitalis toxicity.
Unequivocal Toxic Effects

Presence of ventricular arrhythmias is the definite evidence of digoxin toxicity.
Ventricular premature contractions (VPC) are the earliest and most common mani-
festations of digitalis toxicity with least specificity.
Ventricular bigemini and multifocal VPCs (see Fig. 29.7).
Ventricular tachycardia (VT): VT with exit block and bi-directional VT strongly
suggests digoxin toxicity3 (see Fig. 29.8).
Ventricular fibrillation (VF): Digitalis induced VF is rarely recorded in humans.
AV dissociation strongly indicates digitalis toxicity (see Table 29.1).
Table 29.1 ECG in digitalis toxicity
1. Non-paroxysmal junctional tachycardia

2. Second degree AV block (Mobitz type I)
3. Sinoatrial (SA) block
4. Ventricular premature contractions (VPCs) especially bigeminy and multifocal
5. Ventricular tachycardia (VT) especially with exit block and bi-directional VT
6. Atrioventricular (AV) dissociation
1. VPCsmultifocal
1. ST 3. AV
and bigeminy
2. T amplitude dissociation
2. Bi-directional VT
3. T dragged
down
inverted right Unequivocal
mark
appearance
Therapeutic
Digitalis Toxic effects
effects
4. Prolonged PR Excessive/toxic
5. Decreased QTc 1. NP junctional
with occasional tachycardia
U waves 2. PAT with AV 4. 2 AV block-
block Wenkebach type
3. Atrial 5. SA block
fibrillation
Fig. 29.9 | Therapeutic and toxic effects of digitalisVPCs: ventricular premature con-
tractions, VT: ventricular tachycardia, NP: non-paroxysmal, PAT: paroxysmal
atrial tachycardia, ST: ST depression, T amplitude: decreased T amplitude.
Mechanism of Digitalis Induced Arrhythmias

Enhanced automaticity, reentry or delayed after depolarization results in atrial tachy-
cardia with block, non-paroxysmal junctional tachycardia, VPCs, VT, bi-directional
VT, ventricular fibrillation or flutter.
Depression of the pacemaker causes SA node arrest.
Depression of the conduction results in SA block and AV block.
AV dissociation results in suppression of the dominant pacemaker with passive escape
of lower junctional focus or inappropriate acceleration of a subsidiary pacemaker
(see Fig. 29.9).
ELECTROLYTE ABNORMALITIES AND ECG CHANGES: HYPERKALEMIA
It is associated with a distinctive sequence of ECG changes. The correlation between

plasma K and ECG is less reliable, but there is a good correlation between plasma K
levels and surface ECG in experimental hyperkalemia.
V1 V2 V3 V4 V5 V6
Fig. 29.10 | Hyperkalemiatall tented T waves in II, aVF and V V .2 6
At a plasma level of about 5.7 mEq/L: T wave is tall, peaked (tented) and often sym-
metrical with a narrow base ( 0.20 s)4 and a normal or decreased QTc interval,
which is best seen in Leads II, III, and V2V4 (see Fig. 29.10).
At a plasma level of about 7.0 mEq/L: There is reduction in the amplitude of
P wave, intra-atrial conduction delay, prolongation of PR interval, and QRS begins
to widen.
At a plasma level of about 8.4 mEq/L: P wave is no longer recognizable.
At a plasma level of 911 mEq/L:
QRS complex is uniformly widened, with prolongation of both initial and termi-
nal portions, resulting in a pattern that may resemble RBBB, LBBB, left anterior
or left posterior fascicular block or a combination of the four.
In RBBB pattern due to hyperkalemia, initial phase of QRS complex is pro-
longed, while in conventional RBBB, only the terminal portion of the QRS
complex is delayed.
Similarly in LBBB pattern due to hyperkalemia, terminal portion of the QRS
complex is delayed, while in conventional LBBB, only the initial portion of the
QRS complex is prolonged.
Occasionally hyperkalemia induces ST elevation in right precordial leads (V1V2)
stimulating MI, known as the dialyzable current of injury, which disappears after
appropriate treatment5 (see Fig. 29.11).
At a plasma level of 12 mEq/L: SA block, AV block (Wenkebach-type I or Mobitz
type II), junctional or ventricular escape rhythms may be present. However, it
eventually leads to asystole sometimes preceded by undulating ventricular flutter-
fibrillation (see Table 29.2).
Modification of Hyperkalemic Effects by Other Electrolytes

Hypocalcemia frequently accompanies hyperkalemia in patients with renal insuf-
ficiency, which aggravates AV and intraventricular conduction disturbances and
facilitates the appearance of ventricular fibrillation.
V1 V4
V2 V5
V3 V6
Fig. 29.11 | elevated

Advanced hyperkalemiatall and peaked T waves (best seen in V ) and
3
ST segment in V (dialyzable current of injury), widened QRS
1
complexes and flat P waves.
Table 29.2 ECG in hyperkalemia
1. Tall tented T waves with narrow base

2. Reduced P wave amplitude, which eventually disappears
3. Prolonged of PR interval
4. Normal or decreased QTc interval
5. Widened QRS complex resembling RBBB or LBBB
6. ECG changes best seen in II, III, V2V4 leads
Hypercalcemia with hyperkalemia may also present in some patients with renal
insufficiency due to the overzealous therapy with calcium or associated secondary
hyperparathyroidism which may counteract the effects of hyperkalemia and prevent
ventricular fibrillation.
Similarly, hypernatremia may counteract the effects of hyperkalemia, while hypona-
tremia may augment the effects of hyperkalemia on AV and intraventricular con-
duction disturbances.
HYPOKALEMIA
ECG also serves as a reasonably satisfactory guide to serum K levels in hypokalemia

and there is a reasonable correlation between plasma K level 2.3 or 3.0 mEq/L and
ECG changes. The ECG changes are a reflection of the K gradient across the cell
membrane and hence indicate the ratio of extracellular and intracellular K. Hypokalemia
is characterized by:
Gradual depression of ST segment, decrease of T wave amplitude (flattening of
T wave) with occasional T wave inversion.
Prominent upright U waves, best seen in V2V4 due to prolonged repolarization of
Purkinje fibers (see Fig. 29.12). Sometimes, the sinus beat that follows the VPC
shows a prominent U wave and may be the only ECG clue to hypokalemia.
QT interval is usually normal; QU interval is prolonged4 that may predispose to
torsades de pointes.
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 29.12 | Hypokalemia with ST segment depression, prominent U waves (amplitude

more than T waves) especially in V V .
2 3
Hypokalemia also predisposes to various tachyarrhythmias similar to antiarrhyth-

mic drugs including quinidine and digitalis:
Ectopics: supraventricular (22%) and ventricular ectopics (28%).6
Similar to digitalis toxicity: nonparoxysmal atrial tachycardia with AV block and
AV dissociation due to a combination of increased automaticity of ectopic pace-
makers and AV conduction disturbance.
Serious ventricular arrhythmias including VT, torsades de pointes and ventricular
fibrillation in patients with severe hypokalemia.7
Hypokalemia which frequently occurs in AMI and predisposes to arrhythmias is due to:
Intense sympathetic stimulation by the circulating epinephrine that shifts K into
the skeletal muscle and liver.8,9
Due to treatment with thiazide diuretics7 or administration of sodium bicarbonate
during resuscitation.10
Surawicz et al attempted quantitative analysis of ECG pattern of hypokalemia and
proposed a diagnostic criteria.11
ST segment depression of 0.5 mm
U wave amplitude of 1 mm
U wave amplitude T wave amplitude in the same lead.
The ECG was considered to be typical of hypokalemia if three of the above features
were present in two leads. It was considered compatible with hypokalemia if two of
the above features or one related to the U wave were present. When serum K level was
2.7 mEq/L, the ECG was typical in 78% and compatible in 11% (see Table 29.3).
Modification of Hypokalemic Effects by Other Electrolytes

ST segment is prolonged in hypokalemic patients with hypocalcemia, without affect-
ing its arrhythmogenic effects.6
Table 29.3 ECG in hypokalemia
1. Prominent upright U waves

2. Normal QT interval
3. Gradual ST depression
4. Decrease amplitude/flattening of T waves
5. Best seen in V2V4
Normal Hypercalcemia
I I
II II
III III
QT 0.36 s QT 0.26 s
QTc 0.41 QTc 0.36
Fig. 29.13 | HypercalcemiaQT interval is shortened.
HYPERCALCEMIA
The serum Ca2 level affects the duration of phase 2 of the action potential which
determines the duration of ST segment and thereby affects the duration of QT interval.
This was initially recognized by Carter and Andrus in 1922.12
Hypercalcemia shortens the phase 2 action potential thereby shortening the QT
interval (see Fig. 29.13). QT interval correlates reasonably with serum Ca2 level, if
other known factors affecting QT interval, such as age, sex, heart rate, myocardial
disease, drugs and other electrolytes are eliminated.4
Of the three intervalsQT, Q-oT (Q to the onset of T wave), Q-aT (Q to the apex
of the T wave), Q-aT interval has greatest accuracy and correlates best with the Ca2
level.13
ST segment is shortened and occasionally depressed with T wave inversion.14

Severe hypercalcemia (serum Ca2 15 mg/dl) is often associated with T wave
changesflattened, notched or inverted.15
Cardiac arrhythmias are uncommon in patients with hypercalcemia. However, ven-
tricular fibrillation, second or third degree AV blocks have been reported in severe
hypercalcemia.16,17
HYPOCALCEMIA
It prolongs phase 2 action potential duration thereby:

Prolonging the QT interval and ST segment (see Fig. 29.14). Similarly, Q-aT is
more accurate and correlates best with serum Ca2 level.
Hypocalcemia may be associated with hypokalemia, in which case ECG also shows
ST segment depression, T wave inversion and prominent U waves.
Hypocalcemia is often associated with hyperkalemia in chronic renal disease, in
which case ECG also reveals prolonged ST segment and tall tented T waves (see
Table 29.4).
Hypocalcemia Normal
I I
II II
III III
QT 0.48 s QT 0.36 s
QTc 0.52 QTc 0.41
Fig. 29.14 | HypocalcemiaQT interval is prolonged.

Table 29.4 Hypercalcemia and Hypocalcemia
Hypercalcemia Hypocalcemia
1. Shortened QT interval 1. Prolonged QT interval

2. Shortened ST segment 2. Prolonged ST segment
3. T wave changes with severe hypercalcemia 3. Prominent U waves when associated with
hypokalemia
4. Arrhythmias-vent fibrillation and AV blocks 4. Tall tented T waves when associated with
in severe hypercalcemia hyperkalemia
1. ST, flat T 1. QT (Q-aT)

2. U 1mm 2. Shortened ST
amplitude and T 3. T changes
3. QU interval
4. Atrial and
ventricular
arrhythmias Hypokalemia (K) Hypercalcemia (Ca)
Electrolytes
1. Tall tented T Hyperkalemia (K) Hypocalcemia (Ca)

2. Flat P
3. Prolonged PR
4. Widened QRS
resemble bundle 1. QT (Q-aT)
branch blocks 2. Prolonged ST segment
5. ST in V1V2 (DCI) 3. Associated with K and K
6. 2 AV block
7. SA block
Fig. 29.15 | Common electrolyte abnormalities and ECG changesDCI: dialyzable current of injury, Q-aT:
Q to the apex of T wave interval, ST: ST elevation, ST: ST depression.
HYPERMAGNESEMIA
There are no specific ECG characteristics due to mild to moderate isolated abnormal-
ities in serum Mg2 levels. Hence, ECG effects of hypermagnesemia may be dominated
by the Ca2 levels. However, severe hypermagnesemia (serum Mg level 15 mEq/L)
can cause AV and intraventricular conduction disturbances which may culminate in
complete heart block and cardiac arrest.18
HYPOMAGNESEMIA
It is usually associated with hypocalcemia or hypokalemia and as such isolated hypo-

magnesemia may not be recognized on ECG. It can potentiate certain digoxin toxic
arrhythmias.
Thus, the serum electrolyte imbalance (hyperkalemia, hypokalemia, hypercalcemia

and hypocalcemia) causes distinctive ECG changes (see Fig. 29.15).
REFERENCES
1. Wirth KE. Relevant metabolism of cardiac glycosides. In: Erdmann E, Greeff K, Skou JC, eds.
Update in Cardiac Glycosides, 17851985. New York: Springer-Verlag; 1986:257262.
2. Lown B, Wyatt NF, Levine HD. Paroxysmal atrial tachycardia with block. Circulation 1960;21:
129143.
3. Rosenbaum MB, Elizari MV, Lazzari JO. Mechanism of bi-directional tachycardia. Am Heart J
1969;78(1):412.
4. Vander Ark CR, Ballantyne F III, Reynolds EW Jr. Electrolytes and the electrocardiogram. Cardiovasc
Clin 1973;5:269294.
5. Levine HD, Wanzer SH, Merrill JP. Dialyzable currents of injury in potassium intoxication resem-
bling acute myocardial infarction or pericarditis. Circulation 1956;13(1):2936.
6. Davidson S, Surawicz B. Ectopic beats and atrioventricular conduction disturbances in patients with
hypopotassemia. Arch Intern Med 1967;120(3):280285.
7. Redleaf PD, Lerner IJ. Thiazide-induced hypokalemia with associated major ventricular arrhthmias.
Report of a case and comment on therapeutic use of bretylium. JAMA 1968;206(6):13021304.
8. Brown MJ, Brown DC, Murphy MB. Hypokalemia from beta 2-receptor stimulation by circulating
epinephrine. N Engl J Med 1983;309:14141419.
9. Vick RL, Todd EP, Luedke DW. Epinephrine induced hypokalemia: relation to liver and skeletal
muscle. J Pharmacol Exp Ther 1972;181(1):139146.
10. Thompson RG, Cobb LA. Hypokalemia after resuscitation from out-of-hospital ventricular fibrilla-
tion. JAMA 1982;248(21):28602863.
11. Surawicz B, Braun AH, Crum WB et al. Quantitative analysis of the electrocardiographic pattern of
hypopotassemia. Circulation 1957;16(5):750763.
12. Carter EP, Andrus EC. QT interval in human electrocardiogram in absence of cardiac disease.
JAMA 1922;78:1922.
13. Nierenberg DW, Ransil BJ. Q-aTc interval as a clinical indicator of hyperkalemia. Am J Cardiol
1979;44:243248.
14. Lind L, Ljunghall S. Serum calcium and the ECG in patients with primary hyperparathyroidism.
15. Ahmed R, Yano K, Mitsuoka T et al. Changes in T wave morphology during hypercalcemia and its
relations to the severity of hypercalcemia. J Electrocardiol 1989;22(2):125132.
16. Voss DM, Drake EH. Cardiac manifestations of hyperparathyroidism, with presentation of a previ-
ously unrelated arrhythmia. Am Heart J 1967;73:235.
17. Crum WD, Till HJ. Hyperparathyroidism with Wenckebachs phenomenon. Am J Cardiol 1960;
6:836.
18. Agus ZS, Morad M. Modulation of cardiac ion channels by magnesium. Annu Rev Physiol 1991;
53:299307.
CHAPTER 30
A RRHYTHMIAS
1. SINUS NODAL DISTURBANCES 4. PRE-EXCITATION SYNDROME

AND ARRHYTHMIAS 580 (PES) 606
i. Sinus Tachycardia 580 Accessory Pathways (AP) 607
ii. Sinus Bradycardia 581 i. Concealed Accessory
iii. Sinus Arrhythmia 581 Pathways 608
iv. Sinus Pause or Sinus Arrest 582 ii. Pre-Excitaion Syndrome 609
v. Sinoatrial (SA) Exit Block 583 5. NARROW QRS TACHYCARDIA 622
vi. Wandering Pacemaker 583 i. Irregular tachycardia 622
vii. Sick Sinus Syndrome ii. Regular tachycardia 622
(BradycardiaTachycardia 6. VENTRICULAR ARRHYTHMIAS 622
Syndrome) 584 i. Premature Ventricular
viii. Sinus Node Reentry Tachycardia 585 Complexes (PVCs) or
2. ATRIAL ARRHYTHMIAS 586 Ventricular Premature
i. Premature Atrial Contractions Beats (VPBs) 622
(PACs) 586 ii. Ventricular Tachycardia (VT) 630
ii. Atrial Tachycardias (AT) 587 iii. Idioventricular Rhythm (IVR) 640
iii. Atrial Flutter (Afl) 589 iv. Ventricular Flutter (Vfl) and
iv. Atrial Fibrillation (Af) 593 Ventricular Fibrillation (Vf) 641
3. AV JUNCTIONAL ARRHYTHMIAS 598 7. WIDE QRS TACHYCARDIA 642
i. AV Junctional Escape Beats 598 i. Regular Wide QRS Tachycardia 642
ii. AV Junctional Rhythm 599 ii. Irregular Wide QRS Tachycardia 643
iii. AV Junctional Premature Beats 8. HEART BLOCK 644
or Premature AV Junctional AV Block 644
Beats 600 REFERENCES 655
iv. AV Junctional Tachycardia 601
v. AV Nodal Reciprocating
(Reentrant) Tachycardia
(AVNRT) 603
1. SINUS NODAL DISTURBANCES AND ARRHYTHMIAS
i. Sinus Tachycardia
In normal sinus rhythm, the heart rate is between 60 and 100 beats/min.
A sinus rhythm of 100 beats/min with constant PR interval and normal P wave
is defined as sinus tachycardia (see Fig. 30.1). Sinus tachycardia is usually non-
paroxysmal, which is accelerated and terminated gradually.
ARRHYTHMIAS 581
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 30.1 | Sinus tachycardiasinus rhythm with a rate of 110/min.

It is common in infancy and early childhood and is the normal reaction to a variety of
physiological or pathophysiological stresses such as exercise, anxiety, fever and anemia.
It is due to the accelerated phase 4 diastolic depolarization of sinus nodal cells.
Inappropriate sinus tachycardia: It is a persistent increase in resting heart rate unre-
lated to or out of proportion with the level of physical, emotional, pathological or
pharmacological stress. The cause is multifactorial, but main mechanisms are (i)
Enhanced automaticity of the sinus node,1 and (ii) Abnormal autonomic regulation
of the sinus node with excess symapathetic and reduced parasympathetic tone.2
Postural orthostatic tachycardia syndrome (POTS): It is a part of wide spectrum of
autonomic dysfunction (other spectrum being orthostatic hypotension).3 POTS is said
to be present when the heart rate increases by 30 beats/min of the baseline heart rate
or 120/min within 10 minutes of upright tilt in the absence of postural hypotension.
ii. Sinus Bradycardia

A sinus rhythm of 60 beats/min with normal P wave contour occurring before each
QRS complex with a constant PR interval is defined as sinus bradycardia (see Fig. 30.2).
It frequently occurs in healthy young adults, particularly well trained athletes.
It is due to decrease sinus node discharge, resulting from excessive vagal or decreased
sympathetic tone (see Table 30.1).
iii. Sinus Arrhythmia

It is defined as the variation in sinus rhythm between the longest and shortest cycle (PP
or RR intervals) on a resting ECG exceeding 0.12 s or the maximum cycle length minus
minimum cycle length divided by minimum cycle length exceeding 10% (see Fig. 30.3).
P wave morphology is normal with a constant PR interval (120 ms) since the focus
of discharge remains within the sinus node.
V5
Fig. 30.2 | Sinus bradycardia at a rate of 50/min.

Table 30.1 Sinus tachycardia and sinus bradycardia
Condition Common causes Salient ECG findings
1. Sinus tachycardia Infants and early childhood fever, Sinus rhythm of 100 beats/min,
anemia, exercise, anxiety, acute myocardial normal P waves and constant
infarction (AMI), heart failure PR interval
2. Sinus bradycardia Well-trained athletes, AMI (inferior MI) Sinus rhythm of 60 beats/min,
normal P waves and constant
PR interval
P P P P P P
P P P
Fig. 30.3 | Sinus arrhythmiavarying PP interval (non-respiratory).

It is due to rhythmic fluctuation in vagal tone mediated through Bainbridge reflex.
It is of two types: respiratory form and non-respiratory form.
Respiratory or phasic sinus arrhythmia: Cycle length (PP interval) shortens
during inspiration and lengthens with expiration. Breath holding eliminates the
cycle length variation.
Non-respiratory or non-phasic sinus arrhythmia: It is characterized by variation in
PP interval unrelated to respiratory cycle, and may be the result of digitalis toxicity.
It is most common in children and decreases with advancing age.
The loss of sinus rhythm variability is a risk factor for sudden cardiac death, which
can also occur in patients with acute intracranial lesions4 (see Table 30.2).
iv. Sinus Pause or Sinus Arrest

It is due to a disorder of impulse formation as a result of slowing or cessation of spon-
taneous sinus nodal automaticity (see Fig. 30.4).
It is recognized by a pause in the sinus rhythm.
Sinus node can be involved by degenerative fibrotic changes, MI, digitalis toxicity or
excessive vagal tone.
ARRHYTHMIAS 583
Table 30.2 Sinus arrhythmia
Common causes Salient ECG findings
Children and acute intracranial lesions 1. Variation of RR or PP interval of 0.12 s

due to fluctuation in vagal tone
2. Normal P waves and constant PR interval
Fig. 30.4 | Progressive sinus bradycardia and sinus arrest which resulted in ventricular
escape rhythm.
v. Sinoatrial (SA) Exit Block

It is due to a conduction disturbance during which an impulse formed within the
sinus node fails to depolarize the atria or depolarizes with delay.
It is recognized by a pause due to the absence of normally expected P wave.
First degree SA exit block: It cannot be recognized by ECG as SA node discharge is
not recorded.
Second degree SA exit block type I (Wenkebach): PP interval progressively shortens
prior to the pause and the duration of the pause is 2 PP cycles (see Fig. 30.5).
Second degree SA exit block type II: The duration of pause equals approximately
two, three or four times the normal PP cycle consistent with 2 : 1, 3 : 1, or 4 : 1 SA
exit block (see Fig. 30.6).
Third degree SA exit block: It can present as complete absence of P waves, but is
difficult to diagnose with certainty without sinus node electrograms.
Acute myocarditis or infarction involving the atrium, excessive vagal tone, and drugs
such as quinidine, procainamide or digoxin can produce SA exit block (see Table 30.3).
vi. Wandering Pacemaker

It indicates shift of dominant pacemaker from sinus node to the latent pacemakers
usually atrial or AV junctional tissue. Only one pacemaker at a time controls the
rhythm in contrast to AV dissociation.
There is a change in the contour of the P wave i.e. it becomes inverted or merged
with the QRS complex (leads I, II), and there is cyclical increase in RR interval
with gradual shortening of PR interval (120 ms) (see Fig. 30.7).
PR PR
PR
PR
pause
Fig. 30.5 | Second degree type I SA exit blockshortening of PP interval followed by

a pause and the duration of the pause is less than twice the shortest cycle
length. The cycle after the pause exceeds the cycle before the pause. PR
interval is normal and constant.
P
P P P P PR
Fig. 30.6 | Second degree type II 2 : 1 SA exit blockPause is twice the basic PP inter-
val. PR interval is normal and constant.
Table 30.3 Sinoatrial exit block
1. AMI involving atria Pause due to absence of expected P wave,

2. Increased vagal tone 2nd degree exit block is usually recognized
3. Drugs: quinidine, digoxin,
procainamide
R R R
P P' P'
R
R R R
P' P'
P P
Fig. 30.7 | Wandering pacemakervarying P wave contour (inverted P to upright P)

and gradual shortening of PR interval.
Often, it occurs in young individuals particularly athletes and is due to an aug-

mented vagal tone.
vii. Sick Sinus Syndrome (BradycardiaTachycardia Syndrome)

It is due to sinus node dysfunction with SA and AV conduction abnormalities, which
may manifest as persistent sinus bradycardia interspersed with sinus arrest or SA exit
ARRHYTHMIAS 585
Afl Afl
Fig. 30.8 | Sick sinus syndromeBradycardia interspersed with intermittent sinus

arrest and junctional escape beats (dots), followed by tachycardia with a
short spell of atrial flutter (Afl).
Table 30.4 Sick sinus syndrome
1. Drugs: digitalis, quinidine, beta blockers Sinus bradycardia interspersed with sinus
arrest, SA exit block or paroxysms of atrial
flutter or fibrillation
2. Hyperkalemia
3. Ischemia or AMI, pericarditis, cardiomyopathy,
collagen disease, surgical injury
SNRT Abrupt termination of

SNRT
aVR
aVL
P' P' P P
I
V1 P' P' P' P' P P P P
Fig. 30.9 | inSinus node reentry tachycardia (SNRT) and its abrupt terminationP wave
SNRT similar to sinus P wave.
block, or paroxysms of rapid regular or irregular atrial tachyarrhythmias (usually atrial

flutter or fibrillation) (see Fig. 30.8 and Table 30.4). More than one of these can be
recorded in the same patient on different occasions.
viii. Sinus Node Reentry Tachycardia

It accounts for 510% of SVT.
The rate is usually slower than other causes of SVT with a range of 80200 beats/min,
and an average of 130140 beats/min (see Fig. 30.9).
P waves are identical to sinus P waves.
2 type I:
1. Varying P contour
1. PP progressively
2. Gradual PR
2. Pause: 2 PP cycles
3. Cyclical RR
3. Constant PR
2 type II:
1. Pause: 2, 3 or SB interspersed
4 times PP cycle SA exit block Wandering with Sa, SAEB,
2. Constant PR (SAEB) pacemaker Af or Afl
1. P similar to sinus P
2. PR shorter SNRT Sick sinus syndrome
3. RP longer Sinus nodal
disturbances
and arrhythmias
Sinus tachycardia Sinus arrhythmia
1. 100/min SB: Sinus 1. PP 0.12s

Sinus arrest (Sa)
2. Normal P bradycardia 2. Max CLMin
3. Constant PR CL/Min CL = 10%
1. 60/min
Pause in sinus
2. Normal P
rhythm
3. Constant PR
Fig. 30.10 | ECG diagnosis of sinus nodal disturbances and arrhythmiasSNRT: sinus node reentry
tachycardia, Af: atrial fibrillation, Afl: atrial flutter, Max CL: maximum cycle length, Min CL:
minimum cycle length.
PR interval is related to tachycardia rate, but generally RP interval is longer with a

shorter PR interval.
Vagal maneuvers and adenosine can slow and terminate the tachycardia.
They are usually initiated and terminated abruptly by a premature atrial contraction.
(see Fig. 30.10).
2. ATRIAL ARRHYTHMIAS
i. Premature Atrial Contractions (PACs)

It is a common atrial arrhythmia occurring in about 0.4% normal individuals5 (see
Fig. 30.11).
It can occur in fevers, emotional stress, thyrotoxicosis, alcohol, and tobacco, or caf-
feine consumption.
PAC is characterized by P wave that occurs before the next expected sinus impulse
with its contour differing from that of sinus P wave.
If premature atrial focus is high in the atrium, the premature P waves are upright
and if the premature atrial focus is low in the atrium, P waves are inverted.
When PACs occur early in the cardiac cycle, P are superimposed on T waves
(hence the admonition search the T for P), which deforms the T waves slightly.
ARRHYTHMIAS 587
V1
P R P R R P R
Fig. 30.11 | Premature

interval.
atrial contractions (P)with PR of 120 ms and short RP
However often such PACs are blocked before reaching the ventricle and can be
misinterpreted as a sinus pause or sinus exit block.
Early occurring PACs may trigger atrial tachycardia, Afl or fibrillation.
Usually, PAC initiates a ventricular complex with a normal or basic QRS configuration
(In BBB, the basic QRS complex will be wide and slurred and PAC will like wise
initiate a QRS complex of BB type).
PR interval of the conducted PAC is usually prolonged (120 ms) i.e. it follows
the general rule: RP interval is inversely related to the PR interval. Thus a short
RP interval produced by an early PAC is followed by a long PR interval.
The PACs have less than fully compensatory pauses (the duration of the pause after
PAC is less than twice the PP interval) as the premature P wave resets the sinus cycle
early.
However, occasionally fully compensatory pause can occur due to delay in the reset
of the sinus cycle.
Rarely, an interpolated PAC may occur, in which the pause after the PAC is very
short and the interval bounded by normal sinus initiated P waves on either side of
the PAC is slightly longer than or equal to one normal PP interval.
PACs that follow every sinus beat cause atrial bigeminy (see Table 30.5).
ii. Atrial Tachycardias (AT)

They are classified into focal atrial tachycardia and multifocal atrial tachycardia.
a) Focal Atrial Tachycardia

Focal atrial tachycardia constitutes 1015% (but more in children) of the SVTs with
an atrial rate of 150200 beats/min (see Table 30.6).
P wave contour is different from that of the sinus P wave. A positive or biphasic P wave
in aVL and a negative or biphasic P wave in V1 favors RA origin, while a positive P
in V1 and a negative P wave in lead I or aVL favors LA origin. Negative P waves in
inferior leads are suggestive of a caudal origin, while positive P waves in these leads
suggest a cranial origin6 (see Fig. 30.12).
PR interval is influenced by the tachycardia rate.
It has the capability of developing AV block without interrupting the tachycardia
(atrial tachycardia with block), i.e. as the atrial rate increases, AV conduction becomes
impaired.
Table 30.5 Premature atrial contractions (PACs)
1. Alcohol, tobacco or 1. Premature P is different from sinus P wave, which may be

caffeine consumption upright or inverted depending upon the site of origin
2. Fevers 2. Slightly deforms the T wave when it superimposes on it
3. Thyrotoxicosis 3. PR is usually 120 ms with short RP interval
4. Digitalis toxicity 4. PAC initiates normal or basic QRS complex
5. Ischemia 5. Compensatory pause is not full
6. CHF 6. It can trigger atrial tachycardia, atrial flutter or atrial fibrillation
7. COPD
Table 30.6 Focal atrial tachycardia
1. Alcohol ingestion 1. P wave differs from the sinus P wave and may be inverted or upright
depending upon the site of origin
2. Digitalis toxicity 2. Atrial rate is 150200/min
3. MI 3. It has the capability of developing AV block without interruption i.e.
as atrial rate increases AV conduction becomes impaired
4. COPD 4. Due to abnormal automaticity or micro-reentry
5. Surgical atriotomy scar
I aVR V1 V4
II aVL V2 V5
P
III aVF V3 V6
P P
Fig. 30.12 | Focal atrial tachycardiainverted P most obvious in II, III and aVF leads
with narrow QRS complexes at a rate of 150/min.
The mechanism of focal tachycardia could be due to an abnormal automaticity or

micro-reentry and both varieties are amenable for catheter ablation (see Table 30.7).
Clinically, it may present as paroxysmal or persistent (incessant) AT. Automatic AT
tends to be incessant especially in children.
ARRHYTHMIAS 589
Table 30.7 Differential diagnosis of automatic and reentry atrial tachycardia (AT)
Automatic (ectopic) atrial tachycardia Reentry atrial tachycardia
1. Morphology of P is similar in all leads 1. Initial P differs from the subsequent P

2. Warm-up (gradual acceleration of the 2. Warm-up and cool-down are absent
rate of tachycardia) and cool-down
are present
3. Vagal maneuvers (carotid sinus massage) 3. Vagal maneuvers do not terminate AT and can
do not terminate AT, but can produce produce AV block
AV block
4. Resetting of AT by a premature stimulus 4. Premature stimulus does not reset AT, but
may terminate the AT
5. Pacing cannot terminate the AT 5. Pacing may suppress the AT
6. Occurs in digitalis toxicity (usually AT 6. Less common and may be due to atrial
with AV block), MI, COPD, alcohol fibrosis (with pulmonary disease) or surgical
ingestion atriotomy scars
P' R R R R
II P' R P' P' P'
Fig. 30.13 | Multifocal atrial tachycardiavarying P waves and PR interval with defi-
nite isoelectric base line.
b) Multifocal Atrial Tachycardia (MAT) or Chaotic

Atrial Tachycardia (CAT)
It is characterized by usual atrial rates of 100130 beats/min.
The rhythm is irregular with totally irregular PP intervals and may be confused with
atrial fibrillation; however the rate is usually not excessively rapid.
There are multifocal premature beats, atleast three different P wave morphologies
with changing PR interval in one lead and isoelectric base line between P waves
(see Fig. 30.13).
This tachycardia commonly occurs in older patients with COPD and CHF. Unusual
causes include digoxin toxicity and theophylline administration.
It has been suggested that MAT is the result of DAD (delayed after depolarization)
trigger induced automaticity7 (see Table 30.8).
iii. Atrial Flutter (Afl)

It is a rapid regular atrial tachyarrhythmia with:
Usual atrial rate of 250300 beats/min.
Most common AV conduction ratios (i.e. the ratio of flutter wave to conducted ven-
tricular complexes) are 2:1 and 4:1 and most often occurs in an even number e.g. 2:1,
4:1, (see Fig. 30.14); while 3:1 or 5:1 ratios are rare. But alternating 2:1 and 4:1 ratios
Table 30.8 Multifocal atrial tachycardia
1. Older patients with COPD, CHF 1. Atrial rate: 100130/min

2. Rarely in digitalis toxicity, 2. Totally irregular rhythm and may be confused with atrial
aminophylline administration fibrillation
3. Atleast three different P waves with varying PR interval
in one lead and isoelectric base line between P waves
4. Due to delay after depolarization
II
Afl Afl Afl Afl
Fig. 30.14 | Atrial flutter (Afl) with 4 : 1 and 2 : 1 block.
Table 30.9 Atrial flutter (Afl)
1. Mitral valve disease 1. Atrial rate: 250350/min

2. Congenital heart disease 2. Regular saw toothed flutter waves without isoelectric
base line in between them
3. Cardiomyopathy 3. Even number AV conduction (2 : 1 and 4 : 1 commonest)
4. CAD (less frequent) 4. Best visualized in II, III, aVF, and V1 leads
5. Surgical atriotomy scar
6. Pericariditis
7. Thyrotoxicosis
8. Alcohol ingestion
are common generating a bigemini pattern. In young children and rarely in adults,
1:1 AV conduction may occur.
The ventricular response becomes irregular with the occurrence of Wenckebach
phenomenon.
Regular saw toothed flutter waves without an isoelectric interval in between
flutter waves (vs multifocal AT) are best visualized in leads II, III, aVF, or V1 (see
Table 30.9).
The combination of abrupt slowing of the ventricular rate and an increased rate of
atrial flutter during carotid sinus massage strongly supports the diagnosis of Afl.
Occasionally, carotid sinus massage will cause atrial flutter to convert to atrial fibril-
lation (Af ) and very rarely sinus rhythm follows.
ARRHYTHMIAS 591
Incidence and Etiology

The overall incidence of Afl is 0.37%. It is more common in men (2.5 times).
It increases markedly with age, from 5/100,000 in 50 yrs old to 587/100,000 in
80 years old.8
It occurs in 2535% of patients with Af.9
It is associated with underlying atrial abnormalities secondary to mitral valve disease,
congenital heart disease, cardiomyopathy, and less frequently in CAD. It may occur in
thyrotoxicosis, alcoholism, pericarditis, following surgery for congenital heart disease
(especially TOF, TGA, or ASD).10
However, lone atrial flutter (no structural heart disease or precipitating cause) can
also occur (though rare).6
Types of Afl
Atrial flutter can be classified depending upon the electrophysiological and clinical
properties.
a) Electrophysiological classification
a) Depending upon the mechanism: Afl is a macro-re-entrant AT and depending
upon the re-entry circuits used, it is grouped into cavotricuspid isthmus (CTI)
dependent Afl and non cavotricuspid isthmus (NCTI) dependent Afl.
CTI-dependent Afl: They are all amenable for catheter ablation, and rapid overdrive
pacing can terminate the arrhythmia. Depending upon the re-entry circuits, CTI-
dependent Afl has the following varieties:
Counterclockwise reentry or typical Afl
Clockwise reentry or atypical Afl
Double wave reentry Afl
Lower loop reentry Afl
Counterclockwise reentry atrial flutter is the commonest and others are less com-
mon or rare.
(i) Counterclockwise reentry or common or classic or typical Afl:11
The CTI-dependent Afl is caused by a macro re-entrant right atrial circuit around
the tricuspid annulus, i.e. the impulse travels in counterclockwise direction down the
RA free wall inferiorly to atrial septum, from there it travels through the isthmus
bounded by crista terminalis (i.e. the area between SVC and IVC), coronary sinus os
on one side (forming the posterior barrier) and tricuspid annulus on the other side
(forming the anterior barrier) and Afl is known as common or classic or typical Afl.
Counterclockwise Afl is characterized by dominant negative flutter waves in inferior
leads and a positive flutter deflection in V1 with transition to a negative deflection in
V6 at the rate of 250350 beats/min.
(ii) Clockwise reentry or atypical or reverse typical Afl:12
In this CTI-dependent Afl, the re-entrant circuit travels in the opposite direction
i.e. clockwise direction.
This type of Afl is characterized by positive flutter waves in inferior leads, wide and
negative flutter waves in V1 with transition to positive waves in V6.
(iii) Double wave reentry Afl:13
In this arrhythmia, two flutter waves simultaneously occupy the usual flutter pathway.
This arrhythmia is transient, usually terminating within three to six complexes, but
may rarely deteriorate into Af.
(iv) Lower loop reentry Afl:14
In this arrhythmia, the re-entry wave front circulates around the IVC due to conduc-
tion across the crista terminalis, and unusual ECG patterns occur.
Non-cavotricuspid dependent Afl or incisional macro-re-entry Afl:11

It is caused by macro-re-entry circuits that do not use CTI. They are less common and
most related to an atrial scar, which creates conduction block and a central obstacle for
reentry.
It is common in patients with prior cardiac surgery involving the atrium such as
repair of congenital heart disease ASD, MV surgery, or atrial maze procedure.
The resulting arrhythmia is known as lesion-related or incisional macro-re-entry AT.
CTI-dependent Afl is also common in patients with prior atrial surgery and may
coexist with incisional macro-reentrant atrial tachycardias.
The flutter waves on ECG usually differ from that of CTI-dependent flutter, but
can resemble typical patterns. However, definitive diagnosis requires intracardiac
mapping.
It is also amenable to catheter ablation but recurrences are more common than CTI-
dependent Afl.
b) Depending upon the atrial rate and ability to entrain and interrupt Afl with
atrial pacing: Two types have been described:15
Type I Afl (common or classic): In type I, the atrial rate is 250320/min with a
mean of 300/min. It can be entrained and interrupted by atrial pacing.
Type II Afl (uncommon): In type II, usual atrial rate is 320350/min, but it
may occasionally be as fast as 450/min. It cannot be entrained and interrupted by
atrial pacing. It may occur as the fore runner for chronic atrial fibrillation (see
Fig. 30.15).
Clinical classification: Clinically, Afl is classified as paroxysmal (brief), persistent and

chronic form and therapeutic approaches are influenced by the clinical pattern.
Paroxysmal Afl is common with type I Afl and have high success rate of reversion to
sinus rhythm.
Persistent Afl occurs in chronic heart diseases, thyrotoxicosis or pulmonary
embolism.
Chronic Afl occurs in the setting of advanced heart disease and with type II
atrial flutter, which is often a forerunner of chronic Afl (see Table 30.10 and
Fig. 30.16).
ARRHYTHMIAS 593
iv. Atrial Fibrillation (Af)

a) Incidence:
Af is the most common sustained cardiac arrhythmia encountered in clinical practice
with an overall incidence of 0.42% which is associated with an increased morbidity
and mortality.
It is found in 1% of persons older than 60 years to more than 5% of patients older than
69 years.16
As per Framingham data, the overall chance of developing Af over a period of two
decades in patients older than 30 years is 2%.17
V5
AfI AfI AfI AfI
Fig. 30.15 | Atrial flutter (Afl-type II).

Table 30.10 Types of atrial flutter (Afl)
Depending upon the mechanism Depending upon the atrial rate Clinical classification
1. Cavotricuspid isthmus (CTI) dependent 1. Type I: 250320/min 1. Paroxysmal

i) Counterclockwise reentry Afl 2. Type II: 320350/min 2. Persistent
ii) Clockwise reentry Afl 3. Chronic
iii) Double wave reentry Afl
iv) Lower loop reentry Afl
2. Non-CTI dependent
Incisional macro Type I:

Clockwise (Typical):
reentry: Related to 1. 250320/min
ve Afl in II, III, aVF
atrial scar, more 2. Atrial pacing
and V6; ve Afl in V1
recurrences abolishes
Counter clockwise
(Typical): ve Afl in II, III, Depending upon Depending upon
Classification of Afl
aVF and V6; ve Afl in V1 the mechanism the atrial rate
Paroxysmal: 48 hours Type II:

Clinical 1. 320350/min
Persistent: 2 days 2. Atrial pacing
to weeks cannot abolish
Chronic: months- 3. Forerunner to
forerunner to chronic Af chronic Af
Fig. 30.16 | Classification of atrial flutter (Afl)fl: flutter waves, Af: atrial fibrillation.
b) Etiology
A history of CHF, valvular heart disease and stroke, left atrial enlargement, abnor-
mal mitral or aortic valve function, hypertension and advanced age have been found
to be independent risk factors for prevalence of Af.
Af was found in 29% of patients with isolated MS, 16% in isolated MR, 52% in
patients with combined MS and MR, and in only 1% of patients with aortic valve
disease.18
Af also occurs in CAD (517%, especially with CHF, atrial infarction, post CABG);
cardiomyopathy, thyrotoxicosis (look for thyrotoxicosis in recent onset Af ), alcohol
intake (holiday heart syndrome) and drugs such as digoxin and sympathomimetics.
c) Mechanism of Af
The genesis of Af is explained by multiple-wavelets hypothesis of Moe (1962):19 Af
involves several simultaneous and consistently shifting wave fronts that twist, block and
split to form new wave fronts. The rhythm is sustained when the number of wavelets is
large enough so that the probability of all wave fronts dying out at the same time is low.
This hypothesis was substantiated by Allessie et al in 198520 (see Fig. 30.17).
Persistence of Af depends on the:
1. Mass and width of excitable tissue i.e. size of the atria. Larger the size, easier is to
sustain Af.
2. Electrical wave length of the atria which is equal to conduction velocity effective
refractive period. Electrical wave length is 1216 cm for the normal sinus rhythm.
Vagal stimulation, sympathetic stimulation and alcohol ingestion (through sympa-
thetic stimulation) decreases the effective refractory period of the atria and
thereby decreasing the electrical wave length of the atrial tissue. Shorter wave
lengths of the atria predisposes to Af.
In Af, the electrical wave length of the atria averages 7.8 cm.
Multiple
wavelets
Fig. 30.17 | Genesis of atrial fibrillation.

ARRHYTHMIAS 595
Vagal stimulation Size of atria LAE/RAE
Electrical
Electrical wave
heterogeneity Sustenance of Af
length of atria
of atria
Genesis of Af Electrical
Advanced age refractiveness Vagal stimulation
of atria
Multiple wavelets
Sympathetic
Alcohol ingestion
stimulation
Fig. 30.18 | Mechanism of atrial fibrillation (Af)LAE: left atrial enlargement, RAE: right atrial enlargement.
3. Electrical heterogeneity of the atria: Presence of IVC, SVC orifices in RA and pul-
monary veins in LA causes electrical heterogeneity of the atria which facilitates the
breakup of the wave fronts into new ones that are necessary to sustain Af.
Vagal stimulation decreases the atrial refractoriness non-uniformly, resulting in
electrical heterogeneity which facilitates the sustenance of atrial fibrillation.
Advanced age facilitates the electrical heterogeneity of the atria (see Fig. 30.18).
d) ECG Features
Af is a totally irregular atrial rhythm characterized by:
Grossly disorganized atrial activity which results in fibrillatory (f) waves that are totally
irregular and vary in size and shape from beat to beat with the absence of normal
P waves, and are best seen in leads V1, II, III and aVF.
The atrial rate ranges from 400600/min with variable ventricular response due to
variable AV conduction resulting in irregularly irregular ventricular rhythm (irregu-
lar RR interval). Hence, in the absence of discernible atrial activity (f waves), a grossly
irregular ventricular rhythm still suggests the presence of Af.
Aberrant conduction tends to occur when a long ventricular cycle is followed by a
short cycle, the short cycle terminated by an aberrantly conducted beat, which is
referred as Ashman phenomenon21 (see Fig. 30.19). A series of short cycles, if short
enough may generate runs of aberrantly conducted beats mimicking VT.
In Af, if the ventricular cycle length prolongs, then VPC may occur. This phenome-
non is known as rule of bigeminy.
The ventricular rate in Af is usually 120180/min, but can accelerate to 200/min
in the presence of WPW syndrome with conduction down the accessory pathway.
The QRS complex during Af will be similar to that recorded during sinus rhythm,
usually a narrow QRS complex. However, a wide QRS complex occurs if associated
with BBB or antidromic variety of WPW syndrome (antegrade conduction over the
accessory pathways) or Ashman phenomenon. Wide QRS complex in Af results in
irregular wide QRS tachycardia.
V1
R R R R
ACB
Fig. 30.19 | Ashmans phenomenon in atrial fibrillationlongshort cycle sequence

ending in an aberrantly conducted beat (ACB with RBBB pattern).
Table 30.11 Atrial fibrillation (Af)
1. Valvular heart disease 1. Irregular atrial rhythm

2. CHF 2. Absence of normal P waves, but presence of
fibrillatory (f) waves
3. Hypertension 3. Atrial rate 400600/min with variable ventricular rate
(usually 120180/min)
4. Advanced age 4. Usually initiates narrow QRS complex, but wide QRS if
associated with BBB or antidromic WPW syndrome
or Ashman phenomenon
5. Cardiomyopathy 5. Best seen in V1, II, III, and aVF
6. CAD
7. Thyrotoxicosis
8. Alcohol intake
9. Drugs: digitalis, sympathomimetics
Lone Af: Af occurring in the absence of identifiable cause is known as lone Af and
carries a good prognosis22 (see Table 30.11).
e) Classification
Based on ECG criteria
Coarse Af: Size of waves similar to flutter waves (i.e. 1 mm) (see Fig. 30.20).
Fine Af: Size of f waves 1 mm (see Fig. 30.21).
Discernible Af: No visible f waves, but gross irregularly irregular ventricular complexes.
Clinical classification: It is helpful from therapeutic point of view.
Paroxysmal Af: It could be short standing (lasting from seconds to 1 hour) or long
standing (lasting from 1 hour to 48 hours). Spontaneous termination of Af can
occur. It is further grouped into:
Group I: First episode of Af
Group II: Recurrent attacks of Af in untreated individuals
Group III: Recurrent attacks of Af in treated individuals.
Persistent Af: It lasts for 2 days to weeks and self termination is unusual, but rever-
sion to sinus rhythm should be the aim of therapy.
ARRHYTHMIAS 597
R R R f R f R f f f
Fig. 30.20 | Atrial fibrillation (coarse)f waves 1 mm in size.

R R R R
V1
Fig. 30.21 | Atrial fibrillation (fine).

Table 30.12 Types of atrial fibrillation
ECG classification Clinical classification
1. Coarse Af 1. Paroxysmal
2. Fine Af 2. Persistent
3. Discernible Af 3. Chronic or permanent
Coarse Aff 1 mm Fine Aff <1 mm
VPC occurs if vent. Discernible AfNo

cycle length Based on ECG visible f but irregular
Rule of bigeminy vent. complexes
Due to
Classification
modifications
Lone AfNo
Aberrantly conducted identifiable cause
beat in short cycle Paroxysmal
Clinical
Ashman phenomenon Af 48 hours
Chronic/permanent
months to years
Persistent Af
2 days to weeks
Fig. 30.22 | Classification of atrial fibrillation (Af)vent.: ventricular, f: fibrillatory waves.

Chronic or permanent Af: It persists for months to years and reversion to sinus
rhythm is usually not possible and ventricular rate control is the aim of therapy (see
Table 30.12 and Fig. 30.22).
The common atrial arrhythmias can be diagnosed at the bed side from the ECG
changes. In both premature atrial contration (PAC) and focal atrial tachycardia (FAT),
P differs from the sinus P, while three different P waves with varying PR in a lead are
4. Deforms T when it is 4. Even number AV conduction

superimposed on it 2 : 1, 4 : 1 commonest
5. Initiates normal or 5. Best seen in II, III, aVF and V1
basic QRS complex
1. Atrial rate: 250300/min

1. P differs from sinus P 2. Regular saw toothed fl
2. PR 120 ms with waves
short RP 3. No isoelectric base line in
3. C P is not full between fl waves
Afl
1. Atrial rate : 400600/min
PAC with varying vent. rate
2. Ir Ir rhythm
Atrial arrhythmias Af 3. Best seen in V1, II, III and aVF
1. P differs from sinus P 3. No Normal P, but f waves
FAT
2. Atrial rate: 150200/min
MAT 4. Initiates normal QRS
3. AV conduction is complex
impaired as atrial rate 5. Initiates wide QRS complex
increases if associated with BBB, AD
4. Due to abnormal WPW synd or Ashman ph
automaticity or micro-
re-entry 1. Totally irregular rhythm 4. Three different P with varying
2. Atrial rate: 100300/min PR in one lead
3. Due to DAD 5. Isoelectric base line in
between P waves
Fig 30.23 | Diagnostic features of atrial arrhythmiasPAC: premature atrial contraction, FAT: focal atrial
tachycardia, MAT: multifocal atrial tachycardia, Afl: atrial flutter, Af: atrial fibrillation, CP:
compensatory pause, DAD: delayed after depolarization, BBB: bundle branch block, AD
WPW synd: antidromic Wolff Parkinson White syndrome, ph: phenomenon, f: fibrillatory waves,
fl: flutter waves, Ir Ir: irregularly irregular.
diagnostic of multifocal atrial tachycardia (MAT). In Afl, the atrail rate is usually 250300/
min with regular saw toothed flutter waves, while in Af, the atrial rate is 400600/min
with irregularly irregular rhythm (see Fig. 30.23).
3. AV JUNCTIONAL ARRHYTHMIAS
The common AV junctional arrhythmias are AV nodal reciprocating tachycardia,

junctional rhythm, junctional premature beats and junctional tachycardia.They may
occur due to ectopic focus or reentry phenomenon (see Fig. 30.24).
i. AV Junctional Escape Beats

a) Mechanism
A latent pacemaker in N region of AV node can become the dominant pacemaker by
default (passive mechanism) or usurpation (active mechanism). When a decreased
ARRHYTHMIAS 599
Typical Atypical
Escape beats Junctional rhythm
AVNRT Latent pacemaker Premature beats
Reentry AVJA Ectopic focus
Junctional
tachycardia
Non-paroxysmal Focal/paroxysmal
Fig. 30.24 | Types and mechanism of AV junctional arrhythmias (AVJA)AVNRT: AV

nodal reentrant tachycardia.
number of impulses arrive at the AV node as a result of slowing of sinus node discharge
or due to the interruption of propagation of the normal impulses along its usual
course, latent pacemaker (here the N region of AV node):
Escapes and initiates depolarization passively by default or
Capture pacemaker control actively by usurpation by increasing its discharge rate of
impulses resulting in AV junctional escape beats.
They are usually precipitated by long pauses (e.g. as in sinus bradycardia), slow phase of
sinus arrhythmia, intermittent SA block, sinus arrest, partial AV block or atrial fibrillation
with slow ventricular rate.
b) ECG Findings
The ECG shows pauses longer than normal PP interval, interrupted by a normally
conducted QRS complex with absent, retrograde, fusion or sinus P waves not con-
ducted to the ventricle.
Fusion P waves are frequent and are recognized by their shape which is intermediate
between that of sinus P waves and P waves of escape pacemaker. They occur when one
part of the atrium is activated by one pacemaker and another part by another pacemaker.
If P waves precede the QRS, they have a PR interval generally 0.12 s (see Fig. 30.25).
The interval from the last normally conducted beat to the AV junctional escape beat
gives the initial discharge rate of the AV junctional focus, and usually the interval from
the last normally conducted beat to the AV junctional escape beat gives the initial dis-
charge rate of the AV junctional focus, and usually occurs at a rate of 3560 beats/min.
AV junctional escape rhythm is usually regular. However, the intervals between the
subsequent escape beats gradually shorten due to a warm-up phenomenon.
ii. AV Junctional Rhythm

It results if the AV junctional escape beats continue for a period of time. It is defined
as at least three junctional escape beats in a row.
P P' P' P P
Fig. 30.25 | AV junctional escape beats (P) precipitated by a long pause of sinus
bradycardia. PP interval between junctional beats is longer than normal
PP interval and PR is 0.12 s.
II
P' P' P' P' P' P'
Fig. 30.26 | AV junctional rhythmretrograde P occurring after normal QRS complex

at a rate of 50/min.
The usual rate is 3560 beats/min with normally conducted QRS complexes (see
Fig. 30.26).
AV dissociation can be seen if QRS complexes occur independent of the atrial dis-
charges.
The AV junctional escape beats or AV junctional rhythm serves as a safety mecha-
nism to prevent the occurrence of ventricular asystole as a result of the increased
vagal tone or heart block or pathological sinus bradycardia.
iii. AV Junctional Premature Beats or Premature AV

Junctional Beats
They are seen in normal subjects and in patients with structural heart disease. They are
characterized by an impulse that arises prematurely in the AV junction which attempts
antegrade or retrograde conduction.
If unimpeded, the AV junctional premature impulse discharges the atrium to pro-
duce a premature retrograde P wave and a narrow premature QRS complex.
The retrograde P wave can occur before (by 0.12 s see Fig. 30.27), during (i.e.
concealed within the QRS complex with slight aberration, see Fig. 30.28) or after
QRS complex (i.e. appear in the ST segment, see Fig. 30.29).
The P waves are usually inverted in leads II, III, and aVF; isoelectric or slightly neg-
ative in leads I and V6; and upright in right precordial leads.
The compensatory pause is usually not full and interpolated junctional premature
complex can also occur.
The QRS complexes are narrow except when aberrant intraventricular conduction
occurs.
When P waves precede QRS complex, the distinction from PACs may be difficult and
similarly when aberrant intraventricular conduction is present and the P waves are
within or after QRS complexes, the distinction from PVCs may be impossible without
intracardiac recordings (see Table 30.13).
ARRHYTHMIAS 601
II
IP
P'
Fig. 30.27 | AV junctional premature beatsthe first premature complex is preceded

by negative P wave and followed by a shorter compensatory pause. The sec-
ond (6th premature complex) is an interpolated (IP) one conducted with
aberration but no visible P wave.
Fig. 30.28 | AV junctional premature beatsconducted with slight aberration, (arrow)

and a shorter compensatory pause but no visible P waves.
aVF
P
Fig. 30.29 | AV junctional premature beatretrograde P follows premature QRS complex

with some degree of ventricular aberration and shorter compensatory pause.
Table 30.13 AV junctional arrhythmias
AV junctional escape beats Premature AV junctional beats
1. Pauses longer than normal PP interval and 1. Premature retrograde P waves which may
interrupted by normally conducted QRS occur before, during or after QRS complex
complexes with absent, retrograde, fusion and compensatory pause is usually not full
P or sinus P waves
2. P is inverted in II, III, aVF; upright in right
precordial leads; isoelectic or negative in I, V6
2. If P precedes QRS, PR is 0.12 s 3. QRS complex is normal
3. Usually have regular rhythm with a rate
of 3560/min
iv. AV Junctional Tachycardia

It consists of focal or paroxysmal junctional tachycardia and non-paroxysmal junctional
tachycardia.
a) Focal Junctional Tachycardia

It is a rare entity which arises from the AV node or His bundle.
V1
II
V5
Fig. 30.30 | Focal junctional tachycardia at a rate of 150/min with narrow QRS complex.
Onset of tachycardia occurs with isorhythmic AV dissociation (arrows).
I aVR V1 V4
V5
II aVL V2
III aVF V3 V6
Fig. 30.31 | Focal Junctional tachycardia at a rate of 190/min with narrow QRS complex.
It is also known as automatic or paroxysmal junctional tachycardia.
It may occur in children or young adults with congenital heart diseases such as ASD,
VSD (congenital junctional ectopic tachycardia) and postoperatively (postoperative
junctional ectopic tachycardia).23
Abnormal automaticity or triggered activity is the mechanism of this arrhythmia.
The ECG features include a heart rate of 110250 beats/min with narrow QRS
complexes or typical BBB conduction pattern. AV dissociation is often present (see
Figs 30.30 and 30.31).
b) Non-paroxysmal Junctional Tachycardia

It is also known as accelerated AV junctional rhythm which is characterized by:
A narrow QRS complex tachycardia with a rate of 60130 beats/min (see Figs
30.32 and 30.33).
It shows a typical warm-up and cool-down pattern and cannot be terminated by
pacing maneuvers.
ARRHYTHMIAS 603
P' P' P' P' P'
II
Fig. 30.32 | Non-paroxysmal junctional tachycardia at a rate of 62/min with negative

P waves preceding the QRS complex.
P P P P P P
II
Fig. 30.33 | Non-paroxysmal junctional tachycardia at a rate of 88/min with negative

P waves after QRS complex.
Table 30.14 AV junctional tachycardia
a) Focal junctional tachycardia a) Focal junctional tachycardia

1. Occurs in children and young adults with 1. Rate is 110250/min
ASD, VSD or postoperatively
2. Usually, it has narrow QRS or typical BBB
conduction pattern
3. Often, AV conduction dissociation is present
b) Non-paroxysmal junctional tachycardia b) Non-paroxysmal junctional tachycardia
1. Ischemia (inferior) 1. Narrow QRS at a rate of 60130/min
2. Myocarditis 2. Warm-up and cool-down patterns are
common
3. Digitalis toxicity 3. Cannot be terminated by pacing
4. COPD with hypoxia
5. Hypokalemia
Similar mechanism of enhanced automaticity or triggered activity.

It is present in digitalis toxicity (earliest sign), myocardial ischemia (inferior infarc-
tion), myocarditis, hypokalemia and COPD with hypoxia.
Wenckebach conduction can occur in patients with digitalis toxicity (see Table 30.14).
v. AV Nodal Reciprocating (Reentrant) Tachycardia (AVNRT)

It is the most common cause for SVT (60%), which is usually not associated with struc-
tural heart disease. It is also more common in females.
It is characterized by an abrupt onset and offset with a regular rate of 140250
beats/min (commonly 180200 beats/min in adults).

The underlying pathophysiology of AV nodal reentry tachycardia is the presence of
dual pathways in the region of AV node: fast and slow pathways.

Fast pathway with a longer refractory period appears to be located near the apex
of Kochs triangle.
Compact
atrioventicular node
Bundle of His
Fast-pathway
Right
atrium
Tricuspid
annulus
Right
Coronary- Slow-pathway
ventricle
sinus
ostium
Fig. 30.34 | Fast- and slow-pathways for genesis of AVNRT.
II
Fig. 30.35 | AVNRT at a rate of 190/min with a narrow QRS complex. P waves not visible.
Slow pathway with a shorter refractory period extends inferoposterior to the AV
node and stretches along the septal margins of the tricuspid annulus at the level
of or slightly superior to the coronary sinus (see Fig. 30.34).
AVNRT is classified into typical and atypical depending upon the reentry circuit
traverses:
a) Typical AVNRT (SlowFast AV Node Reentry)

During typical AVNRT, a premature atrial impulse is blocked in the fast pathway,
allowing the anterograde conduction in the slow pathway. After conduction through
the slow pathway to the His bundle and ventricle, the impulse is briskly conducted
back to the atrium through the fast pathway in the retrograde direction. As the retro-
grade conduction is rapid, the subsequent atrial activity begins soon after the onset of
ventricular activation that causes:
RP interval shorter than PR interval which is 70 ms.
In about 50% retrograde P waves are not detected on surface ECG (see Fig. 30.35).
In about 50%, P waves occurring just before (rarely) QRS complex, or buried in the
QRS complex, distort QRS complex forming a pseudo-r (pseudo RBBB pattern) inV1.
P waves are inverted in inferior leads.
Often initiated by a premature atrial impulse with prolonged PR interval (see Fig.
30.36).
ARRHYTHMIAS 605
II P P P P
Fig. 30.36 | Onset of AVNRT (P) at rate of 136/min after an atrial premature beat (arrow)
with a long PR interval.
Table 30.15 AVNRT
1. Can occur in structurally normal heart.

2. Usually, RP interval is 70 ms and shorter than PR interval.
3. P wave occurs before (rarely), during or after QRS complex producing
pseudo-r in V1 and pseudo-s in inferior leads.
4. P waves are inverted in inferior leads.
5. Often initiated by a premature atrial impulse with a prolonged PR interval.
Infrequently, both antegrade and retrograde circuits are composed of slow pathways
(i.e slowslow AV node reentry) producing:
Long RP interval of 70 ms but shorter than PR interval in most cases and
P wave inscribed after QRS complex results in a pseudo-s (slurring of S wave) in
inferior leads.
b) Atypical AVNRT (FastSlow AV Node Reentry)

It is less common and occurs in 510%. During atypical AVNRT, the impulse travels
the fast pathway and conducts back to the atrium through the slow pathway retro-
gradely, producing:
A long RP interval, which is longer than PR interval and
Negative P waves in Leads III, and aVF, prior to QRS complex (see Table 30.15).
Common Features of AV Junctional Arrhythmias

P waves occur before, during or after QRS complex.
P waves are upright in aVR and inverted in inferior leads (see Fig. 30.37).
PR is 120 ms if P precedes QRS complex.
Usually, they have a narrow QRS complex or a typical BBB pattern.
AV dissociation can occur.
The commonest AV junctional arrhythmia is the AV nodal reentrant tachycardia
(AVNRT) which accounts for about 60% of all supraventricular arrhythmias. In typi-
cal AVNRT, RP interval IS 70 ms and shorter than PR interval. In AV junctional
escape beats, PP interval is normal PP interval. A continuity of AV junctional
beats results in junctional rhythm with a rate of 3560/min. Junctional tachycardia is
a narrow QRS tachycardia (see Fig. 30.38).
aVR aVR aVR
AN REGION AN or N-H NH REGION
aVF aVF aVF T
P P
Fig. 30.37 | Morphology of P wave and QRS complex in junctional arrhythmiasP waves are usually
upright in aVR and inverted in aVF (inferior leads) with normal or basic QRS complex. P waves
precede QRS complex in high junctional focus (AN region) and follow QRS complex in low
junctional focus (NH region) or buried in QRS complex.
1. Heart rate of >60130/min 1. Heart rate of 110250/min

2. Narrow QRS 2. Narrow QRS or typical 1. P occurs before, during, or
3. Wenckebach conduction BBB pattern after QRS with a rate of
can occur in digitalis 3. AV dissociation 3560/min
toxicity often occurs 2. PP > normal PP
3. PR is < 0.12 s if P
precedes QRS
Paroxysmal 4. Normal QRS complex
AVJ rhythm
Nonparoxysmal AVJ tachycardia AVJ escape beats
3560/min
1. In 50% P is
AVJA
undetected in ECG 1. P occurs before, during
2. In 50% P occurs or after QRS
before, during or 2. P in II, III, aVF; upright in
after QRS producing AVJ premature
AVNRT V2,V2; isoelectric or in I, V6
pseudo-r in V1 and beats
3. Usually normal QRS
pseudo-s in II, III, complex
aVF
3. P in II, III, aVF 1. Heart rate of 140250/min
4. R P <70 ms and 2. Often initiated by premature
shorter than PR atrial impulse with PR
3. Narrow QRS complex
Fig. 30.38 | Diagnostic

tachycardia.
features of AV junctional arrhythmias (AVJA)AVNRT: AV nodal reentrant
4. PRE-EXCITATION SYNDROME (PES)
The pre-excitation syndrome is due to the presence of extra nodal accessory path-
ways which can occur in the following form:
Concealed form
Manifest form producing Wolff-Parkinson-White (WPW) syndrome
ARRHYTHMIAS 607
The presence of concealed accessory pathways account for 30% of the patients with
apparent SVT, while the reported incidence of manifested PES is 0.150.25% of
the general population24 with a higher prevalence of 0.55% in the first degree rela-
tives of the patients with accessory pathways.25
The PES is found in all age group, more common in males.
Majority of the individuals with PES have normal hearts, but is also found in con-
genital heart diseases such as Ebsteins anomaly (510%26), MVP (7%27) and cardiomy-
opathies (DCM and HCM-4% in HCM28). It is also reported in cardiac tumors
(rhabdomyoma) and tuberous sclerosis.29 Other congenital heart diseases in which
PES has been reported include ASD, TGA, tricuspid atresia, VSD, TOF and COA.30
Accessory Pathways (AP)

These represent the developmental abnormality of AV ring and consist of small fibers
resembling normal myocardium that can act as pathways of conduction. They are clas-
sified on the basis of their location along the mitral and tricuspid annulus. AP have their
atrial site of origin along the mitral and tricuspid annulus, tend to ramify prior their
insertion into the ventricular myocardium (either LV or RV).
a) Location
On the basis of their location, they are classified into left sided (or left ventricular) and
right sided (or right ventricular):
LV free wall (left lateral): The accessory pathways located in the LV free wall are
the commonest (56%).

RV free wall: The accessory pathways in the RV free wall constitutes 21%.
Interventricular septum (IVS): The accessory pathways inserted into the IVS
constitute 24%, Posterior septal wall: 18%, anterior septal wall: 2%, and mid
septum: 4%.
1015% have multiple pathways. Patients with Ebsteins anomaly often have
right sided multiple accessory pathways in the posterior septum or the postero-
lateral wall.
b) Types
Three types of accessory pathways have been described:
Kent bundle i.e. atrioventricular accessory pathway is the usual or commonest
accessory pathway, bypassing the AV node and extending from the atrium to the
ventricle (see Fig. 30.39). Kent bundle is also found in monkeys, dogs and cats.
James bundle i.e. atriohisian accessory pathway is the uncommon pathway
bypassing the AV node and extending from the atrium to His bundle, which
gives rise to Lown-Ganong-Levine (LGL) syndrome (see Fig. 30.40).
Almost all Mahaim fibers are right sided and consist of (i) nodoventricular/
nodofascicular accessory pathway extending from AV node to the ventricle

(nodoventricular) or RBB (nodofascicular) (see Fig. 30.41) and (ii) fasciculoven-
tricular accessory pathway extending from His bundle or bundle branches to the
Atrium Atrium
AV node AV node
His His
Ventricle Ventricle AHAP

AVAP
Fig. 30.40 | Atriohisian accessory pathway (AHAP)
Fig. 30.39 | Atrioventricular accessory pathway
(AVAP) from atrium to ventricle.
from atrium to His bundle.
Atrium Atrium
AV node AV node
His His
Ventricle Ventricle
NVAP
FVAP
Fig. 30.41 | Nodoventricular accessory pathway
(NVAP) from AV node to ventricle.
Fig. 30.42 | Fasciculoventricular accessory pathway
(FVAP) from His bundle or its branches
to ventricle.
ventricle (see Fig. 30.42). However, Mahaim fibers are atriofascicular pathways
(also known as Brechenmacher tract), usually located in the RV free wall con-
necting anterolateral wall of RA, close to the lateral tricuspid annulus and apical
region of the RV or distal RBB.31 They constitute approximately 8% of the acces-
sory pathways and due to the presence of nodal tissue in these fibers, they display
decremental conduction (antegrade or retrograde) which is not characteristic of
other accessory pathways.32
i. Concealed Accessory Pathways

The patients with concealed accessory pathways are capable of only retrograde conduc-
tion from the ventricle to the atrium. Hence, these are not apparent in the ECG dur-
ing sinus rhythm as typical ECG manifestations of PES/WPW syndrome are absent.
However, it can still participate in the reentrant circuit to produce an AV reciprocating
tachycardia (AVRT), and paroxysmal supraventricular tachycardia (PSVT) in which:
Tachycardia rate is unusually faster (200/min),
QRS complex is normal and
ARRHYTHMIAS 609
Inverted P waves occur after QRS complex on the ST segment or early T wave espe-
cially in inferior and lateral leads.
In majority of the patients, the accessory pathways are located in LV free wall and in
the posteroseptal area.
The treatment is similar to AVNRT and PES and is amenable to catheter ablation.
ii. Pre-Excitaion Syndrome

It is a manifest form of presence of accessory pathways. It occurs when the atrial
impulse activates whole or some part of the ventricle (antegrade conduction) or when
the ventricular impulse activates whole or some part of the atrium (retrograde conduc-
tion) earlier than expected if the impulse traveled through normal conduction system
(i.e. SA node-atrium-AV node-His bundle-ventricle). The activation of ventricle or
atrium is possible only in the presence of accessory pathways. PES can present with
sinus rhythm i.e. WPW syndrome or with tachyarrhythmias.
a) PES With Sinus RhythmWPW Syndrome

ECG manifestations
In patients with accessory pathways, the impulse may be conducted only through
normal route i.e. atrium-AV node-His bundle-ventricle (concealed accessory path-
ways), only through accessory pathways (giving rise to full pre-excitation) or simul-
taneously through normal route and accessory pathways (resulting in fusion beats,
i.e. delta waves).
With increasing conduction through accessory pathways, the QRS complex widens
and PR and HV intervals shorten as in WPW syndrome, and with increasing con-
duction through normal route as during exercise, PR and HV intervals lengthen
and QRS complex shortens.
Increasing pre-exctitation results in progressive shortening of PR interval and
widening of QRS complex without change in the interval from P to the end QRS
complex is known as concertina effect which usually occurs in intermittent PES
(see Fig. 30.43).
Short PR interval 120 ms with a normal P wave. The duration of PR interval equals
the duration of P wave or its initial portion especially in fully pre-excited complexes.
R R
R
R R
II R
P P P P P P
NC APC
Fig. 30.43 | Intermittent pre-excitation syndrome with concertina effect. The first com-
plex (NC) is conducted through normal AV node pathway alone, the sixth
through accessory pathway alone (APC, fully pre-excited), while the rest are
due to progressive pre-exctation without change in the P-end QRS interval.
Wide QRS complex 120 ms with a delta wave in its initial portion, and normal
terminal portion. A normal q wave is seldom found in pre-excited complexes and
presence of q waves in V6 virtually excludes the PES.33
Delta wave, a fusion beat is due to the depolarization of ventricle in part by the wave
front traveling along the normal conduction route with a normal physiological AV
delay (i.e. atrium-AV node-His bundle-ventricle) and in part by the wave front trav-
eling along the accessory pathway (i.e. atrium-AP-ventricle). The delta wave repre-
sents the ventricular activation from atrium through accessory pathway.
Duration of delta wave is 0.020.07 s. In PES, delta waves should be present in
all leads. However, they become isoelectric and are overlooked in those leads
which are perpendicular to initial QRS forces.
Negative delta waves resemble abnormal Q waves of myocardial infarction (MI).
Hence, negative delta waves in right precordial leads mimic anterior MI (see Fig.
30.44), in aVL stimulate lateral MI (see Fig. 30.45) and in inferior leads they mimic
an inferior MI (see Fig. 30.46). The large upright delta wave and positive QRS
complex in V1 may simulate true posterior MI or RBBB or RVH (see Fig. 30.47).
I aVR V1 V4
d d
II aVL V2 V5
III aVF V3 V6
Fig. 30.44 | WPW syndrome with short PR interval and negative delta waves in right
precordial leads simulating anterior MI.
I aVR V1 V4
II aVL d V2 V5
III aVF V3 V6
Fig. 30.45 | WPW syndrome with short PR interval and negative delta waves in aVL
simulating lateral MI.
ARRHYTHMIAS 611
I aVR V1 V4
II d aVL V2 V5
III d aVF d V3 V6
Fig. 30.46 | WPW syndrome with short PR interval and negative delta waves in inferior
leads simulating inferior MI.
I aVR V1 d V4
II aVL V2 V5
III aVF V3 V6
Fig. 30.47 | WPW syndrome (type A) with short PR interval, upright delta waves and
positive QRS complexes (tall R) in V simulates true posterior MI or RVH.
1
Tall R waves in V1 and V2 simulating RVH, RBBB or posterior infarction is

described as type A WPW syndrome. Negative QRS complex and delta waves in
V1 and upright in V5, V6 simulating LBBB is described as type B WPW syndrome
(see Fig. 30.48).
Secondary STT changes that are generally directed opposite to that of delta waves
may be found, but are more common with tachyarrhythmias. The altered sequence
of ventricular activation in these patients results in secondary repolarization abnor-
malities. As the duration of QRS complex increases, the T wave becomes more
negative.
V1 d V4
aVR
I
II aVL V2 V5
III d V3 V6
aVF
Fig. 30.48 | WPW syndrome (type B) with short PR interval, negative QRS complexes
and delta waves in V and upright in V simulating LBBB.
1 6
aVR V1 d d V4
I
d d
II aVL V2 d V5
d d d
III aVF V3 V6
Fig. 30.49 | WPW syndrome with left lateral accessory pathwayshort PR interval,
positive delta waves and QRS complex in V and isoelectric or negative
1
delta waves in I, aVL and V5.
Localization of accessory pathways during sinus rhythm:34

Accessory pathways located in the LV (left sided) have positive (ve) delta wave and
QRS complex in V1 further.
(i) the presence of isoelectric or negative delta waves in I, aVL, V5, and V6 localizes
accessory pathway in left lateral wall (see Fig. 30.49).
(ii) while early QRS transition i.e. in V2, V3: localizes accessory pathway in the sep-
tum and if negative delta wave and QRS complex are also present in II, III and
aVF, indicates the presence of accessory pathway in the left posteroseptal wall (see
Fig. 30.50).
ARRHYTHMIAS 613
I aVR R V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 30.50 | WPW syndrome with left posteroseptal accessory pathwayshort PR

interval, positive delta waves and QRS complex in V with negative delta
1
waves in inferior leads and early QRS transition in V2.
I aVR V1 V4
d d
II aVL V2 V5
III aVF V3 V6
Fig. 30.51 | WPW syndrome with RV free wall accessory pathwayshort PR interval,
negative delta waves and QRS complex in V with left axis (30) and late
1
QRS transition in V5.
Accessory pathways located in the RV (right sided) have negative ( ve) delta wave
and QRS complex in V1, further.
(i) LAD and late QRS transition i.e. in V5, V6, localizes accessory pathway in RV free
wall (see Fig. 30.51).
(ii) While early QRS transition, i.e. in V2, V3, localizes accessory pathway in the septum
If negative delta wave and QRS complex are also present in II, III and aVF;
accessory pathway is located in the right posteroseptal wall (see Fig. 30.52) or
If axis is inferior, accessory pathway is located in the right anteroseptal wall
(see Figs 30.53 and 30.54).
I aVR V1 V4
II aVL V2 V5
d
III aVF V3 V6
d
Fig. 30.52 | WPW syndrome with right posteroseptal accessory pathwayshort PR

interval, negative delta waves and QRS complex in V and inferior leads
1
with early QRS transition in V3 simulating LBBB.
I aVR V1 V4
d
d
II aVL V2 V5
III aVF V3 V6
Fig. 30.53 | WPW syndrome with right anteroseptal accessory pathwayshort PR, nega-
tive delta waves, and QRS complex in V with inferior QRS axis.
1
b) PES with Tachyarrhythmias

The tachycardias, which occur in PES include:
Reciprocating or reentry tachycardia i.e. AVRT (80%), which can be orthodromic
(9095%) or antidromic (510%)
Af (1530%) which may degenerate into VF35
ARRHYTHMIAS 615
Lead V1
Negative delta Positive delta waves

and QRS complex and QRS complex
Right ventricle Left ventricle
Isoelectric
Negative Negative or negative
delta waves Left Inferior delta waves delta waves
and QRS in axis axis and QRS in in I, aVL,
II, III, aVF II, III, aVF V5, and V6
Posteroseptal RV free wall Anteroseptal Posteroseptal Lateral
Fig. 30.54 | Localization of accessory pathways in WPW syndrome (PES with sinus rhythm).
Fig. 30.55 | Orthodromic AVRTantegrade conduction of reentrant impulse through

normal route and its retrograde conduction through accessory pathway
producing narrow QRS tachycardia.
Afl (5%) and

VT (uncommon)
Orthodromic AVRT: It is due to the antegrade conduction of reentrant impulse
from the atrium to the ventricle through normal conduction route and its retrograde
conduction from ventricle to the atrium through the accessory pathway, which results
in narrow QRS SVT (see Fig. 30.55).
The ECG characteristics are
Tachycardia in PES is often initiated by premature atrial or ventricular complexes
(see Fig. 30.56).
II
Fig. 30.56 | Orthodromic AVRT initiated by a premature atrial complex (P).

RPR
I aVR V1 V4
R R
II aVL V2 V5
III aVF V3 V6
Fig. 30.57 | Orthodromic AVRTNarrow QRS tachycardia at a rate of 186/min. P waves

after QRS complex on the depressed ST segment with RP interval PR
interval.
Regular rate of 150250 beats/min (usually faster than AVNRT). Delta waves no
longer observed and duration of QRS complex is normalized.
Short PR interval of 120 ms. RP interval is 70 ms and shorter than PR interval (see
Fig. 30.57).36 (PR is RP when retrograde pathway is slow as in antidromic AVRT).
P waves occur after, not during QRS complex. Inverted P waves in II, III and aVF with
positive P waves in aVR and aVL (in posteroseptal pathway) or inverted P waves in I
(in left lateral pathway).36
Presence of QRS alternans, i.e. alteration of R wave amplitude during tachycardia.37
Secondary STT changes, i.e. ST segment depression and T wave inversion are common.
Sudden onset and termination.
Adenosine, beta blockers, calcium channel blockers and digitalis prolong the conduc-
tion and refractive period of AV node, while quinidine, procainamide and disopyra-
mide (Class IA sodium channel blockers) prolong the conduction and refractive
period of accessory pathway and help in differentiating narrow QRS tachycardias.
Localization of accessory pathway during AVRT: It may be done on the basis of
secondary STT changes, and localization of inverted P waves.
ST segment depression of 2 mm in V4V6: Accessory pathway is located in the left
lateral wall (sensitivity: 64%, specificity: 60%) (see Fig. 30.58).
Inverted or notched T wave in V2: Accessory pathway is located in the anteroseptal
wall (sensitivity and specificity: 100%).
ARRHYTHMIAS 617
v4
I aVR V1
V5
R R II R R aVL R R V2
T T
V6
III aVF V3
T T
Fig. 30.58 | Orthodromic AVRTNarrow QRS tachycardia at a 180/min with upstroke

slurring of QRS complex and alteration of R wave amplitude suggest
orthodromic AVRT, while ST segment depression of 2 mm in V4V6 and
inverted T waves in V5V6 localizes to left lateral accessory pathway.
T wave inversion in II, III, and aVF: Accessory pathway is located in the right pos-
teroseptal wall (sensitivity: 63%, specificity: 84%).
Negative P waves in II, III and aVF with upright P waves in aVR and aVL: Accessory
pathway is located in the posteroseptal wall; while negative P waves in I localize the
accessory pathway to the left lateral wall.
Antidromic AVRT
(i) It constitutes 510% of AVRT and is due to the antegrade conduction of reen-
trant impulse from the atrium to the ventricle along the accessory pathway and its
retrograde conduction from the ventricle to the atrium through normal conduc-
tion route, produces a wide QRS tachycardia (see Fig. 30.59).
(ii) One third of these patients may have multiple accessory pathways with a high
incidence of atrial and ventricular fibrillation.
(iii) The accessory pathways are located far away from AV node and no patient with a
posteroseptal accessory pathway has antidromic AVRT.38
(iv) QRS morphology is similar to fully pre-excited complex.
(v) In rare type of antidromic AVRT (see Fig. 30.60), two or more accessory path-
ways are used both for antegrade and retrograde conduction, also resulting in
wide QRS tachycardia (see Table 30.16).
WPW syndrome with Af and Afl: Wolf, Parkinson and White (1930) mentioned
atrial fibrillation in their original description of the syndrome. If the ventricular rate is
unusually rapid (200/min) during Af, wide QRS complex pre-excitation should be
suspected as this is possible only in the presence of a short effective refractive period of
Fig. 30.59 | Antidromic AVRTantegrade conduction of reentrant impulse along the

accessory pathway and retrograde conduction through normal route pro-
ducing wide QRS tachycardia.
V4
I aVR V1
II aVL V5
V2
III aVF V6
V3
Fig. 30.60 | Antidromic AVRTwide QRS tachycardia at a rate of 250/min.

the accessory pathway. The occurrence of Af is facilitated by the presence of reentrant
tachycardia.
The QRS complexes are wide as the atrial impulses are conducted to the ventricles
through the accessory pathway during Af and Afl in most cases.
The QRS complexes are wide due to an aberrant ventricular conduction (see
Fig. 30.61).
Ventricular fibrillation may develop in patients of WPW syndrome due to rapid
ventricular rate during Af and Afl or due to the presence of multiple accessory
pathways.
ARRHYTHMIAS 619
Table 30.16 Etiology and characteristics of AVRT
Common cause Orthodromic AVRT Antidromic AVRT
1. Can occur in structurally 1. Constitutes 9095% of AVRT 1. Constitutes 510% of AVRT

normal heart
2. Ebsteins anomaly 2. Sudden onset and termination 2. Regular tachycardia, unless
associated with Af or Afl with
variable AV conduction
3. MVP 3. Regular rate of 150250/min 3. Wide QRS complexes
4. Cardiomyopathies 4. Short PR (120 ms)
(DCM and HCM)
5. Cardiac tumors 5. RP 70 ms and shorter than PR
(rhabdomyoma)
and tubersclerosis
6. Other CHD: ASD, VSD, 6. P waves after QRS complex
tricuspid atresia, TGA,
TOF, COA
7. Absent delta waves and
normalization of QRS complex
8. R wave alternans
9. Often associated with
secondary STT changes
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 30.61 | WPW syndrome with atrial fibrillationwide QRS tachycardia at an irregular
rate of about 200/min. There is slurring of the upstroke of QRS complexes
after long pauses.
WPW syndrome with Af may be mistaken for VT. However, very rapid (200/min)
and gross irregularity of the ventricular response occurs during Af rather than during VT.
WPW syndrome with Afl, the rhythm is regular with AV conduction of 2 : 1 or 1 : 1
and may be mistaken for paroxysmal VT. However, the AV conduction of 1 : 1 in Afl is
rare in the absence of accessory pathways.
aVR V1 V4
I R
V2 V5
II aVL
III V3 V6
aVF
Fig. 30.62 | Mahaim tachycardia (Nodoventricular) at a rate of 186/min, LBBB pattern

QRS complex with 30 axis, late QRS transition, R in I and rS in V .
1
c) Mahaim Tachycardia
A sinus impulse may travel from RA to AV node with normal delay, but is followed
by premature excitation of basal part of the ventricle as the impulse travels through
Mahaim fibers resulting in a delta wave with normal PR interval. However, no pre-
excitation (no delta wave) is generally apparent during sinus rhythm due to slow
conduction and decremental properties of this pathway.
But ECG may reveal short PR interval, narrow QRS complex with delta wave,
late QRS transition (as accessory pathway is located in RV) and decremental
conduction.
During pre-excitation tachycardia, the absence of retrograde conduction in these
pathways produces only an antidromic AVRT, and is characterized by anterograde
conduction from the atrium to the ventricle over the accessory pathway and retro-
grade conduction from the ventricle over the RBB-His bundle-AV node to the atrium,
producing:
LBBB pattern with superior axis (0 to 75)
Late QRS transition (positive QRS complex after V4)
R in I and rS in V1 (see Fig. 30.62)
RP longer than PR interval, as a result of longer A-V interval (due to long conduc-
tion time over the accessory pathway) and shorter V-A interval.
A delay in retrograde conduction due to RBBB, increases the length of the
tachycardia circuit i.e. prolongs the V-A interval and tachycardia can become
incessant.39
PR interval is normal; HV interval is shortened with slight ventricular pre-excitation
manifested by slurring of the initial QRS complex in pre-excitation due to fasciculo-
ventricular Mahaim fibers. No specific arrhythmias have been associated with this
accessory pathway.
ARRHYTHMIAS 621
d) Lown-Ganong-Levine (LGL) Syndrome

It is characterized by short PR interval with normal P wave and normal QRS complex
with short AH interval (see Fig. 30.63). The atriohisian pathway may be demon-
strated anatomically, but it is insignificant in the genesis of tachycardia.
e) Permanent form of AV Junctional reciprocating

Tachycardia (PJRT)
It is an incessant form of narrow QRS SVT with short PR interval but RP interval
exceeding PR interval (similar to atrial tachycardia) (see Fig. 30.64).
It is usually due to the presence of posteroseptal accessory pathway (most often in the
right ventricle).40
Tachycardia is usually initiated by a premature complex or lengthening of PR interval
and is maintained by orthodromic conduction, i.e. antegrade conduction over the
normal AV conduction route and retrograde conduction along the accessory pathway.
It does not respond to vagal stimulation (i.e. carotid sinus massage).
I aVR V1 V4
PR
II aVL V2 V5
PR PR
III aVF V3 V6
Fig. 30.63 | LGL syndrome with short PR interval and normal QRS complexes.
R R R PR
P
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 30.64 | Permanent form of AV junctional reciprocating tachycardia (PJRT)Narrow

QRS tachycardia with short PR interval and RP interval PR interval.
5. NARROW QRS TACHYCARDIA
The QRS duration is 120 ms and consists of:

i. Irregular tachycardia
It includes:
Atrial fibrillation
Atrial flutter with variable AV conduction
Atrial tachycardia with variable AV block or Wenkebach block
Multifocal atrial tachycardia (MAT).
ii. Regular tachycardia

It consists of:
Sinus tachycaradia
Atrial flutter with fixed AV conduction
Atrial tachycardia
AVNRT
AVRT (orthodromic).
Differential diagnosis: The AVRT can be differentiated from other common regular
narrow QRS tachycardia by the presence of delta waves and P wave morphology and
its relation with RP and PR intervals (see Table 30.17, Figs 30.65 and 30.66). The
intravenous adenosine and vagal stimulation have different responses among the vari-
ous causes of regular narrow QRS tachycardia (see Figs 30.67 and 30.68).
The presence of delta wave is the most characteristic feature of WPW syndrome.
The typical AVRT has to be differentiated from other causes of narrow QRS tachycar-
dia, while the antidromic AVRT, WPW syndrome with Af and Mahaim tachycardia
with their characteristic features can be differentiated from the ventricular tachycardia
(see Fig. 30.69).
6. VENTRICULAR ARRHYTHMIAS
Ventricular arrhythmias include:

Premature ventricular complexes or Ventricular premature beats
Ventricular tachycardia (VT)
Ventricular flutter/fibrillation
i. Premature Ventricular Complexes (PVCs) or Ventricular

Premature Beats (VPBs)
PVCs are also known as ventricular premature contractions (VPCs).
They are the commonest ventricular arrhythmias occurring in 0.8% of normal individ-
uals of 16 years to 50 years age.

They can occur in 33% of men and 15% of women with exercise.
ARRHYTHMIAS 623
Table 30.17 Differential diagnosis of narrow QRS regular tachycardia
Features AVRT AVNRT AT
1. Rate (not much useful 150250/min Less than AVRT Usually 180/min
for differential diagnosis)
2. P waves P waves after, not during In 50% not detected. P in I, aVL and
QRS complex, P in II, III, In 50% occurs before, P in V1 in left AT.
aVF with P in aVR, aVL during or after QRS P or biphasic in
(in posteroseptal AP), P pseudo-r in V1 or V1, aVL and P or
in I (in left lateral AP) pseudo-s in II, III, biphasic in aVL in
aVF P in II, III, aVF right AT
3. Atrial rate faster than No No Yes
ventricular rate
4. RPPR intervals i) RP is 70 ms and i) RP is 70 ms and i) RP is 70 ms
RP PR RP PR and usually
PR
ii) RP PR in PJRT ii) May be 70 ms ii) But RP may
and RP PR be PR
in atypical form iii) Varying PR
in MAT
5. Delta waves May be present Absent Absent
6. QRS alternans Present Absent Absent
7. STT changes
i) ST 2 mm i) May be present i) Usually absent i) Usually absent
ii) T inversion ii) Usually present with ii) May be present ii) Usually absent
septal accessory
pathways
8. Vagal stimulation No effect or terminate No effect or terminate Does not terminate,
(carotid sinus massage) but may cause
transient AV block
They can occur in AMI, during fibrinolytic therapy, CHF, cardiomyopathy and MVP.
They can be provoked by a variety of medications (digitalis), electrolyte imbalance, and
excessive use of tobacco, caffeine or alcohol.
ECG Recognition
PVC is characterized by:
The premature occurrence of wide bizarre QRS complex (duration usually 120 ms)
with ST segment and large T wave opposite in direction to the abnormal QRS complex
i.e. when QRS complex is upright, ST segment is depressed and T wave is inverted;
and when QRS complex is negative, ST segment is elevated and T wave is upright.
However, the QRS complex of the PVC may be narrow when it arises from the ven-
tricular septum or fascicles, which is known as a fascicular beat. PVCs arising from
the anterior fascicle resemble RBBB with left posterior fascicular block and those
arising from the posterior fascicle resemble RBBB with left anterior fascicular block.
R R
OR
P' P'
Typical AVNRT: RP is < 70 ms and < PR. P waves Atypical AVNRT: RP may be
may occur before, during or after QRS complex >70 ms & > PR. P waves are
inverted in inferior leads
R R
P' P'
AVRT: RP is >70 ms but < PR. P waves usually after, PJRT: RP is >70 ms > PR. P
not during QRS complex waves are inverted in inferior leads
R R R R
OR
P P
fl fl fl fl
P' P'
Atrial tachycardia: RP < or > PR. P waves may occur Atrial flutter with flutter (fl) waves
before or after QRS complex usually inverted in inferior leads
Fig. 30.65 | PAVNRT:

wave morphology and its relation with RP and PR intervals in narrow QRS tachycardia
AV nodal reentrant tachycardia, AVRT: AV reentry tachycardia, PJRT: permanent
form of AV junctional reciprocating tachycardia.
PVC is not preceded by premature P wave, but may be preceded by a non-conducted

sinus P wave. Retrograde conduction of ectopic ventricular impulse to the atrium
often occurs resulting in retrograde P wave which is usually hidden in the ventricu-
lar complex, but occasionally atrial capture occurs and inverted P wave is observed
following PVC.
PVC is usually followed by a full compensatory pause, i.e. the interval between the
sinus P wave immediately before the PVC and the first sinus P wave after the PVC
is equal to twice the sinus cycle length (see Fig. 30.70). However; in bigeminy i.e.
interpolated PVC, it is less than full, but long enough for PVC to occur. The
bigeminy disappears when the heart rate increases as the long diastolic (RR) inter-
vals shorten as per the rule of bigeminy. Occurrence of PVCs after long RR inter-
vals and their disappearance when the RR intervals shorten is known as the rule of
bigeminy39 (see Fig. 30.71).
PVCs usually have fixed coupling interval, i.e. the interval between the normal QRS
complex and the premature QRS complex (variation does not exceed 0.08 s).41
Variable coupling interval occurs due to parasystole (see Table 30.18).
ARRHYTHMIAS 625
Narrow QRS tachycardia

(QRS duration <120 ms)
Regular tachycardia?
Yes No
Visible P waves? Atrial fibrillation

Atrial tachycardia/flutter with
Yes variable AV conduction
MAT
Atrial rate > ventricular rate
Yes No
Atrial flutter or
Analyze RP interval
Atrial tachycardia
Short Long
(RP shorter than PR) (RP longer than PR)
Atrial tachycardia (AT)

RP <70 ms RP >70 ms PJRT
Atypical AVNRT
AVRT
AVNRT AVNRT
Atrial tachycardia
Fig. 30.66 | Differential diagnosis of narrow QRS tachycardiaAVRT: AV reentry tachycardia, AVNRT: AV
nodal reentrant tachycardia, PJRT: permanent form of AV junctional reciprocating tachycardia.
Regular narrow QRS

tachycardia
IV Adenosine
No change Gradual slowing then Sudden Persisting AT with

in rate reaccelaration of rate termination transient high
grade AV block
1) Inadequate dose 1) Sinus tachycardia 1) AVNRT 1) Atrial flutter

2) Consider VT 2) Focal AT 2) AVRT 2) AT
(fascicular or high 3) Nonparoxysmal 3) Focal AT
septal origin) junctional 4) SNRT
tachycardia
Fig. 30.67 | Response to IV adenosine in regular narrow QRS tachycardia and its differential diagnosis
AVRT: AV reentry tachycardia, AVNRT: AV nodal reentrant tachycardia, AT: atrial tachycardia,
SNRT: sinus node reentry tachycardia.
Regular narrow
QRS tachycardia
No effect or Vagal stimulation No effect, but may

may terminate (carotid sinus massage) AV block and reveal fl
waves more clearly
AVNRT AVRT No effect Does not terminate, Atrial flutter

but cause transient
AV block
PJRT
AT
Fig. 30.68 | Effect of vagal stimulation (carotid sinus massage) on regular narrow QRS
tachycardia and its differential diagnosisAVRT: AV reentry tachycardia,
AVNRT: AV nodal reentrant tachycardia, AT: atrial tachycardia, PJRT: per-
manent form of AV junctional reciprocating tachycardia, fl waves: flutter
waves.
1. Normal P
2. Short PR: <120 ms
3. Wide QRS >120 ms
4. Delta waves 1. Normal P
1. Short PR
5. Secondary STT 2. Short PR: <120 ms
2. RP > PR
changes 3. Normal QRS
3. P inverted in
II, III, aVF
WPW synd Sinus rhythm LGL synd
PJRT
Wide QRS Narrow QRS
PES
tachycardia tachycardia
AVRT
Mahaim WPW synd Antidromic
tachycardia with Af AVRT 4. P waves after,
not during QRS 1. Regular rate
5. No delta waves of 150250/min
1. RP > PR 1. Irregular 1. Regular rate 6. Normaliztion of 2. Short PR
2. LBBB ventricular rate of 150250/min QRS 3. RP >70 ms, but
pattern QRS of > 200/min 2. Wide QRS 7. QRS alternans <PR
complex 2. Wide QRS similar to fully 8. Secondary
2. Late QRS with slurring of preexcited STT changes
transition upstroke after complex
3. R in I, rS in long pauses
V1
Fig. 30.69 | Classification and characteristics of pre-excitation syndrome (PES)AVRT: AV reentry

tachycardia, PJRT: permanent form of AV junctional reciprocating tachycardia, WPW synd:
Wolff Parkinson-White syndrome, LGL synd: Lown Ganong Levine syndrome, Af: atrial
fibrillation.
ARRHYTHMIAS 627
I aVR V1 V4
PVC
PVC PVC
II aVL V2 V5
PVC PVC PVC
III aVF V3 V6
PVC PVC
PVC
Fig. 30.70 | Premature ventricular contractions (PVC) with wide QRS complex, STT
opposite in direction to the QRS complex and full compensatory pause.
Fig. 30.71 | Rule of bigeminyoccurrence of PVCs after long RR intervals.

Table 30.18 Premature ventricular complex (PVC)
Common causes Salient ECG findings and types
1. Can occur in normal individuals 1. Premature occurrence of wide bizarre QRS complex
with exercise
2. AMI, during fibrinolytic therapy 2. Not preceded by premature P wave, but may be by
non-conducted sinus P wave
3. CHF 3. Usually followed by a full compensatory pause
4. Cardiomyopathy 4. Has fixed coupling interval
5. MVP 5. PVC can be uniform/multiform; unifocal/multifocal;
right ventricular/left ventricular; bigeminy/
trigeminy/quadrigeminy
6. Digitalis toxicity
7. Electrolyte imbalance
8. Excessive use of alcohol,
caffeine or tobacco
Types of PVCs
i) Bigeminy, trigeminy, quadrigeminy, pentageminy
Bigeminy refers to the presence of a pair of a normal and a premature complex (i.e.
interpolated PVC).
Fig. 30.72 | PVCs in bigeminy (upper tracing) and trigeminy (lower tracing).
Fig. 30.73 | PVCs in couplet.
II
Fig. 30.74 | PVCs in triplets or salvos with increased risk for ventricular tachycardia/
fibrillation.
Trigeminy indicates PVC following two normal beats (see Fig. 30.72).
Quadrigeminy is PVC following three normal beats.
Pentageminy refers to the presence of PVC following four normal beats.
ii) Couplets, triplets or salvos
Couplet: Two successive PVCs are termed as a pair or a couplet (see Fig. 30.73).
Triplet: Three successive PVCs are called triplet. Triplets are also called salvos and
considered as nonsustained VT if they occur upto 30 s (see Fig. 30.74).
iii) Depending upon the polarity of the premature complex
Predominantly positive premature QRS complex in V1: Origin of PVC is usually from
the LV.
Predominantly negative premature QRS complex in V1: Origin of PVC is usually
from the RV.
ARRHYTHMIAS 629
Fig. 30.75 | Multiform PVCs with different QRS contours.

LV: +ve QRS RV: ve QRS
complex in V1 complex in V1
Bigeminyinterpolated
Uniform
Trigeminyfollowing 2 Couplets2
normal beats successive PVCs
PVCs
Quadrigeminyfollowing Triplets (salvos)3
3 normal beats successive PVCs
Pentageminyfollowing Multiform
4 normal beats
Pleomorphic-different
Multifocal in origin
QRS contours
Fig. 30.76 | Types of premature ventricular contractions (PVCs)RV: right ventricular

origin, LV: left ventricular origin.
iv) Depending upon the frequency of the PVCs42

Class 0: No PVCs
Class I: Rare, 1 PVC/hour
Class II: Infrequent: 19 PVCs/hour
Class III: Intermediate: 1029 PVCs/hour
Class IV: Frequent: 30 PVCs/hour
v) Depending upon the forms of PVCs42

Class A: PVCs of uniform morphology, or unifocal in origin.
Class B: PVCs of multiform, pleomorphic having different contours or mulitfocal in
origin (see Fig. 30.75).

Class C: Repetitive forms of PVCs: couplets, triplets or salvos.
Class D: Non sustained VT: runs of 3 consecutive PVCs up to 30 s.
Class E: Sustained VT: runs of PVCs of 30 s (see Fig. 30.76).
Estimation of Risk of PVCs

It is based upon the frequency and/or forms of PVCs.42
VPCs may function as triggering events to initiate potentially lethal ventricular
arrhythmias (VT, Vf ) (see Fig. 30.77) when the myocardium is susceptible, and when
Vf
Fig. 30.77 | Early PVCs (arrows), R-on-T phenomenoninitiating ventricular fibrilla-

tion (Vf).
PVCs are frequent (Class IV), multifocal, multiform, or in couplets and salvos. Hence
when PVCs are 30/hour, treatment may be initiated even in the absence of struc-
tural heart disease.
Differentiation of PVCs from Premature Supraventricular

Complexes (SVCs) with Aberrant Ventricular Conduction (AVC)
A premature P is usually preceded by abnormal QRS complex when the ectopic beat is
supraventricular (atrial or junctional) in origin. In the absence of identifiable P waves
(when the ectopic focus is located in AV junction or ventricle), a fully compensatory
pause following premature complex favors PVC. However, the absence of fully com-
pensatory does not exclude PVC with retrograde depolarization of SA node. In such an
event, retrograde P may be identifiable after QRS complex and RP interval 0.20 s is
suggestive of PVC and if RP interval is 0.11 s, the premature complex is likely to be
AV junctional.43
QRS complex of RBBB pattern with an rSR in V1 favors SVC with AVC, while con-
cordant QRS complexes (either all positive or all negative) in the precordial leads are
diagnostic of PVCs44 (see Fig. 30.78).
ii. Ventricular Tachycardia (VT)

It arises in the specialized conduction system distal to the bifurcation of the His bundle
or in the ventricular muscle or in combination of both (see Fig. 30.79).
It is due to the disorders of impulse formation and conduction.
VT is rare in individuals without structural heart disease (non-sustained VT can occur
1 in 67,000 population), but is common in ischemic heart disease (AMI: 628%)
and cardiomyopathy.
It can also occur in valvular heart disease, MVP, congenital heart disease, during
reperfusion therapy (fibrinolytic therapy, PTCA and CABG) and can be provoked by
various medications including digoxin and quinidine and electrolyte imbalance such
as severe hypokalemia and hyperkalemia.
There is an increased risk of sudden cardiac death in patients with VT and structural
heart disease, reduced left ventricular function, increased QT interval dispersion, spon-
taneous ventricular arrhythmias, and presence of late potentials on signal averaged ECG.
ARRHYTHMIAS 631
V1 V4
V2 V5
V3 V6
Fig. 30.78 | Supraventricular complex with aberrant ventricular conductionatrial fibril-

lation with two complexes conducted after long pauses with aberration
mimics PVCs. However RBBB pattern in V1 favors supraventricular complex.
Aorta
PA
LA
Ventricular tachycardia
RA LV
RV
Left ventricular damage

Myocardial infarction
Myocarditis
Fig. 30.79 | Genesis of ventricular tachycardia.

ECG Recognition
VT is characterized by the occurrence of three or more consecutive wide bizarre shaped
premature ventricular complexes with QRS duration of 140 ms and ST segment
and T wave opposite in direction to the abnormal QRS complex (see Fig. 30.80).
I aVR V1 V4
II aVL V2 V5
III aVF V3 V5
Fig. 30.80 | Ventricular tachycardia: wide QRS complex at a rate of about 150/min.
PVC VT
Fig. 30.81 | Initiation of monomorphic ventricular tachycardia (VT) by a PVC (arrow) with
premature index of 1.
It is often initiated by PVCs and sometimes by supraventricular impulses. Premature

index (PI coupling interval/QT interval ratio) of PVC initiating VT is usually 1
(see Fig. 30.81), and longer PI does not initiates VT.45 It has been found that a short-
long cycle sequence often precedes the onset of VT.46 The short cycle consists of a
sinus beat followed by a PVC and long cycle consists of compensatory pause of the
PVC and next sinus beat i.e. a sequence of sinus beat-PVC-compensatory pause-
sinus beat-VT occurs especially at the onset of polymorphic VT.
ARRHYTHMIAS 633
Table 30.19 Ventricular tachycardia
1. IHD, during fibrinolytic therapy, 1. 3 PVCs at a ventricular rate of 70250/min

PTCA, post-CABG
2. Cardiomyopathy 2. Often initiated by PVCs
3. MVP 3. Wide QRS complex of 140 ms
4. Congenital heart disease 4. Usually regular rhythm, but interrupted by fusion
and captured beats
5. Digitalis toxicity 5. Atrial activity is independent of ventricular activity
6. Quinidine toxicity 6. LAD in frontal QRS axis
7. Severe hypokalemia and hyperkalemia
It is usually regular with a ventricular rate of 70250/min (usually 100/min).

Atrial activity is independent of ventricular activity (i.e. AV dissociation, usually
1:1 conduction) or the atria can be depolarized retrogardely by the ventricles (in
about 25%).
The regular rhythm of the VT may be interspersed by occasional fusion and captured
beats in about 5% of the patients with VT.47 Fusion beats (also known as Dressler
beats) indicate activation of the ventricle from different foci, with one of the foci of
ventricular origin, resulting in QRS complexes of intermediate contour. The capture
beat has a normal QRS complex as it is supraventricular in origin.
VT usually has LAD in frontal plane.
If VT occurs in MI, Q waves may be present.
In certain circumstances, SVT (with aberrant conduction or antidromic AVRT) can
mimic VT (see Table 30.19).
Types of VT
(a) Depending upon the duration of VT: It can be sustained or non-sustained.
Non-sustained VT: Runs of VT last up to 30s. They can occur in individuals with-
out structural heart disease and may be self terminating.
Sustained VT: Runs of VT last for 30s, usually with ventricular rate of 100/min
and often occurs in patients with structural heart disease.
(b) Depending upon the QRS morphology: VT can be uniform or monomorphic,
multiform or polymorphic.
(i) Monomorphic or uniform VT: QRS contours are unchanging. Various types of
monomorphic VT are as follows:
Sustained monomorphic VT occurs in acute or chronic ischemic heart disease, idio-
pathic dilated or hypertrophic cardiomyopathy and less frequently in inflammatory
or infiltrative diseases or as a primary electrical disturbance.
Non-sustained monomorphic VT can occur in individuals with structurally normal heart.
LBBB pattern VT is characterized by r wave in V1 is broader than 30 ms, there is notch-
ing of S wave in V1 with r to nadir of S 60 ms and qR or qS in V6.48 (see Fig. 30.82).
r V1 V6
R
>0.03 sec
Notch or
slur
S
>0.06 sec
Fig. 30.82 | Characteristic of monmorphic LBBB pattern VTr 30 ms, notching of
S and r to nadir of S 60 ms in V with qR in V .
1 6
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 30.83 | Monomorphic VT with LBBB pattern and inferior axis arising from RVOT at
a rate of 210/min.
LBBB Pattern VT occurs in:

Bundle branch reentry tachycardia associated with dilated cardiomyopathy. It is a
form of monomorphic sustained VT, characterized by retrograde conduction over the
LBB and antegrade conduction over RBB producing LBBB contour with frontal axis
of about 30.
RVOT tachycardia is characterized by LBBB QRS morphology with an inferior axis
and is often found in individuals with structurally normal hearts (see Fig. 30.83). Two
types of RVOT tachycardia has been describedrepetitive monomorphic VT and exer-
cised induced VT.
Repetitive monomorphic VT are often non-sustained and benign. It is often due to
early or delayed after depolarizations (see Fig. 30.84).
ARRHYTHMIAS 635
Fig. 30.84 | Repetitive monomorphic VT with LBBB pattern at a rate of 160/min.

Paroxysmal VT or exercised induced VT is also referred as catecholamine-sensitive
tachycardia that are usually suppressed by blockers and calcium channel blockers.
Arrhythmogenic RV dysplasia (ARVD) is characterized by LBBB contour with RAD
and inverted T waves in right precordial leads. It occurs predominantly in young males.
However in sinus rhythm, ECG exhibits complete or incomplete RBBB with T wave
inversions in V1V3.49
RBBB pattern VT: It is characterized by monophasic R or biphasic qR, Rs or Rr in
V1, R/S 1 in V6 with a frontal QRS axis between 90 to 90 (see Fig. 30.85).50
This type of VT occurs as
Variant form of bundle branch reentry tachycardia with antegrade conduction over
the LBB and retrograde conduction over the RBB.
Idiopathic LV tachycardia has RBBB morphology with a superior axis originating
near the posterior fascicle of the LBB at the inferior basal septum, hence sometimes
referred as fascicular tachycardia (see Fig. 30.86). It can be paroxysmal and can be sus-
tained once initiated. It is sensitive to verapamil. Generally, the prognosis is good.
Isthmus tachycardia is similar to LVOT tachycardia found in patients with MI.
The site of origin is between the basal inferior septum and the mitral annulus (see
Table 30.20).
(ii) Multiform or polymorphic or pleomorphic VT: QRS contours vary randomly
and from the management point of view, these are subclassified into:
Polymorphic VT with normal QT interval
Polymorphic VT with prolonged QT interval
Polymorphic VT with normal QT interval: It is most frequently caused by acute
ischemia or MI and rarely arrhythmogenic RV dysplasia.
Idiopathic polymorphic VT or familial catecholaminergic polymorphic VT has
normal QT interval.
It is usually initiated during sinus tachycardia by PVC with a short coupling interval.
It is poorly tolerated and tends to quickly degenerate into VF.
Polymorphic VT with prolonged QT interval: Torsades de pointes (TDP) is the clas-
sical example (see Fig. 30.87).
It was originally described as a syndrome characterized by prolonged QT interval.51
It is characterized by QRS complexes of changing amplitude that appears to twist
around the isoelectric line.
R R
aVF
V1
V2
V3
V4
V5
V6
S S
Fig. 30.85 | Vandanddeep

1 6V sign in monomorphic VT with RBBB pattern (monophasic R in V 1
S in V ).
6
It is frequently non sustained occurring with a rate of 200250/min.

It is often the late onset PVC that initiates TDP and is usually due to early after
depolarization (see Figs 30.88 and 30.89).
Females are more susceptible for the development of TDP than males in the ratio
of 3:1.52
The clinical conditions known to predispose TDP are congenital long-QT syndrome,
antiarrhythmic drugs which prolong QT interval (class IA: quinidine is the common-
est, class IC: propafenone, class III: sotalol, ibutilide, dofetilide and amiodarone
amiodarone is the least cause), bradycardia, hypokalemia, and hypomagnesemia.
Poisoning with organophosphorus compounds,53 intracranial hemorrhage54 and
hypothyroidism55 are the other predisposing conditions.
IV magnesium is the initial treatment of choice for TDP from an acquired cause fol-
lowed by temporary ventricular or atrial pacing.56
(c) Depending upon the polarity of the QRS complex
Bidirectional VT: It is an uncommon VT in which polarity of the QRS complex varies
in alternate complexes.
ARRHYTHMIAS 637
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 30.86 | Monomorphic VT with RBBB pattern arising from left posterior septum at a
rate of 210/min.
Table 30.20 Therapeutic classification of monomorphic VT
Type depending upon the

Origin and onset ECG pattern
drug sensitivity
1. Adenosine sensitive VT Mostly RVOT LBBB contour with inferior axis

2. Verapamil sensitive VT Post fascicle of LBB at RBBB contour with superior axis
the inferior septum
3. Catecholamine or Propranolol Exercise induced from LBBB contour (if from RVOT) or
sensitive VT RV or LV RBBB contour (if from LV)
4. Undifferentiated VT i.e. usually not Paroxysmal exercise LBBB contour with inferior axis
responding to any drug induced usually from RV
It is characterized by RBBB pattern alternating its polarity from (60 to 90) to

(120 to 130)
It has a regular rhythm with a ventricular rate of 140200/min.
It is due to severe digitalis toxicity (and indicates poor prognosis) and severe myocardial
disease (see Fig. 30.90).
(d) Narrow QRS VT and Fascicular VT: VT arising from the fascicles may have a
narrow QRS complex ( 110 ms) and diagnosis is established by the presence of AV
dissociation, fusion beats and HV interval shorter than during the sinus rhythm.57
However, VT originating from the fascicles may have usual characteristics of VT. VT
of left anterior fascicle is suggested by RBBB pattern with inferior axis and VT of left
posterior fascicle is suggested by RBBB pattern with superior axis58 (see Fig. 30.91).
Fig. 30.87 | Polymorphic VT with prolonged QT intervalTorsades de pointes.
Fig. 30.88 | Late or end diastolic PVCalso high risk for initiating polymorphic VT
especially Torsades de pointes.
SB
PVC
TDP
Fig. 30.89 | Late onset PVC initiating Torsades de pointes (TDP)SB: sinus beat.
Localizing the Site of Origin of VT
1. LV origin of VT: RBBB pattern of QRS complex.
q in I and V6 is associated with anterior origin of VT.59
R in I, V1 and V2 is associated with posterior origin of VT.59
ARRHYTHMIAS 639
V2
Fig. 30.90 | Bidirectional ventricular tachycardia usually occurs in severe digitalis toxi-
city or severe myocardial disease.
RVOT tachycardia: BBB reentry ARVD: RAD & T

inferior axis tachycardia: +30 axis in V1, V2
LBBB pattern: 1. Short CI PVC initiates

1.V1-r >30 ms, r-S 2. Acute ischemia/MI
>60 ms and slurring of S 3. Poorly toleratedVf
2.V6-qR or qS
Nonsustained Normal QT
Sustained: >30 s
upto 30 s
Monomorphic VT Polymorphic
Variant BBB reentry
tachycardia
RBBB pattern: Bidirectional QT (TDP)
Isthmus tachycardia 1. V1R or qR, Rs, Rr
2. V6R/S <1
Idiopathic LV 1. Regular140 1. Non sustained200250/min
tachycardia 200/min 2. Late onset PVC initiates VT
2. RBBB pattern
3. Due to severe
digitalis toxicity 3. Predisposing conditions:
Cong long QT synd, AAD
(IA, IC and III), HR, K, Mg,
OP poisoning, ICH and
hypothyroidism
Fig. 30.91 | Types and characteristics of ventricular tachycardia (VT)RVOT: right ventricular outflow
tract, BBB: bundle branch block, RBBB: right bundle branch block, LBBB: left bundle branch
block, ARVD: arrhythmogenic right ventricular dysplasia, RAD: right axis deviation, CI: cou-
pling interval, PVC: premature ventricular contraction, TDP: Torsades de pointes, AAD:
antiarrhythmic drugs, OP: organophosphorous poisoning, ICH: intracranial hemorrhage,
Cong long QT synd: congenital long QT syndrome, MI: myocardial infarction, Vf: ventricular
fibrillation, K: hypokalemia, Mg: hypomagnesemia.
Inferior axis suggests the origin of VT from left anterior fascicle.58

Superior axis suggests the origin of VT from left posterior fascicle.58 VT
arising from or near left posterior fascicle may have LBBB pattern QRS
complex.60
2. RV origin of VT: LBBB pattern of QRS complex

Inferior axis suggests the origin of VT from RVOT.
30 axis suggests the origin of VT from bundle branch.
iii. Idioventricular Rhythm (IVR)

Arrhythmia of ventricular origin operating independently (under the control of the
ventricular pacemaker) at a slow or accelerated rates (20110/min) is known as
idioventricular rhythm (IVR). It is classified as slow or accelerated IVR.
Slow IVR: When ventricular rate is less than normal (2050/min), it is known as
slow IVR (see Fig. 30.92). It is found in normal individuals or in conditions of meta-
bolic or electrolyte derangement, and correction of the precipitating factors usually
terminates the arrhythmia.
Accelerated IVR (AIVR): When the ventricular rate is 60110/min, IVR is known as
accelerated IVR, which hovers within 10 beats of sinus rate, so that the control of the
cardiac rhythm shifts between these two competing pacemaker sites61 (see Fig. 30.93).
The AIVR is transient and intermittent, with a regular or irregular ventricular
rhythm.
II
Fig. 30.92 | Slow idioventricular rhythm with a ventricular rate of 46/min.

I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 30.93 | Accelerated idioventricular rhythm at a rate of 90/min.

ARRHYTHMIAS 641
As the rate is slow, captured and fusion beats are seen, often occurring at the onset
and termination of the arrhythmia.
The onset of AIVR is usually gradual (non paroxysmal) and it usually occurs in
the presence of sinus bradycardia when the ventricular rate exceeds the sinus rate
due to slowing of sinus node, SA block or AV block.
The termination of the rhythm also occurs gradually as the dominant sinus
rhythm accelerates or when the ectopic ventricular rhythm decelerates.
Due to slow ventricular rate and gradual onset, more rapid ventricular arrhythmias
are rarely seen.
This arrhythmia usually occurs in patients with structural heart disease such as AMI
(836%62, 90% during first few hours after reperfusion63) myocarditis, hypertension,
rheumatic heart disease and congenital heart disease.64 It also occurs in digitalis
toxicity.65 However, it does not affect the clinical course or prognosis of the disease
entity, and treating the underlying condition usually terminates the arrhythmia.
iv. Ventricular Flutter (Vfl) and Ventricular Fibrillation (Vf)

These are terminal arrhythmias that usually terminate fatally within 35 min unless
rapid initiation of emergency measures are taken promptly.
Vf commonly occurs in the setting of coronary heart disease (acute ischemia or
advanced chronic ischemic heart disease) or nonischemic cardiomyopathy.
VT commonly precedes the onset of Vf, but may develop during late onset PVCs,
hypoxia, atrial fibrillation with rapid ventricular responses in WPW syndrome,
R-on-T pacing or asynchronized cardioversion, or electrical accidents due to
improper grounding of electrical devices, or as proarrhythmic effects of antiarrhyth-
mia drugs.
It can occur in any age group in infants, young people, athletes, and persons without
known structural heart disease.66
Persons in lower socioeconomic strata are a greater risk for cardiac mortality.67 Sudden
cardiac death is generally due to Vf, which occurs most frequently in the morning and
may be related to increased platelet aggregability (see Table 30.21).
Table 30.21 Ventricular fibrillations (Vf)
Etiology Salient ECG findings
1. Any age 1. Irregular undulations of varying contour

and amplitude
2. CAD 2. No definite QRS complexes and T waves
3. Cardiomyopathy
4. Hypoxia
5. Af, VT, R-on-T PVC can degenerate into Vf
6. Antiarrhythmic drugs
7. Asynchronized cardioversion
8. Electrical accidents (due to improper grounding)
ECG Recognition
(a) Ventricular fibrillation (Vf)
Vf is recognized by the presence of irregular undulations of varying contour and
amplitude without distinct QRS complexes, ST segment and T waves at a rate of
150500/min.
Vf may be coarse initially but over the time it loses its amplitude and becomes fine
(0.2 mV in amplitude), and chances of successful defibrillation and survival rates
are decreased (see Fig. 30.94).
Rapid polymorphic VT may be confused with Vf.
(b) Ventricular flutter (Vfl)
Ventricular flutter presents as sine waves, i.e. large regular zigzag oscillations with-
out clear cut definitions of QRS complex and T waves, occurring at a rate of
150300/min (usually 200/min) (see Fig. 30.95).
Rapid VT may be difficult to distinguish from ventricular flutter.
7. WIDE QRS TACHYCARDIA
The QRS duration is 120 ms and is classified into regular and irregular.
i. Regular Wide QRS Tachycardia

It consists of :
VT
SVT with BBB: AT, Afl with fixed AV conduction
Coarse Vf
Fine Vf
Fig. 30.94 | Ventricular fibrillations (Vf)coarse and fine.
II Vfl
Fig. 30.95 | Sine waves in ventricular flutter (Vfl).

ARRHYTHMIAS 643
SVT with Aberrant ventricular conduction (see Fig. 30.96)

Antidromic AVRT (see Fig. 30.97)
Mahaim tachycardia
ii. Irregular Wide QRS Tachycardia

It consists of :
Atrial fibrillation with BBB or aberrant ventricular conduction
Atrial flutter/atrial tachycardia with varying AV conduction and BBB
Atrial fibrillation with WPW syndrome (see Fig. 30.98)
Polymorphic VT with normal QT interval
Torsades de pointes
I aVR V1 V4
II aVL V2 V5
III V3 V6
aVF
Fig. 30.96 | SVT with aberrant ventricular conduction at a rate of 146/minQRS com-
plex is 118 ms with rsR pattern (partial RBBB) in V .
1
V4
I aVR V1
II aVL V5
V2
III aVF V6
V3
Fig. 30.97 | Regular wide QRS tachycardia at a rate of 250/minantidromic AVRT.

I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Fig. 30.98 | Irregular wide QRS tachycardia: atrial fibrillation with WPW syndrome.
Differential diagnosis: It is essential to differentiate ventricular tachycardia from the
supraventricular tachycardia with aberrant conduction from the therapeutic as well as
from the prognostic points of view (see Table 30.22 and Fig. 30.102). The wide QRS
tachycardia with negative concordance is diagnostic of VT, while a positive QRS con-
cordance can also occur in WPW syndrome (see Figs 30.99 and 30.100). The ECG
morphology in V1 and V6 also helps to distinguish VT from SVT with aberrant con-
duction (see Fig. 30.101).
8. HEART BLOCK
Heart block is due to the disturbance of impulse conduction which can be permanent
or transient. Heart block most commonly occurs:
Between the sinus node and atria: SA block
Between the atria and ventricles: AV block
Within the atria: Intraatrial block or
Within the ventricles: Intraventricular block
AV Block
During AV block, the block can occur in the AV node, His bundle, or bundle
branches. It occurs when the atrial impulse is conducted with delay or is not con-
ducted at all to the ventricle at a time when the AV node is not physiologically refrac-
tory. The heart block is classified depending upon its severity into first degree, second
degree, and third degree or complete AV block. All degrees of AV block may be inter-
mittent or persistent.
ARRHYTHMIAS 645
Table 30.22 Differential diagnosis of wide QRS tachycardiaVT vs SVT
Features Diagnostic findings
1. Ventricular rate SVT tends to be faster than VT

2. Rhythm regularity Generally, VT tends to be regular (except TDP), while SVT
most often is irregular (regular rhythm in AT and Afl with
fixed AV conduction, antidromic AVRT)
3. Onset of tachycardia SVT is initiated by premature P wave, while PVC initiates VT.
In VT, first wide QRS complex is preceded by a sinus P
wave with a PR interval that of the conducted sinus
complex
4. QRS duration Usually 140 ms in VT, while it is 140 ms in SVT (except
in preexistent BBB and antidromic AVRT)
5. AV dissociation AV dissociation with capture and fusion beats is a hall
mark of VT
6. P and QRS relation In VT: atrial activation depends on ventricular discharge, e.g.
2:1 VA block, while in SVT ventricular activation depends
on atrial discharge, e.g. 2:1 AV block
7. Frontal QRS axis LAD usually occurs in VT (sensitivity: 100%, specificity: 90%)
8. QRS configuration
a) Concordant pattern in a) Negative QRS concordant is diagnostic of VT, while
precordial leads (V1V6) positive QRS concordant can also occur in WPW
syndrome. However, right superior axis (90 to 180)
and positive concordance is 100% specific for VT.68
b) RBBB contour b) In VT: monophasic R or biphasic qR, Rs, or Rr in V1 with
and R/S 1 in V6 are present, while in SVT; QRS
complex is triphasic in V1
c) LBBB contour c) In VT: V1 has r 30 ms, notching of S wave with r to nadir
of S 60 ms and V6 has qR or qS, while in SVT, the initial
positive wave (r) is 30 ms, there is rapid smooth descent
of S wave without a notch and the distance from r to nadir
of S is 60 ms. Besides r during SVT is r during sinus
rhythm, while r during VT is r during sinus rhythm
9. VAT 0.08 s in VT and 0.08 s in SVT
10. Presence of structural VT is more likely
heart disease or MI
11. IV adenosine or vagal stimulation Usually, termination or slowing of wide QRS tachycardia
of supraventricular origin
a) First Degree AV Block

It can occur in individuals with structurally normal heart and rheumatic fever (see
Table 30.23).
It is due to delayed conduction of atrial impulse to the ventricles, which is characterized
by prolongation of PR interval by 0.20 s at normal heart rate and normal QRS com-
plexes both in duration and configuration (Fig. 30.103).
V1
V1
V2
V2
V3
V4
V3
V4
V5
V5
V6
Fig. 30.99 | Wide QRS tachycardia with

negative concordance in VT.
V6
Fig. 30.100 | Wide QRS tachycardia with

positive concordance in VT.
In general, prolonged PR interval is constant, but may vary inversely with RP inter-
val during sinus arrhythmia, which is referred too as floating PR. It may shorten
when the heart rate increases and prolong when the vagal tone is increased (see
Fig. 30.104).
At times, PR interval may exceed PP interval, a phenomenon known as skipped
P waves.
Clinically, prolonged PR interval can result from a conduction delay in:
AV node (most common cause prolonging the A-H interval),
His Purkinje system (least common cause prolonging the H-V interval) or both, and
Occasionally within the atria (intraatrial conduction delay) and seen in patients
with an endocardial cushion defect.69
QRS complex has a bundle branch block pattern if the conduction delay is in the His-
Purkinje system.
ARRHYTHMIAS 647
r V1
V1
0.03 sec
Narrow r
30 ms
Notch or
slur
Rapid
smooth
descent
S S
0.06 sec
SVT
VT
Wide QRS Configuration in VT & SVT in V1
V6 R
V6
r
R
q No q
VT SVT
Wide QRS Configuration in VT & SVT in V6
Fig. 30.101 | Differentiation of ventricular tachycardia (VT) from supraventricular

tachycardia (SVT) with LBBB contour on the basis of QRS configuration
in V1 and V6..
Delayed conduction over the both bundle branches can rarely produce prolonged
PR interval without significant QRS complex aberration.
b) Second Degree AV Block

It is characterized by intermittent failure of conduction from atria to ventricles and is
further subdivided into:
Mobitz type I (Wenckebach phenomenon)
Mobitz type II
Mobitz type I or Wenckebach phenomenon
It is more common and occurs in hypoxia of any cause, increased vagal tone (well-
trained athletes), with medications (digitalis, quinidine, and procainamide), hyper-
kalemia, rheumatic fever, myocarditis besides CAD (especially inferior MI, more
often with RV MI, see Table 30.24).
It also occurs in congenital heart disease, such as ASD and Ebsteins anomaly.
Wide QRS tachycardia

(QRS duration 120ms)
Regular or irregular
Regular Irregular
1 to 1 AV relationship? 1. Atrial fibrillation

2. Atrial flutter/AT variable
conduction and
i) BBB or ii) antegrde conduction
via accessory pathways
Yes or unknown No
QRS morphology Ventricular rate Atrial rate ventricular

in precordial leads atrial rate VT rate *AT, *Atrial flutter
Typical See precordial leads for LBBB pattern:

RBBB or *Concordance *R in V1 30 ms
LBBB *No R/S pattern *R to nadir of S VT
SVT *Onset of R to nadir VT in V1 60 ms
longer than 100 ms *qR or qS in V6
RBBB pattern:
*qR, Rs or Rr in V1 VT
*Frontal axis:90
to 90
Fig. 30.102 | Differential diagnosis of wide QRS tachycardia.

Table 30.23 First degree AV block
Etiology Salient ECG findings
1. Structurally normal heart 1. Prolonged PR interval of 0.20 s

2. Rheumatic fever 2. Normal QRS complex
In general, it is more benign and does not progress to more advanced forms of AV
block.
Wenckebach periodicity can occur in any cardiac tissue and is seen more frequently
in AV node than in sinus node.
ECG recognition
i) PR interval:
It is characterized by progressive prolongation of PR interval until a P wave is
blocked.
ARRHYTHMIAS 649
I aVR V1 V4
P R
II aVL V2 V5
P R P R
III aVF V3 V6
Fig. 30.103 | First degree AV blockprolonged PR interval.
R R R
P P P
R R R
P P P
Fig. 30.104 | First degree AV block with varying PR interval.
Table 30.24 Second degree AV block
Features Mobitz type I Mobitz type II
a) Etiology 1. Well-trained athletes 1. Acute anterior myocardial infarction

2. Digitalis, quinidine, procainamide toxicity
3. Rheumatic fever
4. Hyperkalemia
5. CAD
6. Myocarditis
7. ASD, Ebsteins anomaly
b) ECG findings 1. Progressive prolongation of PR interval 1. Constant PR interval
2. As PR lengthens, RR shortens 2. Wide QRS complex
3. Wenckebach conduction ratio of 3:2 3. Fixed AV conduction of 2:1, 3:1
The increment in the conduction time is greatest in the second beat of the
Wenckebach group, and subsequently there is a decrement in the increment of
the conduction time, i.e. the absolute increase in the conduction time decreases
progressively in the subsequent beats.
ii) The relation between PR and RR intervals:
There is a progressive shortening of the RR interval until a P wave is blocked.
There is a decrement in the RR interval, even though there is increment in the
conduction time, i.e. as the PR lengthens, RR interval shortens.
iii) RR interval containing the blocked P wave is shorter than the sum of two PP
intervals.
The duration of the pause produced by the non-conducted P wave is less than
twice the interval of the last conducted beat preceding the blocked P wave, which
usually has the shortest interval, i.e. the longest PP interval (from non-conducted
P to P of next Wenckebach group) is less than twice the shortest PP interval pre-
ceding the blocked P wave. The sequence between one pause and the next is
referred to as Wenckebach period.
In atypical Wenckebach type, the increment in the PR interval of the last conducted
beat is increased rather than getting decreased and lengthening of the last RR (PP)
interval occurs instead of its shortening.
Most common Wenckebach conduction ratio is 3:2, but any (x1) conduction
can occur, e.g. 4:3, 5:4.
iv) The site of block is usually in the AV node, proximal to His bundle and QRS com-
plex is normal. Exercise or atropine (which increases the atrial rate) tends to
decrease type I 2 AV block, while type II increases.70 (see Fig. 30.105).
Mobitz type II
It is less common, and usually associated with organic heart disease and frequently
occurs in the setting of an acute anterior MI.
It is frequently progressive, and often antedates the development of Stokes-Adams
syndrome and complete AV block, the site of which as a rule is infranodal.
II P R P R P R P P R
III
Fig. 30.105 | Mobitz

menon.
type I second degree AV block with typical Wenckebach pheno-
ARRHYTHMIAS 651
ECG recognition
There is no progressive lengthening of PR interval. It may be normal or prolonged
but remains constant prior to the blocked P wave.
Isolated P waves may fail to conduct or fixed pattern of conduction (2:1, 3:2) may occur.
As the usual site of block is infranodal, QRS complexes are wide, and when the QRS
complex is narrow, the site of block more likely in the His bundle (in 2735%71) (see
Figs 30.106 and 30.107). Most patients have associated BBB and block is distal to
the His bundle.72
When two or more consecutive P waves are blocked (3:1 or higher), it indicates
advanced AV block (see Table 30.24).
P R P
P R
II
V1
Fig. 30.106 | Mobitz type II second degree AV block with 3:2 conduction and LBBB
pattern QRS complex as the site of block is infranodal.
I aVR V1 V4
II aVL V2 V5
P R P R
III aVF V3 V6
Fig. 30.107 | Mobitz type II second degree AV block with 2:1 conduction, prolonged PR
interval and normal QRS complex as the block is in His bundle.
c) Complete or Third Degree AV Block

It could be due to acquired or congenital causes (see Table 30.25).
i) Acquired causes:
In adults, drug toxicity (digitalis), CAD and degenerative process (Lenegres disease:
sclerodegenerative process of the conduction system; Levs disease: calcification and
sclerosis of the conduction system in elderly) are the most common causes of com-
plete AV block.
Surgery (surgical correction of congenital anomalies, prosthetic valve implantation),
electrolyte disturbances (hyperkalemia), myoendocarditis, cardiomyopathy (DCM)
tumors, Chagas disease, diphtheria, rheumatoid nodules, calcific AS, myxedema,
polymyositis, and infiltrative diseases, such as amyloidosis, sarcoidosis, scleroderma
can cause complete AV block.
ii) Congenital Causes:
These are often associated with corrected TGA and VSD. It is inherited in infants
born to mothers with systemic lupus erythematosis.73
ECG recognition: Complete AV block can be at the level of AV node (usually in the
congenital causes), within the bundle of His or distal to it in the Purkinje system (usu-
ally in the acquired causes). If the block is in the main bundle branches, it is called
bilateral bundle branch block and if the block involves the RBB and two divisions of
LBB, it is called trifascicular block (see fascicular blocks, Chapter 26).
Complete AV block occurs when no atrial activity (P waves) is conducted to the
ventricles, which results in complete AV dissociation (i.e. independent beating of
the atria and ventricles).
Table 30.25 Complete AV block
Acquired causes:
1. Coronary artery disease 1. Complete AV dissociation
2. Degenerative process 2. Atrial focus rate: 60100/min
3. Digitalis toxicity 3. Ventricular focus:
4. Hyperkalemia i) In acquired causes: block is below His bundle
5. Myoendocarditis with wide QRS complex,and ventricular rate is
6. Calcified aortic stenosis 40/min
7. Infiltrative diseases ii) In congenital causes: block is above His bundle
8. Chagas disease with narrow QRS complex and ventricular rate is
4060/min
Congenital causes:
1. Corrected transposition of great arteries
2. Ventricular septal defect
3. Infants born to mother with systemic
lupus erythematosis
ARRHYTHMIAS 653
The atrial focus (pacemaker) can be sinus, ectopic (tachycardia, atrial flutter, atrial
fibrillation) or AV junction, and the atrial rate is usually 60100/min (see Fig. 30.108).
The ventricular focus (pacemaker) is usually located just below the region of the
block, which can be above or below the His bundle.
Acquired complete AV block occurs most commonly distal to the His bundle and
the ventricular rate is 40/min with wide QRS complexes as in acute anterior MI
(see Fig. 30.109). But in inferior MI, most often the block is proximal to the His
bundle and QRS complexes may be narrow.
The ventricular rate may be increased by exercise or vagolytic agents when the block
is above the His bundle and the pacemaker is high in AV junction as in congenital
causes.74
Congenital complete AV block usually occurs proximal to His bundle.
The ventricular rates vary from 4060/min with normal QRS complexes, which
are more stable (see Figs 30.110 and 30.111).
Absent Q waves in left precordial leads, but present in right precordial leads in
cTGA.
P P P P P P P P
P
V1
V2
Fig. 30.108 | Complete AV block with wide QRS complex (RBBB pattern), regular atrial
rhythm at a rate of 88/min and regular ventricular rhythm at rate of
37/min.
II P
P
III P
P P
Fig. 30.109 | Complete AV block with wide QRS complex, regular atrial rate of 60/min
and ventricular rate of 36/min.
T waves may be deeply inverted or coving in right or mid precordial leads.

There is no arithmetic relationship between P and QRS, i.e. no periods of syn-
chronization as in acquired AV block.
At times, the firing rate of the two foci are similar and the P waves and QRS rates are
similar (a condition known as isorhythmic dissociation), which makes the diagnosis
of complete AV block difficult (see Fig. 30.112).
I
P P P P
II
P P P P P
III
P P P
P P
Fig. 30.110 | Congenital complete AV block with narrow QRS complexregular atrial
rate of 60/min and regular ventricular rate of 46/min.
II R R R R
P P
P P P P
After exercise
II R R R R
Fig. 30.111 | Congenital complete AV block with narrow QRS complex and regular
ventricular rhythm at a rate of 50/min and atrial rate of 88/min. After exer-
cise, the ventricular rate increased to 70/min unlike acquired complete
AV block.
ARRHYTHMIAS 655
1. Complete 3. Vent. focus

1. Progressive of 1. PR 0.20 s
AV dissociation @: 40/min
PR and of RR 2. Normal QRS
2. Atrial focus 4. Wide QRS
2. RR with blocked complex
@: 60100/min complex
P sum of 2
PP intervals
Type I 1st degree Acquired
3. 3:2 commonest CR
4. Normal QRS
complex 2nd degree AV block Complete
5. Exercise the block
Type II Congenital
1. Constant PR: 3. Wide QRS 1. Complete AV 4. Narrow

normal or PR complex usual dissociation QRS complex
2. Fixed CR: 2:1 4. Exercise 2. Atrial focus @: 5. Vent @
or 3:2 the block 60100/min with exercise
3. Vent. focus @:
4060/min
Fig. 30.112 | AV blocktypes and characteristics-Vent:

increases, : decreases.
ventricular, @: rate, CR: conduction ratio, :
REFERENCES
1. Morillo CA, Klein GJ, Thakur RK, et al. Mechanism of inappropriate sinus tachycardia; role of
sympathovagal balance. Circulation 1994;90(2):87377.
2. Sgarbossa EB, Yamanouchi Y, Rejna T, et al. Autonomic imbalance in patients with inappropriate
sinus tachycardia. J Am Coll Cardiol 1995;26(1):A52.
3. Shen WK, Low PA, Jahangir A, et al. Is sinus node modification appropriate for inappropriate sinus
tachycardia with features of postural orthostatic tachycardia syndrome? Pacing Clin Electrophysiol
2001;24(2):21730.
4. Frank JI, Ropper PH, Zuniga G. Acute intracranial lesions and respiratory sinus arrhythmia. Arch
Neurol 1992;49(11):120003.
5. Hiss RG, Lamb LE. Electrocardiographic findings in 122,043 individuals. Circulation 1962;25:
94761.
6. Tang CW, Scheinman MM, van Hare GF, et al. Use of P wave configuration during atrial tachycardia
to predict site of origin. J Am Coll Cardiol 1995;26(5):131524.
7. Scher DL, Arsura EL. Multifocal atrial tachycardia: Mechanisms, clinical correlates, and treatment.
Am Heart J 1989;118(30):57480.
8. Granada J, Uribe W, Chyou PH, et al. Incidence and predictors of atrial flutter in general population.
J Am Coll Cardiol 2000;36(7):224246.
9. Saxon LA, Kalman JM, Olgin JE, et al. Results of radiofrequency catheter ablation for atrial flutter.
Am J Cardiol 1996;77(11):101416.
10. Garson A, Bink-Boelkens M, Hesslein PS, et al. Atrial flutter in the young: a collaborative study of
380 cases. J Am Coll Cardiol 1985;6(4):87178.
11. Saoudi N, Cosio F, Waldo A, et al. A classification of atrial flutter and regular atrial tachycardia
according to electrophysiological mechanisms and anatomical bases: a Statement from a Joint Expert
Group from the Working Group of Arrhythmias of the European Society of Cardiology and North
American Society of Pacing and Electrophysiology. Eur Heart J 2001;22(14):116282.
12. Saoudi N, Nair M, Abdelazziz A, et al. Electrocardiographic patterns and results of radiofrequency
catheter ablation of clockwise type I atrial flutter. J Cardiovasc Electrophysiol 1996;7(10):93142.
13. Cheng J, Scheinman MM. Acceleration of typical atrial flutter due to double-wave reentry induced by
programmed electrical stimulation. Circulation 1998;97(16):158996.
14. Cheng J, Cabeen WR Jr, Scheinman MM. Right atrial flutter due to lower loop reentry: mechanism and
anatomic substrates. Circulation 1999;99(13):170005.
15. Waldo AL, Helnthorn RW, Plumb VJ. Atrial flutter: Recent observations in man. In Joseph ME,
Wellens HJJ, eds. Tachycardias: Mechanisms, Diagnosis, Treatment. Philadelphia: Lea & Febiger,
1982:11335.
16. Atrial fibrillation: Current understandings and research imperatives. The National Heart Lung and
Blood Institute Working Group on Atrial fibrillation. J Am Coll Cardiol 1993;22(7):18304.
17. Kannel WB, Abbott RD, Savage DD, et al. Epidemiologic features of chronic atrial fibrillation: the
Framingham study. N Engl J Med 1982;306(17):101822.
18. Diker E, Aydogdu S, Ozdemir M, et al. Prevalence and predictors of atrial fibrillation in rheumatic
valvular heart disease. Am J Cardiol 1996;77(1):968.
19. Moe GK. On the multiple wavelets hypothesis of atrial fibrillation. Arch Int Pharmacodyn 1962;
140:18088.
20. Allessie MA, Lammers WJEP, Bonke FIM, et al. Experimental evaluation of Moes multiple wavelet
hypothesis of atrial fibrillation. In: Zipes DP, Jalife J, eds. Cardiac Electrocardiography and Arrhythmias.
New York: Grune and Stratton, 1985:26575.
21. Gouaux JL, Ashman R. Auricular fibrillation with aberration simulating ventricular paroxysmal
tachycardia. Am Heart J 1947;34:36673.
22. Kopecky SL, Gersh BJ, McGoon MD, et al. The natural history of lone atrial fibrillation: A population
based study over three decades. N Engl J Med 1987;317(11):66974.
23. Ruder MA, Davis JC, Eldar M, et al. Clinical and electrophysiologic characterization of automatic
junctional tachycardia in adults. Circulation 1986;73(5):9307.
24. Krahn AD, Manfreda J, Tate RB, et al. The natural history of electrocardiographic pre-excitation in
men. The Manitoba Follow-up Study. Ann Intern Med 1992;116(6):45660.
25. Vidaillat HJ Jr, Pressley JC, Henke E, et al. Familial occurrence of accessory atrioventricular pathways
(pre-excitation syndrome). N Engl J Med 1987;317(2):659.
26. Lev M, Gibson S, Miller RA. Ebsteins disease with Wolff-Parkinson-White syndrome. Am Heart J
1955;49:724.
27. Gallagher JJ, Pritchett ELC, Sealy WC, et al. The preexcitation syndromes. Prog Cardiovasc Dis 1978;
20(4):285327.
28. Frank S, Braunwald E. Idiopathic hypertrophic subaortic stenosis: clinical analysis of 126 patients
with emphasis on the natural history. Circulation 1968;37(5):75988.
29. Bharati S, Bauernfeind R, Josephson M. Intermittent preexcitation and mesothelioma of atrioven-
tricular node: a hitherto undescribed entity. J Cardiovasc Electrophysiol 1995;6(10 Pt 1):82331.
30. Giardina ACV, Ehlers KH, Engle ME. Wolff-Parkinson-White syndrome in infants and children.
A long term follow-up. Br Heart J 1972;34(8):83946.
31. McClelland JH, Wang X, Beckman KJ, et al. Radiofrequency catheter ablation of right atriofascicular
(Mahaim) accessory pathways guided by accessory pathway activation potentials. Circulation 1994;89:
265566.
32. Murdock CJ, Leitch JW, Teo WS, et al. Characteristics of accessory pathways exhibiting decremental
conduction. Am J Cardiol 1991;67(6):50610.
33. Bogun F, Kalusche D, Li Y-G, et al. Septal Q waves in surface electrocardiographic lead V6 exclude
minimal ventricular preexcitation. Am J Cardiol 1999;84(1):1014, A9.
34. Xie B, Heald SC, Bashir Y, et al. Localization of accessory pathways from the 12-lead electrogram using
a new algorithm. Am J Cardiol 1994;74:161.
35. Campbell RW, Smith RA, Gallagher JJ, et al. Atrial fibrillation in the preexcitation syndrome. Am J
Cardiol 1977;40(4):51420.
ARRHYTHMIAS 657
36. Prystowsky EN, Miles WM, Heger JJ, et al. Preexcitation syndromes: mechanisms and management.
Med Clin North Am 1984;68(4):83193.
37. Kay GN, Pressley JC, Packer DL, et al. Value of the 12 lead electrocardiogram in discriminating
atrioventricular nodal reciprocating tachycardia from circus movement atrioventricular tachycardia
utilizing a retrograde accessory pathway. Am J Cardiol 1987;59(4):296300.
38. Packer DL, Gallagher JJ, Prystowsky EN. Physiologic substrate for antidromic reciprocating tachycardia.
39. Miles WM, Zipes DP. Atrioventricular reentry and variants: Mechanisms, Clinical features, and
Management. In: Zipes DP, Jalife J, eds. Cardiac Electrophysiology: From Cell to Bedside, 3rd ed.
Philadelphia: WB Saunders, 2000:63855.
40. Shih HT, Miles WM, Klein LS, et al. Multiple accessory pathways in the permanent form of junctional
reciprocating tachycardia. Am J Cardiol 1994;73(5):3617.
41. Langendorf R, Pick A, Winternitz M. Mechanism of intermittent ventricular bigeminy. I.
Appearance of ectopic beats dependent upon length of cycle, the rule of bigeminy. Circulation
1955;11:422.
42. Myerburg RJ, Kessler KM, Luceri RFM, et al. Classification of ventricular arrhythmias based on
parallel hierarchies of frequency and form. Am J Cardiol 1984;54(10):13558.
43. Scherf D, Cohen J. The Atrioventricular Node and Selected Cardiac Arrhythmias. Orlando: Grune &
Stratton, 1964.
44. Marriott HJL, Thorne DC. Dysrhythmic dilemmas in coronary care. Am J Cardiol 1971;27(3):32730.
45. Qi WH, Fineberg NS, Surawicz B. The timing of ventricular premature complexes initiating chronic
ventricular tachycardia. J Electrocardiol 1984;17:377.
46. Gomes JA, Alexopoulos D, Winters SL, et al. The role of silent ischemia, the arrhythmic substrate
and short-long sequence in the genesis of sudden cardia death. J Am Coll Cardiol 1989;14:
161825.
47. Fisch C. Electrocardioagraphy of Arrhythmias. Philadelphia: Lea & Febiger, 1990:131.
48. Kindwall KE, Brown J, Josephson ME. Electrocardiographic criteria for ventricular tachycardia in wide
complex left bundle branch block morphology tachycardia. Am J Cardiol 1988;61(15):127983.
49. Metzger JT, de Chillou C, Cheriex E, et al. Value of 12-lead electrocardiogram in arrhythmogenic right
ventricular dysplasia and absence of correlation with echocardiographic findings. Am J Cardiol 1993;72:
9647.
50. Wellens HJ, Bar FW, Lie KI. The value of the electrocardiogram in differential diagnosis of a tachycardia
with a wide QRS complex. Am J Med 1978;64:27.
51. Fontaine G. A new look at torasdes de pointes. Ann NY Acad Sci 1992;644:15777.
52. Makkar RR, Fromm BS, Steinman RT, et al. Female gender as a risk factor for torasdes de pointes
associated with cardiovascular drugs. JAMA 1993;270(21):25907.
53. Ludomirsky A, Klein HO, Sarelli P, et al. Q-T prolongation and polymorphous (torsades de pointes)
ventricular arrhythmias associated with organophosphorus insecticide poisoning. Am J Cardiol 1982;
49:1654.
54. Di Pasqale G, Pinelli G, Andreoli A, et al. Torsade de pointes and ventricular flutter-fibrillation fol-
lowing spontaneous cerebral subarachnoid hemorrhage. Int J Cardiol 1988;18(2):16372.
55. Pechter RA, Osborn LA. Polymorphic ventricular tachycardia secondary to hypothyroidism. Am J
Cardiol 1986;57(10):883.
56. Choue CW, Kim SG, Fisher JD, et al. Comparison of defibrillator therapy and other therapeutic
modalities for sustained ventricular tachycardia or ventricular fibrillation associated with coronary
artery disease. Am J Cardiol 1994;73(15):10759.
57. Weiss J, Stevenson WG. Narrow QRS ventricular tachycardia. Am Heart J 1986;112(4):8437.
58. Cohen HC, Gozo EG, Pick A. Ventricular tachycardia with narrow QRS complex (left posterior fas-
cicular tachycardia). Circulation 1972;45(5):103543.
59. Josephson ME, Horowitz LN, Waxman HL, et al. 12 lead electrocardiogram in localizing site of origin.
Circulation 1981;64(2):25772.
60. Zivin A, Goyal R, Daoud E, et al. Idiopathic left ventricular tachycardia with left and right bundle
branch block configurations. J Cardiovasc Electrophysiol 1997;8(4):4414.
61. Grimm W, Marchlinski FE. Accelerated idioventricular rhythm, bi-directional ventricular tachycardia.
In: Zipes DP, Jalife J, eds. Cardiac Electrophysiology: From Cell to Bedside. 2nd ed. Philadelphia,
WB Saunders, 1994:9206.
62. Lichstein E, Ribas-Meneelier C, Gupta PK, et al. Incidence and description of accelerated ventricular
rhythm complicating acute myocardial infarction. Am J Med 1975;58(2):1928.
63. Goldberg S, Greenspon AJ, Urban PL, et al. Reperfusion arrhythmia: a marker of restoration of antegrade
flow during intracoronary thrombosis for acute myocardial infarction. Am Heart J 1983;105:2632.
64. Massumi RA, Ali N. Accelerated isorhythmic ventricular rhythms. Am J Cardiol 1970;26(2):17085.
65. Schamroth L. Genesis and evolution of ectopic ventricular rhythms. Br Heart J 1966;28(2):24457.
66. Wever EF, Hauer RN, Oomen A, et al. Unfavorable outcome in patients with primary electrical disease
who survived an episode of ventricular fibrillation. Circulation 1993;88(3):10219.
67. Hallstorm A, Boutin P, Cobb L. Socioeconomic status and prediction of ventricular fibrillation survival.
Am J Public Health 1993;83(2):2458.
68. Akhtar M, Shenasa M, Jazayeri M, et al. Wide QRS complex tachycardia. Ann Intern Med 1988;
109(11):90512.
69. Waldo AL, Kaiser GA, Bowman FO Jr, et al. Etiology of the P-R interval in patients with endocardial
cushion defect. Circulation 1973;48(1):1926.
70. Lagendorf R, Cohen H, Gozo EG. Observations on second degree atrioventricular block, including new
criteria for the differential diagnosis between Type I and Type II block. Am J Cardiol 1972;29(1):1119.
71. Narula OS, Samet P. Wenckebach and Mobitz type II AV block due to block within His bundle and
bundle branches. Circulation 1970;41(6):94765.
72. Zipes DP. Second-degree atrioventricular block. Circulation 1979;60(3):46572.
73. Goble MM, Dick M II, McCune WJ, et al. Atrioventricular conduction in children of women with
systemic lupus erythematosus. Am J Cardiol 1993;71(1):948.
74. Scherlag BJ, Lazzara R, Helfant RH. Differentiation of A-V junctional rhythms. Circulation 1973;
48(2):30412.
BASIC INVESTIGATIONS
6B. RADIOLOGY OF THE HEART AND GREAT VESSELS

31. Introduction and evaluation of heart 661
32. The pulmonary vasculature 684
33. Cardiac calcification 693
34. Evaluation of extracardiac structures and chest X-ray in other views 701
CHAPTER 31
I NTRODUCTION AND
EVALUATION OF H EART
CARDIAC IMAGING EVALUATION OF CHEST

TECHNOLOGIES 661 ROENTGENOGRAM 663
TECHNICAL FACTS INVOLVED Cardiac Size, Contours, Borders,
IN CHEST ROENTGENOGRAM 662 Chambers, and Great Vessels 663
Cardiac Fluoroscopy 663 REFERENCES 682
CARDIAC IMAGING TECHNOLOGIES
The discovery of X-rays by Wilhelm Conrad Roentgen on 8 November 1895 revolu-

tionized the field of medical diagnosis.1 Soon after its discovery, Francis H Williams in
1896 first showed the importance of X-rays in cardiac imaging for determining the
heart size.2 Since then, chest roentgenogram has become a routine part of medical
workup. The development of new technologies such as echocardiogram, radio isotope
scanning, computed tomography (CT), and magnetic resonance imaging (MRI) have
once again revolutionized cardiac imaging which permits functional and anatomically
detailed examinations of the heart and great vessels that is not possible with plain X-ray
film. However in spite of these advances, the plain chest radiograph continues to be in
vogue (see Table 31.1).
Because it provides unique and valuable information about the structure and func-
tion of the heart and thoracic vessels.
Table 31.1 Present day usefulness of X-ray chest
Chest X-ray is useful for evaluation of:

1. Structure and function of the heart and great vessels
2. Valvular, myocardial, and pericardial calcification
3. Cardiac size and chambers enlargement
4. Pulmonary arterial and venous hypertension
5. Valvular heart disease, LV failure and pulmonary edema
6. Congenital heart disease
7. Evaluation, and monitoring in ICU of patients with cardiac disease, post-operative
cardiac surgery and implanted cardiovascular devices
662 BASIC INVESTIGATIONS: RADIOLOGY OF THE HEART AND GREAT VESSELS
It is readily available and relatively inexpensive even though with low sensitivity.
It presents an opportunity to identify subtle or overlooked cardiac pathology including
significant vascular and pericardial calcification, cardiac size, chamber enlargement and
evidence of pulmonary arterial or venous hypertension.
It often helps to confirm a clinical diagnosis of valvular heart disease, LV failure and
pulmonary edema.
In recent years, the bedside portable chest roentgenogram has gained special impor-
tance in the evaluation and monitoring of patients with cardiac disease in the intensive
care unit (ICU), including post operative cardiac patients and others with implanted
cardiovascular devices.3,4
TECHNICAL FACTS INVOLVED IN CHEST ROENTGENOGRAM
Conventional PA (frontal, posteroanterior) view of chest X-ray is taken with the sub-
ject erect and in full inspiration at a distance of 6 ft (or 72 inches) from the source of
X-rays (from X-ray tube to the film).
Distance: If the distance is 6 ft, as in bedside portable X-rays (distance is 40 inches)
cardiac shadow spuriously appears enlarged because of greater beam divergence.
Projection: Both PA (posteroanterior) and AP (anteroposterior) views cause car-
diac magnification, but this is greater for AP view. In PA view chest X-ray, the film
is in-front of the patient, while in AP view chest X-ray (as in bedside portable X-ray),
film is placed behind the patient, in which the heart is away from the film, X-ray
beam is more diverging and the cardiac shadow looks larger.
Position of the patient: The size looks bigger if X-ray is taken in supine position
as in bedside portable X-ray. Combination of a short focus, film distance and AP
projection cause greater magnification.
Degree of inspiration: Shallow inspiration makes the heart look bigger.
Strength of X-ray tube kilo voltage (kV): In conventional chest X-ray, low kV
(6080 kV) is used, which gives high contrast demonstrating lungs and bones well,
but penetrating the mediastinum poorly. In high kV (120150 kV) chest X-ray,
there is less contrast, but improves the visualization of mediastinum and hidden
areas of the lungs.
The diastolic image of the heart: The chest X-ray taken at random largely records
the diastolic image of the heart.
Radiation exposure to the patient in conventional PA view chest X-ray is 0.1 rad per
film.
Other views of X-ray chest evaluation are left lateral, right anterior oblique (RAO) and
left anterior oblique (LAO).
Chest X-ray in RAO projection is performed with the patient in a 45 oblique
relationship to the film cassette, i.e. right shoulder towards the film cassette.
Chest X-ray in LAO projection is performed with the patient in a 60 oblique rela-
tionship to the film cassette, i.e. left shoulder towards the film cassette.
INTRODUCTION AND EVALUATION OF HEART 663
Cardiac Fluoroscopy
It is used to assess the dynamic features of the heart, for the detection of cardiovascu-
lar calcification and for evaluation of valve prosthesis and pacemakers. However due to
significant radiation risk to patient and examiner, the cardiac fluoroscopy has gives its
way to more advanced and safe cardiac imaging modalities, such as echocardiogram.
EVALUATION OF CHEST ROENTGENOGRAM
The plain X-ray chest is usually evaluated in frontal projection (PA view) (see Fig. 31.1)
and should be systematically evaluated as follows for:
Cardiac size, borders, chambers, and great vessels
Cardiac contour
Pulmonary vasculature
Cardiac calcification
Extra-cardiac features such as pleura, trachea, domes of the diaphragm, fundus of
the stomach, bony abnormalities and position of the patient.
However, X-ray chest in other views such as left lateral, right anterior oblique (RAO) and
left anterior oblique (LAO) views are also helpful in the evaluation of cardiac disorders.
Cardiac Size, Contours, Borders, Chambers and Great Vessels

1. Cardiac Size
Direct measurement of heart size in plain film radiographs has become obsolete and is
only of historical importance as more accurate analysis of cardiac chamber dimensions
and volume can be made with other imaging techniques such as echocardiography, radio
isotope scanning, CT and MRI. However, the plain film radiographs are still a valuable
tool for identifying an enlarged heart that is abnormal. The heart size is assessed by:
i) Measuring the transverse diameter expressed as an absolute value or a cardio-thoracic
ratio.
ii) Measuring heart volume.
Aorta
Superior
vena cava Pulmonary artery

Right Right ventricle
atrium Left ventricle
Fig. 31.1 | Diagrammatic representation of cardiac silhouette in PA view.

TDh1
TDt
TDh2
Fig. 31.2 | Measurement of transverse diameter of

the heartsum of widest distance of the
Fig. 31.3 | Measurement of transverse diameter
of the thorax (TDt)measured above
right heart border from mid line (TDh1) the costophrenic angles.
and widest distance of the left heart
border from mid line (TDh2).
a) Transverse diameter of the heart: The maximum transverse diameter of the heart
is obtained by adding the widest distance of the right heart border from the midline
and left heart border to the midline (see Fig. 31.2).
The midline is drawn through mid point of the spine from the sternum to the
diaphragm.
The normal transverse diameter of the heart ranges from 10 cm (in a small thin indi-
vidual) to 16.5 cm (in a heavy tall person)5 with a mean of 15.5 cm in men and 15 cm
in women.
A measurement of 10% beyond these values is abnormal.
As the normal differences of transverse diameter in systole and diastole is 0.30.9 cm,
6
a change of 1.5 cm between the examinations is significant.

b) Cardiothoracic (CT) ratio: It is expressed as the ratio between the maximum
transverse diameter of the heart divided by the maximum transverse diameter of
the thorax.7 The maximum transverse diameter of the thorax is obtained above the
costophrenic angles (see Fig. 31.3).
The normal average CT ratio is:
0.50 in adults
0.50 in children
0.60 in neonates
0.57 in supine AP chest radiograph.
i) A normal heart may appear large because of small AP diameter due to:
Pectus excavatum (see Figs 31.4 and 31.5) or
Straight back syndrome.
ii) The heart may appear small
Even though it is enlarged due to the downward displacement of cardiac apex as in AR.
Fig. 31.4 | PA viewsuggestive of mild car- Fig. 31.5 | Lateral viewconfirms pectus excavatum
(arrows) and narrow AP diameter of the
diomegaly in pectus excavatum.
chest responsible for false cardiomegaly
in PA view.
Fig. 31.6 | Apparent small sized (tubular) heart in COPD (emphysema).

Because of a large AP diameter in COPD (see Fig. 31.6) or due to severe dorsal
kyphosis in elderly patients.
In Addison disease or anorexia nervosa due to the absence of brown fat.
c) Cardiac volume The heart volume can be calculated from the PA and lateral chest
radiographs by using the following formula:
1bd K M
V
a
where
V heart volume expressed in ml/m2 body surface area.
l long diameter of the heart measured from the junction of the right atrium and
superior vena cava to the apex of the heart in PA chest film.
b broad diameter of the heart (or short axis) in PA chest film which is equivalent to
b1 b2. b1 is the perpendicular from the right cardiophrenic angle to the long
b2
d
b1 I
Fig. 31.7 | Measurement of long (l) and broad (b) diameters

of the heartl: from the junction of right atrium
Fig. 31.8 | Depth (d) of the heartgreatest
width in lateral view.
and superior vena cava to the apex of the heart,
b: is a perpendicular from l to the right cardio-
phrenic angle (b1) and to the junction of left atrium
and main pulmonary artery (b2).
diameter and b2 is the perpendicular from the junction of the left atrium and
main pulmonary artery to the long diameter (see Fig. 31.7).
d depth of the heart (or the greatest width), which is measured in lateral view
(see Fig. 31.8).
K constant (0.4) for ellipsoid shape of the heart.
M magnification factor as both PA and AP views cause cardiac magnification.
a body surface area in square meters.
The normal calculated heart volume5,8 is:
550 ml/m2 body surface area in men and
500 ml/m2 body surface area in women.
The normal long diameter is 1015.5 cm with an average of 13 cm, which usually
increases in LV hypertrophy.
The normal broad diameter (short axis) is 711 cm with an average of 9 cm, which
may be increased in mitral stenosis even when the transverse diameter is normal.
The normal depth is 711 cm with an average of 9 cm, which is increased in real
cardiac enlargement as in mitral stenosis, but not in conditions such as sternal depres-
sion which may result in increase transverse diameter of the heart (see Table 31.2).
2. Cardiac Contour
Any significant deviation from the normal cardiovascular contour may serve as a clue
to the cardiovascular diseases.
i) A boot shaped heart, Coeur en sabot (Dutch peasants wooden shoe with
upturned toe) is characteristic of tetralogy of Fallot due to the right ventricular
enlargement (see Fig. 31.9).
Table 31.2 Evaluation of cardiac size
Features Normal values
1. Transverse diameter of heart (average) 15.5 cm in males

15 cm in females
2. Cardio-thoracic ratio 0.50
3. Cardiac volume 550 ml/m2 in males
500 ml/m2 in females
Fig. 31.9 | Boot shaped heart in tetralogy

of Fallot.
Fig. 31.10 | Globular shaped heart in Ebsteins anomaly.
MPA
LAE
Fig. 31.11 | An egg shaped cardiac

silhoutte in transposi-
Fig. 31.12 | Straightening of the left heart border (mitralization)
due to left atrial enlargement (LAE) and main pul-
tion of great arteries. monary artery (MPA) dilatation in mitral stenosis.
ii) A triangular or a large rounded (or globular) heart with a narrow pedicle is
diagnostic of Ebsteins anomaly (see Fig. 31.10).
iii) An egg shaped cardiac silhouette in transposition of great arteries (see Fig. 31.11).
iv) A straightening of left heart border (mitralization) due to left atrial enlarge-
ment together with main pulmonary artery dilatation is characteristic of mitral
stenosis with pulmonary hypertension (see Fig. 31.12).
RSVC LVV
Fig. 31.13 | Snow man appearance in total anomalous pul-

monary venous connectionRSVC: dilated right
Fig. 31.14 | Cottage loaf appearance in
total anomalous pulmonary
superior vena cava, LVV: dilated left vertical venous connection.
venous channel.
Fig. 31.15 | Unfolding of aorta (arrow). Fig. 31.16 | Fusiform aneurysm of aorta (arrow).
v) Snow man appearance or cottage loaf appearance in total anomalous pul-
monary venous connection (see Figs 31.13 and 31.14).
vi) A typical shelf-like configuration of the heart in LAO view is due to right
atrial enlargement.
vii) A bulge along with the cardiac border with a retrosternal double density is
diagnostic of left ventricular aneurysm.
viii) Unfolding of aortic arch is a feature of atherosclerosis or chronic hypertension
(see Fig. 31.15) and has to be differentiated from fusiform aneurysm of aorta
(see Fig. 31.16).
ix) A flask-like, globular silhouette or water bottle appearance with smooth and
featureless heart borders is due to pericardial effusion (see Fig. 31.17).
As the effusion extends to the pulmonary bifurcation, the hilar structures are
obscured, and in contrast to massive cardiomegaly, hilar vessels are not obscured.
Fig. 31.17 | Flask shaped heart in pericardial effusion.

Table 31.3 Abnormal cardiac contour
Features of cardiac contour Causes
1. Boot shaped heart Tetralogy of Fallot

2. Flask-like or water bottle appearance with a smooth Pericardial effusion
featureless cardiac border
3. Triangular or a large rounded heart with a narrow pedicle Ebsteins anomaly
4. Snow man or cottage loaf appearance Total anomalous pulmonary venous
connection
5. Egg shaped heart Transposition of great arteries
6. Mitralization of left heart border Mitral stenosis with PH
7. Shelf-like configuration of cardiac shadow Enlarged right atrium (in LAO view)
8. Retrosternal double density with a bulge along the Left ventricular aneurysm
cardiac border
9. Convex double density in the right portion of the Enlarged left atrium
cardiac silhouette
Normally, the subepicardial fat merges imperceptively with the mediastinal fat,
as the two fat planes are separated by only 2 mm thick stripe of the peri-
cardium. In pericardial effusion in lateral view, the retrosternal space is nar-
rowed or obliterated and subepicardial fat is displaced posteriorly, which may
be visible as a wide opaque vertical band between the anterior border of the
heart and mediastinum. This is known as epicardial fat pad sign, which is
highly specific for pericardial effusion (see Table 31.3).
3. Cardiac Borders, Chambers, and Great Vessels

The cardiac borders consist of right and left heart borders (see Figs 31.18 and 31.19).
a) Right heart border: It is formed by:
i) Superior vena cava (SVC): A faint slightly concave line of SVC descends from the
sternoclavicular region close to the shadow of the vertebral column and blends with
SC
AA
Az
A PA AAo PA
LB
S
LA
RA RA
LV RV LV
Fig. 31.18 | Borders of the heart-RA: right atrium,

S: superior vena cava, A: ascending
Fig. 31.19 | Borders of the heart with line
drawingAAo: ascending aorta,
aorta, Az: azygous vein, AA: aortic arch, RA: right atrium, PA: main pul-
PA: main pulmonary artery, LB: left monary artery, LV: left ventricle,
bronchus, LA: left atrium, LV: left ven- RV: right ventricle.
tricle, SC: subclavian artery.
Table 31.4 Cardiac borders in X-ray chestfrontal projection
Right heart border Left heart border
1. Superior vena cava (SVC) 1. Aortic knuckle

2. Right atrium 2. Main pulmonary artery
3. Ascending aorta and azygous vein 3. Left atrial appendage
when dilated 4. Left ventricular contour
5. Left subclavian artery when dilated
6. Persistent left SVC when present
upper right atrial convexity. The lateral border of the SVC normally lies within 1 cm of
the spine and in a good inspiratory film SVC can be clearly separated from the RA.
ii) Raigh atrium (RA): In frontal projection, RA forms a gentle convexity with the
adjacent right middle lobe (see Table 31.4). The superior border blends above with
SVC and inferior border blends below with IVC, meeting the diaphragm at a slightly
acute angle.
In left lateral view; it is not border forming, while it forms the posteroinferior
heart border and anterosuperior heart border in RAO and LAO views respectively
(see Table 31.5).
Right atrial enlargement (RAE) commonly occurs in valvular heart diseases and
Ebsteins anomaly (see Figs 31.20 and 31.21). Radiographically, RAE is considered:
When it bulges 5.5 cm to the right of the midline9 or
When RA border occupies 3 intercostal spaces
An enlarged RA may cause bulging of the right upper anterior border of the cardiac
shadow in LAO view and may produce a typical shelf-like configuration.
Table 31.5 Cardiac borders in X-ray chest in other views
Heart borders Lateral view RAO view LAO view
1. Anterior border
Above Anterior margin of MPA Right ventricular outflow Right atrium
and ascending aorta tract and MPA
Below Right ventricle Sinus portion of RV Right ventricle
2. Posterior border
Above Left atrium Right atrium Left atrium
Below Left ventricle Left atrium Left ventricle
3. Superior border Arch of aorta
MPA: main pulmonary artery.
RAE
Fig. 31.20 | RAE in Ebsteins anomaly RA is

5.5 cm to the right of midline.
Fig. 31.21 | RAE in valvular heart disease (arrow).
iii) Ascending aorta and azygous vein: Structures which are border forming but are
normally not visualized clearly in the frontal projection include ascending aorta and
azygous vein.
(a) Ascending aorta normally lies within the cardiac silhouette and is superimposed
on the SVC which forms a convex border above the RA.
The aortic valve and annulus, and coronary arteries are not visible as they lie
deep in the mediastinum.

After 40 yrs of age, ascending aorta may be elongated which may bulge laterally
beyond SVC. However, dilated ascenting aorta is more common in aortic

regurgitation and Marfan syndrome (see Figs 31.22 and 31.23).
The prominence of ascending aorta in 40 yrs of age is a good sign of aortic
aneurysm or post-stenotic dilatation (see Figs 31.2431.26).
(b) The azygous vein is an elliptical structure at the right tracheobronchial angle. It
ascends in the right paravertebral sulcus and arches forward over the right main
stem bronchus to enter the back of the SVC.
Normal-sized
aortic arch
Dilated
ascending
aorta
Large left
ventricle
Fig. 31.22 | Dilated ascending aorta and enlarged LV in aortic regurgitation (diagrammatic).
Fig. 31.23 | Dilated ascending aorta in a patient

with Marfan syndrome (arrows).
Fig. 31.24 | Aneurysm
in syphilis.
of ascending aorta (arrow)
Fig. 31.25 | Sacular aneurysm of aorta (arrow). Fig. 31.26 | Post stenotic dilatation of ascending
aorta in aortic stenosis (arrow).
Normally, it measures 0.71.0 cm in erect and 1.01.3 cm in the supine position.

The azygous vein and hemiazygous vein (its left sided equivalent) which receive
intercostal veins, become visible when it is enlarged in:
SVC and IVC obstruction
The absence of intrahepatic portion of IVC
Portal vein obstruction and
Both LVF and RVF. The dilatation of the azygous vein parallels the changes
in pulmonary venous pressure, which makes the azygous vein a useful guide
for the development of CHF.
iv) Right ventricle (RV)
(a) In frontal projection: Right ventricle is not border forming in frontal view
and cannot be directly visualized. Normally, right ventricle lies anteriorly and
is border forming in left lateral and oblique views. However, there are indirect
signs of right ventricular enlargement (RVE) in frontal projection also, which
include:
(i) Left ventricle is displaced posteriorly and to the left, pushing the left heart
border laterally and cardiac apex superiorly. (ii) Right atrium is pushed to the
right. (iii) With further RVE, left ventricle is rotated posteriorly and right ven-
tricle may form the cardiac apex.
This results in widening of the cardiac shadow (i.e. increasing TD of the heart),
increasing the broad diameter of the heart and left cardiophrenic angle becom-
ing more acute (see Fig. 31.27).
(b) In left lateral view, right ventricle is border forming in the subxiphoid region,
which usually extends superiorly to a point about 1/3rd of the distance between
the diaphragm and the suprasternal notch (see Fig. 31.28).
Ao
PA
RV LA
LV
Fig. 31.27 | Right ventricular enlargement in PA

viewthere is an increase in trans-
Fig. 31.28 | X-ray chest lateral view of a normal
individualRV: right ventricle, LV:
verse and broad diameters of the left ventricle, LA: left atrium, PA:
heart with an acute left cardiophrenic pulmonary artery, Ao: aorta, arrow
angle (arrow). indicates normal retrosternal space.
Fig. 31.29 | Right ventricular enlargement in lateral viewdilated RV encroaching upon

retrosternal space (white arrow) together with LAE (black arrows) in a
patient of mitral stenosis.
Table 31.6 Radiological signs of right ventricular enlargement in X-ray chest
In PA view Other views
1. Pushing of the left heart border laterally 1. Enlarged right ventricle encroaches upon the
retrosternal space in lateral view
2. Pushing of right atrium to the right 2. Increase of convexity of anterior border of the
cardiac silhouette in LAO and RAO views
3. Right ventricle may form the cardiac apex
4. Increase in transverse and broad diameters
of the heart
5. Cardiophrenic angle becomes more acute
As right ventricle enlarges, curvature of the anterior border increases, cardiac

shadow assumes a globular configuration encroaching upon the retrosternal
space (see Fig. 31.29).
However, the retrosternal space may also be obliterated in a patient with a small
AP diameter or pectus excavatum despite the absence of RVE.

(c) In RAO view, the anterior border of the heart is formed by the sinus portion of
the RV inferiorly and right ventricular outflow tract and main pulmonary artery
superiorly.10
(d) In LAO view, the anterior heart border is formed by right atrium above and right
ventricle below.
LAO view is a superior projection for the detection of RVE, which is character-
ized by an increase in the convexity of the anterior border of the cardiac silhou-
ette (see Table 31.6).
b) Left heart border: It is made up of four visible convex curves, which are as follows
from above downwards: aortic arch or knuckle, arc of main pulmonary artery, left atrial
appendage and the contour of the left ventricle.
RAA
Fig. 31.30 | Right aortic arch (RAA) with absent

aortic knuckle on left side (arrow).
Fig. 31.31 | Enlarged left superior intercostal vein
(arrow, nipple sign).
i) The arch of aorta: In PA view, the aortic arch is seen as a projection beyond the left
margin of the mediastinal shadow, which is known as aortic knuckle or knob. It repre-
sents the left posterolateral portion of the aortic arch with a diameter of 23 cm. At
the level of the aortic arch, the trachea is displaced slightly to the right.
Unfolding of aorta is the prominent aortic arch, which is wider and higher than
normal and may even reach the level of clavicle, with conspicuous ascending aorta
protruding further to the right than normal, and descending aorta appearing on the
left with a tortuous or serpentine configuration. It is seen in older individuals with
atherosclerosis, systemic hypertension or significant aortic regurgitation (see Fig. 31.15).
Right aortic arch: When a right aortic arch is present, the trachea is displaced
slightly to the left (instead of to the right) with absent aortic knuckle on the left
side11 (see Fig. 31.30).
Left superior intercostal vein: When this vein is enlarged and becomes prominent,
it is visible as a small bump or nipple on the aortic knob, measuring 23 mm in
diameter (see Fig. 31.31). This is often visualized due to the increased central venous
pressure or increased blood flow (similar to dilated azygous vein on the right side) as
in SVC syndrome, IVC obstruction or deep mediastinal venous obstruction. It is
also visualized in 410% of normal individuals.12
In coarctation of aorta, the engorged aortic knob and post-stenotic dilatation of
descending aorta may cause a 3 sign on the aorta and an E sign on the barium
filled esophagus, both depicting the site of coarctation13 (see Figs 31.32 and 31.33).
ii) Aorticopulmonary window: It is a variably sized concave indentation immedi-
ately below the aortic knuckle, which is bordered superiorly by the inferior margin of
the aortic arch and inferiorly by the upper margin of the left pulmonary artery.
It contains important anatomical structures which include left recurrent laryngeal
nerve, ligamentum or ductus arteriosus, and ductus node.
Enlargement of the ductus node or ligamentum arteriosus makes this concave space
into a convex bulge and left recurrent laryngeal nerve may be involved.
Fig. 31.32 | 3ascending

sign (upper left arrow) and dilated
aorta (right middle arrow)
Fig. 31.33 | Eesophagus
sign (arrows) on the barium filled
in lateral view in coarcta-
in coarctation of aorta. tion of aorta.
Fig. 31.34 | Normal main pulmonary artery (arrow).
iii) Main pulmonary artery: The left main pulmonary artery is located immediately
below the aorticopulmonary window, which is identified as a small to moderate-sized,
smoothly marginated arc (pulmonary arc) arching over the left main bronchus (see
Fig. 31.34).
When it is dilated, it forms a prominent outward bulge due to (see Table 31.7)
The increased pulmonary blood flow as a result of left-to-right shunts (as in ASD,
VSD, PDA)
Pulmonary valvular stenosis (i.e. poststenotic dilatation) (see Fig. 31.35)
Increased pulmonary artery pressure as in Eisenmengers physiology, or due to other
causes of pulmonary hypertension
Idiopathic pulmonary artery dilatation
And sometimes in Marfan syndrome (besides involving ascending aorta).
Table 31.7 Main pulmonary artery (MPA) abnormalities
MPA dilatation MPA hypoplasia
1. Left-to-right shunts 1. Transposition of great arteries

2. Valvular pulmonary stenosis 2. Truncus arteriosus
3. Pulmonary artery hypertension 3. Pulmonary atresia
4. Idiopathic dilatation 4. Tetralogy of Fallot
5. Marfan syndrome (rare cause)
Ao
Fig. 31.35 | Dilated main pulmonary artery

(arrow) in pulmonary stenosis.
Fig. 31.36 | Hypoplasia of main pulmonary artery
(arrow) in TOF with oligemic lung fields
but prominent ascending aorta (Ao).
Fig. 31.37 | Absence of triad of contours at the base in transposition of great arteries
giving rise to a narrow vascular pedicle.
Hypoplasia of pulmonary artery: The main pulmonary artery border may be flat or
not seen at all in transposition of great arteries, truncus artriosus, TOF, and pulmonary
atresia11 (see Figs 31.36 and 31.37).
iv) Left atrial appendage: It forms a smooth and slightly concave segment of the left
heart border located immediately below the left main bronchus and MPA (see Table 31.8).
Superior Aorta
Right Right ventricle

atrium Left ventricle
Fig. 31.38 | Enlarged left atrial appendage in mitral stenosis (diagrammatic).
Table 31.8 Radiological signs of left atrial enlargement in X-ray chest
1. Mitralization (straightening) of left heart border together with dilated main

pulmonary artery (as in mitral stenosis)
2. Elevation of left main bronchus, resulting in increase of carinal angle
3. Causes a convex shadow of double density in the right portion of cardiac
silhouette
4. Posterior displacement of barium filled esophagus in lateral and RAO views
Enlarged
pulmonary
trunk
Distended Splaying
pulmonary of carina
veins
Double shadow Enlarged

of left atrial left atrium
enlargement
Fig. 31.39 | Enlarged left atrium elevating the left main bronchus and forming a convex
shadow of double density within the right heart border (diagrammatic).
In lateral views, LA forms the superior aspect of the posterior heart border, which is
often obscured by the converging pulmonary veins (the posterior border of LA lies
immediately anterior to the pulmonary venous confluence).
In left atrial enlargement, left atrial appendage which forms the concave left heart
border is staightened (see Fig. 31.38) or bulges laterally elevating the left main bronchus
and increasing the carinal angle (normal carina angle is 75) (see Fig. 31. 39).
Enlarged left atrium also causes the straightening of the left heart border (mitral-
ization) together with dilated main pulmonary artery as in mitral stension (see
Fig. 31.40).
MPA
LAE
Fig. 31.40 | Enlarged LA causes straight-

ening of the left heart border
Fig. 31.41 | LAE forms convex double shadow (lower
straight white arrow) within enlarged the right
together with dilated main heart border (curved arrow). LA appendage
pulmonary artery (MPA). (upper straight arrow) bulges laterally.
Fig. 31.42 | LAE (Barium swallowlateral view)

causing posterior displacement of
Fig. 31.43 | LAE (Barium swallowRAO view)
causing posterior displacement
esophagus (arrow). of esophagus (arrow).
Conditions simulating enlargement of left atrial appendage include pericardial

fibroma or cyst, lymphoma, thymoma, mediastinal or pleural neoplasms.
Congenital absence of pericardium also causes the bulging of LA appendage.
Other radiological signs of LA enlargement include:
LA enlarges towards the right forming a convex shadow of double density, which may
be within the right heart border, at the right heart border, outside the right heart
border or at the right midclavicular line (see Fig. 31.41). The borders of the RA and LA
can be differentiated by tracing the inferior border of the RA which blends with the
IVC, while the left atrial shadow crosses the midline towards the left side of the heart.
Enlarged LA causes posterior displacement of barium filled esophagus in RAO
and lateral views (see Figs 31.42 and 31.43).
Aorta
Superior

Right ventricle
Right
atrium Enlarged left ventricle
Obtuse left CP angle
Fig. 31.44 | Left ventricular enlargement with increase in long and transverse diame-
ters of the heart and obtuse left cardiophrenic (CP) anglediagrammatic
representation in PA view.
Fig. 31.45 | LVE in PA view with increase transverse diameter and obtuse left car-
diophrenic angle (arrow).
v) The left ventricular border: Left ventricle forms the left heart border below the
left atrial appendage and forms a mildly convex border as it extends to the diaphragm.
However, the left ventricular border blends seamlessly with the left atrial appendage
without a specific landmark to differentiate between these two.
Left ventricle forms the posteroinferior heart border below the left atrium and just
above the diaphragm in left lateral and LAO views, while IVC forms the posterior
heart border in left lateral projection.
Radiological signs of left ventricular enlargement (LVE) are as follows:
In LVE, the left heart border is displaced laterally and the apex is displaced inferiorly
(downwards and outwards) widening the left cardiophrenic angle i.e. it becomes
more obtuse (while in RVE it is more acute).
Increase of long diameter of the heart (13 cm) besides increase in transverse diam-
eter of the heart in frontal projection (see Figs 31.44 and 31.45).
Elongation of left ventricular shadow, overlapping the spine and obliterates the
posteroinferior cardiophrenic recess in LAO and left lateral views (most specific
Fig. 31.46 | LVE in lateral viewenlarged LV

extending below the diaphragm
Fig. 31.47 | Left ventricular enlargement in lateral
view: enlarged left ventricle encroach-
(arrows) together with LAE. ing the spine and obliterating the pos-
terior cardiophrenic recess (arrows).
Table 31.9 Radiological signs of left ventricular enlargement in X-ray chest
PA view Oblique and lateral views
1. Left heart border is displaced 1. Overlapping of the spine and obliteration of

laterally and cardiac apex inferiorly posteroinferior cardiophrenic recess in LAO and
lateral views
2. Widening of left cardiophrenic angle 2. Extension of LV shadow posteriorly by 1.5 cm beyond
the outline of upper portion of IVC in lateral view,
i.e. Hoffman-Rigler sign
3. Increase in transverse and long 3. Posterior displacement of barium filled esophagus in
diameters of the heart lateral projection by enlarged left ventricle and
left atrium
radiological sign) (see Figs 31.46 and 31.47). However, this can also occur due to the
downward extension of markedly enlarged left atrium and moderate-severe pericardial
effusion.
In LVE, the left ventricle extends posteriorly 1.5 cm beyond the outline of
the upper portion of IVC, i.e. Hoffman-Rigler sign in left lateral view. A 2 cm verti-
cal line is drawn upwards along the IVC from the point where the posteroinferior
portion of left ventricle crosses IVC. The distance between the LV posterior border
and upward vertical is measured, which is normally 1.5 cm, while in LVE, it is usually
1.5 cm. However, Hoffman-Rigler sign can also be present in poor positioning
of the patient for lateral chest film or RV enlargement may displace left ventricle
posteriorly.14
In barium swallow with oblique views, normal left ventricle does not usually dis-
place the esophagus, but rather it overlaps or lies posterior and lateral to it. But
when both left atrium and left ventricle are enlarged, the barium filled esophagus is
pushed backwards in one long curve (see Table 31.9).
PA view:
1. Straightening of
LHB with dilated
Lateral and RAO
MPA
views:
2. Elevation of
1. Posterior
LMB carinal
displacement of Ba
PA view: angle
filled esophagus
1. >5.5 cm to the 3. Convex shadow of
right of midline double density within
2. Occupies 3 or outside RHB
ICS
RAE LAE
LAO view: PA view:
1. Right upper 1. TD and LD of the
anterior border Cardiac heart
of cardiac shadow chambers 2. Left CP angle >
2. Typical shelf obtuse
like configuration
RVE LVE
Other views:
1. Overlapping of spine
and obliteration of
posterior CP recess in
lateral and LAO views
PA view: Other views:
2. Extension of LV
1. TD and BD of 1. Encroaches
shadow posteriorly by
the heart retrosternal space
>1.5 cm (Hoffman-
2. Left CP angle > in lateral view
Rigler sign)
acute 2. In convexity of
anterior border of
cardiac silhouette in
LAO and RAO views
Fig. 31.48 | Radiological diagnosis of cardiac chambers enlargementRAE: right atrial enlargement, LAE:
left atrial enlargement, RVE: right ventricular enlargement, LVE: left ventricular enlargement,
ICS: intercostal spaces, Ba: barium, LHB: left heart border, RHB: right heart border, MPA: main
pulmonary artery, LMB: left main bronchus, TD: transverse diameter, BD: broad diameter, LD:
long diameter, CP: cardiophrenic, PA: posteroanterior, RAO: right anterior oblique, LAO: left
anterior oblique.
vi) Other structures forming left heart border

The left subclavian artery which extends from the clavicle to the aortic arch is bor-
der forming along the upper left portion, above the aortic arch. Though it forms a
concave border with the lung, not usually appreciated in frontal views, until it dilates
and bulges laterally in post-ductal coarctation of aorta or becomes tortuous because
of atherosclerosis or hypertension.
Persistent left SVC causes vertical or a smooth convex left supra-aortic border (see
Fig. 31.48).
REFERENCES
1. Roentgen WB. New Forms of Radiation. Wurzburg, Germany: Wurzburger Physical Medical Society;
December 18, 1895.
2. Williams FH. A method for more fully determining the outline of the heart by means of a fluoro-
scope together with other uses of this instrument in medicine. Boston Med Surg J 1896;135:
335337.
3. Henry DA. Radiologic evaluation of the patient after cardiac surgery. Radiol Clin North Am 1996;
34(1):119135.
4. Henschke C, Yankelevitz DF, Wand A, et al. Accuracy and efficiency of chest radiography in the
intensive care unit. Radiol Clin North Am 1996;34:2127.
5. Jefferson K, Rees S. Clinical Cardiac Radiology. 2nd ed. London, Butterworths, 1980.
6. Gammill SL, Krebs C, Meyers P, et al. Cardiac measurements in systole and diastole. Radiology
1970;94(1):115120.
7. Kabala JE, Wilde P. Measurement of heart size in the anteroposterior chest radiograph. Br J Radiol
1987;60(718):981986.
8. Keats TE, Enge IP. Cardiac mensuration by the cardiac volume method. Radiology 1965;85(5):
850855.
9. Stanford W, Galvin JR. The radiology of right heart dysfunction: Chest roentgenogram and com-
puted tomography. J Thorac Imag 1989;4(3):719.
10. Murphy MI, Blue LR, Ferris EJ, et al. Sensitivity and specificity of chest roentgenogram criteria for
right ventricular hypertrophy. Invest Radiol 1988;23(11):853856.
11. Steiner RM, Gross GW, Flicker S, et al. Congenital heart disease in adult patient: The value of plain
film chest radiology. J Thorac Imaging 1995;10(1):125.
12. Chasen MH, Charnsangave G. Venous chest anatomy: Clinical implications. Eur J Radiol 1998;
27(1):214.
13. Figley MM. Accessory roentgen signs of coarctation of aorta. Radiology 1954;62(5):671687.
14. Hoffman RB, Rigler LG. Evaluation of left ventricular enlargement in the lateral projection of the
chest. Radiology 1965;85:93100.
CHAPTER 32
THE PULMONARY VASCULATURE
1. NORMAL PULMONARY ii. Decreased PBF 687

VASCULARITY 684 iii. Abnormal PBF Patterns 687
2. ABNORMAL PULMONARY 3. PULMONARY INTERSTITIAL
VASCULARITY 685 EDEMA 690
i. Increased PBF 686 REFERENCES 692
Even though pulmonary vasculature is the most difficult portion to analyze because of its
complex nature and overlapping of interstitial, arterial and venous structures, the clear
visualization of the pulmonary blood vessels on the chest film helps in the assessment
and diagnosis of various cardiovascular disorders (see Fig. 32.1).
1. NORMAL PULMONARY VASCULARITY
The normal radiographic anatomy consists of:

i) The main pulmonary artery which bifurcates into left pulmonary artery (LPA)
and right pulmonary artery (RPA) within the mediastinum.
ii) The LPA then courses to the left and posteriorly and hence its borders are just vis-
ible above the middle of the left hilum. However in lateral projection, the LPA passes
over the left main stem (principal) bronchus and parallels the aortic arch.
iii) The RPA, which has a horizontal course within the mediastinum, divides into lobar
branches proximal to the right hilum. In lateral view, the RPA forms a round or
elliptical opacity anterior to the right main stem bronchus.
iv) The transverse diameter of right descending PA (RDPA), which is visualized
immediately above the origin of the right middle lobe branch, is 1015 mm with a
variation of 1 mm in males and 914 mm with a variation of 1 mm in females.
It is a useful parameter to judge the pulmonary blood flow1 (see Fig. 32.2).
v) There is a tree-like gradual branching of intrapulmonary arteries, which parallel
the bronchi, tapering gradually from the hilum towards the periphery of the lung.
The intrapulmonary arteries and bronchi (segmental bronchi) subtend the same
broncho-pulmonary segment and both are of approximately of the same diameter
with a ratio of 1.2:1.0 (artery: bronchus).2
THE PULMONARY VASCULATURE 685
RDPA
Fig. 32.1 | Normal pulmonary vas- Fig. 32.2 | Measurement of right descending
pulmonary artery (RDPA) to judge
culature.
pulmonary blood flow.
vi) The pulmonary veins course centrally in the interlobular septa and converge in
the posterior aspect of the LA 23 cm below the hila. Though the pulmonary veins
are larger than the arteries, they branch less frequently and are not related to the
broncho-arterial unit. The veins in the upper lobes are usually lateral to or super-
imposed on the pulmonary artery branches, and often it is difficult to distinguish
a vein from an artery.
vii) In outer third of the lungs, both pulmonary arteries and veins are too small to be
seen clearly on the chest x-rays. The normal ratio of the central (inner third) and
peripheral (outer third) arteries is 5:3 or 5:2. Normally, the diameter of the ves-
sels in the first anterior intercostal space below the first rib is 3 mm.
viii) In normal erect individuals, the upper zone vessels are smaller than in the lower
zones (bases). The normal ratio of caliber of the vessels between lower and upper
lung zones is 5:1 and is partly due to:
The effects of gravity (increased distribution of blood to the bases of the
lungs) and
Differential intraalveolar pressure (higher intraalveolar pressure in upper lung
zones than in the lower lung zones. The pressure difference between the apex
and the base of the lung is approximately 22 mmHg in normal adults in erect
position.3
ix) In supine and prone chest films, blood flow appears equal in both upper and lower
lung zones, even though it is the greatest in the dependent position or posterior
third of each lung which is better appreciated with axial CT imaging.
2. ABNORMAL PULMONARY VASCULARITY
It could be due to volume changes with normal pulmonary blood flow (PBF) pattern or
changes in distribution with abnormal PBF pattern (see Fig. 32.3).
i. Increased PBF
It occurs in left-to-right shunts, e.g. ASD, VSD, PDA; admixture lesions, e.g. TGA,
PAPVC TAPVC; increased cardiac output states, e.g. chronic anemia, AV fistula,
hyperthyroidism and pregnancy4 (see Figs 32.4 and 32.5).
The volume of PBF is proportional to the caliber of the pulmonary arteries with no
significant changes in pressure, resistance or flow pattern.
The right descending pulmonary artery is dilated and the artery/bronchus ratio is
greater than 1 especially in the outer third lung fields.
This phenomenon is also known as shunt vascularity, in which both upper and lower
lung zones receive increased blood flow with the change of ratio of PBF between
these two zones from normal 5:1 to 4:1 or 3:1.
However, in smaller left-to-right shunt of 1.8, abnormal pulmonary vascularity
may not be detected.
Fig. 32.3 | Dilated main pulmonary artery and its main branches.
MPA
Fig. 32.4 | Pulmonary plethora i.e. increased Fig. 32.5 | Pulmonary plethora i.e. increased pulmo-
nary flow (arrows) in transposition of great
pulmonary flow (arrows) with dilated
main pulmonary. arteries.
ii. Decreased PBF

When PBF is reduced due to pulmonary outflow tract obstruction (e.g. PS, pulmonary
atresia), or an intracardiac right-to-left shunt (e.g. TOF), pulmonary arteries and veins
are reduced in size (see Fig. 32.6).
The central vessels are narrow, and the artery/bronchus ratio is 1 with non-visible
peripheral vessels, but more radiolucent lungs.
Reduced PBF may be generalized as in TOF or Ebsteins anomaly (see Fig. 32.7), or
may be regional as a result of pulmonary embolism, emphysema, tumor invasion or
vasculitis.
In patients with markedly decreased PBF as in pulmonary atresia or chronic pul-
monary thrombo-embolism, collaterization occurs, i.e. small tortuous bronchial col-
lateral vessels, which arise from the descending aorta, develop in the upper medial
lung zones (see Table 32.1).
iii. Abnormal PBF Patterns

These reflect increased pulmonary vascular resistance, and could be due to pulmonary
arterial hypertension, AV fistula, development of collaterals and pulmonary venous
hypertension.
Fig. 32.6 | Oligemia i.e. decreased pul- Fig. 32.7 | Oligemic

anomaly.
lung fields in Ebsteins
monary blood flow in TOF.
Table 32.1 Abnormal pulmonary vascularity
Increased pulmonary vascularity Decreased pulmonary vascularity
1. ASD, VSD, PDA 1. Tetralogy of Fallot

2. Total anomalous pulmonary venous 2. Pulmonary atresia
connection and partial anomalous 3. Tricuspid atresia
pulmonary venous connection 4. Ebstein anomaly
3. Truncus arteriosus 5. TGA with pulmonary stenosis
4. Transposition of great arteries (TGA)
with VSD
Centralization
Due to pulmonary arterial hypertension, the central arteries including main pulmonary
artery, LPA, RPA and second order branching vessels are dilated, while the more distal
branches constrict, with decreased peripheral blood flow and more radiolucent lung
fields in the outer third. This phenomenon is known as centralization of pulmonary
vascularity (see Fig. 32.8).
It occurs in severe pulmonary arterial hypertension (primary or secondary),
Eisenmengers syndrome, COPD, or chronic recurrent pulmonary thrombo-
embolism (see Fig. 32.9).
Lateralization
Asymmetrical PBF due to unilateral decrease or absence of PBF occurs in patients
with pulmonary artery branch stenosis or atresia, hemitruncus, after creation of a
shunt (such as Blalock-Taussig, Waterston or Potts shunt).
Lateralization of PBF on the left side occurs in valvular pulmonary stenosis, in which
the blood flow through the stenotic valve is directed towards the LPA (see Fig. 32.10).
Similarly, preferential blood flow is often towards the left side in PDA, as the ductus
is oriented towards the origin of LPA in most of the patients.
The paucity of the pulmonary vascularity in the diseased lung with the obstructed
pulmonary artery is known as Westermark sign.
Localization
A localized abnormal PBF pattern can also occur e.g. congenital pulmonary arteriovenous
fistula in right lower lobe.
Fig. 32.8 | Dilated MPA (centralization) and Fig. 32.9 | Dilated central pulmonary arteries (C) while
peripheral pulmonary arteries (arrows) are
right descending pulmonary artery
(arrow heads). insignificant in Eisenmengers syndrome.
Fig. 32.10 | Lateralization of PBFprominent

left pulmonary artery in valvular
Fig. 32.11 | Cephalization of PBFprominent upper
lobe veins (Antler sign) (arrow) in mitral
pulmonary stenosis (curved arrow). stenosis.
Collateralization
Development of bronchial collateral vessels from the descending aorta in the upper
medial lung zones occurs in patients with markedly decreased PBF as in TOF with
pulmonary atresia.
Cephalization
Radiographically, cephalization or redistribution of PBF to the upper lobes is the earliest
sign of pulmonary venous hypertension (see Fig. 32.11). Radiological changes in the
pulmonary vascularity are useful in the estimation of pulmonary venous pressure.
When pulmonary venous pressure rises to 1318 mmHg (normal: 912 mmHg),
the pulmonary blood flow is redirected into the upper lobes in erect position and ante-
riorly in supine position, so the normal difference in size between the smaller upper
lobe and larger lower lobe vessels is reversed, i.e. a phenomenon of cephalization
occurs.5 A clue to the recognition of redistributed blood flow is the increased diameter of
blood vessels in the first intercostal space by 3 mm. The redistribution of PBF occurs
due to following mechanisms:5
The fluid leaks from the pulmonary veins into the interlobular spaces (interstitium)
with increase in the pulmonary venous pressure, first in the lower lobes because of the
gravitation effects. This fluid accumulation decreases the pulmonary compliance and
increases the interstitial pressure, which restricts the blood flow to the lower lobes.
Fluid accumulation also results in hypoxia, which causes arterial spasm and the basilar
vessels constrict significantly, forcing the blood to flow upward.
Cephalization usually occurs in three conditions:
(i) Left sided obstructive lesions: mitral stenosis, aortic stenosis
(ii) Left ventricular failure: due to CAD, cardiomyopathy and
(iii) Severe mitral regurgitation, even before pump failure of the left ventricle occurs
(see Table 32.2).
Table 32.2 Pulmonary vascularityAbnormal distribution
Abnormal pulmonary vascularity Causes
1. Centralization Pulmonary hypertension, Eisenmengers

syndrome; chronic recurrent pulmonary
thromboembolism
2. Localization Congenital pulmonary AV fistula
3. Lateralization Pulmonary artery branch stenosis or atresia,
hemitruncus; Blalock-Taussig, Waterston or
Potts shunt; valvular pulmonary stenosis
4. Cephalization Mitral stenosis, aortic stenosis, severe mitral
regurgitation, left ventricular failure
Both Lateralization and Localization

It occur in scimitar syndrome (gives a crescent like shadow in the right lower lung field
in partial anomalous pulmonary venous connection with hypoplasia of right lung and
dextroposition).
3. PULMONARY INTERSTITIAL EDEMA
With the elevation of pulmonary venous pressure above 18 mmHg, pulmonary

interstitial edema occurs which is characterized by distinct Kerley B lines (see Figs
32.12 and 32.13).
They are thickened interlobular septa, which appear as thin horizontal lines present
at both lung bases (costophrenic angles) perpendicular to the lateral pleural surface
in the frontal chest film.6
Kerley B lines can also occur in noncardiac diseases, such as sarcoidosis, interstitial
pnuemonitis, asbestosis and lymphatic spread of the tumor.
In long standing severe pulmonary venous hypertension as in severe mitral stenosis,
often Kerley A lines as well as pulmonary hemosiderosis are evident. Kerley A lines
are straight lines up to 4 cm running from the apex towards the hilum.
Pulmonary alveolar edema: With further elevation of pulmonary venous pressure
above 25 mmHg; leakage of fluid from the interstitial spaces into the pulmonary air
spaces occurs, which leads to alveolar edema.
Radiographically pulmonary alveolar edema is characterized by butterfly or batwing
appearance in the inner two thirds of the lungs, i.e. central perihilar in distribution7
(see Fig. 32.14). As outer 1/3rd of the lung is better aerated, has better pumping
effect due to more efficient lymphatic drainage and is more compliance than the
inner 1/3rd of the lung, the fluid concentrates preferentially in the central portion of
the lung.8
Prominence
of upper lobe
blood vessels
Enlarged hilar
Ground glass vessels
appearance of
alveolar edema
Enlarged cardiac
silhouette
Septal or
kerley B lines
Fig. 32.12 | Pulmonary interstitial and alveolar edema (Diagrammatic).
Fig. 32.13 | Pulmonary interstitial edema (arrow)

peribronchial cuffing and Kerley B
Fig. 32.14 | Pulmonary alveolar edema (batwing
appearance, arrows) with right pleural
lines (KB). effusion.
Asymmetrical pulmonary edema is usually due to morphological changes in the lung

parenchyma, e.g. emphysema, pulmonary thromboembolism, therapeutic irradiation.
An attempt has been made to distinguish cardiac pulmonary edema from non-cardiac
pulmonary edema from the x-ray chest film.
In cardiac pulmonary edema, the edema is perihilar in distribution with extension
to the cardiophrenic angles (pleural effusion), pulmonary vascular redistribution,
septal (Kerley) lines, and cardiomegaly. While in noncardiac etiology, the pul-
monary edema usually has a peripheral distribution with no cardiomegaly, no septal
lines and pleural effusion.9 In fluid overload, the alveolar edema may be perihilar,
but cardiophrenic angles are spared.
Besides, the pulmonary capillary wedge pressure (PCWP) is usually 18 mmHg,
and edema fluid/serum protein ratio is 0.5 in cardiac pulmonary edema, while
PCWP is 18 mmHg, and edema fluid/serum protein ratio is 0.7 in non-cardiac
pulmonary edema.10
REFERENCES
1. Chang CH. The normal roentgenographic measurement of the right descending artery in 1085 cases.
Am J Roentgenol 1962;87:929.
2. Woodring JH. Pulmonary artery-bronchus ratio in patients with normal lungs, pulmonary vascular
plethora, and congestive heart failure. Radiology 1991;179(1):115122.
3. Chen JTT. Essentials of Cardiac Roentgenology. Boston: Little Brown, 1987.
4. Baron MG. Plain film diagnosis of common cardiac anomalies in the adult. Radiol Ciln North Am
1999;37(2):401420.
5. Sharma S, Bhargava A, Krishnakumar R, et al. Can pulmonary venous hypertension be graded by the
chest radiography? Clin Radiol 1998;53(12):899902.
6. Kerley PJ. Radiology in heart disease. BMJ 1933;2:594.
7. Fleischner FG. The butterfly pattern of acute pulmonary edema. Am J Cardiol 1967;20(1):3946.
8. Milne ENC, Pistolesi M. Reading the Chest Radiograph: a physiologic approach. St. Louis. Mosby-
Year Book, 1993:950.
9. Morgan P, Goldman L. Pulmonary edema and acute respiratory distress syndrome. Radiol Clin North
Am 1991;29(5):943963.
10. Sibbald WJ, Cunningham DR, Chin DN. Non-cardiac or cardiac pulmonary edema? A Practical
approach to clinical differentiation in critically ill patients. Chest 1983;84(4):452461.
CHAPTER 33
CARDIAC CALCIFICATION
VALVULAR CALCIFICATION 693 ii) Left Atrial Calcification 696

i) Mitral Valve Calcification 695 VASCULAR CALCIFICATION 697
ii) Aortic Valve Calcification 695 i) Calcification of the Aorta 697
iii) Calcification of the Pulmonary ii) Calcification of the Pulmonary
Valve 695 Artery 698
iv) Calcification of the Tricuspid iii) Coronary Artery Calcification 698
Valve 695 PERICARDIAL CALCIFICATION 699
MYOCARDIAL CALCIFICATION 696 TUMOR CALCIFICATION 700
i) Left Ventricular Calcification 696 REFERENCES 700
The cardiac calcification is mostly dystrophic and occasionally metastatic. The dys-
trophic calcification usually occurs in dead or degenerative tissue with normal levels
of serum calcium. The cardiac calcification is detected by chest roentgenography,
especially in lateral views. The cardiac calcification could be:
Valvular calcification
Myocardial calcification
Vascular calcification and
Pericardial calcification.
VALVULAR CALCIFICATION
Radiographically, visible calcium within a cardiac valve suggests the presence of hemo-
dynamically significant stenosis. The calcification of the left sided valves is common,
while right sided valvular calcification is uncommon. Calcified valves can be visualized
in PA, lateral and LAO views. However, they are best seen fluoroscopically.
Radiological identification of valvular calcification

A line drawn on the lateral chest film from the anterior costophrenic angle through
the hilum to the lung apex will separate the anterosuperior calcified aortic valve
from the posteroinferior calcified mitral valve (see Fig. 33.1).
Divide the heart into six portions on the lateral view film: aortic valve is identified in
the upper middle row, while the mitral valve is visible in the lower posterior row.
In PA view chest film, aortic valve occupies a more cranial position, close to the
spine, while the mitral valve is lower and some what more laterally to the left.
AV
45
MV
Fig. 33.1 | Calcified aortic valve (white arrowhead)
lies anterosuperior to the line drawn from
anterior costophrenic angle through hilum
to the lung apex in lateral chest film, while
Fig. 33.2 | Identification of valvular calcification
in PA view or fluoroscopyAV: aortic
calcified mitral valve (black arrowheads)
valve, MV: mitral valve.
is posteroinferior to this line.
AV
MV
Fig. 33.3 | Identification

valve.
of valvular calcification in LAO viewAV: aortic valve, MV: mitral
In PA view or in fluoroscopic examination with patient turned 15 to the left and an
imaginary line drawn from the junction between left atrial appendage and left ven-
tricle (i.e. point of opposing movement in fluoroscopy) on the left side border down-
wards to the patients right at an angle of 45. The linear calcified aortic valve is
situated just above this line while crescent calcified mitral valve is just below and left
of this line (see Fig. 33.2).1
In LAO view calcified aortic valve is best seen, which lies at the intersection of a
vertical line through the center of the heart shadow and a horizontal line through
the top of the left ventricular arc, while the calcified mitral valve occupies posterior
third of the heart shadow at a lower level (see Fig. 33.3).1
CARDIAC CALCIFICATION 695
Fig. 33.4 | Mitral valve calcification in PA

view (black arrowheads).
Fig. 33.5 | Aortic annulus calcification
(arrows) in lateral view.
i) Mitral Valve Calcification

It is usually due to rheumatic valvulitis and senile degeneration (see Fig. 33.4).
In rheumatic valvulitis, the calcification appears as clump-like or linear, measuring
about 24 cm in diameter. It is more common in mitral stenosis, and posterior valve
leaflet is more commonly involved, which may extend to the adjacent posterior
ventricular wall.
Mitral annular calcification is seen in individuals older than 40 years as a wavy, O-,
J-, or C-shaped opacity especially in women, and rarely causes any hemodynamic
disturbances.
ii) Aortic Valve Calcification

It occurs in rheumatic valvulitis, congenital bicuspid aortic valve, senile degeneration
(older than 65 years), syphilis, ankylosing spondylitis and following bacterial endo-
carditis. Only first three causes stenosis.
A thick irregular semilunar ring-like calcification with a central bar or knob is
typical of a calcified stenotic bicuspid aortic valve, which is found in 65% of
patients with congenital aortic stenosis.
Aortic annular calcification is typical of degenerative process in elderly individual
and may extend into the descending aorta and interventricular septum (see Fig. 33.5).
iii) Calcification of the Pulmonary Valve

It occasionally occurs in severe valvular PS with gradients 80 mmHg or in long
standing severe pulmonary hypertension.
iv) Calcification of the Tricuspid Valve

It is unusual and rheumatic valvulitis is the most common of all the causes. Tricuspid
annular calcification is rare and usually occurs in long standing valvular pulmonary
stenosis, ASD or RV hypertension (see Table 33.1).
Table 33.1 Valvular calcification
Structure involved Causes
1. Mitral valve Rheumatic mitral stenosis

2. Mitral annulus Elderly female
3. Aortic valve Aortic stenosis: rheumatic, congenital, senile
4. Pulmonary valve Severe valvular pulmonary stenosis (rheumatic or
congenital), chronic severe pulmonary hypertension
5. Tricuspid valve Rheumatic tricuspid stenosis
6. Tricuspid annulus Chronic valvular pulmonary stenosis, atrial septal defect,
right ventricular hypertension
Fig. 33.6 | Myocardial calcification due to left ventricular aneurysm (arrows).
MYOCARDIAL CALCIFICATION
The dystrophic calcification usually occurs in LV wall and LA.
i) Left Ventricular Calcification

Myocardial calcification is most frequently due to left ventricular aneurysms as a
result of large myocardial infarction, and occurs in 8% of the infarcts of more than
6 years old2 (see Fig. 33.6). It is localized to the apical and anterolateral aspects of
the left ventricular wall. It is usually curvilinear and is located within the periphery
of the infarct or aneurysm.
Myocardial calcification can also occur in chronic renal failure and following cardiac
trauma, especially involving the anterior wall of the right ventricle.3
ii) Left Atrial Calcification

It is usually due to rheumatic carditis and is associated with mitral stenosis or regurgitation.
Table 33.2 Myocardial calcification
Site of calcification Causes
1. Left ventricle Left ventricular aneurysm, chronic renal failure, cardiac

trauma
2. Left atrium Rheumatic carditis, organized thrombus, myxoma
Fig. 33.7 | Ascending aorta calcification (arrow).
Left atrial calcification is usually thin and curvilinear and forms a shell around the
circumference of the chamber or is confined to the left atrial appendage.4
Less often, calcification of an organized thrombus within left atrium adherent to the
chamber wall can occur (see Table 33.2).
VASCULAR CALCIFICATION
Calcification of the aorta and coronary arteries is common and is always associated
with atherosclerosis, although not correlated with its severity.
i) Calcification of the Aorta

It is commonly due to atherosclerosis. But it can also occur in syphilis, sinus of Valsalva
aneurysm, Takayasu arteritis, and calcified ductus arteriosus.5
In atherosclerosis, calcification usually occurs in the region of the arch in individuals
older than 50 years. It is identified as a thin curvilinear opacity near the lateral border
of the arch. However, when calcification is located deep to the aortic border, aortic
dissection may be present.
In syphilis, calcification of the ascending aorta occurs and is often associated with
aortic regurgitation6 (see Fig. 33.7).
ii) Calcification of the Pulmonary Artery

The origin of the main pulmonary artery occasionally calcifies following right ventricu-
lar outflow tract (RVOT) surgery for total correction of TOF. Calcification of the main
pulmonary artery can also occur in severe long standing pulmonary hyperension.7
iii) Coronary Artery Calcification

The chest film though relatively inexpensive, has low sensitivity for identification of
coronary artery calcification when compared with other imaging modalities like fluo-
roscopy, CT, especially the electron beam or ultrafast CT (EBCT).8 Visualization of
the coronary arteries in plain chest film is severely limited by superimposed structures,
low contrast resolution and motion.
A calcified left anterior descending coronary artery is seen as a double line of calci-
fication along the anterior border of the heart in lateral view (see Fig. 33.8).
The left main coronary artery (LMCA) and its proximal branches may be visible just
below the left main stem bronchus at the left of left atrial appendage in PA chest film.
Fluoroscopy had 82% accuracy in the detection of significant coronary artery disease,9
while EBCT is 85100% sensitive for the detection of significant coronary artery
stenosis10,11 (see Table 33.3).
Fig. 33.8 | Coronary artery calcificationcalcification of left anterior descending (arrow

heads) and left circumflex (arrows) arteries in lateral view.
Table 33.3 Vascular calcification
Site of calcification Causes
1. Aorta Atherosclerosis
Syphilis
Takayasu arteritis
2. Pulmonary artery Long standing pulmonary hypertension, post corrective
surgery for tetralogy of Fallot
3. Coronary arteries (left anterior Atherosclerosis
descending, left main coronary artery)
PERICARDIAL CALCIFICATION
Pericardial calcification is secondary to the organized blood or exudate in the pericardium,

and is most often associated with previous inflammation or blunt trauma.12 The com-
mon causes are:
Viral infection especially Coxsackie or influenza A and B
Granulomatous disease: TB, histoplasmosis
Hemopericardium following trauma
Autoimmune disease: SLE, Rheumatic heart disease
Constrictive pericarditis: Calcification is present up to 50%,12 especially as a result
of tubercular pericarditis.
Occasionally, intrapericardial teratomas and cysts calcify.
Pericardial calcification is most abundant along the RA and RV borders, and in the AV
groove (see Figs 33.9 and 33.10). It is usually best visualized in lateral view (see Fig.
33.11). Pericardium over the LV is usually free of calcification because of its vigorous
Fig. 33.9 | Pericardial calcification in PA

view (arrow).
Fig. 33.10 | Pericardial calcification in atrioventricular
groove in lateral view (arrow).
Fig. 33.11 | Pericardial calcification in LAO view (arrow).

Table 33.4 Pericardial calcification
Pathogenesis Causes
1. Inflammation (pericarditis) Granulomatous: tuberculosis, histoplasmosis

Viral: Coxsackie, influenza A and B
Autoimmune: systemic lupus erythematosis, and Rheumatic fever
2. Cardiac trauma Hemopericardium
3. Constrictive pericarditis Tubercular etiology
4. Intrapericardial tumors Teratomas
pulsations. As pericardium is absent behind the LA, calcification rarely occurs along
the LA border. In contrast, myocardial calcification is usually localized to the LV and
rarely seen over the RA or RV (see Table 33.4).
TUMOR CALCIFICATION
About 10% of the LA myxomas calcify, which may appear as a speckled pattern or
a round clump of calcium mimicking mitral annular or valve calcification.13
REFERENCES
1. Sosman MC. Roentgenogical aspect of acquired valvular heart disease. Am J Roentgenol 1939;43:47.
2. Lasser A. Calcification of the myocardium. Hum Pathol 1983;14(9):824826.
3. Jing J, Kawashima A, Sickler K, et al. Metastatic cardiac calcification in a patient with chronic renal
failure undergoing hemodialysis: Radiographic and CT findings. AJR Am J Roentgenol 1996;170(4):
903905.
4. Leonard JJ, Katz S, Nelson D. Calcification of the left atrium: its anatomic location, diagnostic
significance and roentgenologic demonstration. N Eng J Med 1957;256(14):629633.
5. Rubin GD. Helical CT angiography of the thoracic aorta. J Thorac Imaging 1997;12(2):118149.
6. Chen JTT. The significance of cardiac calcifications. Appl Radiol 1992;21:1119.
7. Roberts HC, Kauczor HU, Schweden F, et al. Spiral CT of pulmonary hypertension and chronic
thromboembolism. J Thorac Imaging 1997;12(2):118127.
8. Stanford W, Thompson BH. Imaging of coronary artery calcification: its importance in assessing
atherosclerotic disease. Radiol Clin North Am 1999;37(2):257272.
9. Aldrich RF, Brenski JF, Battaglini JW, et al. Coronary calcification in the detection of coronary
artery disease and comparison with electrocardiographic exercise testing. Circulation 1979;59(6):
113124.
10. Broderick LS, Shemesh J, Wilensky RL, et al. Measurement of coronary artery calcium with dual
slic helical CT compared with coronary angiography, evaluation of CT scoring methods, inter-
observer variations and reproducibility. Am J Roentgenol 1990;167:439.
11. Mautner GC, Mautner SL, Froehlich J, et al. Coronary artery calcification: Assessment with
electron beam CT and histomorphometric correlation. Radiology 1994;192(3):619623.
12. McComb BL, Steiner RM. Pericardial disease. In: Goodman I, Putman C, eds. Critical Care Imaging,
3rd ed. Philadelphia, WB Saunders, 1992.
13. Raynen K. Cardiac myxomas. N Eng J Med 1995;33(24):16101617.
CHAPTER 34
EVALUATION OFE XTRACARDIAC
STRUCTURES AND C HEST X- RAY
IN OTHER V IEWS
EVALUATION OF EXTRACARDIAC EVALUATION OF CHEST X-RAY IN

STRUCTURES 701 OTHER VIEWS 704
1. Bronchi and Sinuses 701 1. Chest X-ray in Left Lateral
2. Situs 701 Projection 705
3. Pleura 701 2. Chest X-ray in RAO View 706
4. Bones and Joints 703 3. Chest X-ray in LAO View 706
5. Soft Tissues Over the Chest 704 REFERENCES 707
EVALUATION OF EXTRACARDIAC STRUCTURES
1. Bronchi and Sinuses

A combination of bronchiectasis, sinusitis (from X-ray PNS) and dextrocardia is
known as Kartageners syndrome.1 Dextrocardia is the presence of right sided heart.
2. Situs
When both abdominal viscera and atria are in normal position, it is known as situs solitus.
Radiographically, situs solitus is identified by visualization of both aortic knuckle and
fundus of the stomach on the left side (see Figs 34.1 and 34.2). However, the presence
of longer and narrow left bronchus on the left side is more accurate of the presence
of situs solitus, while in situs inversus it lies on the right side (see Fig. 34.3).
In dextrocardia with situs solitus, the fundus of the stomach and aortic knuckle
remains on the left side with right sided heart (see Figs 34.4 and 34.5).
In dextrocardia with situs inversus, the fundus of the stomach and aortic knuckle lie
on the right side with right sided heart (see Figs 34.6 and 34.7).
3. Pleura
A right sided pleural effusion is often present with left heart failure.
702 BASIC INVESTIGATION: RADIOLOGY OF THE HEART AND GREAT VESSELS
Right Left
Descending
aorta
Apex
Liver
Fundus Liver Stomach
Fig. 34.1 | Chest X-ray PA viewnormal position and Fig. 34.2 | Normal position and situs solitus
(Diagrammatic).
situs solitus with liver on the right side and
fundus of the stomach on the left side.
LB RB
RB LB
Situs solitus
Situs inversus
Fig. 34.3 | Determination of situs from bronchus morphologypresence of left bronchus

which is longer and narrow on the right side indicates situs inversus.
Right Left
AK
Descending
aorta
Apex
S
L
Stomach
Liver
Fig. 34.4 | Dextrocardia with situs solitusright sided heart

with fundus of the stomach (S) and aortic knuckle Fig. 34.5 | Dextrocardia with situs solitus
(Diagrammatic).
(AK) on the left side and liver (L) on the right side.
EVALUATION OF EXTRACARDIAC STRUCTURES 703
Right Left
AK
AAo Descending
PT aorta
DAo
Apex
Apex
Stomach Liver
S L
Fig. 34.6 | Dextrocardia with situs inversusDAo:

Fig. 34.7 | Dextrocardia with situs
inversus (Diagrammatic).
descending aorta, PT: pulmonary trunk,
L: liver, S: fundus of the stomach, AK:
aortic knuckle, AAo: ascending aorta.
Fig. 34.8 | Vanishing tumor (arrow) in congestive heart failure.

Congestive heart failure may be associated with a pseudo-tumor or vanishing
tumor due to interlobar collection of pleural fluid (see Fig. 34.8). As CHF improves,
the tumor disappears.
4. Bones and Joints

Notching of the ribs is the erosion of lower borders of the ribs, which can occur due to
enlarged intercostal arteries, veins or nerves.
i) Commonest cause of notching of ribs is coarctation of aorta, in which case it is
known as Docks sign.2 It is due to dynamic dilatation and tortuosity of the posterior
intercostal arteries.
Notching is bilateral between 3rd and 8th posterior ribs, when coarctation is located
distal to the left subclavian artery (usual position) (see Figs 34.9 and 34.10).
Fig. 34.9 | Notching of the inferior margins of posterior Fig. 34.10 | Notching of the ribs (arrows,
magnified view).
ribs (arrows)PA view in coarctation of aorta.
Table 34.1 Evaluation of extracardiac structures
Features Structures to be examined or etiology
1. Situs Fundus of the stomach, left main bronchus

2. Pleural effusion Right sided: in left heart failure
Bilateral: in severe congestive heart failure (CHF)
3. Vanishing tumor CHF
4. Notching of the ribs Coarctation of aorta, superior vena caval syndrome,
intercostal neurofibromatosis
Unilateral rib notching is present only on the right side when coarctation narrows
the orifice of the left subclavian artery and collaterals fail to develop on the left side.
The rib notching in anomalous origin of right subclavian artery distal to coarctation
is unilateral (only on the left side) as collaterals fail to develop on the right side.
If rib notching occurs, in abdominal coarctation of aorta, it is confined to lower ribs
only.
ii) Superior vena caval syndrome also causes rib notching of venous origin.
iii) Neurofibromatosis can also produce rib notching by the intercostal neurofibromas.
5. Soft Tissues Over the Chest

Severe edema in the soft tissue over the chest occurs as a part of anasarca in patients
with renal failure (see Table 34.1).
EVALUATION OF CHEST X-RAY IN OTHER VIEWS
Structures of the heart which cannot be evaluated in frontal view of chest X-ray can be
evaluated in the left lateral, RAO and LAO views.
Aorta
Ao Pulmonary
artery
PA
Left atrium
RV LA Left
ventricle
LV Right
ventricle
Posteroinferior
cardiophrenic
recess
Fig. 34.11 | Chest X-ray lateral view in a normal individual-
black arrow: retrosternal space, white arrow:
posteroinferior cardiophrenic recess.
Fig. 34.12 | Chest X-ray lateral view
(Normal and diagrammatic).
1. Chest X-ray in Left Lateral Projection

i) The Anterior Border
The anterior border is formed by right ventricle in the subxiphoid region extending
superiorly to a point about 1/3rd of the distance between the diaphragm and the
suprasternal notch. The enlarged right ventricle may obliterate the retrosternal space
(see Figs 34.11 and 34.12).
The normal right atrium is not border forming in this projection.
Anterior margin of main pulmonary artery and ascending aorta lie above the right
ventricle; but due to abundant mediastinal fat, these structures are not clearly visu-
alized in a normal person. In patients with severe emphysema, main pulmonary
artery and ascending aorta may be well outlined.
ii) The Arch of Aorta

It is clearly outlined superiorly.
Inferior margin of the posterior aortic arch is often visible posteriorly.
Also, the superior margin of left pulmonary artery is visualized in the semilunar
lucency of the aorticopulmonary window.
The descending aorta is not usually visible clearly as it lies adjacent to the spine and in
the posterior mediastinal fat. However, descending aorta may be better visualized in
the patients with tortuous or calcified aorta.
iii) Posterior Border

The upper posterior border is formed by the left atrium, which appears as a shallow
convex bulge and is anterior to the pulmonary venous confluence.
The posteroinferior heart border just above the diaphragm is formed by the left ven-
tricle, which appears as a long convex bulge.
Aorta
Superior vena cava
Pulmonary artery
Left atrium
Right atrium
Right ventricle
Left
ventricle
Fig. 34.14 | Chest X-ray RAO view (Normal and dia-

Fig. 34.13 | Chest X-ray RAO view. grammatic).
iv) Lateral Projection

It is also useful for the identification of valvular calcification. Barium filled esopha-
gus can be used for the visualization of enlarged left atrium and left ventricle.
2. Chest X-ray in RAO View

Chest X-ray in RAO view is performed with the patient in a 45 oblique relationship to
the film cassette, i.e. right shoulder towards the film cassette (see Figs 34.13 and 34.14).
i) The Anterior Border of the Heart
It is formed by the sinus portion of the right ventricle inferiorly, and RVOT and main
pulmonary superiorly.3
ii) The Posterior Border
It is formed by right atrium superiorly and left atrium inferiorly. RAO view is usu-
ally used for the evaluation of left atrial enlargement.
iii) This View Permits
The optimal visualization of a calcified mitral or tricuspid valve.
The aortic arch is foreshortened in this projection, so the aortic arch and proximal
descending aorta are often superimposed and not visualized.
3. Chest X-ray in LAO View

Chest X-ray in LAO view is performed with the patient in a 60 oblique relationship
to the film cassette, i.e. left shoulder towards the film cassette.
i) The Anterior Border of the Heart

It is formed by right atrium above and right ventricle below.
This view is superior for detecting right ventricular enlargement, which is character-
ized by an increase in the convexity of the anterior border of the cardiac silhouette.
Aortic triangle
Aorta
Aortic window
Pulmonary artery
Right atrium
Left atrium
Left ventricle
Right ventricle
Fig. 34.15 | Chest X-ray LAO view.
Fig. 34.16 | Chest X-ray LAO view (Normal and diagrammatic).

An enlarged right atrium may cause bulging of the right upper anterior border of
the cardiac shadow and may produce a typical shelf-like configuration.
ii) The Posterior Border

It is formed by left atrium superiorly and left ventricle inferiorly.
This view is useful for diagnosing the presence of left ventricular enlargement.
The enlarged left ventricle overlaps the spine, and posteroinferior cardiophrenic
recess may be obliterated
iii) Visualization of Other Structures in LAO View

The aortic and pulmonary valves are in profile in this view, so that aortic and pul-
monary valve calcifications can be visualized (see Figs 34.15 and 34.16).
The aorta and pulmonary artery are seen as two arches one above the other separated
by a lucent subaortic window, in which trachea and left bronchus can be outlined.
The aortic arch is also in profile in this projection, so that the abnormalities of the
arch, including dissection, aneurysm and coarctation can be detected especially with
angiography.
The ventricular septum is also in profile in this LAO view, hence septal defects and
right and left ventricular functions can be evaluated with angiography.
REFERENCES
1. Elliott LP, Jue KL, Amplatz K. A roentgen classification of cardiac malpositions. Invest Radiol 1966;
1(1):1728.
2. Dock W. Erosion of ribs in coarctation of aorta. A note into the history of a pathognomic sign. BHJ
1948;10:148.
3. Murphy ML, Blue LR, Ferris EF, et al. Sensitivity and specificity of chest roentgenogram criteria for
right ventricular hypertrophy. Invest Radiol 1988;23(11):853856.
I NDEX
A rhythm 232, t232 CTI dependent 591

Arrhythmias 580, see also individual irregularly irregular 233 non CTI dependent 592
arrhythmias regularly irregular 232 paroxysmal 592
Arterial pulse 225, f226 radial pulse synchronicity 245 persistent 592
absent or delayed femoral pulse 245, volume 244, t244 type I 592
f246 hyperkinetic pulse 245 type II 592
character 233, t235 pulsus magnus 245 Atrial infarction 544, f545
anacrotic pulse 236, f236 pulsus parvus 244, t244 diagnostic criteria 544
bisferiens pulse 236, f237 wave pattern 226, t227 Atrial tachycardia 587, t588
dicrotic pulse 238, f238 in ascending aorta 226, f227 focal 587, f588, t588
pulsus alternans 239, f239 in peripheral artery 226, f227 MAT 589, f589, t589
compound 239 Arterial supply of the heart 34, f35, t34 premature atrial contractions 586,
partial 239 divergent coronary anatomy 38 f587, t588
total 239 LCA 34 Auscultation 354
pulsus bigeminus 238, f239 coronary angiogram f36, f36 characteristics of cardiac sounds 355
Brokenbrough sign 239 LAD 35 factors affecting 355
pulsus paradoxus 240, t241 LCx 35 frequency 355, t356
mechanism 241, f242, f243 measurements 39, t39 human acoustic acuity 354, t355
reversed 244, t244 RCA 37 dynamic auscultation 361, see also
total 244, t244 AV nodal branch 34 dynamic auscultation
pulsus tardus 233, f234 conus artery 34 examination 358
water hammer pulse 234, f234, f235 coronary angiogram f36 identification of systole and
condition of the vessel wall 245 PDA 34 diastole 359
definition 225 PLV 34 methods 359
examination 228 RA branch 37 Levine and Harveys inching 359
brachial 228, f229 RV branch 37 selective listening 359
carotid 228, f229 SA nodal branch 34 posture of the patient 360, f360, f361
dorsalis pedis 229, f230 Atrial arrhythmias 586, f598 principles 354, 355
femoral 229, f229 Atrial fibrillation 593 stethoscope 356, f357
popliteal 229, f230 classification 591, f593, t593 bell 356, f357
posterior tibial 229, f230 chronic or permanent 597 binaural 358
radial 228, f228 coarse 596, f597 diaphragm 357, f357
genesis 225 discernible 596 tubing 357, f357
peripheral signs of aortic fine 596, f597 technique 354
regurgitation 246 paroxysmal 596 topographical sites 358, f359
abdomen 248 persistent 596 AV junctional area 47, 50
BP 247 ECG 595 AV junctional arrhythmias 598,
eyes 247 Ashmans phenomenon 595, f596 f599, f600
head and neck 247 lone atrial fibrillation 596 AV junctional escape beats 598,
lower limb 248 rule of bigeminy 524 f599, t601
pulse 246 etiology 594, t596 ECG 599
upper limb 247 incidence 593 mechanism 598
rate 231 mechanism 594, f595 AV junctional premature beats 600,
bradyarrhythmias 232 Atrial flutter 589, f590, t591 f601, t601
bradycardia 231 etiology 591 AV junctional rhythm 599, f600
pulse deficit 232 incidence 591 AV junctional tachycardia 601, t603
tachyarrhythmias 231 types 591, t593, f593 focal 601, f602
tachycardia 231 chronic 592 non paroxysmal 602, f603
Note: f indicates figures and t indicates tables.

INDEX 709
AV nodal reciprocating tachycardia Pickwickian syndrome t169 sternoclavicular area 310, t311
(AVNRT) 603, t605 Under weight 169 palpation 316, f317
atypical 605 waist circumference 163 aortic area 326, f327
common features 605, f606 short stature 165 sounds 326
etiology and characteristics t605 causes 166, t166 thrills 327, f327, t328
pathophysiology 603, f604 Ellis van Creveld syndrome t166, apex f317, 318
types and mechanism f606 f167 absent 318
typical 604, f604 Noonan syndrome t166 character 318, t307
AV node 50 tall stature 163 heaving t318, f319, 320, 331
AN region 50 homocystinuria 163, t164 hyperdynamic t318, 319,
N region 50 Klinefelters syndrome 163, f163, f319, 331
NH region 50 t164 OS 321, t321
Marfan syndrome 163, f163, t193 pericardial knock 320
B Turner syndrome f191, t191 pericardial rub 322
Basic electrophysiological principles 66 Bundle branches 51, f52 S1 321
action potentials 67 blood supply 51, t52 S3 320, t320
extracardiac ion concentration t66 LBB 51 S4 320, t320
in Purkinje fibers 69 RBB 51 site and extent 318
in SA node 69 Bundle of His 51 sounds 316, t321
intracardiac ion concentration t66 distal 51 thrills 316, t328
mechanism of automaticity 70 middle 51 tumor plop 321
origin and sequence of cardiac proximal 51 ectopic areas 328
activation 71 in PDA 329
atrial depolarization 71 C LA 329
atrial repolarization 71 Cardiac cycle 77, t77 LV 328
decremental conduction 71 atrial diastole 81 RA 329
ventricular depolariztion 71 atrial systole 81 epigastrium 328, f329
ventricular repolarization 71 correlations f78, f80 left parasternal area 322
phases 67, f68, t68 ECG changes 82 grading 323, f324, t324
transmembrane potentials t67 ventricular diastole 79 in MR 324, f325
Biventricular hypertrophy 513, f514 ventricular systole 78 lift 322, f324
features of LVH 513 Cardiac imaging 661 sounds 326
LA abnormality 513 fluoroscopy 663 lower left sternal area 326
Blood pressure (arterial) 249 introduction 661 sounds 326
component 249, t249 technical facts 662 thrills 326, t328
definition 249 technologies t661 pulmonary area 326, f327
determinants 250 usefulness of X ray chest t661 sounds 327
measurements 250 Cardiac tamponade 126, f126, 564, f564 thrills 327, t328
ambulatory BP monitoring 261, t262 Cardinal symptoms 85, t86 sternoclavicular areas 328
continuous non invasive BP importance of history taking 85 Chest 299, f301
monitoring 260, f261 Cardiovascular pulsations 306 Inspection 299, f301
direct 250 Inspection 306, f307 abnormalities 300, t301, f301, f302
flush method 260 aortic area 310, t310 breast abnormalities 303, t303, f304
indirect 251 apical 306, t307 cutaneous lesions 303
auscultatory 252, f252 absent 308, t308 distended vessels 304, f304
in special circumstances 256 displacement 308, t309 shape 300, f301
lower limb 256, f257 double 308 palpation 315
palpatory 251 extent 309 distended vessels 316
upper limb 247, f256 lateral retraction 308 shape 316
variable BP recordings 257, t257 normal 307, t307 Chest pain 87
self monitoring 261 ectopic areas 313 aggravating and relieving factors 98
ultrasound Doppler method 260 beneath the left clavicle 314 associated symptoms 100, t101
Build and stature 162 LA 314 causes 87, f87
build 166 LV 314 character and mode of onset 93
BMI 162 RA 314 definitive typical anginal pain 101
Cushing syndrome t164 epigastric 312, t313, f313 differential diagnosis t88
indices 162 aortic 313 duration 89, f89
Laurence Moon Biedle syndrome cardiac 313 functional classification 98
t169 hepatic 313 linked angina 99
obese 166 left parasternal 311, f311, t312 location 90, f91
over weight 168 pulmonary area 310, t310 noncardiac chest pain 101
710 INDEX
Chest pain (contd.) D effects on murmurs 413

patient gestures 100, f100 Diastolic murmur 431, t431, f433 pharmacological effects 420
radiation 90 classification 432 amyl nitrate inhalation 420
Chest roentgenogram 662, see X-ray chest EDM 432, f432 effects on heart sounds 420
Conduction system of heart 47, f48, t48 AR 433 effects on murmurs 420
Conjunctiva 177 causes 433 postural changes 415
conjunctivitis 178 functional PR 434 knee elbow position 417
pallor 200 late or presystolic 440 left lateral recumbent position 417
petechiae 177, f178 causes 440, f441 effects on heart sounds 417
suffusion 177 complete heart block 441 effects on murmurs 417
Constrictive pericarditis 387, f388, MS 440 sitting up and leaning forward 417
565, f565 TS 441 effects on heart sounds 417
Continuous murmur 441, f444, t444 MDM 435, f435 effects on murmurs 417
causes 442 Austin flint murmur 439 squatting 416, f416
ALCAPA 445 causes 436, t436 effects on heart sounds 416
AV fistula 446 increased flow across AV valves 438 effects on murmurs 416
bronchial collaterals 445 MS 440, f441, t442 sudden lying down 415
coronary cameral fistula 446 organic PR 440, f441 effects on heart sounds 415
left-to-right shunt with MV TS 441 effects on murmurs 415
obstruction 446 pandiastolic or holodiastolc 435 sudden standing 416
localized arterial obstruction 443 Digits 200, t203 types of bed side maneuver 412
mammary souffl 449, f449, t449 arachnodactyly 200, f201 Valsalva maneuver 413, f414
PDA 444, f444, t444, t445 brachydactyly 202 effects on heart sounds 414
RSOV 445 broad thumbs and toes 202, f203, effects on murmurs 414
venous hum 448, f448, t449 t203 phases 414
venous shunts 442 clench hand 203
portosystemic shunts 446, f447 clindactyly 201, f201 E
TAPVC 446 fingerized thumbs 202, f202 Ears 185, t186
Cornea 178 phocomelia 203, f204 cauliflower ears 186, f186
arcus juvenalis 178, f179 polydactyly 201, f201 deafness 187
arcus senilis 179, f179 Raynauds phenomenon 204 ear lobe crease 185, f186
clouding 179 sclerodactyly 204, f204 low set ears 186, f187, t186
Cyanosis 147, t152 single thumb like digit 202, t202 Electrocardiogram 474
central 148 syndactyly 201, f201 effect of heart position 484, t485
associations 149, f149 Digitalis 568, f569 clockwise rotation 486, f486, t485
differentiation from pulmonary effects 568 counter clockwise rotation 486,
causes 153, t154 mechanism 572 f486, t485
etiology 149, f150 therapeutic 568, f570, f571 horizontal heart 485
O2 saturation 149 toxic 569, f571, f572, t572 intermediate heart 485
pathogenesis 150, f151 unequivocal toxic effects 571, f571, vertical heart 485
site 149 f572 electrical axis 485
types t152, 148 Dynamic auscultation 361, t411 hexaxial reference system 481, f481
definition 147 changes in cardiac cycle length 418 method of determination 482
evaluation 156, f156 effects on heart sounds 419 classical 483, f483
age of appearance 156 effects on murmurs 419, f419 equiphasic 482, f482
aggravating factors 157 isometric exercise 417 simplified 484
associations 157 effects on heart sounds 418 normal 484
distribution 157 effects on murmurs 418 intervals 479, f480, t481
relieving factors 157 methods 417, f418 LAD 484
squatting 158 physiological response 418 PP 479
squatting equivalents 158, f158 Muller maneuver 415 PR 479
methemoglobinemia 153 effects on heart sounds 415 QRS 479
diagnosis 155 effects on murmurs 415 QT 479
etiology 154, t155 methoxamine and phenylephrine 421 QU 479
normal physiology 153 effects on heart sounds 421 RAD 484
presentation 154 effects on murmurs 421 RR 479
treatment 155 methods 421 VAT 480, f481
mixed 153 physiological response 421 normal 486
peripheral 148 normal respiration 412 normal variants 487, f487
etiology 148 effects on heart sounds 412 anxiety 489
INDEX 711
children 486, f487, t487 unipolar esophageal leads 470, genu valgum 211, f212
deep respiration 489 f471 pes cavus 210, f210
early repolarization 487, f488, t488 unipolar intracardiac leads 471 rocker bottom foot 210, f211
hyperventilation 489 unipolar limb leads 468, f469 Fibrous skeleton of heart 16, f16, t16
infants 486, t487 transmission factors 464, t465 components and attachments 16
juvenile pattern 487 cardiac 464 fibrous rings 16
postprandial 489 cellular 464 left fibrous trigone 17
P 474, t475 extra cardiac 464 right fibrous trigone 17
abnormal P 490, f491 physical 465 extensions 17
biatrial 494, f495, t495 Extracardiac sounds 402 Frank Starling Law of heart 75
dextrocardia 491, f491 mediastinal crunch 404
left atrial abnormality 491, f492, pacemaker sounds 403 G
t492, f493 pericardial rub 403, f404 Gestures and signs 170, f171, t171
right atrial abnormality 493, causes 403 Gowers sign 170, f171
f493, t492 clinical recognition 403, f404 Levines sign 170, f171
waves 474 components 403, f404 Gums 189
Q 476, t476 mechanism of production 403 cyanosis 189
R 476 Extremities 200 hypertrophy 189, f190
S 477 Eyes 176
segments 480 enophthalmos 177 H
PR 480 exophthalmos 176, f175 Heart 3
ST 481 hypertelorism 176, f187, t177 gross anatomy 3
T 477, t478 nystagmus 177 external features 4, f5, f6
abnormal T 495, t495 Eye lids 177 borders 6
flat 496 lid lag 177 chambers 5 see also individual
inversion with ST changes 496 ptosis 177, f178 chambers 7
inversion without ST changes 497 Kearn-sayre syndrome 177, t178, crux 4
tall T 495, f495 f177 sulci 4
U 478, t478 Klippel Feil syndrome 177, t177 surfaces 4
abnormal U 497, t497 xanthelasma 177, f178 location 3
inverted 497, f498 size 3
prominent 497, f498 F weight in females 3
Electrocardiography 459 Facial appearance 172, t172 weight in males 3
Electrophysiology of the heart 461 ape like 174 Heart blocks 644
see also basic electrophysiology butterfly rash 173, f174 1st degree AV block 645, f649
of heart dull expressionless face 173, f173 2nd degree AV block 647, t649
action potentials 464, f465 elfin facies 175 type I 647, f649
cardiac activation 464 expression of fright and anxiety 174, type II 650, f651
origin 464 f175 complete AV block 652, t652
sequence 464 facial dysmorphism 172, f172 acquired 652, f653
electrical activity 461 facial edema 172 congenital 652, f653
depolarization 461, f462 facial flushing 174 ECG recognition 652
repolariztion 463, f463 grotesque facial features 175 types and characteristics f655
resting cell 461, f462 malar rash 173, f174 Heart murmurs 404 see also
electrocardiographic grid 472 mid facial growth deficiency 176 individual murmurs
extracellular ion concentration 463 mongoloid facies 175, f172 characteristics 406
history 459, t459 moon face 174, f175 configuration 410
intracellular ion concentration 463 Fascicular blocks 523, f524, 525 intensity 409
instrument 466 bifascicular 528 length 406
radio ampliflier 466 RBBB with LAFB 528, f528 location 407
string galvanometer 466 RBBB with LPFB 529, f529 pitch 410
introduction 459 LAFB 524, f525, t525 timing 406
methods of recording t466 Warner criteria 526 transmission 411
precautions 472, t473 LPFB 526, f526, t527 definition 404
recording electrodes and leads 466 WHO/ISFC criteria 527 factors for production 406
bipolar chest 467 multifascicular 527 functional with thrill 409, t410
bipolar limb 467, f467 trifascicular 530, f530 mechanism of production 404, f405,
monitor leads 470, f471 Fatigue 119, f119 t405
relationship between bipolar and Feet 210 classification 406
unipolar limb leads 468, f469 bow legs 210, f211 continuous 441
712 INDEX
Heart murmurs (contd.) evaluation 144 position of the patient 274, f275
diastolic 431 Hoarseness 146 which JVP? 272, f273, t273
systolic 422 causes 146, t147 Vs carotid pulsations 273, t273
Heart sounds 361, f362 Hypercalcemia 576, f576 history 271, t272
S1 362 Hyperkalemia 572, f573, f574, t574 introduction 271
characteristics 363, t363 modifications by other electrolytes 573 diseased conditions 288
determinants 364, t364 Hypermagnesemia 578, f578 acyanotic CHD 291
evaluation 366, f367 Hypertension 262 ASD 291
decreased intensity 368, t369 causes 262, t263 VSD 292, f292
increased intensity 366, t369 classification t263 arrhythmias 288
split 369 complications 267 conduction defects 288
variable 368, t369 definition 262 cardiomyopathy 294
S2 369 mechanism 265, f266, t265 dilated t294
abnormal splitting 369, f369 Hypocalcemia 577, f577, t578 EMF t294
narrow 373, f373 Hypokalemia 574, f575, t576 restrictive t294
persistent 373 modifications by other electrolytes 575 cyanotic CHD 292
reversed 375, f376, f377, t378 Hypomagnesemia 578 Eisenmenger syndrome 292, f292
types 375 PS with intact IVS and right-to-left
wide 374, f375 I shunt 293
wide and fixed 375, f375, t372 Iris 179 TAPVC 293
characteristics 370, t370 Brush fields spots 179, f180 TGA 293, f293
hang out interval 371 CHARGE syndrome t180 TOF 292, f293
normal split 371, f372 coloboma 180, f180 TOF like physiology 292
mechanism 371 tricuspid atresia 293
intensity 379 J pericardial disease t294, 295
determinants 379 Joints 212 cardiac tamponade t294, f295
diminished A2 380, t379 arthritis 213 constrictive pericarditis f294,
diminished P2 380, t379 Jaccords arthritis 213 t294, 295
loud A2 379, t379 gouty arthritis 215, f215 valvular lesions 289
loud P2 380, t379 migrating polyarthritis 213 AR 290, f291
evaluation 381, f381 polychondritis 213 AS 290, f290
AR 381 rheumatoid arthritis 213, f213 MR 289, f290
AS 381 lax joints 212, f213 MS 289, f289
ASD 381 Jugular venous pressure 283 PS 291
biscuspid aortic valve 382 measurement 283, 284, f284 TR 290
cyanotic CHD 383 elevated 285, f285, t285 TS 289
MR 381 normal 284, f284
MS 381 Jugular venous pulse 271 K
PDA 382 analysis 275, t276, f275 Kinetic cardiogram 330
PS 382 a wave 275 apical impulse 330
single S2 377, t378 abnormal a 277, t278 cardiomyopathy 331
VSD 381 absent 278, f279 constrictive pericarditis 332
S3 383, f383 giant 278, f279 double 331, f332
causes 385, t385 prominent 277, f278 hyperdynamic 331, f331
characteristics 383, t383 c wave 276 normal 330, f330
pathological 384 h wave 277 RV hyperkinetic 331
physiological 384 v wave 276 RV sustained 331
clinical recognition 387 abnormal v 279, t280 sustained 331, f332
mechanism of production 384 diminished 280
prerequisites 384 prominent 279, f280 L
theories 384 prominent v and a 280, f280 Left atrium 12, t12
S4 388, f382, f388 x descent 276 development t12
causes 389, t391 abnormal x descent 279, t279 external features 13
characteristics 388 absent 279 shape 13
clinical recognition 390 prominent 279, f279 site 13
mechanism of production 388 y descent 277 internal features 13
prerequisites 389 abnormal y descent 281 fossa lunata 13
theories 389 rapid 281, f281 muscular pectinati 13
Hemoptysis 144, f145 slow 281, f281 pulmonary veins 13
etiology 144 examination 272 LBBB 520, f521
INDEX 713
incomplete 523 cuspal 21 grades 206

WHO/ISFC criteria 522, f522 commissural 21 profile sign 207, f208
Left ventricle 13 types 23 Schamroth window test 207, f208
development t14 closure 21 unidigital 210
external features 13 phases 21 unilateral 209
shape 13 leaflets 20 cyanosis 205
site 13 AML 20 dysplastic 205, f206
internal features 13, f14 commissures 26 koilonychias 205, 206
apical portion 16 PML 20 plummers nail 205
free wall 14 surfaces 20 splinter hemorrhages 206, f207
inflow tract 14 papillary muscles 21 square 205, f206
outflow tract 14 anterolateral 21 strips 205
ventricular septum 14 posteromedial 21 tuft erythema 205, f206
development t14 Molecular basis of muscle contraction 73 Narrow QRS tachycardia 622
Left ventricular hypertrophy 500 muscular contraction 73, f74 differential diagnosis t623, f625
diastolic overload 501, f503 muscular relaxation 74, f75 effects of vagal stimulation f626
diagnostic ECG criteria 502, f503 sliding filament theory 74 irregular 622
Cornell product 505 Myocardial calcification 696, f696, t697 P wave morphology f624
Cornell voltage 505 LA 696 regular 622
Glassglow scoring system 504 LV 696 response to IV adenosine f625
Hernandez Padial 505 Myocardial infarction 533 Neck 190, t191
Koito and Spodick 506 diagnosis in BBB 552, f552 low hair line 191, t191
natural history series 505 LBBB 553, f553, f554, t554 lymphadenopathy 192
Novacode 505 RBBB 552, f552 parotid enlargement 192, f192
Romhilt Estes point score diagnosis during RV pacing 554, f555 short neck 190
system 504 anterior MI 554 thyromegaly 192, f192
Seigels 505 inferior MI 554 webbed neck 191, f191
Sokolow-Lyon 503 ECG changes 533 Nerve supply of heart 40, t40, f42
Sokolow-Lyon grading 504 abnormal Q 534 baroreceptors 43, t44, f45
Talbot 506 abnormal R 534 arterial 45
ECG changes 500, f501 QT dispersion 540 carotid 44
axis 501 ST changes 535 cardiac plexus 40, f41
others 501 T changes 538 deep 41
QRS complex 501 U changes 540 superficial 40
ST-T 501 evolution of ECG changes 540 chemoreceptors 43
in LAFB 507, f507 localization 542 aortic bodies 46
in LBBB 506, f508 anterior MI 535, f536s carotid bodies 46
in RBBB 507, f508 anterolateral MI 535, f537 parasympathetic fibers 43
systolic overload 501, f502 anteroseptal MI 535, f537 peculiarities t41
Lens 181 inferior MI 536, f538 sympathetic fibers 43
premature cataracts 181, f181 posterior MI 538, f539 vasomotor center 45, f44
subluxation 181, f182 posteroinferior MI f539 Nose 185, t186
Lips 187 prognostic value of ECG 555 broad 185, f185
absent philtrum 187, f188 prediction of coronary artery occlusion thin beaked 185, t186
capillary pulsations 187 545
cyanosis 187 ECG correlation 546 O
pallor 187 LAD occlusion 546, 547, f549 Opening snap 321, 392, f394
rhagades 187, f188 LCx occlusion 546, f547 A2-OS interval 393, f394
thick 187 RCA occlusion 546, 547, f547 factors affecting 393
Lymphatic system of heart 28, f29 sensitivity of ECG 555 absent 395
left coronary channel 28 Myocardial ischemia 541, f542 causes 393, f394
main supracardiac channel 29 ECG changes 541 characteristics 392, t392
right lymphatic duct 30 non specific ST-T changes 542 clinical recognition 395
right coronary channel 28 Myocarditis 565, f566 mechanism of production 393
prerequisites 393
M N theory 393
Mitral valve 18, f18, t19, f19 Nails 205 Oral cavity 187
annulus 18 capillary pulsations 206 mucous membrane 188
development 18, t19 clubbing 206, 207, 208 petechiae 177, f178
chordae tendinae 21 causes 208 telangectasia 188
714 INDEX
P Precordial findings 338 Argyll Robertson pupil 181

Palate 189 AR 342, f343, t342 Pulmonary vasculature 684
cleft 189, f190 AS 341, f342, t341 abnormal 685, t687, t690
high arched 190 ASD 343, f344, t343 centralization 688, f688
Palpitation 112 cardiomyopathy 351, t352 cephalization 689, f689
associated symptoms 118, t118 DCM 352 collateralization 689, f610
character 116 HCM 352 decreased PBF 687, f687
definition 112 restrictive 352 increased PBF 686, f686
duration and frequency 114 cyanotic CHD 350 lateralization 688, f689
etiology 112 decreased PBF 349, f350, t349 measurements 684, f685
cardiac causes 112 increased PBF 350, f350, t350 normal 684, f685
non cardiac causes 113 MR 340, f341, t340 pulmonary alveolar edema 690, f691
evaluation 114 MS 338, f339, t338 cardiac 691
mode of onset 115 PDA 346, f347, t346 non cardiac 691
non persistent 114 PS 347, f348, t348 pulmonary interstitial edema 690,
persistent 114 TOF 351, t351 f691
relieving factors 118 VSD 345, f345, t345 Kerley B lines 690, f691
Percussion 333 Precordium 299 Purkinje fibers 51, f52
methods 334 Inspection 299
auscultatory 334, f335 precordial prominence 305 R
direct 334 ossification of ribs 306 RBBB 516, t517, f518
indirect 334, f334 ossification of sternum 306 arrhythmogenic RV dysplasia 519,
scheme 334 Palpation 315 f520
aortic area 336, f336 tenderness 316, t316 Brugada syndrome 519, f520
left border 336 Preexcitation syndromes 606, 609 incomplete 518, f518
LA appendage 337 accessory pathways 607, f607 WHO/ISFC criteria 519
lower part of sternum 337 concealed 608 WHO/ISFC criteria 517
manubrium sternum 337 James 607, f608 Retina 181
pulmonary area 326, f327 Kent 607, f608 angiod streaks 180, t182
right border 335, f335 location 607 arteriosclerotic retinopathy 182, t182
Rotchs sign 337 Mahaim 607, f608 corkscrew retinal arteries 183, t182,
situs 337, f338 antidromic AVRT 617, f618 f184
Pericardial calcification 699, f699, t700 etiology and characteristics t619 fundus examination 181, t182
causes t700 characteristics f626 hypertensive retinopathy 182, f183,
pathogenesis t700 classification f626 t182, t183
Pericardial diseases 562, f566 Lown-Ganong-Levine syndrome 621, large retinal veins 184
Pericardial effusion 563, f563 f621 embolic retinal occlusion 184, f185
Pericardial knock 388, f388 Mahaim tachycardia 620, f620 papilledema 182, t182, f185
Pericarditis 560, f566 orthodromic AVRT 615, f615 Roth spots 182, t182, f184
ECG changes 560 ECG 615, f615 wreath like AV anastamosis 182, t182
ECG variants 562 localization of AP pathways 616, Right atrium 7, t10
atypical 563 f617 development 8
typical 563 permanent form of AV junctional external features 7
evolution 561, t561 reciprocating tachycardia (PJRT) internal features 7, f8
stages 561 621, f621 atrium proper 7
Peripheral edema 215 Wolff Parkinson White syndrome 609, Eustachian valve 7
causes 217 f610, f611, f612, f613, f614 nodes of the heart t9
characteristics 221 ECG 609 openings 9
pathogenesis 216, f217, t216 localization of AP pathways 612, septal wall 7, t8
Starling forces 217 f613, f614, f615 sinus venarum 7
types 218 with atrial fibrillation and atrial tendon of Todaro 9
anasarca 219 flutter 617, f619 Thebesian valve 7
leg edema 219 Prosthetic valve sounds 400, t401 torus aorticus 9
bilateral 219, f220 bileaflet valves 402, f402 triangle of Koch 9
unilateral 220, f221 bioprosthetic valves 402, f402 Right ventricle 10
localized 218 ball-in-cage valves 400, f401 development 12, t8
Phonocardiography 361 closing sounds 400 external features 10
Physical examination 162 opening sounds 400 shape 10, t10
importance 162 tilting disc valves 401, f401 site 10, t10
Posture or attitude 169, f170, t160 Pupils 181 internal features 11, f11, t10
INDEX 715
body 11 variants 109, t109 AS 122

inflow tract 12 orthopnea 109, f110 aortic dissection 120, 126
infundibulum 12 PND 109 arrhythmias 120, 126
supraventricular crest 12 platypnea 110, f111 atrial myxomas 124, f124
Right ventricular hypertrophy 507 tachypnea 110 CAD 120, 125
diagnostic ECG criteria 510, f511, trepopnea 110 complete heart block 128
t511 Sinus nodal arrhythmias 580, f581 HCM 123
Butler Legger 510 sick sinus syndrome 584, f585, t585 MS 123
Milner modified Sokolow-Lyon 510 sinoatrial exit block 583, t584 nitrate syncope 128
natural history series 510 1st degree 583 pacemaker related 128
other 510 2nd degree type I 583, f584 RVOTO 124
diastolic overload 512, f513, f514 2nd degree type II 583, f584 etiopathogenesis 119, t120
ECG changes 508, 509 3rd degree 583 evaluation 137, f137
axis 509 sinus arrhythmia 581, f582, t582 BP measurement 139
others 509 non phasic 582 cardiac catheterization 142
QRS complex 508 phasic 582 carotid massage 139
ST-T 509 sinus bradycardia 581, f582, t582 clinical history 137, t138
in LBBB 511 sinus node reentry tachycardia 585, CT scan 141
in RBBB 510 f585 ECG 141
systolic overload 512, f513 sinus pause or arrest 582, f583 echocardiogram 142
types 511 sinus tachycardia 580, f581, t582 EEG 141
Right ventricular infarct 543, f544 inappropriate 581 electrophysiological studies 141
diagnostic criteria 543 POTS 581 HUTT 139
incidence 543, t543 wandering pacemaker 583, f584 routine blood tests 142
Skin 193, t194 stress testing 142
S cyanosis 200 non cardiac syncope 129, f129
SA node 47 icterus 200 exercised induced 136
anterior internodal bundle 49 nodules 198, t198 metabolic 121, 136
middle internodal bundle 49 Osler nodes 199, f200 hypoglycemia related 136
posterior internodal bundle 49 peripheral emboli 200 hypoxia related 136
Sclera 178 subcutaneous nodules 198, f199 neurological 135, 136
blue 178, f180 subtle small nodule 198 cerebrovascular 135
jaundice 178 pallor 200 migraine related 135
Semilunar valves t24 pigmentation 194, f195 neuralgias 121, 135
annulus 24 angiofibromas 194, f195 seizure disorders 135
commissures 26 bronze 194 psychogenic 121, 136
development t19, 24 caf au luit spots 194 vascular 121, 129
leaflets 25 erythema marginatum 194, f195 carotid sinus hypersensitivity
sinus of Valsalva 26 Janeway lesions 195 133
valve closure 26 multiple lentigines 194 orthostatic 121
Shortness of breath (SOB) 101 symmetrical vitiligo 195 situational 130
angina equivalents 93 texture 195 vasovagal 130, f130
associated symptoms 100, t101 coarse 195 undetermined 121
at rest 108 grooved plucked chicken 196, f196 Systolic murmurs 422, t422, f432
definition 101 hyperextensible 195, f196 classification 422, f422
etiology 104 moist 196 early systolic 422
cardiovascular causes 104, f104 xanthomas 196, t197 causes 422
non cardiovascular causes 104 eruptive 197, f198 holo or pansystolic 428, f429
evaluation 105 tuberous 196 AP window 431
aggravating factors 106 xanthoma striatum palmare 196, causes 433
duration 105 f196 differential diagnosis t429
mode of onset 105 xanthoma tendinosum 197, f197 MR 428
severity 106 Spine 192, t193, f193 PDA with PH 428
functional classification 106 functional scoliosis 193 TR 429
for congenital heart diseases 108 kyphoscoliosis 192 VSD 430
NYHA 106 straight back syndrome 303 late systolic 431
specific activity scale 107 Stair case phenomenon 75 mid sytolic 423, f424
pathogenesis 101, t102 reverse stair case phenomenon 75 causes 424
quantifying the severity t108 Syncope 119 functional 427
relieving factors 111 cardiac 120, 121, f122 innocent 428
716 INDEX
Systolic murmurs (contd.) Z band f55, 59 Ventricular flutter and fibrillation 641,
MR 428 diadic cleft t56, 60, f60 t641
ventricular outflow tract 423, intercalated discs 56, 58 ECG recognition 642, f642
f424, t425 desmosome 58, f58 Ventricular tachycardia 630, t633,
Systolic sounds 362, 396 fascia adherens 58 f631
clicks 399 gap junctions f58, 59 ECG recognition 631, f632
causes 399 sarcolemma 57, f55, t56 genesis 631, f631
characteristics 399 sarcotubular system 59, f59 localizing the site 638
clinical recognition 399, f400 longitudinal sarcoplasmic reticulum types 633, f634
mechanism of production 399 60, t56, f59 bidirectional 636
ejection sounds 396, f397 T system 59 fascicular 637
causes 397 monomorphic 633, f634, t637
characteristics 397, t396 V nonsustained 633
clinical recognition 397 Valves of the heart 17, f18 see also narrow QRS tachycardia 637
aortic 397, t396 individual valves polymorphic 635
pulmonary t396, 398 development t19 sustained 633
mechanism of production 396 general description 17 Torsades de pointes 635, f638
Valvular calcification 693, t696
T radiological identification 693, f694 W
Teeth 188 Aortic valve 694, 695, f694, f695 Wide QRS tachycardia 642, f642, f643
delayed dentition 188 mitral valve 694, 695, f694, f695 differential diagnosis from SVT t645,
malformed teeth 188, t186 pulmonary valve 695 f646, f647
peg shaped teeth 188, t186, f189 tricuspid valve 695 irregular 643, f644
premature dentition 188 Vascular calcification 697, t698 regular 642, f643
widely spaced teeth, 188, f189 aorta 697
Tongue 189 coronary arteries 698, f698 X
color 189 LAD 698 X-ray chest 661
glossoptosis 189 LMCA 698 cardiac borders and chambers 669,
macroglossia 189, f190 pulmonary artery 697 f671, t670, t671
Tracheal tug 329, f330 Venous drainages of heart 31, f31, aorticopulmonary window 675
Tricuspid valve 22, f22, t22 f32, t32 arch of aorta 675
annulus t22, 23 anterior cardic veins 33 ascending aorta 671, f672
chordae tendinae 23 coronary sinus 31 azygous vein 671
types 23 great cardiac vein 33 coarctation of aorta 675, f676
development t19, 22 middle cardiac vein 33 LA appendage 679, f679
leaflets 23 oblique vein of LA 33 LA enlargement 679, f679, f680,
papillary muscles 23 posterior vein of LV 33 f681, t681
Tumor calcification 700 small cardiac vein 33 left heart border 678
Tumor plop 395, t395 Thebesian veins 33 left subclavian artery 682
characteristics 395, t395 Venous pressure 283 left superior intercostal vein 675,
abdominal jugular reflux 286, f286, f675
U t287 LV border 680, f680, f681, t681
Ultrastructure of myocardium 54, t54, f55 estimation 283 MPA 676, f677, t677
cells 54 Gartners method 287 persistent left SVC 682
amoeboid 55, t54 Mays sign 287, f288 RA enlargement 670, t671, f671
contractile t54, 56, t56 Ventricular arrhythmias 622 right aortic arch 675, f675
P 48 idioventricular rhythm 640 right heart border 669
Purkinje 55 accelerated 640, f640 RV 673
contractile proteins t56, 61 slow 640, f640 RV enlargement 673, f673, t674
A band 61, f55 premature ventricular contractions unfolding of aorta 675, f668
H zone 55, f61 (PVC) 622, f624 cardiac contour 666, t669
I band 61, f55 common causes t627 boot shaped 666, f667
M line 62, f55 differential diagnosis from SVT with egg shaped 667, f667
actin 63, f62 aberrent ventricular conduction flask like 668, f669
myosin 62, f62 630, f631 globular 667, f667
myosin isoforms f64, 64 ECG recognition 623, t627 mitralization 667, f667
titin t56, 63 estimation of risk 629, f630 shelf like 668
tropomyosin-troponin complex 63, rule of bigeminy 624, f627 snow man 668, f668
f63 types 627, f629 cardiac size 663, t667
INDEX 717
cardiothoracic (CT) ratio 664, f664 bronchi and sinuses 701, f702 dextrocardia with situs solitus f702
transverse diameter 664, f664 pleura 701 soft tissues 704
volume 665, f666 vanishing tumor 704, f703 in other views 704
extracardiac structures 701 situs 701, f704 LAO 706, f707
bones and joints 703 dextrocardia with situs inversus left lateral 705, f705
notching of ribs 703, f704 f703 RAO 706, f706

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Clinical Examination in

B.N. Vijay Raghawa Rao

B.N. Vijay Raghawa Rao

Formerly Addl. Director, Professor & HOD

Mosby, Saunders, Churchill Livingstone, Butterworth Heinemann and

All rights are reserved. No part of this publication may be reproduced,

Medical knowledge is constantly changing. As new information becomes

Published by Elsevier, a division of Reed Elsevier India Private Limited

Publishing Director: Sanjay K Singh

Typeset by Olympus Infotech Pvt. Ltd, Chennai, India.

Printed and bound at Nutech Photolithographer, New Delhi.

Dr B.N. Vijay Raghawa Rao

It is mans mission to learn to understand

Dr B.N. Vijay Raghawa Rao

PART I BASIC ANATOMY AND PHYSIOLOGY 1

PART 2 THE HISTORY AND SYMPTOMATOLOGY 83

PART 3 GENERAL PHYSICAL EXAMINATION 159

PART 4 JUGULAR VENOUS PULSE 269

PART 5 CARDIOVASCULAR SYSTEM EXAMINATION 297

Chapter 20 Percussion of the precordium and precordial findings in

PART 6A BASIC INVESTIGATIONS: CLINICAL

PART 6B BASIC INVESTIGATIONS: RADIOLOGY OF

PART 1 RFW: rapid filling wave

LCA: left coronary artery CT: cardiac tamponade

TS: tricuspid stenosis OS: opening snap

DAD: delayed after depolarization SVC: superior vena cava

1. Anatomy of the heart 3

1. GROSS ANATOMY OF THE HEART 3 4. THE FIBROUS SKELETON OF

1. GROSS ANATOMY OF THE HEART

Table 1.1 Gross anatomy of the heart

1. Shape Conical hollow muscular organ

3. The fibrous skeleton of the heart

2. EXTERNAL FEATURES OF THE HEART

i. The Sulci of the Heart

Table 1.2 External features of the heart

1. Chambers RA, RV, LA and LV

Brachiocephalic artery Left common carotid artery

Superior vena cava Arch of aorta

Left pulmonary artery

Fig. 1.1 | External features of the heartanterior view (diagrammatic).

Right coronary artery in Left anterior descending

Fig. 1.2 | External features of the heartanterior view.

ii. The Surfaces of the Heart

Arch of aorta Superior vena cava

Left pulmonary artery Right pulmonary artery

Left pulmonary veins

Left auricle Right pulmonary veins

Coronary sulcus Right atrium

Fig. 1.3 | External features of the heartposterior view (diagrammatic).

Aorta Right pulmonary artery

Left pulmonary artery Superior vena cava

Left atrium Right atrium

Coronary sinus and Inferior vena cava

Crux of the heart

Fig. 1.4 | External features of the heartposterior view.

iii. The Borders of the Heart

3. THE CHAMBERS OF THE HEART

i. Right Atrium (RA)

Fig. 1.5 | Interior of right atrium.

Crista terminalis Superior vena cava

Fig. 1.6 | Interior of the right atrium (diagrammatic).

Table 1.3 Development of the right heart

Fetal structures Portion developed