Hypertension & EKG

Hypertension and EKG Evaluation
and Interpretation
Leyda Z. Oquendo-Velez, MD
Mechanism of Disease- Pathophysiology Course
Assistant Professor
UCC School of Medicine
References:
Pathophysiology 5th Edition McCance & Huether-Elsevier/Mosby
Pathophysiology-Heart Disease- 4 th edition L.Lilly-Wolters Kluwer/Lipincott
Williams & Wilkins
REFERENCES
http://medlib.med.utah.edu/kw/ec
g/mml/ecg_v_asyst.html
The Guide to EKG interpretation,
2000 by Ohio University Press
http
http://www.themdsite.com/physici
://www.themdsite.com/physici
ans.htm
http://www.mdchoice.com/ekg/ek
g.asp
http://www.embbs.com/ekg/fileroo
m.html
February 24, 2010 2

Objectives
Identify the new parameters for
hypertension based on JNC 7
Understand the pathophysiology involved
in hypertension
Identify and classify the most common
cardiac dysrhythmias, based on its
presentation
February 24, 2010 3

Cardiovascular Disease Risk
Affects approx. 50 million individuals in the
US.
One billion worldwide.
Normotensive at age 55 have a 90% lifetime

risk for developing HTN (Framingham Heart
Study)
The relation between BP and risk of CVD

events is continuous, consistentand
independent of other risk factors.
February 24, 2010 4
Cardiovascular Disease Risk
The higher the BP, the greater is the chance
of:
heart attack,
heart failure
stroke
kidney disease.
For individuals 40-70 years of age

each increment of 20 mmHg in SBP
10 mmHg in DBP
doubles the risk of CVD
February 24, 2010 5

Hypertension in patients with
cardiovascular and cerebrovascular
diseases
Disease Disease Percentage of
Percentage of
Patients with with
Patients
Hypertension
Hypertension
Acute myocardial infarction & 50-70
Acute myocardial infarction & 50
complications 50-70
complications
Angina pectoris 50-90
Stroke 50 50
Angina pectoris
Sudden coronary death 50
50-90
Valvular disease
Stroke
50
Sudden coronary death
50
Valvular disease
February 24, 2010 6
Trends in the awareness, Rx, and
control of HBP in adults
National Health & Nutrition Examination Survey
NHANES
NHANES II IINHANES
NHANES IIII NHANES
NHANES III
NHANES II NHANES II III NHANES III
(1976-80) (Phase 1) (Phase 2)
(1976-80)
(1976-80) (Phase 1)
(Phase 1) (Phase
(Phase2)
2)
(1988-91) (1991-94)
(1988-91) (1991-94)
Awareness 51% 73%
(1988-91) 68.4%
(1991-94)
Awareness
Treatment 31% 51% 73%
55% 68.4%
53.6%
Awareness 51% 73% 68.4%
10%31%
Treatment
Control 55%
29% 53.6%
27.4%
Treatment 31% 55% 53.6%
Control 10% 29% 27.4%
Control 10% 29% 27.4%
February 24, 2010 7

Classification of BP in individuals
18 years of age
CATEGORY BP (mmHg)
systolic diastolic
Normal <120 and <80
Prehypertension 120-139 or 80-89
Hypertension
Stage1 140-159 or 90-99
Stage 2 >=160-179 or >=100
February 24, 2010 8

Genetic predisposition to HTN is thought to be
polygenetic.
Inherited defects are associated to:
Renal sodium excretion
Insulin and insulin sensitivity-leads to
vasoconstriction-increase peripheral resistance
Activity of the RAAS system
Cell membrane Na and Ca transport
Sympathetic response to neurogenic hormones
Pathophysiology of Hypertension
Genetics &
Environment
Dysfunction of the SNS, Inflammation/Endothelial

Insulin resistance RAAS, natriuretic peptide dysfunction
Vasoconstriction / Renal salt &

inflammation H2O retention
Increased peripheral
Increased blood volume
resistance
Sustained HTN
Role of the sympathetic nervous system in the
pathogenesis of HTN
SNS activity
Catecholamines or
receptor activity
Vascular
HR & TPR Insulin Procoagulant
Remodeling
& vasoconstriction resistance effects
(cytokines; NO)
Endothelial Narrowing of
Dysfunction/ vessels
Tissue ischemia & vasospasm
HTN
Shift in the pressure-natriuresis relationship
Dietary K,
Mg, Ca
Na
Genetics
on diet
Insulin
SNS
resistance
Renal salt
excret
RAA Obesity
Renal glom
Endothelial
& tubular
dysfunction
Dysfunction inflamm
Natriuretic
hormones
BP regulation
The cardiovascular system regulatory
mechanisms:
Baroreceptor reflex:mediation due to aortic
walls and carotid sinuses recepetors in the
walls.
Stretching of baroreceptors with a BP
rise=signals to the medulla
Carotid sinus through CN IX
Aortic arch- through CN X
BP regulation
The sympathetic pathway will be inhibited,
meanwhile the parasympathetic is activate
promoting
Decrease in peripheral vascular resistance
Reduction on cardiac output
BP=CO x TPR
Blood Pressure
Total Peripheral
Cardiac Output
Resistance
CO=SV x HR
Cardiac Output
Stroke Volume Heart Rate

Regulation of systemic blood pressure
Blood Pressure
Cardiac Output Peripheral resistance
Heart Rate Stroke Volume
PNS, SNS Catecholamines

catecholamines
Cardiac Contractility SNS
Venous Return
SNS,
Venous tone
catecholamines
Blood volume thirst
Renal retention
aldosterone, ADH, SNS, NP
Stroke volume
Determined by:
Cardiac contractility
Venous return to the heart-preload
The resistance the left ventricle must
overcome to eject blood into the
aorta=afterload
TPR
Peripheral resistance
Circulating regulators(angiotensin II,
catecholamines)
Direct innervation(alpha1, beta 2)
Local regulators(NO, endothelin, H,
adenosine, PGD)
Blood viscosity
Regulation of systemic blood pressure
Blood Pressure
Peripheral
Cardiac Output
Resistance
circulating direct local

regulators blood
regulators innervation viscosity
NO, endothelin,
angiotensin I alpha-1 receptors
H, O2, Hematocrit
catecholamines Beta-2 receptors
adenosine, PGD
Four systems are directly
responsible for BP regulation
Heart-supplies the pumping pressure
Blood vessel tone-determines systemic
resistance
Kidney-regulates intravascular volume
Hormones-modulate the function of the
other three systems
Abnormal findings in HTN
Heart: Sympathetic overactivity
Blood vessels: Constriction of them in
response to
Increased sympathetic activity
Abnormal regulation of vascular tone(NO,
endothelin, natriuretic factors)
Ion channel defects
Kidney: Retaining excessive water and Na
retention
Failure to regulate appropriately the RBF
Ion channel defects
Innapropiate hormonal regulation (RAAS axis
important hormonal regulator
Renin secretion should be supressed by HTN
Target organ damage in Hypertension
Organ System Manifestations
Heart LVH
HF
MI
Myocardial ischemia
Cerebrovascular Stroke
Aorta and Aortic aneurysm
peripherovascular Aortic dissection
Kidney Nephrosclerosis
Renal failure
Retina Arterial Narrowing
Hemorrhages, exudates,
papilledema
Assess for Major Cardiovascular
Disease (CVD)
Major risk factors: Hypertension
- Smoking Obesity (BMI>= 30
kg/m2)
- Dyslipidemia Physical inactivity
- Diabetes Mellitus Microalbuminuria
- Age >60 year estimated GFR < 60
mL/min
- Sex (men and
postmenopausal Age > 55 for men, > 65
women) female
- Family history of
premature CV Family history of
disease premature CVD
men <55, women < 65
February 24, 2010 25
Asseses for Identifiable Causes of
Hypertension
Sleep Apnea
Drug induced/related
Chronic kidney disease
Primary aldosteronism
Renovascular disease
Cushings syndrome or steroid therapy
Pheochromocytoma
Coarctation of aorta
Thyroid/ parathyroid disease

Medical History
Known duration and History of all
levels of elevated blood medications
pressure. Results and adverse
Patient history effects.
Family history Psychosocial and
Symptoms suggesting environment factors.
causes of hypertension.
History of recent
changes
Dietary assessment

Physical Examination
Two more blood Examination of the heart
pressure measurements. Examination of the lungs
Verification in the
contralateral arm Examination of the
abdomen
Measurement of height,
weight, and waist Examination of the
circumference extremities
Fundoscopic Neurological
examination assessment
Examination of the neck

Lifestyle Modifications
Stop smoking and reduce intake of saturated
fat and cholesterol
Lose weight if overweight
Limit alcohol intake
Increase aerobic physical activity
Limit sodium intake
Maintain adequate intake of K+, Ca++, and
Mg++ for general health

Lifestyle modifications to manage
HTN and SBP reduction
Weight Reduction BMI 18.5
18.5--24.9 Kg.m2 5-20 mmHg/
10 Kg
DASH eating plan Fruits, vegetables,low fat 8-14 mmHg
dairy
Dietary NA reduction Na <= 100 mmol/day 2-8 mmHg

2.4 gm Na or 6 gm Nacl
Aerobic physical 30 min/day at least/ most 4-9 mmHg

activity days
Moderation of Men <= 2 drinks/day 2-4 mmHg

alcohol consumption Women and lighter wgt: <=1

Stages of Hypertension and Treatment
Strategies as Recommended by JNC 7
Blood pressure stages Treatment strategies
Prehypertension (120 to Lifestyle modification*
139/80 to 89 mm Hg) Drug therapy in patients with
Diabetes Mellitus or Chronic
Kidney Disease
Stage 1 (140 to 159/90 to 99 Consider coexisting
mm Hg) conditions
Thiazide--type diuretics for
Thiazide
most patients
Stage 2 (>=160/>=100 mm Consider coexisting
Hg) conditions
Two--drug combination for
Two
most patients
Classification and Management of
BP in Adults
BP Rx without Rx with Lifestyle
Compelling Compelling modificat
Indication Indication ion
Normal No No Yes
Pre HTN No Yes Yes
Stage 1 Thia. Also ACE, Drugs for compelling

ARB, BB, CCB indications:
or comb. Diuretics, ACE, ARB, BB,
Stage 2 2 drugs CCB as needed
Thia + ACE,
February 24, 2010
ARB, BB, CCB 32
Compelling Indications
Heart Failure Thia, BB, ACE, ARB, Aldo Ant.
Post-Myocardial
Infarction BB, ACE, Aldo ant.
High CVD risk Thia, BB, ACE, CCB
DM Thia, BB, ACE, ARB, CCB
Chronic Kidney
Disease ACE, ARB
Recurrent Stroke
Prevention Thia, ACE

Treatment Goals of therapy
Is the reduction of cardiovascular and
renal morbility and mortality.
Persons >= 50 y/o will reach the DBP

goal once SBP is at goal.
The primary focus should be on

achieving the SBP goal.

Treatment Goals of therapy
Targets that are <140/90 mmHg
decrease in CVD complications.
Patients with HTN and DM or renal

disease, the BP goal is < 130/80
mmHg.

Cardiac Dysrhythmias
Sinus Bradycardia
Sinus Tachycardia
Atrial Fibrillation
Atrial Flutter
A-V Blocks
1st degree
2nd degree
3rd degree
Branch Blocks
Complete Right Bundle Branch Block (CRBBB
Complete Left Bundle Branch Block (CLBBB)
Ventricular Tachycardia
Ventricular Fibrillation
Asystole
Myocardial Infarction

Possible order to evaluate an EKG
Check EKG velocity
Check calibration of the machine
Determine the axis
Look for P waves
Determine Heart Rate
Measure PR, QRS, QT
Correlate findings with possible diagnosis

Basic Concepts
Electrocardiograph
Electrocardiogram
Leads:
. Bipolars (I, II, III)
. Unipolars (aVF, aVR, aVL)
. Precordials (V1, V2, V3, V4, V5, V6)
Vectors (pass ways of the different heart
electrical currents)
Axis (the sum of all cardiac vectors)

Summary of sequence of EKG
Interpretation
Calibration
25 mm/sec
Check 1.0 mV vertical box inscription
(normal standard 10 mm)
Each 1 mm vertical box on the EKG paper
represents 0.1 mV
Rhythm
SInus rhythm is present if:
Each P wave is followed by a QRS complex

Each QRS complex is preceded by a P wave
P wave is upright in leads I, II, & III
PR intervals is > 0.12 sec (3 small boxes)
If these criteria are not met, determine type of
arrhythmia
Waves, Complexes, Intervals, Segments
Waves: P, T, U
Complexes: QRS
Intervals: PR, QT
Segments: PR, ST

EKG reading scheme
Axis
HR
Rhythm
Waveform description
Tentative Dx
Comparative studies-
studies-previous EKGs

Intervals
Normal PR=0.12-0.20 sec
(3-5 small boxes
Normal QRS=< 0.10 sec

(=<2,5 small boxes)
Normal QT=<half the R-R interval, if HR is

normal
Normal Decreased in Increased in
0.12-0.20 Preexitation syndrome First degree AV Block
PR sec Junctional rhythm
3-5 small
boxes
=<0.10 sec BBB
QRS =<2,5 small Ventricular ectopic beat
boxes Toxic drug effect
Severe hyperkalemia
Corrected Hypercalcemia Hypocalcemia
QT =<0.44 Tachycardia Hypokalemia
QT sec Hypomagnesemia
Myocardial ischemia
Congenital prolongation of
QT
Toxic drug effect
ST segment or T wave
abnormalities
Inspect for ST elevations
Transmural infarct pattern
Pericarditis
Inspect for ST depression or T wave inversion
Subendocardial ischemia or infarct
Commonly accompany ventricular hyperthrophy
or bundle btanch block
Metabolic or chemical abnormalities
Axis
Normal if QRS is primarily upright in leads
I & II(+90 to -30)
Otherwise , determine axis by
isoelectric/perpendicular method
Axis determination
Leads I and aVF
QRS complex
Normal axis: I Positive - aVF Positive

Left Axis: I Positive - aVF Negative
Right Axis: I Negative - aVF Positive
Extreme Right Axis (No Mans Land):
Land):
I Negative - aVF Negative

Heart Rate
Use one of these methods
1500/(number of mm between two consecutive beats)
25 mm/sec x 60 sec/min/number of mm between

beats
300-150-100-75-60-50
Number of beats in 6 sec X 10

Normal rate=60-100 bpm (bradycardia<60, tachycardia>100)
Rate Determination
Large blocks and number pattern

between two QRS complexes:
300, 150,100,75, 60
EKG Tracing: Count complexes in a 6 second
strip, multiply complex count by 10
Interpretation
Bradycardia: < 60
Normal Sinus Rhythm: 60 - 100
Sinus Tachycardia: > 100

P wave abnormalities
Inspect in leads II & V1 P wave, for left
and right atrial enlaragement
P wave
Atrial depolarization
Shape: Uniform, no notching, no peaking
Height < 2.5 mm
Wide < 0.12 sec
Positive I, II, aVF, V4 to V6
Negative aVR

Common variations of P wave
Relation P wave to QRS
Inversion:
PAC, Junctional rhythm
Tall:
Right atrial enlargement
Wide:
atrial enlargement, decreased atria
Absent P waves:
SA block, Junctional rhythm

PR Interval
AV conduction time
Duration: 0.12 - 0.20 sec
Shortened: < .12 sec:
Lown-
Lown-Ganong
Ganong--Levine syndrome
WPW syndrome
Prolonged: > .20 sec
AV block
Mx: digitalis, beta blockers

QRS wave abnormalities
Inspect for left and right ventricular
hyperthrophy
Inspect for bundle branch block
Inspect for pathologic Q waves-what
anatomic distribution
The corrected QT interval = QT/square
root R-R distance
QRS Complex
Ventricular depolarization
Wide < 0.10 sec
Height 5 30 mm
Free of significant Q waves
Separate from P wave
Wide > 0.12
intraventricular conduction defect
High > 30 mm
ventricular hypertrophy or enlargement
Low < 5 mm
CAD, CHF, myxedema, pericardial effusion, primary amyloidosis,
obesity, emphysema
Significant Q waves: Infarction

3-5 small
boxes
=<0.10 sec BBB
Severe hyperkalemia
Myocardial ischemia
QT
Toxic drug effect
ST Segment
Beginning of ventricular repolarization
ISOELECTRIC: NO DEVIATE BY MORE
THAN 1 mm FROM BASELINE
Elevation:
Injury pattern, think MI
Depression:
subendocardial ischemia
Stress test:
Depression - occult CAD
3-5 small
boxes
=<0.10 sec BBB
Severe hyperkalemia
Myocardial ischemia
QT
Toxic drug effect
QT Interval
ventricular repolarization
Duration: not more than one half the length of
the R-
R-R interval with a sinus rhythm
Shortened: Hypercalcemia, Hyperkalemia
Prolonged:
Congenital
Drugs
Lyte imbalance
CVA
Hypothermia
T Wave
Ventricular repolarization
Same direction of QRS
Asymmetric: Peak closer to the end
Height < 5 mm in standard leads, < 10 mm in
precordial leads
INVERTED: ischemia, PE
Notched: normal in children, pericarditis
Symmetrical, tall: MI, Hyperkalemia, myocarditis.
Flat and depressed: hypokalemia, hypertrophy

3-5 small
boxes
=<0.10 sec BBB
Severe hyperkalemia
Myocardial ischemia
QT
Toxic drug effect
Normal Sinus Rhythm

Mechanisms of Arrhythmia
Development-Bradyarrhytmias
Abnormality Mechanism Examples
Altered impulse Decreased phase 4 Sinus
formation- Decreased depolarization(parasympathetic bradycardia
automaticity stimulation)
Altered impulse Ischemic, anatomic, or drug- 1,2 & 3 AV

conduction- induced impaired conduction Blocks
Conduction blocks
Development-Tachyarrhytmias
Altered impulse
formation-Enhanced
automaticity
Sinus node Increased phase 4 Sinus tachycardia
depolarization
Ectopic focus Acquires phase 4 Ectopic atrial tachycardia
depolarization
Triggered activity
Early afterdepolarization Prolongued action Torsades de pointes

potential duration
Delayed Intracellular calcium APB, VPB, digitalis-
afterdepolarization overload (digitalis tox) induced arrhythmias
Development-Tachyarrhytmias
Altered impulse Unidirectional block

conduction-Reentry plus slowed
conduction
Anatomical Atrial flutter
AV nodal reentrant
tachycardia
Functional Atrial fibrillation

Ventricular fibrillation
Bradyarrhythmias
EKG Pathophysiology Causes
findings involved
Sinus HR < 60 bpm Intrinsic SA node At rest or during sleep is
disease normal
Bradycardia Slowing of the
normal heart Aging, IHD, Intrinsic SA node disease
Cardiomyopathy Highly trained athletes-
rhythm
elevated vagal tone
(decreased
Extrinsic factors: Transient elevated vagal
firing of the SA tone - as a reflex
Medications(antiarrhyth
node) response to pain or fear
mic, BB, CCB);
metabolic
Normal P (Hypothyroidism)
and QRS
Sinus bradycardia
Usually asymptomatic
Except: after a marked reduction of the HR
producing a fall in CO with fatigue, light-
headedness, confusion, or syncope
Sick-Sinus Syndrome-intrinsic SA node
dysfunction, common in elderly,
susceptible to supraventricular
tachycardias AFib, Aflutter
Tachycardia-bradycardia syndrome
Sinus Bradycardia

Sinus Arrhythmia

Tachyarrhythmias
Sinus HR 100-180 Increased Its a response to

Tachycardia bpm sympathetic and/or exercise, fever,
Normal P and decreased vagal hypoxemia,
QRS tone hyperthyroididm,
hypovolemia,
anemia
Atrial Earlier than Automaticity or Usually
premaature expected P reentry in an atrial asymptomatic
beats wave with focus outside SA Electrolyte
abnormal node disturbances
shape Hypoxxemia
Normal P and
QRS
Sinus Tachycardia

Atrial Tachycardia

Atrial Tachycardia

Atrial Premature Beats

Tachyarrhythmias
Atrial HR: 180-350 Many of the impulses Occurs in patients with
flutter bpm reaching the AV node preexisting heart disease
that is in its refractory Asymptomatic usually with
period HR <100 bpm; higher may
cause palpitations, dyspnea
and weakness
Atrial Atrial 350- Many of the impulses Potentially dangerous
fibrillation 600 reaching the AV node arrhythmia
discharges/ that is in its refractory
min period Rapid ventricular rates may
P waves not Some of the impulses compromise the CO
discernible conduct in an
irregular pattern.
Wandering reentrant
circuits within the atria
Tachyarrhythmias
Paroxysmal Atrial 140-250 Reentry involving the AV
Supraventricular bpm node, atrium or and
Tachycardia Narrow QRS accesory pathwat between
the atria and ventricles
AV nodal In some people presents a The most
reentrant slow and a fast-conducting common cause
tachycardia pathways of PSVT in
adults
Atrial Fibrillation with Fast Ventricular
Response

Atrial Flutter

Atrioventricular Conduction System
Impaired conduction between the atria and
ventricles cause these types of AV blocks.
AV Blocks
AV EKG findings Pathophysiology Causes
Block involved
First PR > 0.20 sec Prolongation of the normal Reversible-vagal tone,
> 5 small boxes delay between atrial and nodal ischemia, drugs
ventricular depolarization Structural-MI, Aging
Generally benign &
asymptomatic
Check K
Second Increase in the PR Mobitz I (Wenckebach) Normal in children; in

until a P wave is high vagal tone;
blocked athletes, Hypokalemia,
Hypoxia, MI, DM
Digoxin toxicity & BB
II-Sudden Mobitz II-Usually caused by Usually indicates
intermittent loss of conduction block beyond severe disease
AV conduction, the AV node Hypokalemia, Hypoxia,
with the same MI, DM
length of PR
AV Blocks
AV Block EKG findings Pathophysiolo Causes
gy involved
Third There is no Complete failure MI (inferior wall),
relation between of conduction drugs, aging
the atria and between the atria Lightheadedness,
ventricles and ventricles syncope
QRS normal width Hypokalemia
but HR=40-60
bpm
First Degree AV Block
February 24, 2010 100

Second Degree AV Block
(Mobitz I)
February 24, 2010 101

Second Degree AV Block
(Mobitz II)
February 24, 2010 102

February 24, 2010 103
Third Degree AV Block
February 24, 2010 104

Junctional Rhythm
February 24, 2010 105

Atrioventricular Reentrant Tachycardias
Ventricular PR < 0.12 sec Atrial impulses can

Preexcitatiion (short) pass in an
Syndrome QRS with a anterograde direction
slurred wpstroke to the ventricles
(delta wave) through both the AV
Some accesory node and ventricles
patterns do not (which are stimulated
have the delta earlierr).
wave
Ectopic Atrial Morphologically Automaticity of an Can be paroxysmal or
Tachycardia different P wave atrial focus or reentry can persist.
Can be seen in a 24-
hr holter; healthy
people
Atrioventricular Reentrant Tachycardias
Multifocal Irregular rhythm Abnormal automaticity Common in severe
Atrial with at least in several foci within pulmonary disease and
Tachycardia three different P the atria in hypoxemia
waves
morphologies
Atrial average
>100 bpm
An isoelectric
line between P
waves
distinguishes
from A fib.
Bundle BranchBlocks
EKG Pathophysiology
RBBB Normal R in V1 Normal depolarization of
Small Q in V6 the right ventricle does
not occur.
The initial forces of
depolarization are
directed toward the left
ventricle instead of the
right.
LBBB Normal depolarization of
the left ventricle does not
occur.
The initial forces of
depolarization are
directed toward the right
ventricle instead of the
left.
Bundle Branch Block
LBBB:
QRS > 0.12
QRS negative in Lead V1 & positive in V6
No Q wave
Dx CAD, HBP, Cardiomyopathy, severe AVD
RBBB
QRS greater than 0.12
M-shaped QRS in V1 (rSR pattern)
Wide S wave Lead V6
Dx CAD, Valvular Disease or Idiopathic
February 24, 2010 109

February 24, 2010 110
Left Bundle Branch Block
February 24, 2010 111

February 24, 2010 112
Right Bundle Branch Block
February 24, 2010 113

Ventricular Arrhythmias
EKG Pathophysio Causes
logy
Ventricular Every alternanate beat = bigeminy Ventricular focus Usually benign, present in
Premature To normal beats preceding = fires an action healthy people, in aging
Beats trigeminy potential May indicate structural
Three normal beats heart disease-increased in
preceding=quadrigeminy frequency in relation with
Two consecutive=couplets the severity depreseed
cardiac contractlity, Vagal
Three= trilpets hyperactivity
Sudden death with HF or
MI, Anesthesia
Ventricular P absent Wide QRS > 0.12 sec Having a duration > 30
Tachycardia Rate 100-200 bpm or faster sec-severe symptoms:
Regular QRs-Monomorphic syncope-sustained VT
Changes in shape-polymorphic- Self-terminated-Non
Torsades de pointes sustained VT, Aging,
Hyperkalemia,
Hypercalcemia, Hypoxia
Anesthesia, Vag
Sudden death with HF or
MI,
Ventricular P absent, QRs usually not Aging, Hyperkalemia,
Fibrillation observable, Hypercalcemia, Hypoxia,
VagSudden death with HF
or MI
Ventricular Premature
Beats
February 24, 2010 115

Ventricular Tachycardia
February 24, 2010 116

Torsades de Pointes is a rapid ventricular rhythm caused by low potassium,
medications (those that block potassium channels), or congenital
abnormalities (e.g., Long QT Syndrome) that lengthen the QT interval. The
rate is a variable 250 to 350 per minute, in brief episodes.
February 24, 2010 117
February 24, 2010 118
February 24, 2010 119
February 24, 2010 120
Coronary ischemia
Deep, Symmetric T-wave inversion
ST depression
ST Elevation
>1mm limb
>2mm precordial leads
Q Waves
New LV strain pattern or LBBB
Anatomic distribution
Inferior: II, III, aVF
Anterior: I, aVL, V1-V6
Lateral: I, aVL, V5, V6
Posterior: no indicative changes
February 24, 2010 121

Localization of a Myocardial
Infarction
Anatomic site Leads altered Coronary artery
involved
Inferior II, II V1 RCA
Anteroseptal V1-V2 LAD
Anteroapical V3-V4 LAD (distal)
Anterolateral V5-V6, I,V1 CFx
Posterior V1-V2 (tall R wave, RCA
not Q wave)
February 24, 2010 123
Hyperkalemia
February 24, 2010 124

T
H
A
N
K
S
February 24, 2010 125

Hypertension &amp; EKG

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Hypertension &amp; EKG

Uploaded by

Copyright:

Available Formats

Hypertension and EKG Evaluation

February 24, 2010 2

February 24, 2010 3

One billion worldwide.

Normotensive at age 55 have a 90% lifetime

The relation between BP and risk of CVD

For individuals 40-70 years of age

February 24, 2010 5

February 24, 2010 7

February 24, 2010 8

Dysfunction of the SNS, Inflammation/Endothelial

Vasoconstriction / Renal salt &

Stroke Volume Heart Rate

Cardiac Output Peripheral resistance

Heart Rate Stroke Volume

PNS, SNS Catecholamines

Blood volume thirst

circulating direct local

February 24, 2010 26

February 24, 2010 27

February 24, 2010 28

February 24, 2010 29

Dietary NA reduction Na <= 100 mmol/day 2-8 mmHg

Aerobic physical 30 min/day at least/ most 4-9 mmHg

Moderation of Men <= 2 drinks/day 2-4 mmHg

February 24, 2010 30

Pre HTN No Yes Yes

Stage 1 Thia. Also ACE, Drugs for compelling

High CVD risk Thia, BB, ACE, CCB

DM Thia, BB, ACE, ARB, CCB

February 24, 2010 33

Persons >= 50 y/o will reach the DBP

The primary focus should be on

February 24, 2010 34

Patients with HTN and DM or renal

February 24, 2010 35

February 24, 2010 36

February 24, 2010 37

February 24, 2010 38

Each P wave is followed by a QRS complex

February 24, 2010 44

February 24, 2010 45

Normal QRS=< 0.10 sec

Normal QT=<half the R-R interval, if HR is

Normal axis: I Positive - aVF Positive

February 24, 2010 50

1500/(number of mm between two consecutive beats)

25 mm/sec x 60 sec/min/number of mm between

Number of beats in 6 sec X 10

Large blocks and number pattern

February 24, 2010 53

February 24, 2010 56

February 24, 2010 57

February 24, 2010 59

February 24, 2010 63

February 24, 2010 72

February 24, 2010 75

Altered impulse Ischemic, anatomic, or drug- 1,2 & 3 AV

Early afterdepolarization Prolongued action Torsades de pointes

Altered impulse Unidirectional block

Functional Atrial fibrillation

February 24, 2010 82

February 24, 2010 83

Sinus HR 100-180 Increased Its a response to

Hypertension & EKG

Hypertension & EKG