Kursk State Medical University

Propaedeutics of Internal
Diseases Department
Professor T.A. Dronova
Lecture
HEART FAILURE

Heart failure
Inability of the heart to maintain

sufficient cardiac output to meet the

demands of the body
Congestive heart failure is a relatively common

disorder (2 million persons in the US treated

for heart failure & 400,000 new cases each
year)

Heart failure
ETIOLOGY
1. Myocardial dysfunction
2. Ventricular volume overload
3. Ventricular outflow obstruction
4. Ventricular inflow obstruction
5. Obligatory high cardiac output
6. Altered rhythm

Heart failure
ETIOLOGY
Myocardial dysfunction Ventricular volume
overload
(i) Myocardial
infarction
(ii) Hypertension
(iii) Myocarditis
(iv) Cardiomyopathy

(i) Valvular
incompetence (mitral &
aortic) Left ventricle
overload
(ii) Atrial septal defect
Right ventricle
overload

Heart failure
ETIOLOGY
Ventricular outflow
obstruction

Ventricular inflow
obstruction

(i) Systemic or
pulmonary
hypertension
(ii) Aortic or
pulmonary stenosis

(i) Mitral or tricuspid

valve stenosis
(ii) Constrictive
pericarditis
(iii) Restrictive
cardiomyopathy

Heart failure
ETIOLOGY
Obligatory high
cardiac output

Altered rhythm

(i) Anemia,
thyrotoxicosis
(ii) Beri-beri, patent
ductus arteriosus

(i) Atrial fibrillation

HEART FAILURE
Forms
Acute & chronic
High-output & low-output
Right-sided & left-sided (or biventricular heart

failure)
Forward & backward
Systolic & diastolic

Descriptors useful in clinical setting (particularly

early in the patients course)

Late in chronic heart failure without differences

Acute & chronic heart failure

Acute heart failure - developing suddenly in a
previously asymptomatic patient:
Myocardial infarction
Acute valvular regurgitation in infective endocarditis
Acute pulmonary embolus causing obstruction of the

circulation
Cardiac tamponade

Chronic heart failure - developing gradually:

typically observed in patient with dilated
cardiomyopathy or multivalvular heart disease
which develops or progresses slowly

HEART FAILURE
Acute Vs Chronic
Acute heart failure - usually largely systolic &

sudden reduction in cardiac output often results in

systemic hypotension without peripheral edema
Chronic heart failure - arterial pressure tends to
be well maintained, but there is often
accumulation of edema
Despite these obvious differences in clinical
presentation - no fundamental distinction between
acute & chronic heart failure

Left sided heart failure

Reduction in effective left ventricular output for a

given pulmonary venous or left atrial pressure

Acute increase in left atrial pressure pulmonary
congestion or pulmonary edema
Chronic increase in left atrial pressure Kitaevs
reflex: pulmonary vasoconstriction with pulmonary
hypertension
Causes of left heart failure:
1. Ischemic heart disease
2. Systemic hypertension
3. Mitral & aortic valve disease
4. Cardiomyopathies

Left-sided heart failure

Paroxymal noctural
dyspnea &
Orthopnea
Pulmonary
congestion
Weakened or
mechanically overloaded
left ventricle
Left ventricle:
weakened (myocardial infarction)
mechanically overloaded (aortic stenosis)

Right sided heart failure

Reduction in right ventricular output for any given

right atrial pressure

Increased right atrial pressure increased jugular
venous pressure & hepatic congestion
Causes of right heart failure:
1. Secondary to left heart failure (commonest)
2. Chronic lung disease (causing cor pulmonale)
3. Pulmonary embolism or pulmonary hypertension
4. Tricuspid & pulmonary valve disease
5. Arterial septal defect & ventricular septal defect
6. Cardiomyopathy

Right-sided heart failure

Edema,
congestive hepatomegaly,
systemic venous distention
Weakened or
mechanically overloaded
right ventricle
Primarily right ventricular abnormality:
valvular pulmonic stenosis
pulmonary hypertension secondary to pulmonary
thromboembolism

Biventricular or
congestive heart failure
Causes:
1. Disease involving both ventricles (dilated
cardiomyopathy or ischemic heart disease)
2. Disease of the left ventricle leads to chronic
elevation of left atrial pressure pulmonary
hypertension right heart failure
Clinical features - combination
of
right & left heart failure

HEART FAILURE
High-output Vs Low-output
Elevated cardiac output
Causes: hyperthyroidism, severe anemia,
pregnancy, artheriovenous fistulas, beri-beri
(thiamin deficiency), Pagets disease, Gram
negative septicemia
Heart unable to meet the demands placed on it
Patients - warm
with distended superficial veins
High output heart failure is caused by increased demand
Low output heart failure may be caused by pump failure

HEART FAILURE
Low-output Vs High-output
Low-output heart failure - secondary to
ischemic heart disease
hypertension
dilated cardiomyopahty
valvular disease
pericardial disease

James Hopes (1832)

backward pressure theory
Cardiac chambers may fail independently -

imbalance in performance of ventricle

(development of left ventricle failure
consequent to aortic stenosis or of right
ventricle failure secondary to pulmonic
stenosis)
Initial clinical manifestation - damning up of
blood behind affected ventricle
failure of 1 or other ventricle to fill normally &
discharge its contents - elevated atrial &
venous systemic pressure behind failing
ventricle

Mackenzies (1912)
forward failure hypothesis
Clinical manifestation of heart failure to

inadequate delivery of blood into arterial

system
Reduced cardiac output - diminished
perfusion of vital organs (brain - mental
confusion, skeletal muscle weakness,
kidneys - Na & water retention)
Retention of Na & water augments
extracellular fluid volume & ultimately leads
to symptoms of heart failure (by congestion
of organs & tissues)

Heart failure
Precipitating or aggravating factors
Inappropriate reduction of therapy
Administration of a drug with negative inotropic

(beta-adrenoreceptor antagonist) or fluid

retaining properties (NSAIDs, corticosteroids )
Arrhythmia
Myocardial ischemia or infarction
Intercurrent illness (infection)
Pulmonary embolism
Conditions associated with increased metabolic
demand (pregnancy, thyrotoxicosis, anemia)

Heart failure
Clinical features
2 basic factors :
1. Reduced cardiac output
due to decreased heart function
diminished filling of arterial tree ischemia
of the organs
2. Congestion of blood
heart fails to pump the whole coming blood
damming of blood back into venous
system organs congested organs
functions disturbed

Congestive heart failure

Framingham criteria
Major Criteria:
paroxysmal noctural dyspnoe or orthopnea
neck-vein distention
rales (crackles)
cardiomegaly
acute pumlonary edema
S3 gallop
increased venous pressure
prolonged circulation time
hepatojugular reflux

Congestive heart failure

Framingham criteria
Minor criteria:
ankle edema
night cough
dyspnoe on exertion
hepatomegaly
pleural effusion
vital capacity decreased 1/3 from maximum
tachycardia (rate > 120/min)

Congestive heart failure

Framingham criteria
Major or minor criterion:
weight loss > 4.5 kg in 5 days in response to
treatment
Definite diagnosis of congestive heart failure
-presence concurrently:
2 major criteria
or
1 major & 2 minor criteria

Heart Failure Functional Classification

(New York Heart Association)
Class 1 no limitations: ordinary physical
activity without fatigue, dyspnoe or
palpitation
Class 2 slight limitations of physical
activity : comfortable at rest, ordinary
physical activity results in fatigue,
palpitations, dyspnoe or angina
Class 3 marked limitation of physical
activity: although comfortable at rest, less
ordinary activity to symptoms development
Class 4 inability to carry on any physical
activity without discomfort, symptoms
present even at rest, with any physical
activity, increased discomfort

Heart failure
Clinical features
Inspection
may be bulging of pericardium - left

ventricular hypertrophy (not in acute

ventricular failure), cardiomegaly
cyanosis (may be peripheral or central) usually peripheral acrocyanosis

Palpation & percussion

Apex beat is displaced & heaving in

character, if there is left ventricular

hypertrophy (not in acute ventricular failure)
Tachycardia, cardiomegaly by percussion

Auscultation
Basal crepitations heard in auscultation of

lungs
Gallop rhythm : tachycardia, with S3 & S 4

heart sounds

Right heart failure

raised JVP & hypotension
tachycardia
tender smooth hepatomegaly
pitting peripheral edema
ascites & pleural effusion (may be present)

no evidence of pulmonary edema

Left heart failure

Most prominent - signs pulmonary edema
Symptoms :
dyspnea, orthopnoe, paroxysmal noctural

dyspnea
fatigue, weakness
nocturia
pulmonary edema
mostly symptoms due to lung congestion
if rare dyspnea in attacks cardiac asthma

Left ventricular failure

Essentials of diagnosis
Exertional dyspnea
Cough
Fatigue
Ortopnea
Paroxismal nocturnal dyspnea
Cardiac enlargement
Rales
Gallop rhythm
Pulmonary venous congestion

Left heart failure

Dyspnoe (tachypnoea)

Exertional dyspnoe (increased venous return &

relative normal right heart transmits this in
pulmonary circulation)
Left heart failure - damning of blood in pulmonary
veins pulmonary venous congestion fine nerve
endings stimulation around terminal alveoli sensation of breathlessness)
Stopped exercises - venous return diminished,
congestion resides, dyspnoe relieved
Exercise increase venous return heart pump
poorly congestion of the lungs dyspnoe

Left heart failure

Orthopnoe lying flat breathlessness
advanced heart disease
2 circulatory changes on lying flat :
redistribution of fluid occurs from tissue into the
plasma
0,5 liter of blood pooled in leg veins during standing
- returned to effective circulation increased venous
return
heart workload increased - lung congestion &
dyspnoe
upright position - hydrostatic pressure helps in
draining the upper lung zones into the left atrium
- on lying flat hydrostatic effect lost & whole lung
becomes congested & patient becomes breathless

Paroxysmal noctural dyspnoe

episode of breathlessness at night during sleep

redistribution of fluid on lying flat results in increase

venous return to already poor functioning heart
causing pulmonary congestion
reduced hydrostatic effect in pulmonary veins,
which has function to inhibit congestion of the
lungs
depression of nervous system during sleep leads to
reduced awareness of pulmonary congestion; when
the congestion becomes of high degree patient
becomes severe breathless
during sleep, sympathetic system depressed
cardiac rate; reduced heart rate - blood in
pulmonary vessels, resulting in pulmonary
congestion

Pulmonary edema
persistent severe breathlessness of sudden

onset
profuse sweating, skin becomes cold, pale &
cyanosed
expectoration of watery, frothy often bloodstained sputum (pinkish)
acute cardiac failure after myocardial
infarction, myocarditis & acute valvular
regurgitation usually present with pulmonary
edema in previously asymptomatic patient

Right ventricular failure

Essentials of diagnosis

Elevated venous pressure

Hepatomegaly
Dependent edema

Right ventricular failure

Symptoms
Tissue congestion (inability of heart to empty
properly)
cerebral: headache, insomnia, restlessness
pulmonary: cough, dyspnoe
portal: anorexia, nausea, vomiting pain in right
hypochondrium due to hepatic congestion which
stretches the hepatic capsule stimulates pain
receptor & produces pain
renal : oliguria and nocturia
peripheral edema : edema of feet in ambulatory &
sacral region in bed-bound patient

Right ventricular failure

Symptoms
Reduced cardiac output
fatigue
decreased urinary output due to inadequate

blood supply to the tissue

Right heart failure

raised JVP & hypotension
tachycardia
tender smooth hepatomegaly
pitting peripheral edema
ascites & pleural effusion (may be present)

there is no evidence of pulmonary edema

Right heart failure

Clinical examination
Dependent pitting edema (ambulant patients - ankle

edema, bed-bound patients - around thigh & sacrum)

massive accumulation of fluid - pleural effusion,
ascites
raised JVP, positive hepatojugular reflux
evidence of heart disease
signs of right ventricular (cor ball) or biventricular
cardiomegaly
right ventricular gallop rhythm (S4)
functional tricuspid regurgitation (right ventricular
hypertrophy)
tender hepatomegaly

Investigation
ECG : right or left ventricular hypertrophy,signs of

myocardial ischemia or infarction

X-ray chest: prominent upper lobe veins, Kerley B
lines (engorged peripheral lymphatics seen in the
lower lobes)
Fluid in fissures or interlobar effusion (phantom
tumor) - disappears with treatment of left sided
failure
Increase in broncho-ventricular markings (bats
wings or inverted moustache signs ) features of
pulmonary edema
Pleural effusion - bilateral & symmetrical (if
semilateral - usually right sided)
Cardiomegaly

Management
Rest, salt free diet
Oxygen
Diuretics
Vasodilators
ACE inhibitors (prestarium)
Arteriolar dilators (hydralazim)
Venodilators ( isosorbid-5-mononatritrate)
Digoxin

Heart failure
Adaptive mechanism
Frank-Starling mechanism - through an increased in

preload
Myocardial hypertrophy - restores elevated
ventricular wall stress to normal
Distribution of a subnormal cardiac output away from
skin, skeletal muscle, & kidneys with maintenance of
blood flow to vital organs (brain and heart)
Neurohumoral adjustments, which tend to maintain
arterial pressure. This state is often characterized by
a relative reduction in the ratio of mitochondria to
myofibrils

Acute circulatory failure (shock)

Shock - acute circulatory failure with
critical impairment of tissue
perfusion resulting in generalized
cellular hypoxia:
impaired function of heart
inadequately filled heart

Etiology of acute circulatory failure

Types
hypovolumic shock
secondary to major reduction in blood volume: internal
/ external hemorrhage, severe burns, acute
pancreatitis, dehydration (in diabetes ketoacidosis)
normovolumic shock
secondary to capillary damage, arteriovenous shunting
& inappropriate vasodilatation: septic shock (usually
gram negative septicemia), anaphylactic shock
cardiogenic shock
severe heart failure (myocardial infarction, acute
massive pulmonary embolism, pericardial tamponade)

Hypovolumic shock
Clinical features
inadequate tissue perfusion
skin: cold, pale, cyanosis
kidneys: oliguria, anuria
brain: restlessness then confusion, coma
increased sympathetic tone
tachycardia
sweating
metabolic acidosis & tachypnoe

Acute circulatory failure

General features
hypotension (systolic BP < 100mmHg)
tachycardia (>100 per min)
cold clammy skin
rapid shallow respiration
drowsy, confusion, irritability
oliguria (< 30ml/hr )
elevated or reduced CVP

Cardiogenic shock
general features of shock
signs of myocardial failure (raised JVP, gallop

rhythm, basal crepitations, pulmonary edema)

Septic shock
general features of shock
fever & rigors ( maybe hypothermia )
warm skin due to cutaneous vasodilation

Anaphylactic shock
general features of shock
warm skin
utricaria, angioedema, bronchospasms,

wheeze, and facial edema

Determination of type of shock
cardiogenic : raised CVP ( central venous
pressure )
hypovolumic : low CVP

HEART FAILURE
Forward & backward
The clinical manifestation of heart failure

arises as a consequence of inadequate

cardiac output & / or damming up of blood
behind one or both ventricles
These two principal mechanisms are the
basis of the so-called forward & backward
pressure theories of heart failure

HEART FAILURE
Forward & backward
1) ventricular end-diastolic volume & pressure

increase
2) volume & pressure rise in atrium behind failing
ventricle
3) atrium contracts more vigorously (Starlings law)
4) pressure in venous & capillary beds behind
(upstream to) failing ventricle rises
5) transudation of fluid from capillary bed into
interstitial space (pulmonary or systemic) increases

Heart failure
Systolic heart failure (classic heart failure):

impaired inotropic state causes weakened

systolic contraction, which leads to a reduction
in the stroke volume, inadequate ventricular
emptying, cardiac dilatation, & often elevation of
ventricular diastolic pressure
idiopathic dilated cardiomyopathy - systolic heart
failure prototype

Systolic heart failure

Primary abnormality in heart muscle

(cardiomyopathy), lost in the quantity of

normally contracting cells (ischemic heart
disease)
Secondary to a chronic excessive work load
(hypertension & valvular heart disease)

Heart failure
Diastolic heart failure: abnormalities involves

impaired relaxation of the ventricle & leads to an

elevation of ventricular diastolic pressure at any
given diastolic volume
Failure of relaxation can be functional (during
transient ischemia) or caused by a stiffened,
thicken right ventricle
Typical conditions with diastolic failure - restrictive
cardiomyopathy, secondary to infiltrative
conditions (amyloidosis or hemochromatosis),
hypertrophic cardiomyopathy