1. 1
HEART FAILURE
Prof : Dr Mya Mya Aye

2. Heart Failure
 Heart Failure is the state that develops when the
heart cannot maintain an adequate cardiac output
or can do so only at the expense of an elevated
filling pressure. In the mildest forms of heart
failure, cardiac output is adequate at rest becomes
inadequate only when the metabolic demand
increases during exercise or some other form of
stress. Heart failure may be diagnosed whenever a
patient with significant heart disease develops the
signs or symptoms of a low cardiac output,
pulmonary congestion or systemic venous
congestion. 2

3. Cause of heart failure
Coronary artery disease
 Myocardial infarction
 Ischaemia
Hyoertension
Cardiomyopathy
 Dilated (congestive)
 Hypertrophic/ obstructive
 Restrictive – for example, amyloidosis,
sarcoidosis, haemochromatosis
 Obliterative
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4. Valvar and congenital heart disease
 Mitral valve disease
 Aortic valve disease
 Atrial septal defect, ventricular septal defect
Arrhythmias
 Tachycardiac
 Bradycardia (complete heart block, the sick
sinus syndrome)
 Loss of atrial transport – for example, atrial
fibrillation
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5. Alcohol and drugs
 Alcohol
 Cardiac depressant drugs (β blockers, calcium
antagonists)
" High output " failure
 Anaemia, thyrotoxicosis, arteriovenous
fistulae, Paget's disease
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6. Pericardial disease
 Constrictive pericarditis
 Pericardial effusion
Primary right heart failure
 Pulmonary hypertension – for example,
pulmonary embolism, cor pilmonale
 Tricuspid incompetence
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7. Poor ventricular function/ myocardial damage
(e.g post myocardial infarction, dilated cardiomyopathy )
Heart failure
Decreased stroke volume and cardiac output
Neurohormonal response
Activation of sympathetic system Renin angiotensin aldosterone system
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8. •Vasoconstriction: increased sympathetic tone, angiotensin II,
endothelins, impaired nitric oxide release
•Sodium and fluid retention: increased vasopressin and aldosterone
Further stress on ventricular wall and dilatation ( remodelling)
leading to worsening of ventricular function
Further heart failure
Neurohormonal mechanisms and compensatory mechanisms in
heart failure
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9. Liver Vessels Brain
Renin substrate ( angiotensinogen)
Renin
(kidney)
Angiotensin I
Angiotensin converting enzyme
(lungs and vasculature )
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10. Angiotenin II
Vasoconstriction Aldosterone release Enhanced
sympathetic activity
Salt and water retention
Renin-angiotensin-aldosterone axis in heart failure
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11. Types of heart failure
Heart failure can be classified in several ways.
Acute and chronic heart failure
Heart failure may develop suddenly, as in myocardial
infarction, or gradually, as in progressive valvular heart
disease. When there is gradual impairment of cardiac
function, a variety of compensatory changes may take
place.
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12.  The phrase 'compensated heart failure' is
sometimes used to described a patient with
impaired cardiac function in whom adaptive
changes have prevented the development of
overt heart failure. A minor event such as an
intercurrent infection or development of atrial
fibrillation, may precipitate overt or acute
heart failure. Patients with chronic heart
failure commonly experience a relapsing and
remitting course, with periods of stability and
episodes of decompensation.
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13. FACTORS THAT MAY PRECIPITATE OR
AGGRAVATE HEART FAILURE IN
PATIENTS WITH PRE-EXISTING HEART
DISEASE
 Myocardial ischaemia or infarction
 Intercurrent illness (e.g. infection)
 Arrhythmia ( e.g. atrial fibrillation)
 Inappropriate reduction of therapy
 Administration of a drug with negative inotropic properties
(e.g. β - blocker ) or fluid-retaining properties ( e.g. non-
steroidal anti-inflammatory drugs, corticosteroids)
 Pulmonary embolism
 Conditions associated with increased metabolic demand
(e.g. pregnancy, thyrotoxicosis, anaemia)
 Intravenous fluid overload (e.g. post-operative i.v.
infusion) 13

14. Left right and biventricular heart failure
The left side of the heart is a term for the functional
unit of the left atrium and left ventricle, together
with the mitral and aortic valves; the right heart
comprises the right atrium, right ventricle, tricuspid
and pulmonary valves.
Left-sided heart failure. In this condition there is a
reduction in the left ventricular output and /or an
increase in the left atrial or pulmonary venous
pressure. An acute increase in left atrial pressure
may cause pulmonary congestion or pulmonary
oedema; a more gradual increase in left atrial
pressure, however, may lead to reflex pulmonary
vasconstriction, which protects the patient from
pulmonary oedema at the cost of increasing
pulmonary hypertension.
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15. Right – sided heart failure . In this there is a reduction in the right
ventricular output for any given right atrial pressure. Causes of
isolated right heart failure include chronic lung disease
( corpulmonale ), multiple pulmonary emboli and pulmonary
valvular stenosis.
Bventricular heart failure.Failure of the left and right heart may
develop because the disease preocess ( e.g. dilated
cardiomyopathy or ischaemic heart disease) affects both
ventricles, or because disease of the left heart leads to chronic
elevation of the left atrial pressure, pulmonary hypertension and
subsequent right heart failure.
Forward and backward heart failure.
In some patient with heart failure the predominant problem is an
inadequate cardiac output ( forward failure), whilst other
patients may have a normal or near-normal cardiac output with
marked salt and water retention causing pulmonary and
systemic venous congestion ( backward failure).15

16. Diastolic and systolic dysfunction
Heart failure may develop as a result of impaired
myocardial contraction ( systolic dysfunction) but can
also be due to poor ventricular filling and high filling
pressures caused by abnormal ventricular relaxation
(disastolic dysfunction ). The latter is commonly
found in patient with left ventricular hypertrophy and
occurs in many forms of heart disease, notably
hypertension and ischaemic heart disease. Systolic
and diastolic dysfunction often coexist, particularly in
patents with coronary artery disease.
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17. High-output failure
Conditions that are associated with a very high
cardiac output (e.g. a large AV shunt, beri-
beri, severe anaemia or thyrotoxicosis) can
occasionally cause heart failure.
Clinical features
The clinical picture depends on the nature of the
underlying heart disease, the type of heart
failure that it has evoked, and the neural and
endocrine changes that have developed.
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18. A low cardiac output causes fatigue, listlessness
and a poor effort tolerance, the peripheries are
cold and the blood pressure is low. To
maintain perfusion of vital organs blood flow
may be diverted away from skeletal muscle
and this may contribute to symptoms of
fatigue. Poor renal perfusion may lead to
oliguria and ureaemia.
Pulmonary oedema due to left heart failure may
present with breathlessness, orthorpnoea,
paroxysmal nocturnal dyspnoea and
inspiratory crepitations over the lung bases.
The chest radiograph show characteristic
abnormalities and is usually a more sensitive
indicator of pulmonary venous congestion than
the physical signs. 18

19.  In contrast, right heart failure produces a high
jugular venous pressure, with hepatic
congestion and dependent peripheral oedema.
In ambulant patients the oedema affects the
ankles, whereas in bed-bound patients it
collects around the thighs and sacurum.
Massive accumulation of fluid may cause
ascites or pleural effusion.
 Chronic heart failure is sometimes associated
with marked weight loss (cardiac cachexia)
caused by a combination of anorexia and
impaired absorption due to gastrointestinal
congestion; poor tissue perfusion due to a low
cardiac output; and skeletal muscle atrophy
due to immobility. Increase circulation levels
of cytokine tumour necrosis factor have been
found in patients with cardiac cachexia.
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20.  Complications
In advanced heart failure a number of non-specific
complications may occur.
Ureamia. This reflects poor renal prefusion due to
the effects of diuretic therapy and allow cardiac
output. Treatment with vasodilators or dopamine
may improve renal perfusion.
Hypokalaemia. This may be the result of treatment
with potassium-losing diuretics or
hyperaldosteronism caused by activation of the
renin-angiotensin system and impaired
aldosterone metabolism due to hepatic congestion.
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21.  Most of the body's potassium is intracellular, and
there may be substantial depletion of potassium
stores even when the plasma potassium
concentration is in the normal range.
 Hyperkalaemia-This may be due to the effects of
drug treatment, particularly the combination of
ACE inhibitors and spironolactone (which both
promote potassium retention), and renal
dysfunction.
 Hyponatraemia This is feature of severe heart
failure and may be caused by diuretic therapy,
inappropriate water retention, or failure of the cell
membrane ion pump.
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22.  Impaired liver function. Hepatic venous
congestion and poor arterial perfusion frequently
cause mild jaundice and abnormal liver function
tests; reduced synthesis of clotting factors may
make anticoagulant control difficult.
 Tbromboembolism.Deep vein thrombosis and
pulmonary embolism may occur due to the effect
of a low cardiac output and enforced immobility,
whereas systemic emboli may be related to
arrhythmias, particularly atrial fibrillation, or
intracardiac thrombus complication conditions
such as mitral stenosis or LV aneurysm.
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23.  Arrhythmias. Atrial and ventricular arrhythmias
are very common and may be related to electrolyte
changes ( e.g hypokalaemia, hypomagnesaemia ),
the underlying structural heart disease, and the
pro-arrhythmic effects of increased circulation
catecholamines and some drugs (e.g. digoxin).
Sudden death occur in up ot 50% of patients with
heart failure and is often due to a ventricular
arrhythmia. Frequent ventricular ectopic beats and
runs of non-sustained ventricular tachycardia are
common findings in patients with heart failure and
are associated with an adverse prognosis.
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24.  Investigation
Clinical assessment is mandatory before
detailed investigations are conducted in
patients with suspected heart failure,
although specific clinical features are often
absent and the condition can be diagnosed
accurately only in conjunction with more
objective investigation, particularly
echocardiography.
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25. Investigations if heart failure is suspected
Initial investigations
 Chest radiography
 Electrocardiography
 Echocardiography, including Doppler studies
 Haematology tests
 Serum biochemistry, including renal function and
glucose concentrations, liver function tests, and thyroid
function tests
 Cardiac enzymes ( if recent infarction is suspected )
Other Investigation
 Redionuclide imaging
 Cardiopulmonary exercise testing
 Cardic catheterisation
 Myocardial biopsy-for example, in suspected
myocarditis.
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26. Chest X rays examination
The chest x ray examination has an important role in
the routine investigation of patients with suspected
heart failure, and it may also be useful in
monitoring the response to treatment. Cardiac
enlargement (cardiothoracis ratio > 50%) may be
present but there is a poor correlation between the
cardiothoracic ratio and left ventricular function.
Cardiomegaly is frequently absent, for example, in
acute left ventricular failure secondary to acute
myocardial infarction, acute vavular regurgition,
or an acquired ventricular septal defect. An
increased cardiothoracic ratio may be related to
left or right ventricular dilatation, left ventricular
hypertrophy, and occasionally a pericardial
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27. In left sides failure, pulmonary venous congestion occur,
initially in the upper zones (referred to as upper lobe
diversion or congestion). When the pulmonary venous
pressure increases further, usually above 20 mmHg, fluid
may be present in the horizontal fissure and Kerley may
be present in the costophrenic angles. In the presence of
pulmonary venous pressure above 25 mmHg, frank
pulmonary oedema occurs, with a " bats wing"
appearance in the lungs, although this is also dependent
on the rate at which the pulmonary oedema has
developed. In addition ,
pleural effusion occur, normally bilaterally ,but if they
are unilateral the right side is more commonly affected.
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28. Rarely ,chest radiography may also show
valvar calcification, a left ventricular
aneurysm, and the typical pericardial
calcification of constrictive pericarditis.
Chest radiography may also provide
valuable information about non-cardiac
cause of dyspnoea.
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29.  12 lead electrocardiography
The 12 lead electrocardiographic tracing is
abnormal in most patients with heart failure,
although it can be normal in up to 10% of cases.
Common abnormalities include Q waves,
abnormalities in the T wave and ST segment, left
ventricular hypertrophy, bundle branch block, and
atrial fibrillation.
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30.  The combination of a normal chest x ray finding
and a normal electrocardiographic tracing makes a
cardiac cause of dyspnoea very unlikely.
 In patents with symptoms (palpitations or
dizziness), 24 hors electrocardiographic (Holter)
monitoring or a Cardiomemo divice will detect
paroxysmal arrhythmias or other abnormalities,
such as ventricular extrasystoles, sustained or non-
sustained ventricular tachycardia, and abnormal
atrial rhythmas (extrasystoles, supraventricular
tachycardia, and paroxysmal atrial fibrillation).
Many patients with heart failure, however, show
complex ventricular extrasystoles on 24 hour
monitoring
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31. Echocardiography
Echocardiography is the single most useful non-
invasive test in the assessment of left ventricular
function; ideally it should be conducted in all
patients with suspected heart failure. Left
ventricular dilatation and impairment of
contraction is observed in patients with systolic
dysfunction related to ischaemic heart disease
(where a regional wall motion abnormality may
be detected) or in dilated cardiomyopathy (with
global impairment of systolic contraction)> The
left ventricular ejection fraction has been
correlated with outcome and surcival in patients
with heart failure.
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32. Echocardiography may also show other abnormalities,
including valvar disease, left ventricular aneurysm,
intracardiac thrombus, and pericardial disease.
Doppler echocardiography allows the quantitative
assessment of flow across valves and the identification of
valve stenosis, in addition to the assessment of right
ventricular systolic pressure and allowing the indirect
diagnosis of pulmonary hypertension. Doppler studies have
been used in the assessment of diastolic function. Colour
flow Doppler techniques are particularly sensitive in
detecting the direction of blood flow and the presence of
valve incompletence.
Transoesophageal echocardiography allows the detailed
assessment of the atrial, valves, pulmonary veins, and any
cardiac massess, including thrombi.
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33. Haematology and biochemistry
Routine haematology and biochemistry
investigations are recommended to exclude
anaemia as a cause of breathlessness and high
output heart failure. In mild and moderate heart
failure, renal function and electrolytes are usually
normal. In severs ( New York Heart Association,
class IV) heart failure, however, as a result of
reduced renal perfusion, high dose diuretics,
sodium restriction, and activition of the
neurohormonal mechanisms (including
vasopressin), there is an inability to present.
Hyponatraemia is, therefore, a marker of the
severity of chronic heart failure.
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34. Hypokalaemia occurs when high dose diuretics are
used without potassium supplementation or
potassium sparing agents. Hyperkalaemia can also
occur in severe congestive heart failure with a low
glomerular filtration rate, particularly with the
concurrent use of angiotensin converting enzyme
inhivitors and potassium sparing diuretics. Both
hypokalaemia and hyperkalemia increase the risk
of cardiac arrhythmias; hypomagnesaemia, with
long term diuretic treatment, increases the risk of
ventricular arrhythmias. Thyroid function tests are
also recommended in all patients, in view of the
association between thyroid disease and the heart.
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35. Radionuclide methods
Radionuclide inaging- or multigated
ventriculography- allows the assessment of
the global left and right ventricular
function. This allows the assessment of
ejection fraction, systolic filling rate,
diastolic emptying rate, and wall motion
abnormalities.
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36. Angiography, cardiac catheterisation, and myocardial
biopsy
Angiography should be considered in patients with
recurrent ischaemic chest pain associated with heart
failure and in those with evidence of severe reversible
ischaemia or hibernating myocardium. Cardiac
catheterisation with myocardial biopsy can be valuable in
more difficult cases where there is diagnostic doubt-for
example, in restrictive and infiltrating cardiomyopathies
(amyloid heart disease, sarcoidosis ), myocarditis, and
pericardial disease
Pulmonary function tests
Objective measurement of lung function is useful in
excluding respiratory causes of breathlessness, although
respiratory and cardiac disease commonly36 coexist.