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HEART FAILURE

Prof : Dr Mya Mya Aye

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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.

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Cause of heart failureCoronary artery diseaseMyocardial infarction IschaemiaHyoertensionCardiomyopathyDilated (congestive)Hypertrophic/ obstructiveRestrictive – for example, amyloidosis,

sarcoidosis, haemochromatosisObliterative

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Valvar and congenital heart diseaseMitral valve diseaseAortic valve diseaseAtrial septal defect, ventricular septal defect

ArrhythmiasTachycardiacBradycardia (complete heart block, the sick

sinus syndrome)Loss of atrial transport – for example, atrial

fibrillation

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Alcohol and drugsAlcoholCardiac depressant drugs ( blockers, calcium

antagonists)

" High output " failureAnaemia, thyrotoxicosis, arteriovenous

fistulae, Paget's disease

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Pericardial diseaseConstrictive pericarditisPericardial effusion

Primary right heart failurePulmonary hypertension – for example,

pulmonary embolism, cor pilmonaleTricuspid incompetence

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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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•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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Liver Vessels Brain

Renin substrate ( angiotensinogen)

Angiotensin I

Renin

(kidney)

Angiotensin converting enzyme

(lungs and vasculature )

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Angiotenin II

Vasoconstriction Aldosterone release Enhanced sympathetic activity

Salt and water retention

Renin-angiotensin-aldosterone axis in heart failure

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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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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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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. - 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)

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Left right and biventricular heart failureThe 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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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).

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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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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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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.

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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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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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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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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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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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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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Investigations if heart failure is suspectedInitial 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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Chest X rays examinationThe 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 effusion.

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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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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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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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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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EchocardiographyEchocardiography 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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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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Haematology and biochemistryRoutine 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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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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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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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 commonly coexist.