Cardiac Failure

Synonyms :  Cardiac Failure, Cardiac Insufficiency, Congestive Heart Disease - CHD, Congestive Heart Failure - CHF, Heart Failure, Myocardial Insufficiency

Clinical features, Diagnosis, Management, Prognosis, Nutrition, Herbs,

Heart failure is an imprecise term used to describe the state that develops when the heart cannot maintain an adequate cardiac output. In the mildest forms of heart failure cardiac output is adequate at rest and becomes inadequate only when the metabolic demand increases during exercise or some other form of stress. Almost all forms of heart disease may lead to heart failure and it is important to appreciate that the term refers to a clinical syndrome rather than a specific diagnosis. 

Types of Heart Failure 

1. Acute and chronic heart failure 

Heart failure may develop suddenly, as in myocardial infarction, or gradually, as in progressive valvular heart disease or prolonged hypertension. 

When there is gradual impairment of cardiac function a variety of compensatory changes may improve overall cardiac function (activation of the sympathetic nervous system, myocardial hypertrophy, chamber enlargement, activation of the renin-angiotensin-aldosterone system, release of antidiuretic hormone). These mechanisms aim to increase cardiac output either by directly increasing cardiac contractility/heart rate or increasing blood volume and venous return, which then stimulate pumping activity of the heart. 

As long as these compensatory mechanisms manage to maintain normal or near normal cardiac output, the patient is said to have compensated heart failure, which is generally asymptomatic. However a minor event such as an intercurrent infection, physical or emotional stress, inappropriate reduction of therapy or pregnancy, may precipitate overt (symtomatic) decompensated heart failure in this type of patient. Decompensated heart failure eventually develops in most patients when the weakened heart can no longer respond to constant stimulation. 

2. 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, and the right side stands for the right atrium, right ventricle, tricuspid and pulmonary valves. 

         Left-sided heart failure is a reduction in the left ventricular output with consequent increase in the left atrial and pulmonary venous pressure. An acute increase in left atrial pressure may cause pulmonary congestion or pulmonary oedema, but a more gradual increase in the left atrial pressure often leads to reflex pulmonary vasoconstriction which protects the patient from pulmonary oedema at the cost of pulmonary hypertension and right ventricular strain. 

         Right-sided heart failure is a reduction in right ventricular output with subsequent blood stasis in peripheral tissues. Isolated right heart failure may develop as a result of chronic lung disease such as chronic bronchitis and emphysema (so called cor pulmonale). In emphysema there is widespread destruction of alveolar walls leading to reduction in pulmonary vascular bed (pulmonary ‘pipeline?, and increased resistance to blood flow. In chronic bronchitis due to irreversible airway obstruction there is widespread hypoventilation of many areas in the lungs, which in turn leads to cutting off blood flow through them as an autoregulatory mechanism (gas exchange can not occur in these passive areas). 

         Biventricular heart failure is a failure of both sides of the heart developing because the disease process such as cardiomyopathy (progressive weakening of the heart usually of unknown cause) 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.

Heart failure can develop in following circumstances: 

1.       Ventricular outflow obstruction (pressure overload) is found in systemic or pulmonary hypertension and aortic or pulmonary valve stenosis. Initial heart response is hypertrophy (increased muscle mass) to accommodate increased work in maintaining normal cardiac output. At some point this compensatory mechanism will no longer suffice and overt heart failure will follow.

2.       Ventricular inflow obstruction is observed in mitral or tricuspid valve stenosis or more rarely in constrictive pericarditis that results in formation of firm, inelastic connective tissue layer that covers the heart and restricts its expansion. More acute type of ventricular inflow obstruction is cardiac tamponade after ventricular wall rupture in extensive myocardial infarction.

3.       Ventricular volume overload occurs in intracardial shunting of blood (e.g., septal defects ? ‘holes? which can be inborn or acquired as a result of myocardial infarction) or in valvular incompetence with backflow of blood (e.g., mitral or aortic incompetence will eventually lead to left heart failure)

4.       Impaired ventricular function (reduced cardiac contractility) can be a consequence of diffuse myocardial diseases such as myocarditis and cardiomyopathy or localised myocardial disease such as myocardial infarction (reduced cardiac contractility or grave cardiac arrhythmia such as ventricular fibrillation).

Clinical features:  < BACK TO TOP >

       The clinical picture depends on the nature of the underlying heart disease, the type of heart failure that it has produced and the compensatory mechanisms that have developed.

       Low cardiac output causes fatigue, tiredness and poor effort tolerance, pale skin, cold peripheries, low blood pressure, oliguria (reduced volume of urine).

       Left heart failure may cause breathlessness, orthopnoea and paroxysmal nocturnal dyspnoea with late inspiratory crackles over the lung bases (heard on auscultation), cough with pink-tinged or brownish sputum due to presence of traces of blood or ‘heart failure?cells (macrophages filled with haemosiderin) respectively; these features are absent if there is marked pulmonary vasoconstriction. In acute pulmonary oedema the patient presents with extreme dyspnoea, tachypnoea, cyanosis, restlessness and anxiety with a sense of suffocation.

       Right heart failure produces hepatic congestion (moderately enlarged tender liver), peripheral oedema and ascites or pleural effusion (hydrothorax) due to accumulation of fluid. Distribution of peripheral oedema is influenced by gravity and it affects more lower parts of the body (so called dependant oedema). This means that in mobile patients the oedema affects the ankles and shins, whereas in bedbound patients it collects around the sacrum.

Diagnosis:  < BACK TO TOP >

       Clinical findings and physical examination are very indicative.

       ECG shows signs of compensatory heart changes (myocardial hypertrophy, increased heart rate) and sometimes arrhythmias as a complication of the heart failure.

       Chest X-ray is done to detect changes in the heart and lung (cardiac enlargement, pulmonary congestion and oedema).

       Echocardiography is extremely valuable and may demonstrate the underlying problem (e.g., valve abnormalities) or the current status of the heart vitality (e.g., weak contractions, reduced stroke volume, increased end-systolic volume).

Management  < BACK TO TOP >

       Since heart failure is not a disease, management should be directed to the underlying condition (e.g., replacement of damaged valves).

       Physical rest is helpful (bed-rest increases renal blood flow and will often initiate diuresis without any adjustment in diuretic therapy).

       Diuretics are usually the first line of treatment, leading to a reduction in blood and plasma volume, and may also cause a small but significant degree of arterial and venous dilation.

       Angiotensin converting enzyme (ACE) inhibitors (listed earlier) act to prevent the conversion of angiotensin I to angiotensin II, thereby counteracting salt and water retention, peripheral arterial and venous vasoconstriction. A combination of a diuretic and an ACE inhibitor is a preferred option.

       Angiotensin II antagonists (listed earlier) block the action of angiotensin II and have similar effects to ACE inhibitors, but with the advantage of not causing dry cough as a side effect.

       Cardiotonic glycosides (digoxin [Lanoxin]) may be effective in few selected cases of severe heart failure that has not responded to treatment with a diuretic and an ACE inhibitor. 

Heart failure carries a poor prognosis. Although the outlook depends, to some extent, on the underlying cause of the problem, approximately 50% of patients with severe heart failure will die within two years. Many patients die suddenly, often due to malignant ventricular arrhythmias such as ventricular tachycardia and fibrillation, or myocardial infarction. Others may eventually die from pulmonary oedema/respiratory failure, sometimes with superimposed episode of pneumonia.

Prognosis  < BACK TO TOP >

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Nutrition < BACK TO TOP >

Nutrition that alleviate or prevent Cardiac Failure :-
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Herbs < BACK TO TOP >

Herbs that alleviate or prevent Cardiac Failure :-
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