Heart failure represents a major public health problem in industrialized nations. It appears to be the only common cardiovascular condition that is increasing in prevalence and incidence. In the United States, heart failure is responsible for almost 1 million hospital admissions and 40,000 deaths annually.

Heart failure should be distinguished from (1) conditions in which there is circulatory congestion consequent to abnormal salt and water retention but in which there is no disturbance of cardiac function per se and (2) noncardiac causes of inadequate cardiac output, including shock due to hypovolemia and redistribution of blood volume.

The ventricles respond to a chronically increased hemodynamic burden with progressive hypertrophy. With volume overload, the ventricle is required to deliver an increased cardiac output for prolonged periods, e.g., valvular regurgitation, and it develops eccentric hypertrophy, i.e., cavity dilatation, with an increase in muscle mass such that the ratio between wall thickness and ventricular cavity remains relatively constant. With chronic pressure overload, as in aortic stenosis or untreated hypertension, the ventricle develops concentric hypertrophy, in which the ratio between wall thickness and ventricular cavity size increases.

These descriptors are often useful in a clinical setting, particularly early in the patient’s course, but late in the course of chronic heart failure the differences between them become blurred.

Systolic Versus Diastolic Failure

This classification relates to whether the principal abnormality is the inability to contract normally and expel sufficient blood (systolic failure) or to relax and fill normally (diastolic failure). The major clinical manifestations of systolic failure relate to an inadequate cardiac output with weakness, fatigue, reduced exercise tolerance and other symptoms of hypoperfusion, while in diastolic failure they relate principally to an elevation of filling pressures. In many patients, particularly those who have both ventricular hypertrophy and dilatation, abnormalities of contraction and relaxation coexist.

Diastolic heart failure may be caused by increased resistance to ventricular inflow and reduced ventricular diastolic capacity (constrictive pericarditis and restrictive, hypertensive, and hypertrophic cardiomyopathy), impaired ventricular relaxation (acute myocardial ischemia, hypertrophic cardiomyopathy), and myocardial fibrosis and infiltration (dilated, chronic ischemic, and restrictive cardiomyopathy).

High Output Versus Low Output Heart Failure

Low output heart failure occurs secondary to ischemic heart disease, hypertension, dilated cardiomyopathy, and valvular and pericardial disease. High output heart failure occurs in hyperthyroidism, anemia, pregnancy, arteriovenous fistulas, beriberi, and Paget’s disease. In clinical practice, however, low output and high output heart failure cannot always be readily distinguished.

Acute Versus Chronic Heart Failure

The prototype of acute heart failure is the patient who is entirely well but who suddenly develops a large myocardial infarction or rupture of a cardiac valve. Chronic heart failure is typically observed in patients with dilated cardiomyopathy or multivalvular heart disease that develops or progresses slowly. Acute heart failure is usually largely systolic and the sudden reduction in cardiac output often results in systemic hypotension without peripheral edema. In chronic heart failure, arterial pressure tends to be well maintained until very late in the course, but there is often accumulation of peripheral edema.

Right Sided Versus Left Sided Heart Failure

Patients in whom the left ventricle is mechanically overloaded (e.g., aortic stenosis) or weakened (e.g., post myocardial infarction) develop dyspnea and orthopnea as a result of pulmonary congestion, a condition referred to as left sided heart failure. In contrast, when the underlying abnormality affects the right ventricle primarily (e.g., pulmonic stenosis or pulmonary hypertension), symptoms resulting from pulmonary congestion such as orthopnea and paroxysmal nocturnal dyspnea are less common, and edema, congestive hepatomegaly, and systemic venous distention, i.e., clinical manifestations of right sided heart failure, are more prominent. However, when heart failure has existed for months or years, biventricular failure usually results. For example, patients with long standing aortic valve disease or systemic hypertension may have ankle edema, congestive hepatomegaly, and systemic venous distention late in the course of their disease, even though the abnormal hemodynamic burden initially was placed on the left ventricle.

Backward Versus Forward Heart Failure

The concept of backward heart failure contends that in heart failure, one or the other ventricle fails to discharge its contents or fails to fill normally. As a consequence, the pressures in the atrium and venous system behind the failing ventricle rise, and retention of sodium and water occurs as a consequence of the elevation of systemic venous and capillary pressures and the resultant transudation of fluids into the interstitial space. In contrast, the proponents of the forward heart failure hypothesis maintain that the clinical manifestations of heart failure result directly from an inadequate discharge of blood into the arterial system. According to this concept, salt and water retention is a consequence of diminished renal perfusion and excessive proximal tubular sodium reabsorption and of excessive distal tubular reabsorption through activation of the renin-angiotensin-aldosterone system.

Redistribution of Cardiac Output

The redistribution of cardiac output serves as an important compensatory mechanism when cardiac output is reduced. This redistribution is most marked when a patient with heart failure exercises, but as heart failure advances, redistribution occurs even in the basal state. Blood flow is redistributed so that the delivery of oxygen to vital organs, such as the brain and myocardium, is maintained at normal or near-normal levels, while flow to less critical areas, such as the cutaneous and muscular beds and viscera, is reduced. Vasoconstriction mediated by the adrenergic nervous system is largely responsible for this redistribution, which in turn may be responsible for many of the clinical manifestations of heart failure, such as fluid accumulation (reduction of renal flow), low grade fever (redistribution of cutaneous flow), and fatigue (reduction of muscle flow).

Clinical Findings

Tachycardia

Cyanosis of lips and nail beds

Jugular venous distention

Diminished pulse pressure

Third and fourth heart sounds

Pulsus alternans

Pulmonary rales

Cardiac edema

Hydrothorax and ascites

Congestive hepatomegaly

Jaundice

Cardiac cachexia

Cold, pale extremities

CLINICAL MANIFESTATIONS
OF HEART FAILURE

Dyspnea

Orthopnea

Paroxysmal (nocturnal) dyspnea

Cheyne-Stokes respirations (periodic or cyclic respiration)

Fatigue, weakness, and abdominal symptoms

Cerebral symptoms (confusion, headache, insomnia)

In addition to the enlargement of the particular chambers responsible for heart failure, distention of pulmonary veins and redistribution of pulmonary vasculature to the apices is common in patients with heart failure and elevated pulmonary vascular pressures. Also, pleural effusions may be evident and associated with interlobar effusions.

In summary, treatment of congestive heart failure includes:

Cardiac Transplantation

When patients with heart failure become unresponsive to a combination of therapeutic measures, are in New York Heart Association Class IV (symptomatic at rest), and are deemed unlikely to survive one year, they should be considered for cardiac transplantation. Many centers now have one year survival rates exceeding 80%-90%, and five year survival rates over 70%.