1.Failure of the pump itself: In the most frequent circumstance, damaged muscle contracts weakly or inadequately, and the chambers cannot empty properly. In some conditions, however, the muscle cannot relax sufficiently.

2.An obstruction to flow, owing to a lesion preventing valve opening or otherwise causing increased venticular chamber pressure (e.g., aortic valvular stenosis, systemic hypertension, or aortic coarctation); This overworks the chamber behing the obstruction.

3.Regurgitant flow (e.g., mitral or aortic valvular regurgitation) that causes some of the output from each contraction to reflux backward: This necessarily adds a volume workload on the ventricle.

4.Disorders of cardiac conduction ( e.g., heart block) or arrhythmias owing to uncoordinated generation of impulses ( e.g., ventricular fibrillation): These lead to non-uniform and inefficient contractions of the muscular walls.

5.Disruption of continuity of circulatory system (e.g., gunshot wound through the thoracic aorta): This permits blood to escape.

Heart Failure

The above listed abnormalities often culminate in heart failure, an extremely common result of many forms of heart disease. In heart failure, often called congestive heart failure, the heart is unable to pump blood at a rate commensurate with the requirements of the metabolizing tissues or can do so only from an elevated filling pressure. Although usually caused by a slowly developing deficit in myocardial contraction, a similar clinical syndrome is present in some patients with heart failure caused by conditions in which the normal heart is suddenly presented with a load that exceeds its capacity or in which venricular filling is impaired. Congestive heart failure is a common and often recurrent condition with a poor prognosis ( mortality of more than 50% in less than 5 years) that is the underlying or contributing cause of death of an estimated 300,000 individuals are currently being treated. It is the leading discharge diagnosis in hospitalized patients over 65 years of age.

The cardiovascular system acts to maintain arterial pressure and perfusion of vital organs by responding to excessive hemodynamic burden or disturbance in myocardial contractility by a number of mechanisms. The most important are as follows:

The Frank-Starling mechanism, in which the increased preload of dialation helps to sustain cardiac performance by enhancing contractile tissue augmented.
Activation of neurohumoral systems, especially (1). Release of the neurotransmitter norepinephrine by adrenergic cardiac nerves ( which increases heart rate and augments myocardial contractility), (2).activation of renin-angiotensin-aldosterone system and (3). Release of atrial natriuretic peptide.

These adaptive mechanisms may be adequate to maintain the overall pumping performance of the heart at relatively normal levels, but their capacity to sustain cardiac performance may ultimately be exceeded. Most instances of heart failure are the consequence of progressive deterioration of myocardial contractile function (systolic dysfunction) as often occurs with ischemic injury pressure or volume over load or delated cardiomyopathy. The most frequent specific causes are hypertension and IHD. Sometimes however failure results from an inability of the heart chamber to relax expand and fill sufficiently during diastole to accommodate an adequate ventricular blood volume ( diastolic dysfuntion) myocardial fibrosis, deposition of amyloid, or constrictive percarditis. Whatever its basis, congestive heart failure is characterized by diminished cardiac output (sometimes called forward failure ) or damming back of blood in the venous system ( so-called backward failure) or both.