The heart is a part of an elaborate circulatory apparatus that is designed to serve two major functions: first one is usual course of events, to provide the tissues with significant blood carrying oxygen, substrates and nutrients for their metabolic needs, both at rest and during activity and second one is as a temporary expedient, to reapportion the cardiac output according to the physiologic priorities of the movement, example muscular exercise, heat loss, digestion. The same regulatory mechanisms that satisfy physiologic priorities in health also serve to protect vital organs, like heart and brain, when cardiac output is seriously compromised. The heart is remarkable not only for its capacity to adjust rapidly to metabolic need and to varying loads, but also for its durability. Unfortunately, it’s also vulnerable to a wide array of congenital, metabolic, inflammatory, and degenerative disorders —

8That affect its muscular walls, it’s linings, its values, and particularly its nutrient vessels, i. e., the coronary arteries, some cardiac disorders, such as arteriosclerosis of the small coronary arteries, progress slowly and insidiously, and their disease takes a lifetime to become clinically evident. Others such as bacterial infection of the aortic-valve, are often dramatic in onset and catastrophic in their consequences.

In general signs and symptoms of heart diseases are two different kinds those referable to the heart itself such as pain and palpitation, and others that are extra cardiac and originate in congested circulatory beds hypo perfumed organs. Considered out of context each extra cardiac manifestation may be disappointingly non specific for example, breathlessness is a common symptom that is shared by disorders of the heart, the lungs, and the brain.

GENERAL ASPECTS

Heart failure may be considered in clinical physiologic, or biochemical terms. In the clinic, “ HEART FAILURE “” refers to a distinctive constellation of symptoms and physical signs that has emerged in a patient with an underlying cardiac disorder. The hemo dynamic counterpart at that time in an inability of the heart to reach its output to the metabolic needs of the body ( determined as O2 consumption ) even though filling pressures of the heart are adequate. The biochemical equivalent is not as certain as the hemo dynamic, but appears to involve defective conversation by the heart muscle of chemical energy to mechanical work.

The designation heart failure is used as a synonym for myocardial failure. Consequently, heart failure is concerned with a myocardium that is performing inadequately because of either over load or intrinsic disorder. This stipulation automatically excludes syndromes in which the seat of the difficulty is in abnormalities of the heart valves or pericardium or excessive heart rates each of which can compromise the circulation even though cardiac muscle is normal.

Disproportion between hemodynamic load and myocardial capacity to cope with it initiates the sequence that culminates in heart failure. Generally the heart tolerates volume overloads better better than pressure over loads. e.g. volume over load of the left ventricle produced by aortic insufficiency may exist for years without causing distress, in contrast, pressure over load from aortic stenosis generally elicits signs and symptoms of heart failure much earlier. Sustained overloads are also accommodated better than acute overloads. Thus chronic mitral regurgitation caused by rheumatic heart disease may last for years without signs of heart failure, where as the acute mitral regurgitation produced by a ruptured chorda tendinea is opt to precipitate a disastrous syndrome of heart failure.

The myocardium responds differently to volume and pressure loads. Volume overloads generally elicit dilatation followed by hypertrophy; conversely, pressure overloads characteristically elicit hypertrophy until late in the naturally history when dilatation supervenes. Primary myocardial disease generally elicits both dilatation and hypertrophy.

CATEGORIES OF HEART FAILURE

Heart failure is generally identified by its duration ( acute or chronic ), initiating mechanisms, the ventricle that is primarily affected, the characteristic clinical syndrome,and the underlying physiologic derangements

  1. Acute Vs chronic Heart Failure: The manifestations of heart failure usually begins insidiously, blurring at the outset with those of the underlying cardiac disorder and continuing gradually into a chronic state.how ever, the syndrome may also begin acutely, as after myocardial infraction. Between these extremes of acute and chronic heat failure are instances of sub clinical heart failure in which a successful cardio tonic program, compl with self restriction of activity by the patient, minimises signs and symptoms even though cardiac performance remains seriously compromised on the overhand, its not uncommon for the course of chronic heart failure that stem either from lapses in therapy or from progression of the underlying heart disease
    Both acute and chronic heart failure elicit compensatory adjustments. These include increase in peripheral vascular resistance, redistribution of blood flow and increase in erythropoietic activity. But the adaptive mechanisms differ strikingly in type degree and intensity and even in direction. For example acute distension of the left atrium elicits salt and water retention. This distriction between acute and chronic heart failure must be borne in mind when attempting to relate observations on experimental heart failure in animals to the chronic heart failure in man, because of chronic heart failure is generally acute in onset is fulminating in course and is generally ended abruptly by the death of animal
  2. Initiating mechanism generally imposes its own distinctive stamp up on the clinical syndrome. Thus rheumatic heart disease leads to a different constellation of symptoms and signs from that of hypertensive heart disease in turn both have a different natural history from our pulmonate . Indeed, even a single etiology, arteriosclerosis may have distinctly different consequences, progressive narrowing and gradual occlusion of peripheral branches of the coronary arteries be so convert that the characteristic shortness of breath and undue fatigue of left ventricular failure may be misinterpreted as evidence of the general physical decline of advancing age conversely, abrupt closure of a major coronary artery, as a consequence of thrombosis superimposed on an arteriosclerotic plaque, may elicit massive myocardial necrosis, followed by extensive myocardial scanning and unremitting heart failure.
  3. Left Vs Right heart Failure :. With rare exception one ventricle fails before the other. Because of the prevalence of cardiac disorder which over load or damage left ventricle, e.g. coronary arteriosclerosis and hypertension, heart failure usually begins with the left ventricle. Breathlessness, the key clinical expression of pulmonary congestion and Edema , is the most common initial complaint. Conversely, when the right ventricle fails, systemic venous congestion and peripheral Edima generally predominate. Left ventricular failure is the most common cause of right ventricular failure, and breathlessness often improves as right ventricular out put flats and pulmonary congestion diminishes.
    The mechanism by which left ventricular failure causes the right ventricle to fall is not entirely clear, although pulmonary venous and arterial hypertension from the failing left ventricular and the continuity of heart muscle around both ventricles are undoubtedly involved. In contrast to the accepted sequence of left ventricular failure followed by right ventricular failure, it is still debated wheather -isolated right ventricular failure. The latter association is difficult to prove because of the frequent coexistence of independent and unrelated left ventricular disease in patients with right ventricular failure.
  4. Backward Vs Forward heart Failure: some what reminiscent of the fable about the blind men and the elephant is the vintage controversy about Backward versus Forward heart failure. Backward failure calls attention to the damming up of blood in the vein’s proximal to the following ventricle and attributes to this venous congestion a critical role in the evaluation of the syndrome of heart failure., Forward failure assign’s the same pivotal role to a decrease in cardiac output and under filing of the arterial tree. In reality this distinction is meaningless because it is inevitable in a closed circuit that the inability of the heart to sustain the output ( Forward Failure )and the pooling of blood on the venous inflow side ( Backward Failure ).
  5. Low Vs High Output Failure: Cardiac catheterisation in man has made it possible to sort myocardial failure according to the level of the cardiac output. The separation into high and low output failure is concerned with the clinical manifestations, rather than the causes of myocardial failure. But it is also a hemodynamic frame of reference to which the anatomist and the biochemist can relate the myocardial origins of heart failure. For example, high output failure probably has different biochemical bases from low output failure.Now are all types of low output or high output failure apt to have the same biochemical origins. For example it is unlikely that the high output failure of a peripheral arteriovenous fistula has the same anatomic or biochemical beginnings and evolution as the high output failure of severe anemia or malnutrition.
  6. Congestive failure Vs Congested State : Overfilling of both venous circulations, without myocardial failure, is the hallmark of the “congested state. “ it may be included by rapid infusions; it may also occur in the course of “ hyperkinetic “ circulatory states as diverse as severe anemia and peripheral arteriovenous fistula. Similar but less dramatic venous congestion may also complicate Paget’s disease or beriberi. In each of these situations, if an expanded venous volume and heightened venomotor tone, rather than from heart failure.
Assessment of Cardiac Performance

With respect to evaluating performance, the heart may be regarded from three points of view as a pump, as a muscle and as a component of the circulation. Hemodynamic measurements are used to characterise its behaviour as a pump, cardiac output, stroke output, stroke work, stroke power, ventricular end-diastolic pressure, ejection fraction and ventricular end-diastolic volume. To ascertain it’s behaviour as a muscle, principles of muscle mechanics are applied. It’s adequacy as component of the circulation is reflected in the derangements that result from the low cardiac output, the redistribution of blood flow among tissues and organs, organ hypo perfusion, and venous congestion.

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