Understanding Heart Failure, and its Different Types of Symptoms

Heart Failure: It is a clinical syndrome in which an abnormality of cardiac structure or function is responsible for the inability of the heart to eject or fill with blood at a rate commensurate with the requirements of the metabolizing tissues.

HF results in a constellation of clinical manifestations, including in various combinations, circulatory congestion, dyspnea, fatigue, and weakness.

The severities of the clinical manifestations are commonly described according to criteria development by the Association. HF is frequently, but not always, caused by a defect in myocardial contraction, and then the term myocardial failure is appropriate.

The latter may result from a primary abnormally in heart muscle, as occurs in the cardiomyopathies, or in viral myocarditis. HF also results commonly from coronary atherosclerosis, which interferes with cardiac contraction by causing myocardial infarction and ischemia.

HF may also occur in congenital, valvular, and hypertensive heart disease in which the myocardium is damaged by the long standing hemodynamic overload. In other patients with HF,

However a similar clinical syndrome is present but without any detectable abnormality of myocardial function. In some as cases the normal heart is suddenly presented with a mechanical load that exceeds its capacity.

Such as an acute hypertensive crisis, rupture of an aortic valve leaflet, in endocarditis or with a massive pulmonary emobilm.

HF in the presence of normal systolic function also occurs in chronic conditions in which there is impaired filling of the ventricles due to a mechanical abnormality such as tricuspis and mitral stenosis without myocardial involvement, endocardial fibrosis, and some forms of hypertrophic cardiomyopathy .

Type of Heart Failure: It may be described as systolic or diastolic, high out put or low out put acute or chronic right side or left side and forward or back ward.

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

Systolic versus Diastolic Failure: The distinction between these two forms of HF Relates to whether the principle abnormality is the inability of the ventricle to contract normally and expel sufficient blood or to relax and fill normally.

The man infestations of systolic failure related to an inadequate cardiac output with weakness, fatigue, reduced exercises tolerance, and other symptoms of hypoperfusion, while in diastolic.

HF the manifestations relate principally to the elevation of filling pressures in the left and right ventricles. Diastolic HF is usually defined as HF in patients with an ejection fraction > 50%. Diastolic HF may be caused by increased resistance to ventricular.

Inflow and reduced ventricular diastolic capacity impaired ventricular relaxation and myocardial fibrosis and frequently in women than men, especially elderly women with hypertension. In most patient with HF, abnormalities both of contraction and relaxation coexist.

Low – Out Put Versus High Out put Heart Failure:

Low output HF occurs secondary to ischemic heart disease, hypertension, dilated cardiomy opathy, and valvular and pericardial disease, while high out put HF occurs in patients with reduced systemic vascular resistance.

I.e. anemia, hyperthyroidism, pregnancy, arteriovenous fistulas, beriberi, a paget’s disease. In clinical practice, however, low-output high-output HF cannot always be readily distinguished. The normal range of cardiac output is wide (2.2 to 3.5 l/min per m2).

In many patients with low-output HF, the cardiac output may actually be just above the lower limit of normal range at rest (although lower than it had been previously), but fails to rise normally during exertion. On the other hand, in patients with so-called high-output HF,

The output may not exceed the upper limits of normal (although it would have been above normally elevated had it been measured before HF supervened); instead, it may have fallen to within normal limits with HF.

The hemodynamic burden placed on the myocardium by many forms of high-output heart failure resembles that produced by chronic aortic regurgitation.

In addition, thyrotoxicosis and beriberi may also impair myocardial metabolism directly, while very severe anemia many interfere with myocardial function by producing myocardial anoxia especially in the subendocardium and in the presence of underlying obstructive coronary artery disease.

Acute versus chronic heart failure

An example of causes of acute HF is sudden rupture of a cardiac vale learlet secondary trauma or infective endocarditis or a massive myocardial infarction a patient who previously had no cardiac dysfunction.

In acute HF the sudden reduction in cardiac output often results in systemic hypotension without peripheral edema. Chronic HF is typically observed patients with dilated cardiomyopathy. Vascular congestion is common chronic HF, but arterial pressure is ordinarily well maintained until very late.

Right-sided and left-sided heart failure

Many of the clinic manifestations of HF results from the accumulation of fluid upstream to (behind) the ventricles that is initially affected. For example.

Patients in whom the left ventricle is hemodynamically overloaded (e.g. aortic regurgitation) or weakened due to myocyte loss (e.g. post myocardial infarction) develop dyspnea and orthopnea as a result of pulmonary congestion,

A affects the right ventricle primarily (e.g. primary pulmonary hypertension secondary to chronic pulmonary thronboembolism), symptoms resulting from pulmonary congestion hepatomegaly, and systemic venoudistention, i.e. clinical manifestations of right-sided HF, are prominent.

The muscle bundles composing both ventricles are continuous and both ventricles share a common wall, the interventricular septure. The biochemical changes that occur in the myocardium of HF (215).

Usually occur in the myocardium of both ventricles. Therefore when HF has existed for months or years, localization of excess flu behind one ventricle may no longer exist.

Backward versus forward heart failure

A controversy has revolved around the mechanism of the clinical manifestations resulting from HF. The concept of backward HF contents that in HF, one or the other ventricle fails to discharge its contents or fails to till normally.

As consequence, the pressure in the atrium and venous system behind (upstream to) the failing ventricle rise, and retention of sodium at water occurs as a consequence of the elevation of systemic venous and capillary pressures and the resultant transudation of the fluid into the pulmonary or systemic interstitial space.

On the other hand, proponents of the forward HF hypothesis maintain that the clinical manifestations of HF 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 and distal tubular reabsorption of sodium, the latter through activation of the rennin-angiotensin-aldosterone system (RAAS) .

The rate of onset of HF often influences the clinical manifestations. For example, when a large portion of the left ventricle is suddenly destroyed, as in myocardial infarction, the patients may succumb to acute pulmonary edema, a manifestation of backward failure.

If the patient survives the acute insult, clinical manifestations resulting from a chronically depressed cardiac output, including the abnormal retention of fluid within the systemic vascular bed, may develop, which is a manifestation of forward failure.

| Patho-physiology in heart failures and the neuro-hormmal activation and compensatory mechanism in heart failure | symptoms / clinical features of the heart failure |



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