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Chronic Heart Failure
In heart failure, cardiac output is insufficient to meet the needs of the body, or can meet only with increased filling pressure (preload). Compensatory mechanisms may be able to maintain cardiac output at rest, but probably not enough for physical training. Cardiac function eventually declines, and heart failure becomes severe (decompensated). Heart failure primarily diseases of old age. Diagnosis can be difficult to enforce at an early stage because of relatively no symptoms.

Clinical Manifestation
Dyspnea (shortness of breath), accompanied by weakness, fatigue, and peripheral edema (fluid retention in tissues), which is most often seen as a swelling of the legs. Enlarged heart and liver, central venous pressure causes a high jugular venous distension. A Gallop rhythm can be heard due to the high cardiac filling pressures.

Etiology
Heart failure is most often caused by failure of myocardial contractility, as occurs in myocardial infarction, old hypertension, or cardiomyopathy. However, in certain circumstances, even a good myocardial contractility can not meet the needs of the systemic blood throughout the body to meet the metabolic needs of the body. This condition is caused by mechanical problems such as severe valve regurgitation, thiamine deficiency (beriberi), severe anemia, and more rarely, arteriovenous fistula. High cardiac output state that this alone can lead to heart failure, but not too heavy can precipitate heart failure in people with primary heart disease.
Coronary heart disease, hypertension, heart valve disease, and nutritional deficiency is a common cause. Independent risk factor for heart failure are similar to risk factors in coronary heart disease (elevated cholesterol, hypertension, and diabetes), plus the existence of left ventricular hypertrophy on resting electrocardiogram.

Pathophysiology
Approximately 70% of cases are caused by systolic failure, with impaired ventricular function and ejection fraction less than 50%. Decreased myocardial contractility, and depressed ventricular function curve. In diastolic failure, ventricular filling is interrupted, usually due to stiff ventricular wall due to fibrosis or hypertrophy. Contractility may be normal or even increased, and ejection fraction more than 50%. Failed to systolic and diastolic pressures often occur together. Similar clinical manifestations due to both bulk can be achieved only at rest with increased end-diastolic pressure. In severe heart failure and decompensated, bulk normal rest can not be achieved even with substantial increases end-diastolic pressure.

Left Heart Failure
Ischemic heart disease most often on the left ventricle. Decrease in rainfall led to increased end-diastolic left ventricular pressure (preload) and pulmonary venous pressure because of blood 'back' in the pulmonary circulation and cause pulmonary congestion. This condition causes the heart dilated, and increased pulmonary capillary pressure spur the accumulation of fluid in the interstitial lung tissue. Increased blood and fluid in the lungs makes the lungs become heavy, causing dyspnea. Dyspnea only can only occur if the patient is lying flat (orthopnea) because of fluid distributed to the lung. Dyspnea continues that causes the patient awake at night is called paroxysmal nocturnal dypsnea. If the state is heavy, then the increase in capillary pressure to push fluid into the alveoli (pulmonary edema), a life-threatening condition that causes severe dyspnea, which reduces gas exchange and lead to hypoxemia.

Right Heart Failure
Left heart failure increased pulmonary vascular pressure, and can cause pressure overload and right heart failure, a condition called congestive heart failure. Right heart failure itself is associated with chronic lung disease (pulmonary choir), pulmonary hypertension, embolism, and valve disease. Central venous pressure was elevated in right heart failure, seen as distended jugular veins, and causes fluid accumulation in peripheral tissue (peripheral edema), peritoneum (ascites) and liver, causing pain and liver enlargement (hepatomegaly). Ambulatory patients may show pitting edema of the legs (a curve that does not disappear after the leg is pressed with a finger), which subsided when lying down.

Compensation Mechanism
Adaptation mechanism to compensate for decreased function initially, but often dangerous when the situation settled. In the event of disruption of primary myocardial contractility or excessive hemodynamic burden is given in the normal ventricles, the heart will be holding a number of adaptation mechanisms to maintain cardiac output and blood pressure. These mechanisms increase the work of the heart, increasing oxygen demand, which is obviously dangerous in ischemic heart disease.

Starling's law
Decrease in cardiac output and ejection fraction increased preload. Therefore, an increase in heart strength based on Starling's law, which is partially restore cardiac output, but with the consequence of increased filling pressure (end-diastolic pressure).

Neurohumoral system
Initiate a reflex decrease in blood pressure baroreceptors, and stimulates the sympathetic nervous system (catecholamines). This reflex increases the rate of heart rate and contractility, and improve cardiac output. Venoconstriction increased central venous pressure, systemic vasoconstriction and increased total peripheral resistance which helps maintain blood pressure. However, afterload increases, and redistribution of muscle bulk and splanchnic circulation skeletal muscle weakness and fatigue, and impaired renal function. Decrease in renal perfusion caused stimulation of the renin-angiotensin-aldosterone (RAA), which causes elevated levels of renin, angiotensin II and aldosterone. Reduce the renal artery vasoconstriction filtration and urine production (oliguria), and causes the release of renin, which activates angiotensin I. Angiotensin I is converted into angiotensin II, a powerful vasoconstrictor in renal efferent arterioles, which increases sympathetic activity, inhibit the parasympathetic tone (vagal) and stimulates the adrenal glands to produce aldosterone. Aldosterone hold Natrium ion and water reabsorption, thereby increasing blood volume and central venous pressure. Sympathetic stimulation also increases vasopressin (antidiuretic hormone), causing further fluid retention.

Myocardial hypertrophy
Persistent increase in afterload (hypertension, aortic stenosis) causes a thickening of the ventricular wall because the muscle cells increase in size (myocardial hypertrophy). This situation is rarely caused by ischemic heart disease. Although cardiac hypertrophy improved power, but a thicker ventricles are less compliant (flexible) and end-diastolic pressure had increased again to charge adequate, this can cause diastolic failure. Hypertrophy also reduced capillary density, increase the diffusion distance, and lower coronary reserve (the difference between maximum coronary flow with the rest).

Release of Natriuretic Peptide
Atrial natriuretic peptide released from the atrium of the heart in response to stretch, causing natriuresis and dilatation.
Brain natriuretic peptide is also released from the heart, especially of the ventricles, and with similar job with atrial natriuretic peptide. Natriuretic peptide works as a physiological antagonist to the effects of angiotensin II on vascular tone, secretion of aldosterone, and renal Natrium reabsorption.