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The main pathophysiology of heart failure is a reduction in the efficiency of the heart muscle, through damage or overloading. As such, it can be caused by a wide number of conditions, including myocardial infarction , hypertension and amyloidosis. Over time these increases in workload will produce changes to the heart itself:
The heart of a person with heart failure may have a reduced force of contraction due to overloading of the ventricle. In a healthy heart, increased filling of the ventricle results in increased contraction force and thus a rise in cardiac output. In heart failure, this mechanism fails, as the ventricle is loaded with blood to the point where heart muscle contraction becomes less efficient. This is due to reduced ability to cross-link actin and myosin filaments in over-stretched heart muscle.
A reduced stroke volume may occur as a result of a failure of systole, diastole or both. Increased end systolic volume is usually caused by reduced contractility. Decreased end diastolic volume results from impaired ventricular filling; this occurs when the compliance of the ventricle falls. As the heart works harder to meet normal metabolic demands, the amount cardiac output can increase in times of increased oxygen demand is reduced. This contributes to the exercise intolerance commonly seen in heart failure. This translates to the loss of one's cardiac reserve, or the ability of the heart to work harder during strenuous physical activity. Since the heart has to work harder to meet the normal metabolic demands, it is incapable of meeting the metabolic demands of the body during exercise.
A common finding in those with heart failure is an increased heart rate, stimulated by increased sympathetic activity in order to maintain an adequate cardiac output. Initially, this helps compensate for heart failure by maintaining blood pressure and perfusion, but places further strain on the myocardium, increasing coronary perfusion requirements, which can lead to worsening of ischemic heart disease. Sympathetic activity may also cause potentially fatal abnormal heart rhythms. An increase in the physical size of the heart's muscular layer may occur. This is caused by the terminally differentiated heart muscle fibers increasing in size in an attempt to improve contractility. This may contribute to the increased stiffness and thus decrease the ability to relax during diastole. Enlargement of the ventricles can also occur and contributes to the enlargement and spherical shape of the failing heart. The increase in ventricular volume also causes a reduction in stroke volume due to mechanical and inefficient contraction of the heart.