Compensated cardiac failure. A reduction of cardiac output decreases the blood pressure and the venous return, inhibiting the bar receptors and volume receptors respectively. These bring about reflex sympathetic discharge, restoring the cardiac output. The result is a compensated cardiac failure, which occurs only at a higher central venous pressure. The higher central venous pressure represents an accumulation of blood behind the pumping heart (backward failure).
However, because of the compensation, the forward failure subsides.
A major contributor to the pathogenesis of cardiac failure is the retention of salt and water in the body by the kidneys with consequent increase in blood volume. The kidneys retain fluid and Na+ ions when the renal blood flow (RBF) decreases and/or when there is increased discharge of renal sympathetic nerves. The mechanism of renal fluid and water retention involves renin, angiotensin and aldosterone.
If the cardiac function is severely impaired, sympathetic discharge fails to restore cardiac output. This starts off a vicious cycle in which the sympathetic discharge keeps increasing in an effort to restore cardiac output but fails. Rather, the sympathetic discharge leads to an increase in blood volume through renal mechanisms, which imposes a greater load on the heart. The retention of large amounts of fluid and electrolytes causes edema of the myocardium, further impairing myocardial function. This is known as decompensated cardiac failure.