CHF refers to a syndrome arising from hemodynamic abnormalities resulting from the failure of the heart's pumping function. Pulmonary edema is an increase in lung water, resulting from the leakage of fluid from the pulmonary capillaries and venules into the lung's interstitium and alveoli. Mortality from CHF is substantial. Other causes of CHF are listed in Table 1. The failing heart undergoes a number of compensatory changes to maintain perfusion of vital organs before overt clinical evidence of heart failure occurs.
Neurohormonal activation occurs.
Increased levels of angiotensin and aldosterone contribute to fluid and salt retention, as well as vasoconstriction. Peripheral vasoconstriction and sympathetic stimulation result in increased vital organ perfusion at the expense of increasing cardiac work. The retained salt and water increase preload, but in the long term pulmonary and peripheral edema occur. Increased beta receptor stimulation leads to increased heart rates and cardiac work in order to increase and maintain cardiac output. Over time, the increased stimulation leads to decreased receptor density and function.