Therefore, it is important to understand the pathophysiology of heart failure because it serves as the rationale for drug therapy. In order to compensate for reduced cardiac output during heart failure, feedback mechanisms within the body will try to maintain normal arterial pressure by constricting arterial resistance vessels, thereby increasing systemic vascular resistance . Veins are also constricted to elevate venous pressure . Arterial baroreceptors and cardiopulmonary baroreceptors are important components of this feedback system. In heart failure, there is a compensatory increase in blood volume that serves to increase ventricular preload and thereby enhance stroke volume by the Frank-Starling mechanism .
Blood volume is augmented by a number of factors.
Reduced renal perfusion results in decreased urine output and retention of fluid. Furthermore, a combination of reduced renal perfusion and sympathetic activation of the kidneys stimulates the release of renin, thereby activating the renin-angiotensin system . This, in turn, enhances aldosterone secretion. The final outcome of humoral activation is an increase in renal reabsorption of sodium and water.