Furthermore, hypertrophy is associated with structural and biochemical changes, such as apoptosis, which may have deleterious effects in the long term. In response to a volume overload, such as that produced by aortic regurgitation or mitral regurgitation, the left ventricle dilates. Within limits, this response effects a compensatory increase in cardiac output by the Frank-Starling mechanism. Dilatation in the absence of a volume overload is an indication of ventricular failure. Peripheral Mechanisms Both arteriolar constriction and venous constriction occur in congestive heart failure.
Arteriolar constriction serves to maintain blood pressure despite a reduced cardiac output.
A number of mechanisms contribute to an increased vascular tone in congestive heart failure. An increase in sympathetic nervous system activity is a major factor responsible for arteriolar constriction. Constriction causes the blood flow to be redistributed, so that the blood supply to the kidneys, skin, splanchnic organs, and skeletal muscle is reduced. These structures have abundant sympathetic alpha-adrenergic receptors and low metabolic rates and do not produce significant amounts of vasodilating metabolites. In contrast, the brain and heart have few alpha-adrenergic receptors and high metabolic rates and produce a greater amount of vasodilating metabolites.