Peripheral circulatory control mechanisms in congestive heart failure

Two abnormalities occur in the resistance vessels in congestive heart failure. First, there is an increased sympathetic tone to the peripheral resistance vessels. Whether or not sympathetic tone is increased at rest depends on the severity of the heart failure and the symptomatic status of the patient. On the other hand, there appears to be a massive sympathoadrenal discharge during exercise which acts to attempt to maintain blood pressure and perfuse essential organs at the expense of nonessential circulations. The afferent limb of this reflex may originate in active skeletal muscle and be supernormally activated by the products of excessive anaerobic metabolism. Reduced baroreceptor activity in heart failure may preferentially facilitate the expression of this response. Second, there appears to be increased "vascular stiffness" of the peripheral arterioles that may be secondary to an increased vascular sodium content or a manifestation of increased tissue pressure seen in edema. During exercise this stiffness reduces the ability of the resistance vessels to dilate. This leads to a higher level of oxygen extraction which is adequate under basal conditions but is insufficient to meet aerobic needs of active muscle and results in a systemic lactic acidemia. Interventions that reduce sympathetic alpha adrenergic tone or restore normal arteriolar dilator capacity might be expected to have the adverse effect of producing exertional syncope.