The peripheral distribution of cardiac output in heart failure

There are two sets of compensatory mechanisms activated when the heart fails: cardiac mechanisms that try to maintain a normal cardiac output and peripheral circulatory mechanisms that try to maintain blood pressure to perfuse the heart and the brain. The latter are most important during the stress of exercise. During exercise, two patterns of responses are noted: 1) blood vessels supplying active skeletal muscle fail to dilate normally, and 2) blood vessels supplying other visceral organs constrict excessively. The inability of skeletal muscle resistance vessels to dilate normally to a metabolic stimulus is related to sodium and water accumulation in the vessels and to a deconditioning response. These effects probably are at the small artery level. This results in an abnormal metabolic response to exercise. Vasoconstriction in visceral organs is related to neurogenic (sympathetic adrenergic) and humoral (angiotensin, norepinephrine, and vasopressin) mechanisms. The peripheral sympathetic nervous system is the primary determinant of the high plasma norepinephrine levels seen in heart failure. The role of the sympathetic nervous system is to provide for acute vasoconstriction and the renin-angiotensin system is to provide for chronic visceral vasoconstriction. These circulatory mechanisms operate most effectively over different time frames that are either short (sympathetic nervous system), intermediate (renin-angiotensin system), or long (deconditioning, vascular stiffness). When treatment is successful these systems return to normal over similar time frames.