In congestive heart failure the increases in sympathetic outflow and circulating catecholamines cause pronounced vasoconstriction in the renal and splanchnic vascular beds, which in the early stages of the disease permits the patient to engage in limited exercise even though the cardiac output does not increase normally. Eventually the muscle and skin flows also decrease reflexly. The widespread peripheral vasoconstriction augments the afterload of the heart. The cutaneous veins are constricted; together with the augmented circulating blood volume due to abnormal renal retention, this contributes to the increase in central venous pressure. The resulting increase in preload initially improves the filling of the heart and shifts the myocardium along its Starling curve. The peripheral venoconstriction helps explain the increased tolerance to orthostatic stress seen in patients with heart failure. Since these reflex vascular adjustments tend to augment both the pre- and the afterload of the heart, pharmacological agents causing dilatation of the systemic veins and/or of the arterioles improve the performance of the failing myocardium.