Hyperdynamic state in chronic liver diseases

Abstract

Reduced splanchnic arteriolar resistance and increased portal venous outflow have been associated with chronic portal hypertension. This hyperdynamic splanchnic circulatory state is accompanied by a hyperdynamic systemic circulation characterized by a high cardiac index and low systemic vascular resistance. The systemic phenomenon occurs earlier than the regional one, possibly because the increased outflow resistance induced by portal hypertension delays the effect of circulating humoral vasodilators on the splanchnic bed. Several vasoactive substances have been advanced as the vasodilator responsible for the hyperdynamic circulation. Glucagon and bile acids have been found to be potent splanchnic vasodilators in animal studies. However, neither consistently dilates other vascular beds. For example, bile acids are splanchnic--but not systemic--vasodilators. Several studies suggest a role in chronic liver disease for nitric oxide, a potent endogenous vasodilator secreted by endothelial cells. Prostaglandins have also been proposed as the responsible vasodilator. However, mixed results have been seen with experimental suppression of prostaglandin synthesis. For a hyperdynamic state to develop and persist requires not only reduced cardiac afterload, but also an increased venous return. Recently, we found an expanded plasma volume after initial vasodilation in rats with portal hypertension. This 'refill' of the circulation may be intrinsic to development of the hyperdynamic state. Furthermore, this blood volume expansion may be the link between vasodilation and the hyperdynamic circulation.