[Liver cirrhosis and cardiovascular system]

The patient with hepatocellular disease shows marked vasodilatation, accompanied by hyperdynamic circulation and opening of arteriovenous shunts. The effect of these circulatory changes and especially the profound vasodilation has only recently been investigated in detail. In patients with hepatocellular failure the extremities are flushed, the pulses bounding, the cardiac output increased and the blood pressure low. The circulation resembles what found with systemic arteriovenous fistulae. The peripheral vasodilatation and splanchnic venous pooling reduce the effective blood volume so activating baroreceptors. The secondary events which follow the vasodilation include stimulation of the sympathetic nervous system. This serves to counteract the tendency to arterial hypotension and probably contributes to renal hypoperfusion and to the hepatorenal syndrome development. The nature of the concerned vasodilators remains speculative, but is likely to be multiple. Whatever its nature, the substance might be formed by the sick hepatocyte, fail to be inactivated by it or bypass it through intra- or extra-hepatic portal systemic shunts. In cirrhosis the cardiac index and reduced systemic vascular resistance correlate with the Child's grade of liver failure. This article provides an overview of the general vasodilatory state and its effects on various organs. The mechanisms and the different vasoactive substances that might be responsible are also discussed.