Pathophysiological basis of albumin use in cirrhosis

Abstract

During the course of cirrhosis, a progressive reduction of splanchnic vascular resistance takes place in parallel with a deterioration of cardiac function manifested by the disappearance of the hyperdynamic circulation due to a fall in cardiac output. This compromises arterial pressure and determines a homeostatic activation of endogenous vasoconstrictor systems. Cirrhotic patients are prone to developing renal vasoconstriction, decreased renal perfusion and renal failure in response to insults that impairs the effective arterial blood volume such as severe bacterial infections or other clinical events that produce hypovolemia. Although circulatory dysfunction in cirrhosis predominantly affects the kidney, it has also effects on other organs and systems: brain edema and encephalopathy, increased portal pressure and decreased intestinal motility. Albumin infusion is effective in the prevention of circulatory dysfunction after therapeutic paracentesis or acute bacterial infections and in in the treatment of hepatorenal syndrome. This effectiveness may be related to the dual effect of albumin on the cardio-circulatory function, the increase in the cardiac output and in the systemic vascular resistance. The administration of intravenous albumin not only expands the plasma volume and increases cardiac preload and cardiac output but also induces arterial vasoconstriction at the level of splanchnic microcirculation. Moreover, albumin is a powerful antioxidant as well as plays a crucial role in the transport of physiologic substances and disposal of toxic substances. Impairment of albumin function is one of the most characteristic traits of cirrhosis. Administration of exogenous albumin could be beneficial because of its positive effects on microcirculation.