Splanchnic vasodilation and hyperdynamic circulatory syndrome in cirrhosis

Abstract

Portal hypertension is a clinical syndrome which leads to several clinical complications, such as the formation and rupture of esophageal and/or gastric varices, ascites, hepatic encephalopathy and hepato-renal syndrome. In cirrhosis, the primary cause of the increase in portal pressure is the enhanced resistance to portal outflow. However, also an increase in splanchnic blood flow worsens and maintains portal hypertension. The vasodilatation of arterial splanchnic vessels and the opening of collateral circulation are the determinants of the increased splanchnic blood flow. Several vasoactive systems/substances, such as nitric oxide, cyclooxygenase-derivatives, carbon monoxide and endogenous cannabinoids are activated in portal hypertension and are responsible for the marked splanchnic vasodilatation. Moreover, an impaired reactivity to vasoconstrictor systems, such as the sympathetic nervous system, vasopressin, angiotensin II and endothelin-1, plays a role in this process. The opening of collateral circulation occurs through the reperfusion and dilatation of preexisting vessels, but also through the generation of new vessels. Splanchnic vasodilatation leads to the onset of the hyperdynamic circulatory syndrome, a syndrome which occurs in patients with portal hypertension and is characterized by increased cardiac output and heart rate, and decreased systemic vascular resistance with low arterial blood pressure. Understanding the pathophysiology of splanchnic vasodilatation and hyperdynamic circulatory syndrome is mandatory for the prevention and treatment of portal hypertension and its severe complications.

Keywords: Portal hypertension; Splanchnic flow; Splenic circulation; Nitric oxide; Autonomic dysfunction; Cirrhosis; Hyperdynamic circulatory syndrome

Core tip: In cirrhosis, portal hypertension is due to an increase in intrahepatic resistance and splanchnic blood flow. The latter is secondary to arterial splanchnic vasodilatation and the opening of collateral circulation. Though the increase in intrahepatic resistance is the earliest and most important component, at present the only treatment regimes which are available for the control of portal hypertension in cirrhosis, i.e., non-selective beta-blockers, octreotide and terlipressin, act on the splanchnic dynamic component. Thus, understanding the mechanisms that lead to splanchnic vasodilatation and to the hyperdynamic circulatory syndrome is essential for the treatment of the complications of portal hypertension.