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.

Systemic hemodynamics in advanced cirrhosis: Concerns during perioperative period of liver transplantation

“…All transfusion management plans should be handled with great caution, and transplant physicians should very carefully evaluate the effects of increases or decreases of transfusions [60][61][62] . A response time lag due to endothelial injury and permeant breakdown should be considered in LC recipients with long-term PH [63][64][65] . Adequate hydration is also required; dehydration should be avoided because of these patients' peculiar hemodynamics.…”

“…Peculiar hemodynamics in advanced cirrhosis permeant breakdown, and systemic arterial pressure may be effected even by body motion [63][64][65] . Diuretics (e.g., furosemide and potassium-conserving diuretics) and a water-clearance mediator (e.g., tolvaptan) are available [71] .…”

Hospitalizations Due to Cirrhosis: Clinical Aspects in a Large Cohort of Italian Patients and Cost Analysis Report

“…Typical features consist of an irreversible chronic injury of hepatic parenchyma and diffuse fibrosis associated with nodular liver regeneration. The development of portal hypertension, due to increased intrahepatic resistance and splanchnic blood flow [6,7] , is a hallmark in the history of cirrhosis; its presence is associated with the development of severe complications, such as the formation and rupture of esophageal and/or gastric varices, ascites, and hepatic encephalopathy (HE) Keywords Liver cirrhosis · Hospitalization · Epidemiology · Healthcare costs Abstract Background and Aim: Liver cirrhosis is characterized by high morbidity and mortality rates. This study was addressed to evaluate the epidemiological and economic impact of cirrhosis on hospitalizations in a large population in Italy.…”

Cardiac changes in pediatric liver transplant recipients: are they truly irreversible?

“…The haemodynamic changes of systemic vasodilatation in cirrhosis can lead to a reduction in the effective arterial blood volume and compensatory activation of various vasoconstrictor systems [10]; the end result is sodium and water retention as well as volume overload. All of these factors are known to cause cardiac changes, predisposing the cirrhotic patient to the development of cirrhotic cardiomyopathy.…”