Modificările hemodinamice în ciroza hepatică

Abstract

Background: Liver cirrhosis is associated with hemodynamic changes in central and peripheral circulation. These changes include cirrhotic cardiomyopathy, hyperdynamic circulation and peripheral vasodilatation. The pathogenic mechanisms of these abnormalities are multifactorial and include humoral, nervous and vascular dysregulations. Cirrhotic cardiomyopathy suggests a systolic and diastolic dysfunction and electrophysiological abnormalities. It appears to be unmasked by procedures that stress the heart, such as pharmacological vasoconstriction, exercise, and by insertion of transjugular intrahepatic portosystemic shunt. The hyperdynamic circulation is most likely initiated by splanchnic and peripheral vasodilatation, leading to reduction in the effective arterial blood volume. This leads to a diminished renal blood flow in cirrhotic patients, which in turn stimulates the rennin-angiotensin-aldosterone system, sympathetic nervous system, and antidiuretic hormone resulting in renal artery vasoconstriction, sodium retention, and volume expansion. Worsening liver disease results in progressive vasodilatation, making the hyperdynamic circulation and renal artery vasoconstriction more pronounced. These circulatory changes lead to the development of multiple life-threatening complications including hepatorenal syndrome, ascites, spontaneous bacterial peritonitis, gastroesophageal varices, and hepatopulmonary syndrome. Conclusions: Liver cirrhosis is associated with increased cardiac output (hyperdynamic circulation), systolic and diastolic dysfunction and decreased peripheral vascular resistance. These changes influence the evolution of liver cirrhosis and their correction leads to improved prognosis of patients with liver cirrhosis.