The pathophysiology of arterial vasodilatation and hyperdynamic circulation in cirrhosis

Patients with cirrhosis and portal hypertension often develop complications from a variety of organ systems leading to a multiple organ failure. The combination of liver failure and portal hypertension results in a hyperdynamic circulatory state partly owing to simultaneous splanchnic and peripheral...

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Veröffentlicht in:Liver international 2018-04, Vol.38 (4), p.570-580
Hauptverfasser: Møller, Søren, Bendtsen, Flemming
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Bendtsen, Flemming
description Patients with cirrhosis and portal hypertension often develop complications from a variety of organ systems leading to a multiple organ failure. The combination of liver failure and portal hypertension results in a hyperdynamic circulatory state partly owing to simultaneous splanchnic and peripheral arterial vasodilatation. Increases in circulatory vasodilators are believed to be due to portosystemic shunting and bacterial translocation leading to redistribution of the blood volume with central hypovolemia. Portal hypertension per se and increased splanchnic blood flow are mainly responsible for the development and perpetuation of the hyperdynamic circulation and the associated changes in cardiovascular function with development of cirrhotic cardiomyopathy, autonomic dysfunction and renal dysfunction as part of a cardiorenal syndrome. Several of the cardiovascular changes are reversible after liver transplantation and point to the pathophysiological significance of portal hypertension. In this paper, we aimed to review current knowledge on the pathophysiology of arterial vasodilatation and the hyperdynamic circulation in cirrhosis.
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The combination of liver failure and portal hypertension results in a hyperdynamic circulatory state partly owing to simultaneous splanchnic and peripheral arterial vasodilatation. Increases in circulatory vasodilators are believed to be due to portosystemic shunting and bacterial translocation leading to redistribution of the blood volume with central hypovolemia. Portal hypertension per se and increased splanchnic blood flow are mainly responsible for the development and perpetuation of the hyperdynamic circulation and the associated changes in cardiovascular function with development of cirrhotic cardiomyopathy, autonomic dysfunction and renal dysfunction as part of a cardiorenal syndrome. Several of the cardiovascular changes are reversible after liver transplantation and point to the pathophysiological significance of portal hypertension. 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subjects Adrenal Insufficiency
Arterial Pressure
Blood flow
Blood volume
cardiac dysfunction
Cardiac Output
Cardiomyopathy
Cardiovascular system
Cirrhosis
Collateral Circulation
Complications
Humans
Hypertension
Hypertension, Portal - drug therapy
Hypertension, Portal - etiology
Hypertension, Portal - physiopathology
Hypovolemia
Liver
Liver cirrhosis
Liver Cirrhosis - complications
Liver Cirrhosis - physiopathology
Liver diseases
liver failure
Liver Failure - etiology
Liver Failure - physiopathology
Liver transplantation
Multiple Organ Failure
multi‐organ syndrome
portal hypertension
Renal function
Splanchnic Circulation - drug effects
Translocation
Transplantation
Vascular Resistance
Vasoconstrictor Agents - therapeutic use
Vasodilation
Vasodilation - drug effects
Vasodilators
title The pathophysiology of arterial vasodilatation and hyperdynamic circulation in cirrhosis
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