The pathophysiology of arterial vasodilatation and hyperdynamic circulation in cirrhosis

136 Citationer (Scopus)

Abstract

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 result 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. This article is protected by copyright. All rights reserved.

OriginalsprogEngelsk
TidsskriftLiver international : official journal of the International Association for the Study of the Liver
Vol/bind38
Udgave nummer4
Sider (fra-til)570-580
ISSN1478-3223
DOI
StatusUdgivet - apr. 2018

Fingeraftryk

Dyk ned i forskningsemnerne om 'The pathophysiology of arterial vasodilatation and hyperdynamic circulation in cirrhosis'. Sammen danner de et unikt fingeraftryk.

Citationsformater