Why does cirrhosis cause vasodilation
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Wong F. We propose that the high cardiac output and systemic hypotension relate to the marked and dysregulated splanchnic vasodilatation consequent on the development of liver cirrhosis, and as a result of portal hypertension. Hepatic fibrosis causes a marked impairment of portal blood flow into the liver, and maladaptive splanchnic vasodilatation attempts to rectify the associated reduction in hepatic perfusion by increasing blood flow and pressure in the portal venous system.
However, rather than increasing perfusion of the liver, this hyperaemia and hypertension results in incremental shunting of portal blood into the systemic circulation via porto systemic collateral anastamoses. This latter steal becomes extreme in advanced liver disease, where blood flow in the portal vein may even become reversed. This is supported by the correlation of worsening liver function with increases in cardiac output and azygous collateral blood flow, 15 and decreases in hepatic perfusion.
Homeostatic mechanisms, including activation of neurohumoral reflexes, attempt to correct these derangements and lead not to peripheral vasodilatation, but peripheral vasoconstriction with reduced tissue perfusion. Plasma concentrations of vasoconstrictor mediators such as catecholamines, angiotensin II, and endothelin are elevated, and lead to increases in peripheral vascular tone. A transjugular intrahepatic portosystemic shunt TIPSS is inserted to reduce the risk of variceal bleeding by alleviating portal hypertension through increased collateral shunting.
This exacerbates the haemodynamic derangements of cirrhosis, 21 leading to increases in cardiac output, reductions in hepatic sinusoidal perfusion and progressive peripheral vasoconstriction. We would, therefore, suggest that, although liver cirrhosis is associated with a hyperdynamic circulation and low total systemic vascular resistance, marked peripheral arterial vasoconstriction is the dominant clinical picture.
Address correspondence to Dr D. Sherlock S. Cirrhosis of the liver. Oxford Textbook of Medicine. Oxford, Oxford University Press, Peripheral arterial vasodilation hypothesis: a proposal for the initiatio of renal sodium and water retention in cirrhosis.
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