Hepatic, splanchnic and systemic haemodynamic abnormalities in portal hypertension

Jaime Bosch, M. Pilar Pizcueta, Mercedes Fernandez, Faust Feu, Isabel Cirera, Angelo Luca, Joan C. Garcia-Pagán

Research output: Contribution to journalArticlepeer-review


Portal hypertension is characterized by a pathological increase in portal venous pressure that leads to the formation of portosystemic collaterals that divert portal blood to the systemic circulation, bypassing the liver. Increased vascular resistance to portal blood flow is the initiating factor in portal hypertension. Increased resistance along the hepatic and porto-collateral circulation is in part modifiable by pharmacological agents. An additional factor is splanchnic vasodilatation with increased portal blood inflow, which contributes to the maintenance and aggravation of the portal hypertension. Endogenous vasodilators are thought to be responsible for the splanchnic hyperaemia of portal hypertension. Vasodilatation is also prominent in the stomach and lungs, and plays an important role in the pathophysiology of portal hypertensive gastropathy and of the hepatopulmonary syndrome. The systemic circulation is markedly hyperkinetic, with reduced arterial pressure and peripheral resistance and increased cardiac output. The plasma volume is expanded due to renal sodium retention. The expanded plasma volume enables the increase in cardiac output, and represents another mechanism contributing to the increase in portal pressure.

Original languageEnglish
Pages (from-to)425-436
Number of pages12
JournalBailliere's Clinical Gastroenterology
Issue number3
Publication statusPublished - 1992

ASJC Scopus subject areas

  • Gastroenterology


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