The primary hemodynamic abnormality in portal hypertension is increased resistance to portal blood flow. This is the case whether the resistance to portal flow has an intrahepatic cause such as cirrhosis or is due to portal vein obstruction.
Portosystemic shunting should decompress the portal system and thus significantly lower portal pressures. Despite the development of significant collaterals deviating portal blood into systemic veins, portal hypertension is maintained by an overall increase in portal venous flow and thus maintenance of portal hypertension. A hyperdynamic circulation is achieved by tachycardia, an increase in cardiac output, and decreased systemic vascular resistance. Splanchnic dilatation also occurs. Overall, the increase in portal flow likely contributes to an increase in variceal transmural pressure. The increase in portal blood flow is related to the contribution of hepatic and collateral flow; the actual portal blood flow reaching the liver is reduced. It is also likely that hepatocellular dysfunction and portosystemic shunting lead to the generation of various humoral factors that cause vasodilatation and an increase in plasma volume.
Many of the portal hypertension complications can be accounted for by the development of a remarkable collateral circulation.
Collateral vessels may form prominently in areas in which absorptive epithelium joins stratified epithelium, particularly in the esophagus or anorectal region. The superficial submucosal collaterals, especially those in the esophagus and stomach and, to a lesser extent, those in the duodenum, colon, or rectum, are prone to rupture and bleeding under increased pressure. In portal hypertension, the vascularity of the stomach is also abnormal and demonstrates prominent submucosal arteriovenous communications between the muscularis mucosa and dilated precapillaries and veins. The resulting lesion, a vascular ectasia, has been called congestive gastropathy and contributes to a significant risk of bleeding from the stomach.