Portal pressure can be defined by the equation P (portal pressure) = Q (blood flow in the portal venous system) x R (hepatic resistance). Any condition causing increased portal venous flow, or increased hepatic resistance, can develop into portal hypertension. In practice, most conditions associated with portal hypertension are due to a combination of these 2 factors.
In the West, cirrhosis of any etiology is the most common cause of portal hypertension. In the cirrhotic liver, architectural disorganization with nodular regeneration and fibrosis results in a large increase in resistance due to vascular destruction and distortion. The normally smooth, regular vascular channels become tortuous and irregular, which also increases resistance. Further splanchnic arterial inflow and thus flow in the portal vein also increase. Although it appears that increased resistance is the prime factor in cirrhosis, increased flow also contributes to portal hypertension.
Rare conditions causing purely an increased flow into the portal venous system are almost always associated with only mild portal pressure elevation. However, secondary structural changes in the liver microcirculation lead to increased resistance (eg, a splanchnic arteriovenous [A-V] shunt may develop after abdominal trauma). Although significant portal hypertension with this condition has been documented, when the liver is carefully examined in detail, subtle but significant microcirculatory changes are present (eg, collagen deposition in the space of Disse). Conditions associated purely with increased portal venous flow (eg, massive splenomegaly and splanchnic A-V malformations and shunts) are associated with significant portal hypertension only in the presence of secondary intrahepatic microcirculatory changes.