Portal hypertension is a common clinical syndrome associated with chronic liver diseases, and is characterized by a pathological increase in portal pressure that leads to the formation of portosystemic collaterals resulting in shunting of portal blood into the systemic circulation. The increase in portal pressure is due to an increase in vascular resistance and an elevated portal blood flow. The site of increased resistance is variable, and dependent upon the disease process. The site of relative obstruction may be prehepatic, hepatic, or posthepatic. There are several intrahepatic lesions that lead to increased resistance. Some of these lesions are irreversible, like fibrosis, regenerating nodules, and capillarization of the space of Disse; however, there is a functional component, increased vascular tone, which contributes to increased intrahepatic resistance and is potentially reversible. Another important factor contributing to the increased portal pressure is elevated portal blood flow. Peripheral vasodilatation initiates the classical profile of decreased systemic resistance, expanded plasma volume, elevated splanchnic blood flow, and elevated cardiac index, which characterize the hyperdynamic circulatory state. This hyperdynamic circulation is responsible for various complications of portal hypertension.