Pathogenesis of Portal Hypertension: In patients with cirrhosis, portal hypertension results from both an increase in resistance to portal blood flow and enhanced portal blood flow. The increased resistance in the liver results from architectural distortion due to fibrosis and regenerative nodules combined with increased intrahepatic vasoconstriction due to decreased endogenous nitric oxide production and endothelial dysfunction. In the presence of angiogenic factors and increased nitrous oxide production in the splanchnic vascular bed, splanchnic arteriolar vasodilatation and increased cardiac output increase portal venous blood inflow.
Portosystemic Collaterals: Collaterals develop in response to the portal hypertension at sites of communication between the portal and systemic circulations. In comparison to other collaterals, gastroesophageal varices are important due to their risk of rupture and bleeding.
Hepatic Venous Pressure Gradient: The hepatic venous pressure gradient (HVPG) is a measure of portal (sinusoidal) pressure and is obtained by catheterization of a hepatic vein via the jugular or femoral vein. The free hepatic vein pressure is subtracted from the wedged hepatic vein pressure to calculate HVPG, which is normally 3 to 5 mmHg, and an elevated value indicates an intrahepatic cause of portal hypertension. The HVPG predicts the risk of developing varices and overall prognosis (Figure 1). It can also be followed to monitor response to therapy and progression of liver disease. An HVPG value of 10 or greater indicates the patient has developed clinically significant portal hypertension and varices may develop when the HVPG is greater than or equal to 10 to 12 mmHg. The goal of therapy is to reduce the HVPG to less than 12 mmHg or decrease by 20% from baseline values. Due to the invasive nature of the procedure and operator variability, its use is still not widespread in the United States for prognostic or therapeutic monitoring purposes. Clinically, it is used to diagnose portal hypertension and to identify the site of obstruction (prehepatic, intrahepatic, or posthepatic). It is also used to estimate the risk of liver failure following hepatic resection in patients with compensated chronic liver disease.