portal hypertension physiology

Portal hypertension results from a series of physiological alterations due to impeded blood flow in the portal vein, potentially leading to severe complications such as ascites and esophageal gastric varices. Typically, an increase in portal pressure initiates a cascade of complex physiological responses, including vasodilation, alterations in hemodynamics, and disruptions in fluid balance.

Initially, when the portal blood flow faces resistance, the body compensates by vasodilating to reduce vascular resistance and maintain adequate hepatic blood supply. This systemic vasodilation can lower blood pressure, prompting the heart to increase cardiac output, possibly leading to an increased cardiac workload. Moreover, portal hypertension can result in splenic congestion and hyperfunction, impacting the production and equilibrium of blood cells.

As the condition advances, portal hypertension may precipitate ascites formation due to the liver's diminished capacity to synthesize proteins, allowing fluid from the bloodstream to permeate into the abdominal cavity. Concurrently, portal hypertension can cause esophageal gastric varices as the elevated pressure within the portal venous system redirects blood flow through alternative pathways, increasing venous pressure in these areas and leading to venous dilation.

Patients with portal hypertension should avoid strenuous activities and heavy labor to minimize abdominal pressure and prevent the onset or worsening of ascites. They should also maintain a healthy diet, limit salt intake to alleviate ascites symptoms. In cases of abdominal distension or lower limb edema, prompt medical attention and professional treatment are advised. Regarding pharmacological management, adherence to physician guidance is crucial for the judicious use of diuretics and other medications to manage disease progression.