Which mechanism best explains ascites formation in cirrhosis?

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In cirrhosis, ascites mainly arises from portal hypertension that raises hydrostatic pressure in the portal and splanchnic circulation, combined with splanchnic vasodilation that reduces effective arterial blood volume. This perceived low circulating volume triggers compensatory mechanisms such as the renin-angiotensin-aldosterone system, sympathetic activation, and antidiuretic hormone release, promoting sodium and water retention. The result is expansion of the extracellular fluid and fluid movement into the peritoneal cavity. At the same time, liver dysfunction lowers albumin synthesis, causing hypoalbuminemia and a drop in plasma oncotic pressure, which facilitates fluid leakage into the abdomen. Increased hepatic albumin production does not occur in cirrhosis, so that option is incorrect. Pancreatic exocrine insufficiency is not a driver of cirrhotic ascites, and although hyperdynamic circulation with increased cardiac output is a feature, it is not the primary mechanism for ascites formation.