&NA;A unitary hypothesis of the pathogenesis of ascites in cirrhosis is presented that combines and augments the existing overflow and traditional hypotheses. The early circulatory events are increased resistance to sinusoidal blood flow and shift of arterial blood into a splanchnic venous pool with reduction of effective (arterial) intravascular volume (EIVV). The latter stimulates neurohormonal sodium and water retention by the kidney, restoring normal EIVV and expanding total intravascular volume (TIVV). After repeated cycles, normal splanchnic compliance is exceeded and sinusoidal and splanchnic capillary hypertension develop. Hepatic and splanchnic lymph production increases; when these rates exceed the absorptive capacities of the hepatic and retroperitoneal lymphatics and those of the peritoneal cavity, ascites develops. The ascites may, if untreated, be progressive and the start of a vicious circle in which sodium and water are increasingly retained.ASAIO Transactions1989; 35: 161–163.