In a fluid flow network such as the portal system, flow and pressure variables can be calculated in analogy to Ohm's law. Accordingly, the portal pressure depends on the hepatic resistance and the inflow through the splanchnic arterial bed. The latter has little importance in healthy liver because of the highly compliant vascular bed of the liver which passively adapts its diameter (ie, resistance) to flow through distension or shrinking of the organ.1 Thus, doubling of the portal flow results in only minimal changes in the portal pressure. With decreasing compliance of the liver during the development of cirrhosis, the flow increasingly determines the pressure. For instance, if compliance were to approach zero, doubling of the flow would result in doubling of the pressure. Consequently, only advanced cirrhosis may provide the physical basis for the flow to be the chicken, and not the egg.

According to the ‘forward flow hypothesis’ portal hypertension is the result of both an increased hepatic resistance and an increased portal inflow.2 However, the increased hepatic resistance is seen more as an initiating event inducing an increased inflow which then causes most of the portal hypertension. The increased flow could be unrelated to the portal hypertension and could instead be the result of shunting of vasodilating substances causing a hyperdynamic state. The theory is mainly based on the rat model of portal vein constriction which showed 100% shunting and a marked …