Factors influencing peripheral venous pressure in an experimental model

Peripheral venous hypertension and microvascular injury have merged as central features of chronic venous disease. Peripheral venous pressure in the lower limb is controlled by central and peripheral mechanisms. In the current manuscript, we examine the role of peripheral factors, particularly conduit capacitance compliance, focal stenosis, and arterial inflow into the calf.

An experimental venous model using Penrose tubing as a venous analogue was used where the aforementioned parameters could be manipulated. Volume-pressure curves were derived in the static mode. The dynamic model attempted to simulate key pressure parameters of lower limb venous flow.

Decreasing compliance resulted in progressive reduction of conduit capacitance affecting both bending and stretching regimens and the relative distribution between the two, rotating the volume-pressure curve toward the x-axis. Increased postcapillary (arterial) inflow increased conduit pressure. For a given inflow, pressures varied inversely to conduit caliber. Decreased compliance led to a smaller functional caliber at working pressures. Sideline capacitance with stagnant flow connected to the flow channel (simulating calf vein network) did not influence conduit pressure. Focal stenosis increased "venous pressure" if it was narrower than "optimum outflow caliber," defined as the minimum outflow conduit caliber required to balance inflow. Percentage stenosis as traditionally calculated using adjacent lumen as denominator was uncorrelated to pressure increase.

Conduit pressure is increased with smaller native or functional (poor compliance) caliber, focal stenosis, and increased postcapillary inflow. Many of these features appear to be present in limbs clinically suspected of chronic venous disease. The importance of the geometric factor of Poiseuille equation in pressure effects of caliber reduction and collateralization is discussed.