The Importance of Hemodynamic Pressure for the Progression of Venous Insufficiency: Lessons from Physical Analysis of Veins and Waterfalls

Abstract

In phlebology, hydrostatic pressure is regarded as an essential pathogen for the course of "chronic" insufficiency and as a representative of the venous hypertension. Progressive valve insufficiency is attributed to hydrostatic pressure as well as the increase in transmural pressure, which leads to edema formation and metabolic alterations. Hydrostatic pressure does not depend on the column diameter, but only on the height: Pstat = r g h, r: constant, simplified: density. The approach applies at most to static liquids, whereby the blood column in humans rests in the rarest of situations. The far more essential component is the hydrodynamic or hemodynamic pressure, defined with Pdyn = ½ r v2, related to and increasing with the kinetic energy, Ekin = ½ m v2. The aim of this study was to compare well known physical effects from waterfalls to less known forces on veins. Based on sonographic evaluations (14-32 MHz) from the Berlin venous valve study 2016-2020, an analysis of the physical factors of progressive valve damage to the lower extremities was compared with well-known geophysical findings from waterfalls. Ultrasound recordings were analyzed by three independent investigators concerning the main criteria of preexistent lesions, pressure-induced decompensation, and stasis-related degeneration. The effects of static and dynamic forces on leg veins can be differentiated by ultrasound examination. While the hemostatic pressure primarily induces global or at least segmental dilatation, hemodynamic pressure primarily develops focal prereflux dilatations with the typical morphologies of the expansion of the valve sinus, followed by valve zone dilatations up to the loss of valve closure and to the onset of reflux, and finally progressive dilatation below the primary leakage. In the same way, the frequent eccentric vein dilatations with commissural leaks are explained as formation induced by pulsatile forces. The physical processes of waterfalls and (insufficient) leg veins are very similar, since both are driven by gravity and modified by friction. While the hemostatic pressure is nondirectional and can be compensated by nondirectional pressure (eg, compression modalities), the hemodynamic pressure does have a spatial orientation, namely that of the fluid motion, and this even with the square of speed. The forces associated with this, in contrast to pressure, increase with the effective area (F = P × A) and can lead to structural overstress of venous valves and walls, very similar to erosion on the contact surfaces of a waterfall. Phenomena in which the diameter of diseased veins seems to play an empirical role in severity and progression can now be well explained with this new model.