Venous reflux is the most common cause of venous hemodynamic disorders. In this paper 2 issues are discussed: how and where does reflux arise and what are the hemodynamic consequences of retrograde flow. Pressure gradient and incompetent vein connecting both poles of the gradient are the prerequisite for venous reflux to arise. Ambulatory pressure gradient occurs during the activity of the calf muscle venous pump between deep veins of the thigh and the lower leg. Thus the incompetent reflux-carrying vein must connect the popliteal, femoral, profunda femoris, or iliac vein with 1 of the deep veins of the lower leg. Reflux can be considered as shunting of blood from thigh veins into the lower leg veins. The most frequently found incompetent veins are the long and short saphenous veins and perforators communicating with deep veins of the thigh. On the other hand, calf perforators emptying into the deep veins of the lower leg, where the lower pole of the pressure gradient is located, cannot be the feeding source of reflux. A physiological bidirectional flow takes place in calf perforators connecting superficial and deep veins of the lower leg and making them conjoined vessels. Venous reflux produces ambulatory venous hypertension. The quantity of reflux volume and not the localization of retrograde flow in superficial or deep veins is the most important hemodynamic factor. Reflux in superficial veins, when large enough, can cause the most serious symptoms of chronic venous insufficiency including leg ulcers. Plethysmographic findings have shown that incompetence of the femoral and calf perforating veins is hemodynamically unimportant. Large incompetent calf perforators are not the cause of venous abnormality but are the consequence of saphenous retrograde flow.

Chronic Disease↗

PubMedDate not supplied

Conception of the venous hemodynamics in the lower extremity.

Contradictory reports on the significance of several hemodynamic phenomena, such as femoral vein incompetence and incompetent calf perforators, impede orientation in venous hemodynamics. Venous pressure difference arising between the popliteal and the posterior tibial vein during the activity of the calf muscle venous pump was reported for the first time about 50 years ago, but regrettably, this important discovery continues to be unrespected. The venous pressure difference has since been termed ambulatory pressure gradient and seems to be the key factor triggering the venous reflux in the lower limb as well as the process leading to varicose vein recurrence. On the other hand, simultaneous recordings of the mean venous pressure in the posterior tibial and long saphenous veins demonstrated that the pressure curves have been identical at rest, during ambulation, and in the recovery period, a finding typical of conjoined vessels. Bidirectional flow within calf perforators taking place both in healthy subjects and in patients with varicose veins enables a quick equilibration of pressure changes between deep and superficial veins of the lower leg. Reflux disturbing the venous hemodynamics is in various degrees dependent on the quantity of retrograde flow; abolition of reflux restores normal venous hemodynamics. Reflux in superficial veins, if large enough, may cause the most severe form of chronic venous insufficiency. Femoral vein incompetence and incompetent calf perforators per se do not produce ambulatory venous hypertension and do not cause hemodynamic disturbance. This study discusses the controversial issues, tries to define and appraise the principal hemodynamic phenomena (ambulatory venous hypertension, ambulatory pressure gradient, venous reflux, superficial and deep vein incompetence, incompetent perforators), mentions a possible relation between deep vein incompetence and varicose veins, and attempts to present, based on proved facts, a comprehensive picture of the venous hemodynamics in the lower extremity.

Humans↗

PubMedDate not supplied

A critical appraisal of the role of ankle perforators for the genesis of venous ulcers in the lower leg.

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Ankle↗