Calf Muscle Pump: Its Role, Its Limitations—What to Do? By Kenneth J. McLeod, PhD
Reports of chronic venous disorders (CVD) date to biblical times, but beginning with the era of industrialization, CVD has developed into one of the most widespread causes of human disability and discomfort. The breadth of CVD (including lymphatic complications) encompasses spider, reticular and varicose veins, trophic skin changes, leg ulcers, pitting edema, leg pain, joint pain, congestion, skin irritation, and itching, as well as restless legs and muscle cramps.1 Of greater concern, venous stasis can lead to deep vein thrombosis and a greatly increased risk of pulmonary embolism. Epidemiologic studies have shown that more than half of adults in the western world have CVD associated symptoms that are severe enough to reduce their quality of life, with women and the elderly significantly more affected than men.2 Correspondingly, CVD result in substantial medical and economic challenges, with venous insufficiency accounting for more than $3 billion alone in annual direct costs in the U.S
In addition to age and gender, both the duration of daily sitting and standing along with lack of exercise are consistent independent predictors of CVD.4 Postural orthostasis plays a critical role in the development of venous disorders because a principle underlying factor in essentially all venous disorder related conditions is increased venous pressure.5 Despite this, there have been remarkably few interventions developed to prevent venous hypertension. Leg elevation, of course, reduces venous pressure but is generally not viewed as a practical approach for individuals in either the work or home environment. As a result, compression therapy was introduced as a means to reduce systolic pressure peaks and decrease extravasation into the interstitial space. It has, over time, become the gold standard for non-invasive treatment of CVD. Compression interventions include not only stockings, but also multilayer bandage systems, paste bandage systems and pneumatic compressive devices. Compliance with compression stockings and bandaging is typically very poor. While pneumatic compression has historically involved the use of a bulky apparatus, which limited mobility and therefore compliance, new portable technologies are currently under development.
Despite widespread utilization of compression interventions, neither invasive nor non-invasive studies have been able to demonstrate any significant changes in ambulatory venous pressures or venous recovery times resulting from compression therapy.7 This raises the question of the underlying physiologic basis of venous hypertension and what might be the most effective intervention strategies to preclude the numerous health complications associated with CVD.
Venous hypertension is a hydrostatic phenomenon. Three physical factors, relatively unique to humans, influence the development of venous hypertension.8 First, is the location of our heart, which, in upright posture, is sufficiently high in the body with more than 70 percent of the blood in the cardiovascular system remaining below the heart. The large size of our legs (about half our body volume), and the high compliance of human veins, allows most of this blood to collect into the veins of the legs.
Second is the exceptional height of humans, which results in venous columns of blood over one meter in height (distance from feet to right atrium) in even the shortest individuals. Gravity, operating on these fluid columns during orthostasis creates static venous pressures of 100 mmHg or more in the feet and lower legs.
Finally, human skin is extremely compliant; if human skin were stiff (had low compliance) like that in other tall animals (horses, cattle, giraffes, ostrich, etc), high static venous pressures would present minimal difficulties. However, the combination of these three factors means that during orthostasis, the large hydrostatic pressures in the veins and capillaries drive venous and capillary expansion, leading to increased extravasation, and our compliant skin, particular that of women, stretches out, accommodating extensive blood and interstitial fluid pooling to the point where venous return to the heart and cardiac output are compromised.
Further exacerbating this process, both our veins and skin have visco-elastic properties and thus undergo stress-relaxation (often referred to as creep) when exposed to static pressures for extended time periods, leading to additional fluid pooling during extended orthostasis. The rate at which the immediate hydrostatic effects develop is dependent on a number of physiologic and environmental factors. For the initial pooling phase when blood flow is normal, the full hydrostatic effects can take minutes for the veins to fill past the point where the venous valves no longer function; in hot environments, the veins can fill to the point where venous valves become incompetent within several seconds. The slower, stress-relaxation processes occur over a timescale of hours.
Given this hydrostatic basis of venous hypertension, it is clear that compression therapy can serve to reduce effective skin compliance, thereby allowing interstitial pressures to increase, leading to a self-limiting of lower limb blood pooling. However, high interstitial fluid pressures reduce the vascular transmural pressure gradients and physically compress capillaries, resulting in reduced nutritive tissue perfusion.9 Intermittent pneumatic compression can help prevent this loss of nutritive tissue perfusion, but none of the compression approaches address the fundamental physiologic failure leading to the development of venous hypertension.
