Muscle contraction systole at weight-bearing is accompanied by a rise in pressure in all veins of the limb Figure 5. Within the muscular compartment the increase is largest, typically mm Hg, three times higher than the rise in superficial veins. During systole the muscle contraction may cause venous outflow obstruction, further enhancing deep systolic vein pressure. In extreme cases the pressure is raised by more than mm Hg in a fraction of a second.
Competent valves prevent distal flow or outward flow through the perforators. In addition, the higher deep venous pressure does not allow inward flow through the perforating veins during systole. During muscle relaxation diastole the pressure falls below that at rest, especially in the deep veins Figure 5 , ensuing an inward flow through the perforating veins.
In healthy subjects patent vein valves prevent flow in the distal direction in both deep and superficial veins. Figure 5. Schematic representation of normal anatomy and dynamics of lower extremity veins. The simplified venous system consists of superficial veins SV , deep veins DV within muscular compartments M of the calf and thigh, and perforating veins PV. Venous valves VV ensure unidirectional flow of blood in central cent.
The diagram on the right depicts idealized pressure and flow characteristics of different areas of the veins during steady state at passive dependency the leftmost walking-phase symbol and two subsequent walking cycles—during weight-bearing muscle systole and elevation of the leg muscle diastole.
The red line indicates the extremity described. In a passive relaxed state the blood is forced almost solely through the deep system by the pumping action of the heart, often referred to as the vis-a-tergo v-a-t blood flow. AVP-Normal is the normal ambulatory venous pressure in superficial veins. In repeated muscle contractions, as in normal walking, the systolic pressures in the deep and superficial veins will gradually fall and fluctuate at levels considerably below the pressures during a single contraction Figure 5.
The superficial venous pressure in the ankle region during walking is typically 30 mm Hg and is referred to as the ambulatory venous pressure AVP. Superficial and perforator dysfunction Relatively few patients referred to hospital have dysfunction of superficial veins combined with normal valvular function in the perforating veins.
In this group the calf vein pumps are normal and ambulatory venous pressure in the deep veins at the ankle is low, which explains the absence of edema and trophic changes in the skin.
Most patients with venous dysfunction have incompetent valves in both superficial and perforator veins. Although the venous pumps may be normal, the pressure in the deep veins is rapidly restored to the blood column pressure upon standing, because of backfill from the superficial veins Figure 6.
The clinical picture is varicose veins and sometimes leg edema, often in combination with trophic changes. The more extensive and the more distal the venous reflux, the greater the probability of ulcer formation. In steady state at passive dependency blood flows primarily through the deep veins, and the pressure in the veins corresponds, as in healthy subjects, to the hydrostatic pressure from the blood column to the heart.
Consequently, the pressure at rest is not affected by valvular dysfunction. Weight-bearing with muscular contraction causes a steep rise in deep venous pressure, as in healthy subjects. The increase in superficial venous pressure is considerably higher than normal, due to the extensive retrograde flow from the deep venous system through incompetent dilated perforating veins in muscle systole.
During relaxation the pressure in the muscular deep veins falls abruptly, and to a larger extent than in popliteal and superficial veins. This causes an inward flow through the perforating veins, whereas reflux from the popliteal vein is prevented by valves.
The absence of competent valves in the superficial system allows retrograde flow, most often through the saphenofemoral junction. Figure 6. Schematic representation of patients with superficial and perforator venous dysfunction. The most striking difference from healthy subjects is the distal dist. During ambulation there is oscillating flow in incompetent perforators, outward during muscle contraction and inward at muscle relaxation.
Annotations are as in Figure 5. The high retrograde flow in superficial veins during walking refills the deep veins during muscle diastole, greatly enhancing the venous pump capacity by increasing the expelled volume.
The net increase in expelled volume is, however, due to the superficial retrograde circuit and does not represent effectively increased drainage from the extremity. The result of this rapid back-flow is that the systolic pressures in the deep and superficial ankle veins remain high during walking.
Proximal occlusion of the superficial veins normalizes ambulatory venous pressure in these veins and the pressure recovery time after standstill. This effect is the dynamic basis for the detection of superficial venous dysfunction by venous pressure measurements. The pressure test does not, however, assess the patency of the perforating veins. Combined superficial, perforator, and deep dysfunction The deep, perforating, and superficial veins of the leg may all be more or less involved in skin ulcer formation.
Deep venous incompetence is usually secondary to previous deep venous thrombosis, although venous dilatation and subsequent valvular insufficiency may also be the result of increased pressure and flow load from isolated superficial insufficiency.
The latter condition may be reversed following treatment of the superficial veins. The venodynamics are characterized by ambulatory venous hypertension in both superficial and deep veins. In this state the capillary pressure in the upright position is high, the only relief being elevation of the legs.
During walking, the pressures in superficial and deep veins oscillate around the level during passive standing, ie, with minimal net reduction in ambulatory venous pressure Figure 7. Flow in perforating veins is bidirectional, with an outward net flow, as opposed to the situation with superficial and perforator incompetence only Figure 6. The flow in superficial veins may be bidirectional, without net flow, or a net flow directed centrally or distally.
Figure 7. Venodynamics in patients with superficial, perforator, and deep venous dysfunction. During walking, the pressures in superficial and deep veins oscillate around the pressure in the passive upright position, ie, with minimal net reduction in ambulatory venous pressure.
Flow in perforating veins is bi-directional, with outward net flow, the opposite of what is found in patients with superficial and perforator incompetence only Figure 6.
Annotations are as in Figures 5 and 6. Outflow obstruction Venous outflow obstruction may be the result of occluded or partially recanalized veins subsequent to deep vein thrombosis. In proximal outflow venous thrombosis, increased outflow resistance and venous pressure during muscle contraction may lead to venous claudication Figure 8. Ambulatory venous hypertension often leads to distension of the perforators and valve dysfunction.
The pressure and flow is then directed towards the superficial veins, which may become the principal venous conduits. A resulting overload of the superficial veins may lead to dysfunction, including varicose veins. Figure 8 shows mean pressure curves during and after ambulation in the four states listed. The ambulatory venous pressure typically increases from healthy subjects to patients with superficial and perforator dysfunction to those with additional deep venous dysfunction and to those with deep venous obstruction.
These venous pressure profiles, along with the recovery times time from end of walking until the vein pressure reaches the level of passive dependency , with and without superficial venous occlusion occlusion test , form the diagnostic basis of venous pressure measurement.
Figure 8. Schematic illustration of the superficial venous pressure at rest, and during ambulation. The ambulatory venous pressure AVP represents the lowest mean pressure during walking at the site of measurement, and the recovery time RT is the time interval between the termination of walking until the vein pressure reaches the pressure level at passive dependency.
In a recent review article, 41 Levick and Michel argue that sustained fluid absorption into the capillaries from the interstitium does not normally take place except in a few specialized regions like the kidneys and intestines. Rather there is merely a unidirectional fluid shift from the capillaries to the lymphatics via the interstitium. The structural basis for this idea is the endothelial glycocalyx small pore system covering the relatively wider intercellular clefts that form the semipermeable membrane of the capillary wall.
Hence the area for colloid osmotic pressure build-up outside the capillaries is not in the interstitium; it lies within the intercellular clefts. This has important functional consequences. During filtration, the interstitial proteins that may previously have entered the intercellular clefts are washed into the interstitium, effectively reducing the COP just underneath the glycocalyx to a very low level and rendering it insignificant in the fluid balance, and the filtration force is reduced.
In the opposite situation, during the initial phase of absorption, interstitial proteins are trapped in the cleft, like in a sieve, thus building up a large COP which reduces and may stop the fluid transport. These new ideas challenge the relevance of the COPif presented in studies so far. This paper is based on the book chapter StrandenE. Edema in venous insufficiency. In: Wittens C, ed. Best Practice in Venous Procedures. Turin, Italy: Edizioni Minerva Medica; The permission given by the editor is highly appreciated.
Starling EH. On the absorption of fluids from the connective tissue spaces. J Physiol. Aukland K, Nicolaysen G. Interstitial volume: Local regulatory mechanisms. Physiol Rev. Analysis of lymphatic protein flux data.
Estimation of the reflection coefficient and permeability surface area product for total protein. Microvasc Res. Stranden E, Myhre HO. Transcapillary forces in patients with lower limb ischemia. Scand J Clin Lab Invest. Seem E, Stranden E. Transcapillary forces in muscle compartments of lower limbs with deep venous thrombosis. If the thrombosis is at a deeper level and has developed into a pulmonary embolism PE , you should go to your nearest ER immediately. Signs this has happened include:.
Pulmonary embolism is a life-threatening complication of venous thrombosis that takes the lives of up to , Americans each year. This could result in leg pain, persistent swelling, skin sores, and discoloration. Simply book an appointment online or call the clinic at Varicose veins affect about one-quarter of the adult population with symptoms ranging from cosmetic only to discomfort and pain. Sclerotherapy and endovenous ablation are two common treatments to relieve the condition.
A form of eczema, stasis dermatitis usually affects your lower legs after long spells of edema. Often a side effect of vein disorders, stasis dermatitis can lead to skin ulcers on the feet and lower legs. With circulation issues, edema can be a chronic problem that requires medical treatment directly, or for its underlying condition.
It can occur anywhere on the body, but it most often occurs in the lower legs. There are different conditions that can cause edema of the lower legs, and they range from benign to life threatening. Here are some of the most common causes.
Sitting or standing for extended periods can cause fluid retention in the lower legs. When extended sitting is the culprit, edema is caused by blood and other fluids pooling in the tissues.
Because the legs are at a much lower elevation than the heart, and because of a sustained lack of motion, these fluids are unable to return into the rest of the body. When extended standing is the culprit, the edema is caused by excessive pressure on the veins and tissues of the legs, allowing fluids to collect and cause swelling.
To prevent this, it is important to get up and move around every 20 to 30 minutes. Another common cause of lower leg edema is deep vein thrombosis DVT , more simply known as a blood clot. These can occur as a direct result of prolonged sitting, such as on long flights or road trips.
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