Page 53 - Libro 2

3 — Venous Physiology
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Superficial veins
Perforating veins
Obstruction Deep veins
Incompetent perforator
Incompetent superficial valves
Muscle
Incompetent superficial valves
Incompetent deep valves
Rest
Contraction
Relaxation
Figure 3-12 Patterns of venous flow with secondary varicose veins.
increased venous pressure. If residual thrombus is present, the proximal obstruction to blood flow will also add to increased venous pressure in the leg.
VENOUS STASIS ULCERS
The effect of persistent increased venous pressure or venous hypertension is distention of the capillar- ies and increased capillary pressure. This results in slightly opening the junctions between the endothe- lial cells. This will cause plasma proteins to move out of the vascular space and into the tissue. As a consequence to this protein movement, additional fluid will also enter the interstitial space. There are several theories about how the tissue damage occurs, leading to ulceration. One theory involves fibrin accumulating around the capillaries in the interstitial space. This collection of fibrin, termed a fibrin cuff, leads to limited oxygen transfer across the capillaries. Another theory involves the migra- tion and trapping of white blood cells in the capil- laries and venules. The plugging of the capillaries and venules by these white blood cells also results in limited oxygen transfer into the tissue bed. The de- creased oxygen transfer produces tissue ischemia. As the ischemia progresses, ulceration occurs. Venous stasis ulcers are a serious end result of this extreme form of venous disease.
PREGNANCY AND VARICOSE VEINS
During pregnancy, the inferior vena cava and the iliac veins can be compressed by the enlarged uterus while lying supine, particularly in the third trimes- ter. This can produce a continuous venous outflow signal from the legs that is no longer responsive to changes in pressure brought on by respiration. This change in lower extremity venous flow is a result of increased venous pressure due to compression of the pelvic veins. This can be alleviated somewhat by turning the patient on her side so that the weight of the gravid uterus no longer impinges on the venous structures.
Humoral factors circulating during pregnancy cause the veins to be more compliant. This factor plus the increased venous pressure, which occurs later in pregnancy due to the size of the uterus can cause significant venous distention. The final result is a decrease in the velocity of venous flow. This can contribute to the development of a deep venous thrombosis.
Pregnancy does not cause varicose veins. In- creased venous pressure and venous distention can magnify predisposing factors. Thus, varicose veins often first appear during pregnancy. Typically, vari- cose veins become more severe with subsequent pregnancies.
Incompetent deep valves