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Chronic venous insufficiency and hypertensionAny condition obstructing normal venous drainage will lead to a backlog of bloodwhich will increase the pressure within the veins.
This increased pressure will damagethe venous valves which do not have good powers of recovery. As a result an episodeof acute venous hypertension may result in a permanent reduction in the efficiencyof the venous return mechanisms. Reduced efficiency of venous return will lead toa chronic increase in the pressure within the effected peripheral veins.
These factorsexplain why DVT is the most important pathogenic mechanism in the causation ofchronic venous insufficiency. This insufficiency can contribute to the developmentof varicose veins and venous leg ulcers.As a result of the venous insufficiency there is a chronic backlog of blood inthe peripheral veins.
As the volume of blood in these veins increases so doesthe pressure. Increased hydrostatic pressure in the veins in turn increaseshydrostatic pressure in the capillaries. Backlog of blood in the capillaries reducesthe rate of circulation as arterial blood is not able to enter efficiently.
As aresult there is reduced delivery of nutrients and oxygen to the tissues as well asinhibited removal of waste products such as carbon dioxide and nitrates.Increased pressure in the venous ends of capillaries also reduces the rate ofreabsorption of tissue fluid; this increases the volume of tissue fluid resulting inoedema. Oedema in tissues increases the volume of fluid through which nutrientsmust diffuse in order to pass from capillary blood into the tissue cells. Alsooedematous swelling increases the diffusional distance from blood to tissue cells.
This reduces the efficiency of transporting oxygen and nutrients to cells and removingcarbon dioxide and other metabolic waste products. Both of these effects will reducethe viability of tissue cells in the presence of oedema.Increased pressure in a capillary will also lead to dilation of the vessel.
This will stretch the capillary walls and so widen the gaps (or pores) between individualcells which compose the endothelial wall. Increased capillary pore size allowslarger molecules such as proteins to migrate from blood into the tissue spaces. One of the plasma proteins is fibrinogen which can pass through the enlargedpores.
Once in the tissues fibrinogen is converted into the clotting proteinfibrin. Fibrin is composed of long sticky strands which may form a cuff arounda dilated capillary. It may be that the presence of such a 'fibrin cuff' furtherreduces the interchange of oxygen, nutrients and waste products between capillaryblood and tissue fluids and so further reduces tissue viability.