Chronic venous insufficiency and hypertension
\nAny condition obstructing normal venous drainage will lead to a backlog of blood
\nwhich will increase the pressure within the veins. This increased pressure will damage
\nthe venous valves which do not have good powers of recovery. As a result an episode
\nof acute venous hypertension may result in a permanent reduction in the efficiency
\nof the venous return mechanisms. Reduced efficiency of venous return will lead to
\na chronic increase in the pressure within the effected peripheral veins. These factors
\nexplain why DVT is the most important pathogenic mechanism in the causation of
\nchronic venous insufficiency. This insufficiency can contribute to the development
\nof varicose veins and venous leg ulcers.
\nAs a result of the venous insufficiency there is a chronic backlog of blood in
\nthe peripheral veins. As the volume of blood in these veins increases so does
\nthe pressure. Increased hydrostatic pressure in the veins in turn increases
\nhydrostatic pressure in the capillaries. Backlog of blood in the capillaries reduces
\nthe rate of circulation as arterial blood is not able to enter efficiently. As a
\nresult there is reduced delivery of nutrients and oxygen to the tissues as well as
\ninhibited removal of waste products such as carbon dioxide and nitrates.
\nIncreased pressure in the venous ends of capillaries also reduces the rate of
\nreabsorption of tissue fluid; this increases the volume of tissue fluid resulting in
\noedema. Oedema in tissues increases the volume of fluid through which nutrients
\nmust diffuse in order to pass from capillary blood into the tissue cells. Also
\noedematous swelling increases the diffusional distance from blood to tissue cells.
\nThis reduces the efficiency of transporting oxygen and nutrients to cells and removing
\ncarbon dioxide and other metabolic waste products. Both of these effects will reduce
\nthe viability of tissue cells in the presence of oedema.
\nIncreased pressure in a capillary will also lead to dilation of the vessel. This
\nwill stretch the capillary walls and so widen the gaps (or pores) between individual
\ncells which compose the endothelial wall. Increased capillary pore size allows
\nlarger molecules such as proteins to migrate from blood into the tissue spaces.
\nOne of the plasma proteins is fibrinogen which can pass through the enlarged
\npores. Once in the tissues fibrinogen is converted into the clotting protein
\nfibrin. Fibrin is composed of long sticky strands which may form a cuff around
\na dilated capillary. It may be that the presence of such a ‘fibrin cuff’ further
\nreduces the interchange of oxygen, nutrients and waste products between capillary
\nblood and tissue fluids and so further reduces tissue viability.<\/p>\n","protected":false},"excerpt":{"rendered":"
Chronic venous insufficiency and hypertension Any condition obstructing normal venous drainage will lead to a backlog of blood which will increase the pressure within the veins. This increased pressure will damage the venous valves which do not have good powers of recovery. As a result an episode of acute venous hypertension may result in a […]<\/p>\n","protected":false},"author":0,"featured_media":7473,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"video","meta":{"yasr_overall_rating":0,"yasr_post_is_review":"","yasr_auto_insert_disabled":"","yasr_review_type":"","footnotes":""},"categories":[25],"tags":[1476,61,1429,1430,1475],"class_list":["post-7472","post","type-post","status-publish","format-video","has-post-thumbnail","hentry","category-gaming","tag-disease","tag-education","tag-nurse","tag-nursing","tag-venous","post_format-post-format-video"],"yoast_head":"\n