Pathophysiology of Chronic venous insufficiency and Deep venous thrombosis
Chronic venous insufficiency is a condition that describes a dysfunction of the valves in the upper and lower extremities or the inability of the muscles in these regions to exert the required pressure that can force the flow of blood back into the heart. Essentially, the arteries are designed to supply oxygen-rich blood to all parts of the body while the veins are designed to transport the oxygen-deficient blood back into the heart (McPhee& Hammer, 2010). These processes are enhanced by the pressure exerted by the underlying muscles within the upper and lower extremities as well as the ability of the valves within the veins and arteries. These mechanisms prevent the backflow of blood so that there is a continuous movement of blood towards one direction; towards the heart. The occurrence of CVI could be occasioned by two major factors and these are characteristically due to the underlying mechanisms that facilitate the normal flow of blood (Laureate Education, Inc. 2012a).
On one hand is the aspect of the dysfunction of the valves within the veins. The veins are designed to allow the flow of blood towards the heart and prevent the backflow of blood concurrently. When the valves lose this ability, there occurs a situation where the blood within the extremities piles up and gradually the pressure within the veins exceeds the threshold pressure that they can accommodate. This leads to the inflammation of the veins as well as the surrounding tissues with symptoms of increased pain in the affected region (Laureate Education, Inc., 2012a).
On the other hand, the muscles within the extremities may gradually lose their ability to squeeze on the veins and exert the required pressure to facilitate the flow of blood back into the heart. This leads to the reduced speed of blood flow and subsequently causing the pile up of blood within the veins. Once more, inflammation of the veins and surrounding tissues occurs and extreme pain within the region (Huether &McCance, 2012).
Deep Venous Thrombosis (DVT) occurs mainly in the deep veins in regions that are characterized by extensive masses of muscles such as the thighs and calf regions of the lower extremities. In most cases, the a clot forms in the deep veins as a result of either insertion of pacemakers, central nervous catheters or drug injection and in some cases due to natural cases (Laureate Education, Inc. (Executive Producer), 2012a). Once the clot has formed, a blockage of the vein occurs causing sustained pressure that leads to the impairment of the process of blood-flow return. Gradually this leads to the further coagulation due to pile up of blood and the slow speed of movement of blood; two conditions that lead to endothelial injury or dysfunction as well as hyper coagulation (McPhee& Hammer, 2010). These dysfunctions further extend to the valvular system further causing blockage, coagulation and damage. As these problems persist the clot could be pushed towards the vena cava and into the heart leading to a fatal condition.
Venous thrombosis and arterial thrombosis
Venous and arterial thromboses have their primary distinct separation in that they occur in the venous region and the arterial region respectively. Venous thrombosis occurs as a result of the formation of a clot within the nervous system. A decrease in the resistive force within the deep veins accompanied by the low pressure in the veins all lead to the increasing pile up of blood within the veins and subsequently the formation of a clot (Turpie & Esmon, 2011). These clots are usually red in clot and are referred to as red clots that are caused by the oxygen deficient blood and the presence of fibrin the blood within the veins. For arterial thrombosis, they occur in the high pressure arterial region and the formation of a clot is typically influenced by the presence of an underlying injury of the vascular tissue. The clots that occur in arterial thrombosis are white in color and could typically be referred to as white clots due to the presence of fibrin and platelets (Turpie & Esmon, 2011).
The impact of age on the pathophysiology of CVI and DVT
The manifestation of DVT and CVI could be influenced by a combination of factors or at times a single factor. Age is one of the major factors that significantly influence these conditions. With CVI, advancing age is associated with the tear and wear effects of the valves within the veins as well as within the deep lying muscles that are expected to exert the pressure that influences blood flow. The tear and wear effects of advancing age could lead to the decline in the ability of the valves to sustain the backflow of blood and this becomes the primary trigger effect for the accumulation of blood in the lower extremities (McPhee& Hammer, 2010). On the other hand, as a person ages, the muscles in the extremities become weak and may not provide sufficient pressure to sustain blood flow. The outcome is increased pile up of blood in the extremities and increased pressure within the veins which are the ultimate causes of CVI (Laureate Education, Inc. (Executive Producer), 2012a).
With DVT, old age is once more associated with the wearing out of muscles and the regions that have high muscle structure are likely to be affected significantly. As these muscles lose their ability to sustain normal blood pressure levels within the deep veins, accumulation of blood occurs; thus becoming the first point on which a clot can be formed especially due to the inflammatory effects on the walls of the veins (McPhee& Hammer, 2010). In these instances, the nurse has to focus more on helping elderly lifestyles to shun the sedentary lifestyles characterized by minimal physical activity and exercise and adopt lifestyles that can facilitate the optimal functioning of the muscles in the extremities to help sustain normal blood flow (Huether &McCance, 2012). However, for these patients, the use of anticoagulants is important for the short term and even in the long term to prevent the possibility increased coagulation within the veins and sustain a viable flow of blood (Huether &McCance, 2012).
Mind maps: Chronic Venous Thrombosis
Mind map 2: Deep venous thrombosis
References
Huether, S., &McCance, K. (2012).Understanding pathophysiology. St. Louis, Mo: Elsevier.
Laureate Education, Inc. (Executive Producer). (2012a). Alterations of cardiovascular functions PPT lecture. Baltimore, MD: Author.
McPhee, S. J., & Hammer, G. D. (2010). Pathophysiology of disease: An introduction to clinical medicine (Laureate Education, Inc., custom ed.). New York, NY: McGraw-Hill Medical.
Turpie, A. G., & Esmon, C. (2011). Venous and arterial thrombosis-pathogenesis and the rationale for anticoagulation. Thrombosis and haemostasis, 105(4), 586.
