Hemodynamic Disorders PDF
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University of Jordan, School of Medicine
Fatima obeidat
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This document presents a lecture or presentation on Hemodynamic disorders, focusing on thrombosis and embolism, along with their underlying causes, clinical features, and outcomes.
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Fatima obeidat,MD University of Jordan, School of medicine Processes that maintain blood in a fluid, clot-free state in normal vessels while rapidly forming a localized hemostatic plug at the site of vascular injury. The pathologic counterpart of hemostasis is thrombosis, the format...
Fatima obeidat,MD University of Jordan, School of medicine Processes that maintain blood in a fluid, clot-free state in normal vessels while rapidly forming a localized hemostatic plug at the site of vascular injury. The pathologic counterpart of hemostasis is thrombosis, the formation of blood clot (thrombus) within intact vessels. Three elements: 1.The vascular wall. 2. Platelets. 3.The coagulation cascade Primary abnormalities that lead to thrombus formation (called Virchow’s triad): (1) endothelial injury, (2) stasis or turbulent blood flow, and (3) hypercoagulability of the blood Examples: 1. In cardiac chambers after myocardial infarction. 2. Over ulcerated atherosclerotic plaques 3. At sites of traumatic or inflammatory vascular injury (vasculitis). Turbulence leads to arterial and cardiac thrombosis by endothelial injury. Stasis is a major factor in the development of venous thrombi. Important underlying risk factor for venous thrombosis. Primary (inherited) hypercoagulability: young patients (>>Larger leg veins at or above the knee joint. >>>popliteal, femoral, and iliac veins >>> more serious, prone to embolization. >>>cause local pain and edema. >>>Asymptomatic in 50% of patients, recognized after they embolize to lungs. Superficial or the deep veins of the leg. Superficial venous thrombi >>>> in saphenous system, >>>>varicose veins. >>>>rarely embolize >>>>painful, congestion and swelling. >>>> Impaired venous outflow >>>>varicose ulcers 95% of cases originate from thrombi within deep leg veins above knee level. Depending on size, a PE can occlude the main pulmonary artery, lodge at the bifurcation of the right and left pulmonary arteries (saddle embolus), or pass into the smaller, branching arterioles. Recurrence. Most pulmonary emboli (60% to 80%) are small and clinically silent. Large embolus that blocks a major pulmonary artery can cause sudden death. (saddle embolus) Embolic obstruction of medium-sized arteries and subsequent rupture of capillaries can cause pulmonary hemorrhage. Embolism to small end-arteriolar pulmonary branches usually causes infarction. Multiple emboli occurring over time can cause pulmonary hypertension and right ventricular failure (cor pulmonale). Origin of systemic emboli 1.Most systemic emboli (80%) arise from intracardiac mural thrombi; >>>left ventricular infarcts. >>>dilated left atrium 2.Aortic aneurysms 3.Thrombi overlying ulcerated atherosclerotic plaques, 4.10% to 15% unknown origin.