Pulmonary Embolism

Pathophysiology & Complications of PE
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  PULMONARY EMBOLISM Clinical Manifestations, Pathophysiology, Lung changes, Complications.  PATHOPHYSIOLOGY ã Effects of PE on gas exchange (hypoxemia) ã Arteriovenous communications in lungs and heart  –  new vessels bypassing capillaries in the lungs; (in patients with coexisting patent foramen ovale) right to left shunt in the heart. ã V/Q disturbances  –  release of histamine causing bronchospasm, release of serotonin causing vasospasm. In addition, reduced surfactant production leading to atelactasis. ã Fall in cardiac output ã Respiratory alkalosis    –  occlusion or pulmonary artery lead to increase in dead space and impairs elimination of CO2. increase in CO2   reflex increase in ventilation (hyperventilate) ã In some patient when PE is massive, present with hypercapnia .  ã Effects of PE on pulmonary circulation ã Emboli + vasospasm   pulmonary circulation obstruction    increase RV afterload + tachycardia   increase wall stress and RV dilatation   Increase O2 consumption   risk of ischemia. ã Increase in pressure and volume of RV   displacement of interventricular septum   affect distensibility and diastolic filling of LV   reduced cardiac output. ã In pts with co-existing PFO, increased RA pressure may lead to paradoxical embolism to systemic circulation. **Mean pulmonary pressure > 40mmHg   acute RV failure Small PE will only affect hemodynamics if pt have pre-existing cardiac or pulmonary disease that increases pulmonary vascular resistance.  ã L
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