How is pathophysiology of DVT?

Virshow's triad (inflammation, hypercoagulability, endothelial injury), recruitments of platelets release microparticles, venous thrombi form and flourish in an environment of stasis, low oxygen tension, upregulation of proinflammatory genes. Prothrombotic genes (factor V leiden [resistance to AG], prothrombin gene [increase prothrombin concentration], APS antibody most common cause of thrombophilia. Embolization (when the thrombus detach they go to vena cava, RA, RV, pulmonary arterial circulation, cause acute PE, may embolize to arterial circulation by patent foramen ovale/septal defect. Many have no evidence of DVT clot already embolized to lung.) Physiology (arterial hypoxemia, increased Aa gradient, increased anatomic dead space and physiologic dead space, vascular resistance, gas exchange impaired) Pulmonary HTN (pulmonary artery obstruction, tension to right heart buldge to left heart impair filling and compress coronary artery