What is the pathophysiology of venous thromboembolism (VTE)?

Updated: Nov 05, 2020
  • Author: Vera A De Palo, MD, MBA, FCCP; Chief Editor: Vinod K Panchbhavi, MD, FACS, FAOA, FABOS, FAAOS  more...
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A thrombus is a solid mass composed of platelets and fibrin with a few trapped red and white blood cells that forms within a blood vessel. Hypercoagulability or obstruction leads to the formation of a thrombus in the deep veins of the legs, pelvis, or arms.

As the clot propagates, proximal extension occurs, which may dislodge or fragment and embolize to the pulmonary arteries. This causes pulmonary artery obstruction, and the release of vasoactive agents (ie, serotonin) by platelets increases pulmonary vascular resistance. The arterial obstruction increases alveolar dead space and leads to redistribution of blood flow, thus impairing gas exchange due to the creation of low ventilation-perfusion areas within the lung.

Stimulation of irritant receptors causes alveolar hyperventilation. Reflex bronchoconstriction occurs and augments airway resistance. Lung edema decreases pulmonary compliance. The increased pulmonary vascular resistance causes an increase in right ventricular afterload, and tension rises in the right ventricular wall, which may lead to dilatation, dysfunction, and ischemia of the right ventricle. Right heart failure can occur and lead to cardiogenic shock and even death. In the presence of a patent foramen ovale or atrial septal defect, paradoxical embolism may occur, as well as right-to-left shunting of blood with severe hypoxemia.

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