How Does Pulmonary Embolism Occur?

Pulmonary embolism occurs when there is a blockage in the pulmonary artery or its branches, usually caused by a thrombus (blood clot) that originated elsewhere. In deep vein thrombosis (DVT), the thrombus develops in the deep veins, most commonly in the lower extremities. Pulmonary embolism typically occurs when a portion of this thrombus breaks off and enters the pulmonary circulation. Very rarely, pulmonary embolism can result from embolization of other materials into the pulmonary circulation, such as air, fat, or tumor cells.

Large emboli often block the main pulmonary artery, causing a saddle embolism with serious cardiovascular consequences. Conversely, smaller-sized emboli block peripheral arteries and can lead to pulmonary infarction, characterized by intrapulmonary bleeding. Pulmonary infarction occurs in about 10% of cases.

Pulmonary embolism leads to impaired gas exchange due to obstruction of the pulmonary vascular bed, resulting in a ventilation-perfusion mismatch. Alveolar ventilation remains the same, but pulmonary capillary blood flow decreases, leading to hypoxemia.

Additionally, mediators like serotonin are released, causing vasoconstriction (narrowing of blood vessels) and further reducing pulmonary blood flow in unaffected areas of the lung. The local accumulation of inflammatory mediators alters the pulmonary surfactant and stimulates respiratory movements, leading to hypocapnia and respiratory alkalosis.

In pulmonary embolism, pulmonary vascular resistance increases due to mechanical obstruction of the vascular bed by the thrombus and hypoxic vasoconstriction. The pressure in the pulmonary artery increases if the thrombus occludes more than 30% to 50% of the total cross-sectional area of the pulmonary arterial bed.

Risk factors for pulmonary embolism are the same as those for deep vein thrombosis. Virchow’s triad – hypercoagulability (increased blood coagulation), venous stasis, and endothelial damage – provides an understanding of these risk factors. Pulmonary emboli are usually multiple, affecting the lower lobes more frequently than the upper ones, and bilateral pulmonary involvement is more common.

Risk factors for pulmonary embolism can be classified as genetic and acquired. Genetic risk factors include thrombophilia, such as factor V Leiden mutation, prothrombin gene mutation, protein C deficiency, protein S deficiency, and hyperhomocysteinemia. Acquired risk factors include prolonged immobility (such as bed rest for more than three days or extended sitting during travel), recent orthopedic surgery, malignancy, permanent venous catheter, obesity, pregnancy, smoking, and oral contraceptive use.