Pulmonary embolism (PE) is one of the most common etiologies of cardiovascular mortality. It could be linked to several risk factors including advanced age. The pathogenesis of PE is dictated by the Virchow's triad that includes venous stasis, endothelial injury, and a hypercoagulable state. The diagnosis of PE is difficult and is often missed due to the nonspecific symptomatology. Hypoxia is common in the setting of PE, and the degree of respiratory compromise is multifactorial and influenced by underlying cardiac function, clot location, and ability to compensate with respiratory mechanics. Right ventricular dysfunction/failure is the more profound cardiovascular impact of acute PE and occurs due to sudden increase in afterload. This is also the primary cause of death in PE. High clinical suspicion is required in those with risk factors and presenting signs or symptoms of venous thromboembolic disease, with validated clinical risk scores such as the Wells, Geneva, and pulmonary embolism rule out criteria in estimating the likelihood for PE. Advancement in capture time and wider availability of computed tomographic pulmonary angiography and D-dimer testing have further facilitated the rapid evaluation and diagnosis of suspected PE. Treatment is dependent on clinical presentation and initially involves providing adequate oxygenation and stabilizing hemodynamics. Anticoagulant therapy is indicated for the treatment of PE. Treatment is guided by presence or absence of shock and ranges from therapeutic anticoagulation to pharmacologic versus mechanical thrombectomy. The prognosis of patients can vary considerably depending on the cardiac and pulmonary status of patient and the size of the embolus.
Keywords: Virchow's triad; deep venous thrombosis; hypoxia; pulmonary angiography; pulmonary embolism; pulmonary hypertension; thromboembolic disease.
International College of Angiology. This article is published by Thieme.