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Pulmonary embolism (PE) is a potentially fatal obstruction of pulmonary arteries, most commonly from deep vein thrombosis (DVT). It is the third most common acute cardiovascular syndrome after myocardial infarction and stroke, with presentations ranging from asymptomatic to sudden cardiac death.
PE obstructs pulmonary blood flow, increasing right ventricular afterload and causing RV dilation, wall motion abnormality, and potential RV failure. Ventilation-perfusion mismatch leads to hypoxemia. Massive PE with hemodynamic compromise activates the sympathetic axis, causing tachycardia and hypotension. The degree of hemodynamic compromise and RV dysfunction determine mortality risk and guide treatment intensity.
Clinical reasoning begins with pretest probability using the Wells or Geneva score. D-dimer is highly sensitive but non-specific — useful for ruling out PE in low-probability patients. CT pulmonary angiography is the diagnostic standard. Risk stratification (massive, submassive, low-risk) guides treatment: systemic thrombolysis for massive PE, anticoagulation for submassive/low-risk, with catheter-directed therapy for select submassive cases. Key differentials include pneumonia, pneumothorax, ACS, pericarditis, and musculoskeletal pain.
Key imaging focus: Filling defects in pulmonary arteries, RV strain signs, Hampton hump, Westermark sign on CXR