Clinical meaning
Pulmonary embolism causes acute right ventricular pressure overload from mechanical vascular obstruction and vasoactive mediator release. When > 30-50% of the pulmonary vascular bed is occluded, the thin-walled RV fails to generate adequate systolic pressures against the increased afterload. RV dilation causes interventricular septal shift (D-sign), impairs LV filling, and reduces cardiac output. V/Q mismatch from perfused but non-ventilated and ventilated but non-perfused lung units causes hypoxemia. Dead space ventilation increases (high V/Q regions), producing tachypnea. The Wells criteria pre-test probability score guides diagnostic testing: low probability (< 2 points) + negative age-adjusted D-dimer safely excludes PE. CTPA is the definitive imaging test. Risk stratification (PESI/sPESI) combined with RV function assessment and biomarkers determines management intensity from outpatient anticoagulation to systemic thrombolysis.
Diagnosis & workup
Diagnostics & workup: - Wells score: clinical DVT signs (3), PE most likely diagnosis (3), HR > 100 (1.5), immobilization/surgery (1.5), prior VTE (1.5), hemoptysis (1), malignancy (1) - D-dimer with age-adjusted cutoff (age × 10 for > 50 years): rules out PE if score is low and D-dimer negative - CT pulmonary angiography: gold standard; shows filling defect in pulmonary arteries; RV/LV ratio > 0.9 indicates RV strain - V/Q scan for contrast allergy or severe CKD - Echocardiography: RV dilation, McConnell sign, D-shaped septum, TAPSE < 16 mm - Troponin and BNP elevation indicate RV strain (submassive PE) - Bilateral lower extremity compression ultrasound: DVT present in ~50% - sPESI score for outpatient management eligibility (sPESI 0 = low risk)