Pulmonology

Pulmonary Embolism song

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Pulmonary Embolism

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Most pulmonary emboli originate from deep vein thrombosis (DVT) of the proximal lower extremity veins, particularly the iliofemoral system.
Classic presentation is sudden-onset pleuritic chest pain, dyspnea, tachycardia, and hypoxia; massive PE adds hypotension and signs of right heart strain.
The most common EKG finding is sinus tachycardia; the classic but less common finding is S1Q3T3 pattern, reflecting acute right heart strain.
D-dimer is highly sensitive but not specific — a negative D-dimer in a low-probability patient (Wells score ≤4) effectively rules out PE without imaging.
CT pulmonary angiography (CTPA) is the gold-standard diagnostic test for PE; V/Q scan is preferred in patients with renal insufficiency or contrast allergy.
Echocardiography in massive PE shows right ventricular dilation, interventricular septal bowing toward the left ("D-sign"), and McConnell's sign (RV free wall hypokinesis with preserved apex).
Treatment of hemodynamically stable PE is anticoagulation (heparin bridge to warfarin, or direct oral anticoagulants such as rivaroxaban or apixaban); systemic thrombolytics (tPA) are reserved for massive PE with hemodynamic instability.
Saddle embolus lodges at the bifurcation of the main pulmonary artery and is a surgical emergency associated with sudden cardiovascular collapse.
Virchow's triad — hypercoagulability, venous stasis, and endothelial injury — defines the pathophysiologic risk factors underlying PE development.
Factor V Leiden mutation (activated protein C resistance) is the most common inherited thrombophilia predisposing to PE in the United States.