Pulmonary Embolism
Pulmonology / Emergency Medicine
Illness script · Pulmonology / Emergency Medicine
Pulmonary Embolism
Acute obstruction of pulmonary arterial circulation, most often by thrombus from deep veins, causing hypoxia and right heart strain.
This illness script for Pulmonary Embolism covers predisposing factors, classic presentation, mechanism, workup, management, and the clinical pivots that separate it from look-alikes—written for USMLE Step 1 and clerkship reasoning.
01
Predisposing factors
- Virchow's triad: stasis (immobility, long flight), endothelial injury, hypercoagulability
- Major surgery (especially orthopedic), trauma, hospitalization
- Malignancy (especially adenocarcinoma) — unprovoked PE warrants cancer workup
- OCP/HRT use, pregnancy, postpartum period
- Inherited thrombophilia: Factor V Leiden (most common), Prothrombin G20210A, antithrombin III deficiency
- Prior DVT/PE is strongest individual risk factor
02
Presentation
- Classic triad: dyspnea, pleuritic chest pain, hemoptysis (only ~20% have all three)
- Sudden-onset dyspnea is most common symptom; tachycardia most common sign
- Pleuritic pain + hemoptysis suggest peripheral (pulmonary infarction) PE
- Massive PE: hypotension, syncope, elevated JVP, RV heave, loud P2
- Signs of DVT (unilateral leg swelling/tenderness) in ~50% of cases
- Low-grade fever may occur; SpO2 often low but can be normal in submassive PE
03
Pathophysiology
- Thrombus (usually iliac/femoral DVT) embolizes to pulmonary arteries → mechanical obstruction
- Obstruction → increased RV afterload → RV dilation → septal shift → reduced LV preload and CO
- Ventilation-perfusion mismatch → hypoxemia; loss of surfactant → atelectasis
- Massive PE → obstructive shock; right heart failure is primary cause of death
04
Diagnostics
- Start with Wells Score (pretest probability) ± age-adjusted D-dimer to rule out
- CT pulmonary angiography (CTPA): first-line imaging, gold standard for diagnosis
- V/Q scan: use when CTPA contraindicated (CIN risk, pregnancy, contrast allergy)
- ECG: sinus tachycardia most common; S1Q3T3 pattern suggests RV strain (not pathognomonic)
- Echo: RV dilation, McConnell sign (RV free wall hypokinesis with apical sparing) in massive PE
- Troponin + BNT: elevated in RV strain, help risk-stratify submassive PE
05
Management
- Anticoagulation immediately if high suspicion — don't wait for imaging if low bleeding risk
- LMWH (enoxaparin) bridge to warfarin or direct oral anticoagulants (DOACs — rivaroxaban, apixaban) for most
- DOACs now preferred over warfarin for most non-cancer VTE (apixaban or rivaroxaban first-line)
- Massive PE (hemodynamically unstable): systemic thrombolysis (tPA) is definitive; catheter-directed or surgical embolectomy if lysis contraindicated
- Submassive PE (RV strain, hemodynamically stable): anticoagulate; consider catheter-directed thrombolysis if deteriorating
- IVC filter only if absolute contraindication to anticoagulation or recurrence despite therapeutic anticoagulation
06
Clinical pivots
How to separate this script from the look-alikes that show up on exams and on the wards.
Acute MI (STEMI/NSTEMI)
MI: EKG changes in coronary distribution + troponin rise without RV strain pattern; PE: S1Q3T3, RV dilation, CTPA confirms
Pneumothorax
Pneumothorax: absent breath sounds, tracheal deviation, no perfusion defect on imaging; PE: breath sounds intact, CTPA shows clot
Aortic Dissection
Dissection: tearing pain radiating to back, wide mediastinum on CXR, BP differential between arms; PE: pleuritic pain, normal mediastinum
Community-Acquired Pneumonia
Pneumonia: productive cough, fever, lobar consolidation on CXR, responds to antibiotics; PE: sudden dyspnea, wedge-shaped infarct, no response to antibiotics
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Educational use only. This illness script is a study framework, not medical advice. Confirm decisions with current guidelines and your clinical supervisors.