Harvey's Garden

Pulmonary embolism

3 min read

Etiology

  • Most common: Deep vein thrombosis
  • Causes of nonthrombotic embolism
    • Fat embolism
    • Air embolism
    • Amniotic fluid embolism
    • Bacterial embolism
      • Patients with intravenous drug use are at increased risk of developing tricuspid valve endocarditis, giving rise to septic pulmonary emboli
    • Others: pulmonary tumor embolism, pulmonary cement embolism

Tip

Up to 30% of cases may present with no apparent risk factors (eg, hypercoagulability).

Pathophysiology

  • Dual Blood Supply: The lungs are supplied by two circulations:
    1. Pulmonary Arteries: Low-pressure system carrying deoxygenated blood from the RV for gas exchange.
    2. Bronchial Arteries: High-pressure system arising from the aorta; supplies oxygenated blood to the lung parenchyma (bronchi, connective tissue).
  • Pulmonary Infarction:
    • Due to the dual blood supply, PE does not always cause pulmonary infarction (tissue death). The bronchial circulation can often sustain the lung tissue.
    • Infarction is more likely to occur if the bronchial circulation is compromised (e.g., in left-sided heart failure) or if the embolus is very peripheral.
    • When it occurs, it’s typically a hemorrhagic (red) infarct because some blood from the bronchial circulation still leaks into the necrotic area.
    • Clinically, it presents with pleuritic chest pain and hemoptysis. Radiologically, it may appear as a wedge-shaped infiltrate (Hampton’s Hump).

Clinical features

  • Common features of PE
    • Acute onset of symptoms
    • Dyspnea (> 75% of cases)
    • Tachycardia and tachypnea (up to 50% of cases)
    • Sudden pleuritic chest pain (∼ 20% of cases)
    • Cough and hemoptysis
    • Associated features of DVT: e.g., unilaterally painful leg swelling c
  • Features of massive PE (e.g., due to a saddle thrombus)
    • Presyncope or syncope
    • Jugular venous distension and Kussmaul sign
      • RV pressure overload
    • Hypotension and obstructive shock
    • Circulatory collapse

Diagnostics

  • Algorithm:
    • Hemodynamically Unstable: Bedside Echo → if RV strain → Treat.
    • Stable + Low Prob (Wells ≤4): D-dimer (High sensitivity, low specificity). If (-) → Stop. If (+) → CTPA.
    • Stable + High Prob (Wells >4): CTPA immediately. Start empiric anticoagulation before imaging if no contraindications.
  • Initial/Adjuncts:
    • CXR: Usually normal. Rare signs: Hampton Hump (wedge opacity), Westermark Sign (oligemia).
    • ECG: Sinus tach (most common). S1Q3T3 (specific but rare, indicates RV strain).
    • ABG: Respiratory alkalosis (hypocapnia), hypoxia, widened A-a gradient.
  • Confirmatory/Gold Standard:
    • CT Pulmonary Angiography (CTPA): Best initial test for most pts.
    • V/Q Scan: Use if renal failure (Cr elevated), severe contrast allergy, or pregnancy (sometimes).
    • Lower Extremity US: Useful if CTPA contraindicated/unavailable; (+) DVT treats as PE.

Treatment

Reperfusion therapy

  • Indications
    • Massive PE (hemodynamic instability and/or right heart failure) with a low bleeding risk
  • Recombinant tissue plasminogen activator (tPA), e.g., alteplase (preferred)
    • Endothelial-derived TPA is limited primarily to the bronchial circulation, and spontaneous recanalization of the pulmonary artery is a slow process.

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