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


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  • The lung is supplied by dual circulation from both the pulmonary arteries and bronchial arteries. This collateral circulation can help protect against lung infarction as a complication of pulmonary embolism (PE).
  • Distal PEs in small arteries (≤3 mm) are more likely to cause infarction as they may occlude areas distal to the pulmonary-bronchial anastomoses.
  • When a pulmonary infarction does occur, it is typically hemorrhagic (red) rather than ischemic (white) due to the relatively low density of lung tissue and the dual blood supply.

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
  • 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

ECG

ECG changes may be due to right ventricular strain and pressure overload. Most common findings

  • T-wave inversions or flattening
  • Sinus tachycardia
  • Normal ECG
  • S1Q3T3 pattern (neither sensitive nor specific)Pasted image 20230808202409.png Predictors of adverse outcomes: See “High-risk ECG findings in PE.” Other ECG findings in PE: sinus bradycardia (< 60/min); uncommon)

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.