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
Pathophysiology
- 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.
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)
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.