## Pathophysiology of Pulmonary Embolism **Key Point:** Pulmonary infarction does NOT occur in all cases of PE — it occurs in only 10% of cases, typically when there is pre-existing cardiopulmonary disease or when the embolus is large enough to cause wedge infarction. ### Hemodynamic Consequences | Mechanism | Pathophysiology | |-----------|------------------| | **RV afterload** | Acute obstruction of pulmonary vasculature increases pulmonary vascular resistance, causing acute RV strain | | **Hypoxemia** | V/Q mismatch (ventilated but not perfused areas) and intrapulmonary shunting | | **Vasoactive mediators** | Serotonin, thromboxane A₂, and leukotrienes released from platelets cause further pulmonary vasoconstriction | | **Infarction** | Occurs only when collateral circulation is inadequate (10% of cases) | ### Why Infarction is Uncommon 1. Lungs have dual blood supply (pulmonary + bronchial arteries) 2. Rich collateral circulation prevents ischemic necrosis in most cases 3. Infarction requires: - Large embolus occluding distal vessel - Pre-existing cardiopulmonary disease (heart failure, pneumonia) - Compromised bronchial circulation **High-Yield:** Pulmonary infarction is a complication of PE, NOT an inevitable consequence. Most PE patients do not develop infarction. **Clinical Pearl:** When infarction does occur, it typically presents as a wedge-shaped, hemorrhagic consolidation in the lung periphery with pleural involvement. ### Other True Statements - **RV afterload increase:** Acute and can lead to RV dilation and dysfunction - **Hypoxemia:** Universal mechanism of hypoxemia in PE - **Vasoactive mediators:** Important contributor to hemodynamic instability beyond mechanical obstruction [cite:Robbins 10e Ch 4]
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