Regarding the pathophysiology and hemodynamic consequences of pulmonary embolism, all of the following are true EXCEPT:

Question

Accepted Answer

C. Pulmonary infarction occurs in all cases of pulmonary embolism. ## 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]

Answer

A. Hypoxemia results from ventilation-perfusion mismatch and right-to-left shunting

Answer

B. Acute increase in right ventricular afterload occurs due to obstruction of pulmonary vasculature

Answer

D. Release of serotonin and thromboxane A2 from platelets causes pulmonary vasoconstriction

Regarding the pathophysiology and hemodynamic consequences of pulmonary embolism, all of the following are true EXCEPT:

Explanation

Pathophysiology of Pulmonary Embolism

Hemodynamic Consequences

Why Infarction is Uncommon

Other True Statements

Practice similar questions

Join our NEET PG community

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)