Pulmonary Embolism and Right Ventricular Dilation
Yes, pulmonary embolism directly causes right ventricular dilation as part of its pathophysiological cascade, with RV dilation being a key marker of severity and a predictor of adverse outcomes. 1
Pathophysiological Mechanism
- Acute pulmonary embolism causes an abrupt increase in pulmonary vascular resistance when more than 30-50% of the total cross-sectional area of the pulmonary arterial bed is occluded by thromboemboli 1, 2
- This increased afterload leads to immediate right ventricular dilation as the thin-walled, non-preconditioned RV attempts to overcome the sudden pressure increase 1
- The RV dilation is a direct response to increased RV pressure and volume, resulting in increased wall tension and myocyte stretch via the Frank-Starling mechanism 1, 2
- PE-induced vasoconstriction, mediated by thromboxane A2 and serotonin release, further contributes to the pulmonary vascular resistance increase and subsequent RV dilation 1
Hemodynamic Consequences
- The dilated right ventricle has limited adaptive capacity and cannot generate a mean pulmonary artery pressure >40 mmHg 1
- RV dilation leads to prolonged RV contraction time extending into early diastole of the left ventricle 1
- This causes leftward bowing of the interventricular septum, desynchronizing the ventricles and impeding LV filling 1, 2
- The cascade ultimately results in reduced cardiac output, contributing to systemic hypotension and hemodynamic instability in severe cases 3, 4
Clinical Significance of RV Dilation
- RV dilation is a key marker of PE severity and is associated with increased short-term mortality in patients with pulmonary embolism 5
- The prevalence of RV dilation varies by location and extent of embolism: 89% with main pulmonary artery embolism, 64% with bilateral PE, 40% with lobar PE, 23% with segmental PE, and 17% with subsegmental PE 6
- RV/LV ratio is a measurable indicator of RV dilation, with higher ratios indicating more severe dilation 7
- RV dilation can be detected by echocardiography, CT scanning, or indirectly through elevated natriuretic peptide levels 5
Prognostic Implications
- The presence of RV dysfunction as determined by echocardiography is associated with increased short-term mortality (odds ratio = 2.36) 5
- Elevated natriuretic peptides, which reflect RV strain and dilation, are strongly associated with short-term mortality (odds ratio = 7.7) 5
- RV dilation can lead to RV ischemia and further reduced contractility, creating a vicious cycle of worsening hemodynamic compromise 1, 2
- In submassive PE with severe RV dilation (RV/LV ratio >1.9), treatment outcomes may differ compared to cases with mild to moderate dilation 8
Clinical Pitfalls and Considerations
- RV dilation may be more pronounced in systole than diastole in patients with acute PE (median RV/LV ratio 1.010 vs. 0.975) 7
- RV dilation should not be confused with chronic RV enlargement from other causes; acute PE typically presents with acute onset symptoms and other supporting evidence 1
- Not all PE cases cause significant RV dilation; the extent depends on the size, location, and burden of the embolism 6
- RV dilation can persist beyond the acute phase and may contribute to long-term complications such as chronic thromboembolic pulmonary hypertension in approximately 3.8% of patients 3