Right Ventricular Preload Dependence
Yes, the right ventricle (RV) is preload dependent, but it is more sensitive to changes in afterload than to variations in preload. 1
RV Physiological Characteristics
The RV has distinct physiological characteristics that influence its preload dependence:
- Anatomical structure: The RV has a funnel-like configuration with a heavily trabeculated structure, making it more compliant than the LV 1
- Energy expenditure: The RV requires one-sixth the energy expenditure of the LV due to the low-resistance pulmonary circulation 1
- Pressure-volume relationship: The RV pressure-volume loop lacks isovolumic phases of contraction and relaxation, has lower peak systolic pressure, and exists at a higher steady-state volume compared to the LV 1
Preload vs. Afterload Sensitivity
- The RV is highly sensitive to changes in afterload, with minor increases in afterload causing large decreases in stroke volume 1
- The RV has a shallower end-systolic pressure-volume slope than the LV, resulting in greater changes in end-systolic volume with changes in pressure 1
- When pulmonary artery systolic pressure increases acutely, RV stroke volume decreases significantly and arterial elastance increases out of proportion to end-systolic elastance 1
Clinical Implications of RV Preload Dependence
Volume Management
- Traditional misconception: The mantra that "the RV is preload dependent" often leads to inappropriate volume loading in RV dysfunction 1
- Optimal approach: The RV prefers euvolemia with a central venous pressure of 8-12 mmHg 1
- Risks of volume overload: Excessive volume loading can worsen RV dilation and tricuspid regurgitation 1
Hemodynamic Monitoring
- Right ventricular end-diastolic volume index (RVEDVI) correlates better with cardiac index (r=0.61) than pulmonary artery wedge pressure (r=0.42) 2
- RVEDVI more accurately predicts preload-recruitable increases in cardiac output compared to pressure-based measurements 2, 3
- Stroke volume variation (SVV) has better correlation with RVEDVI (R²=0.48) than central venous pressure (R²=0.19) or pulmonary artery diastolic pressure (R²=0.33) 4
Special Considerations in RV Failure
Mechanical Ventilation Effects
- Positive pressure ventilation increases pleural pressure (Ppl), which decreases venous return to the RV 1
- When positive end-expiratory pressure (PEEP) is present, the gradient for venous return is decreased throughout the ventilatory cycle 1
- Increased mean airway pressure can increase pulmonary vascular resistance, further compromising RV function 1
Ventricular Interdependence
- RV dilation causes leftward interventricular septal shift, compromising LV filling and reducing cardiac output 1
- Diuresis reduces ventricular dilation and improves biventricular coupling 1
- In acute RV failure, mechanical flattening with leftward shift of the interventricular septum increases LV end-diastolic pressure and impedes LV diastolic filling 1
Management Principles
- Maintain euvolemia: Target central venous pressure of 8-12 mmHg rather than aggressive volume loading 1
- Consider volume status carefully: In RV infarction, maintain RV preload but avoid excessive volume loading 1
- Avoid factors that reduce preload: Volume depletion, diuretics, and nitrates can have profoundly adverse hemodynamic effects in RV failure 1
- Monitor using volumetric parameters: RVEDVI provides better assessment of preload status than pressure-based measurements 2, 3
- Address afterload: The RV is particularly sensitive to increases in afterload, so managing pulmonary vascular resistance is crucial 1
Pitfalls to Avoid
- Excessive volume loading: Can worsen RV dilation, tricuspid regurgitation, and interventricular dependence 1
- Relying solely on pressure measurements: CVP and PAWP correlate poorly with cardiac output compared to volumetric measurements 2, 5, 3
- Ignoring ventricular interdependence: RV dilation affects LV filling and function 1
- Overlooking afterload: The RV is more sensitive to changes in afterload than preload 1
In summary, while the RV is preload dependent, it is more sensitive to changes in afterload. Optimal management requires careful assessment of volume status using volumetric parameters rather than pressure-based measurements, and maintaining euvolemia rather than aggressive volume loading.