How do increases in Pulmonary Vascular Resistance (PVR) and Systemic Vascular Resistance (SVR) affect preload and afterload?

Effects of Increased PVR and SVR on Preload and Afterload

Increases in Pulmonary Vascular Resistance (PVR) and Systemic Vascular Resistance (SVR) have distinct and significant effects on cardiac preload and afterload, with PVR primarily affecting right ventricular afterload and SVR primarily affecting left ventricular afterload.

Effects of Increased PVR

Impact on Right Ventricular Afterload

• Increased PVR directly increases right ventricular (RV) afterload 1
• The RV is highly sensitive to changes in afterload, with minor increases causing large decreases in stroke volume 1
• Unlike the LV, the RV has a shallower end-systolic pressure-volume slope, making it more vulnerable to afterload increases 1
• Increased PVR can lead to RV-pulmonary arterial uncoupling when the ratio of end-systolic elastance to arterial elastance falls below 0.6-1.0 1

Impact on Preload

• Increased RV afterload from high PVR leads to:
  • RV dilation and potential failure 1
  • Reduced RV stroke volume and cardiac output 1
  • Decreased left ventricular (LV) preload due to reduced pulmonary blood flow 1
  • Leftward shift of the interventricular septum, which further impairs LV filling 1

Effects of Increased SVR

Impact on Left Ventricular Afterload

• Increased SVR directly increases LV afterload 1
• Unlike the RV, the LV is better adapted to handle pressure changes than volume changes 1
• The LV has a steeper end-systolic pressure-volume relationship, allowing it to maintain stroke volume despite increased afterload 1

Impact on Preload

• Increased SVR can affect preload in several ways:
  • Reduced cardiac output may decrease venous return over time 1
  • Increased afterload may cause blood to "back up" in the pulmonary circulation 1
  • When SVR exceeds PVR, it helps maintain RV coronary perfusion during systole 1

Ventricular Interdependence

• The ventricles share a septum, circumferential muscle fibers, and pericardial space, creating interdependence 1
• RV dilation from increased PVR causes:
  • Leftward septal shift
  • Decreased LV compliance
  • Reduced LV filling (preload) 1
• This ventricular interdependence is particularly important in critical care settings 1

Clinical Implications

• In pulmonary arterial hypertension, maintaining SVR greater than PVR is crucial for RV coronary perfusion 1
• In right heart failure, the traditional mantra that "the RV is preload dependent" can lead to inappropriate volume loading, worsening RV dilation 1
• The RV prefers euvolemia with central venous pressure of 8-12 mmHg 1
• In mechanical ventilation:
  • Positive pressure increases PVR by increasing transpulmonary pressure 1
  • Volume loading can reduce PVR in ventilated patients, improving RV output 2

Common Pitfalls and Caveats

• SVR is an unreliable index of true LV afterload as it reflects only peripheral vasomotor tone rather than actual ventricular wall stress during systole 3
• PVR alone does not fully characterize RV afterload; pulmonary arterial compliance and wave reflection also contribute significantly 4
• In acute RV failure, volume loading may worsen ventricular interdependence by increasing RV dilation 1
• When using inotropes that decrease SVR (like milrinone), concurrent use of vasopressors that maintain SVR without increasing PVR (like vasopressin) may be beneficial to maintain RV perfusion 5

In summary, increased PVR primarily affects RV afterload and secondarily reduces LV preload through ventricular interdependence, while increased SVR primarily affects LV afterload with variable effects on preload depending on the clinical context and compensatory mechanisms.