How do you optimize preload to the heart in patients with depressed right ventricular (RV) function?

Optimizing Preload in Patients with Depressed Right Ventricular Function

In patients with depressed right ventricular (RV) function, preload should be maintained at euvolemic levels with a central venous pressure (CVP) of 10-15 mmHg to optimize cardiac output while avoiding RV overdistention. 1

Understanding RV Physiology in Dysfunction

The right ventricle has unique physiological properties that must be considered when managing preload:

• Unlike the left ventricle, the RV is thin-walled and more sensitive to changes in afterload
• The RV is traditionally described as "preload dependent" but this can lead to inappropriate volume loading 1
• RV overdistention can worsen function through several mechanisms:
  • Increased wall tension impairs RV myocardial blood flow 2
  • Ventricular interdependence causes leftward septal shift, compromising LV filling 1
  • Excessive RV dilation worsens tricuspid regurgitation 1

Preload Optimization Algorithm

Step 1: Assess Current Volume Status

• Target CVP: 10-15 mmHg 1
• Evaluate using:
  • Ultrasound assessment of inferior vena cava dimensions and filling dynamics
  • Pulse pressure variation observations
  • Central venous pressure monitoring in response to intervention 1

Step 2: Correct Volume Status Based on Assessment

• If Hypovolemic (CVP <10 mmHg):

  • Administer careful fluid boluses
  • Reassess after each bolus to avoid overcorrection
  • Consider albumin in cases of hypoalbuminemia 1

• If Hypervolemic (CVP >15 mmHg):

  • Implement diuresis to reduce ventricular dilation
  • Diuresis improves biventricular coupling by reducing RV distention 1
  • Consider the FACTT-lite protocol once shock is resolved 1

Step 3: Address Concomitant Factors Affecting RV Function

• Reduce RV Afterload:

  • Early use of inhaled pulmonary vasodilators (epoprostenol or nitric oxide) to improve RV-PA coupling 1
  • Minimize intrathoracic positive pressure ventilation when possible 1
  • Correct acidosis and improve oxygenation to reduce hypoxic pulmonary vasoconstriction 1

• Support RV Contractility:

  • Maintain cardiac index >2.0 L/min/m² (ideally 2.4 L/min/m²) 1
  • Consider inotropic support with agents like dobutamine or milrinone
  • When using inodilators (especially milrinone), consider concomitant vasopressors like vasopressin or norepinephrine to maintain RV perfusion 1

• Optimize Heart Rate:

  • Target heart rate 90-110 beats/min to maximize cardiac output when RV stroke volume is limited 1

• Maintain Coronary Perfusion:

  • Ensure mean arterial pressure >65 mmHg to maintain adequate RV perfusion 1

Pitfalls to Avoid

1. Excessive Volume Loading: The traditional mantra that "the RV is preload dependent" often leads to inappropriate and detrimental volume loading, which worsens RV dilation and tricuspid regurgitation 1

2. Ignoring Ventricular Interdependence: RV distention causes leftward interventricular septal shift, compromising LV filling and reducing cardiac output 1

3. Overlooking RV Ischemia: Excessive preload increases RV wall tension and may impair RV myocardial blood flow, potentially contributing to RV failure 2

4. Delayed Recognition of Need for Mechanical Support: In cases of refractory RV failure despite optimal medical management, early consideration of mechanical circulatory support is preferable to delayed intervention 1, 3

Special Considerations

• Post-Cardiopulmonary Bypass: Transient RV dysfunction is common after cardiac surgery and may require careful preload management 4

• Persistent RV Dysfunction: RV contractile dysfunction may persist even after resolution of acute pressure overload, requiring ongoing careful preload management 5

• Mechanical Ventilation: Positive pressure ventilation increases RV afterload and should be minimized when possible in patients with RV dysfunction 1

By following this approach to preload optimization while simultaneously addressing afterload and contractility, you can maximize cardiac output in patients with depressed RV function while avoiding the detrimental effects of RV overdistention.