How do you manage preload in right ventricular (RV) failure?

Management of Preload in Right Ventricular Failure

In right ventricular failure, preload should be carefully optimized to maintain central venous pressure between 8-12 mmHg, as excessive volume loading can worsen RV dilation and function while inadequate preload can reduce cardiac output. 1

Understanding RV Preload Dependence

The right ventricle has traditionally been described as "preload dependent," but this concept requires careful interpretation:

• While the RV does require adequate filling to maintain stroke volume, excessive preload can be detrimental
• RV distention from volume overload causes:
  • Increased wall tension and myocardial oxygen demand
  • Leftward interventricular septal shift
  • Compromised LV filling
  • Worsened tricuspid regurgitation
  • Reduced RV myocardial blood flow 2

Hemodynamic Targets for RV Preload

The optimal preload management strategy includes:

• Target CVP of 8-12 mmHg 1
• Maintain cardiac index >2.0 L/min/m² (ideally 2.4 L/min/m²) 1
• Ensure adequate RV perfusion with MAP >65 mmHg 1
• Monitor for signs of ventricular interdependence (septal shift on echo)

Algorithm for Preload Management in RV Failure

Step 1: Assess Volume Status

• Evaluate CVP trend and waveform
• Echocardiographic assessment of RV size, function, and septal position
• Consider invasive hemodynamic monitoring in complex cases

Step 2: Manage Based on Volume Status

• If CVP <8 mmHg and signs of hypovolemia:

  • Cautious volume administration (≤500 mL) 3
  • Reassess response to avoid excessive volume loading

• If CVP 8-12 mmHg (euvolemic):

  • Maintain current volume status
  • Focus on optimizing contractility and afterload

• If CVP >12-15 mmHg with RV dilation:

  • Implement diuresis to reduce ventricular dilation 1
  • Consider ultrafiltration if diuretic resistance occurs
  • Target euvolemia to improve biventricular coupling

Pharmacologic Support

• Diuretics: First-line therapy for volume overload to reduce RV dilation and improve biventricular coupling 1

• Inotropic support:

  • Dobutamine (2.5-5.0 μg/kg/min): Improves RV contractility 3
  • Milrinone (0.25-0.75 μg/kg/min): Provides inotropic support with pulmonary vasodilation 3

• Vasopressors:

  • Norepinephrine (0.05-3.3 μg/kg/min): Maintains RV perfusion pressure while supporting systemic pressure 3
  • Vasopressin: Can increase systemic vascular resistance without increasing pulmonary vascular resistance 1

Adjunctive Measures

• Pulmonary vasodilators: Reduce RV afterload to improve RV function

  • Inhaled nitric oxide (5-10 ppm)
  • Inhaled epoprostenol (10-50 ng/kg/min) 1

• Ventilatory strategies:

  • Low tidal volumes (~6 mL/kg)
  • Minimize PEEP (≤10 cmH2O if oxygenation allows)
  • Avoid hypercapnia and acidosis 1

• Pacing strategy:

  • Maintain heart rate 90-110 beats/min to optimize RV stroke volume 1
  • Consider turning off LV lead if ventricular arrhythmias present 1

Advanced Support for Refractory RV Failure

• Mechanical circulatory support:
  • Early RV mechanical support is preferable to delayed intervention 1
  • Options include Impella RP, Protek Duo, or VA-ECMO depending on clinical scenario 1, 4

Common Pitfalls to Avoid

1. Excessive volume loading: The traditional mantra that "the RV is preload dependent" often leads to inappropriate and detrimental volume loading in RV dysfunction 1

2. Inadequate systemic pressure: Maintaining adequate coronary perfusion pressure (MAP >65 mmHg) is essential for RV function, especially when using inodilators 1

3. Ignoring ventricular interdependence: RV dilation causes leftward septal shift that compromises LV filling and reduces cardiac output 1

4. Delayed intervention: Early recognition and intervention for RV failure improves outcomes 1

By carefully balancing preload, optimizing contractility, and reducing afterload, RV function can be supported effectively in patients with right ventricular failure.