What is the best course of treatment for a patient with right ventricular (RV) failure?

Treatment of Right Ventricular Failure

The optimal treatment of RV failure centers on achieving euvolemia (targeting CVP 8-12 mmHg), reducing RV afterload with pulmonary vasodilators, maintaining systemic perfusion pressure with norepinephrine, and avoiding aggressive fluid resuscitation which worsens outcomes through ventricular interdependence. 1

Volume Management: The Critical First Step

Avoid aggressive fluid resuscitation—this is the most common and dangerous error in RV failure management. 1, 2 The traditional teaching that "the RV is preload dependent" leads to harmful volume loading that worsens RV dilation, causes leftward septal shift, compromises LV filling, and reduces cardiac output. 3

• Target euvolemia with CVP 8-12 mmHg, not aggressive volume expansion. 3, 1
• If CVP is genuinely low (assessed by collapsible IVC on ultrasound), administer cautious fluid boluses of ≤500 mL over 15-30 minutes only. 1, 2
• Diuresis is indicated when signs of RV failure and fluid retention are present, as reducing ventricular dilation improves biventricular coupling. 3

The European Society of Cardiology emphasizes that RV distention from excessive volume causes interventricular septal shift that directly compromises LV filling and cardiac output. 1

Vasopressor Support: Maintaining RV Perfusion

Norepinephrine is the vasopressor of choice for hypotensive RV failure, starting at 0.05-3.3 mcg/kg/min. 1, 2 This recommendation is critical because RV coronary perfusion occurs during both systole and diastole, and maintaining systemic arterial pressure at or above RV systolic pressure prevents RV ischemia. 3, 2

• Maintain systemic vascular resistance greater than pulmonary vascular resistance to ensure adequate RV perfusion. 3
• When using inodilators like milrinone that cause systemic vasodilation, concomitant vasopressor support with norepinephrine or vasopressin is necessary to maintain RV perfusion pressure. 3

Inotropic Support: Use With Caution

Dobutamine at 2.5-5.0 μg/kg/min (titrating to 10 μg/kg/min) can improve RV contractility, but the RV has less contractile reserve than the LV, and calcitropic agents have been associated with progressive RV function decline. 3, 2

• Milrinone is FDA-approved for short-term IV treatment of acute decompensated heart failure but carries significant risks. 4
• Milrinone use requires continuous ECG monitoring due to increased ventricular arrhythmias and is only indicated for short-term (<48 hours) treatment. 4
• The combination of inotropes with vasopressors is often necessary, as systemic vasodilation from inodilators can decrease right-sided perfusion pressures. 3

Afterload Reduction: Pulmonary Vasodilators

Inhaled nitric oxide (5-40 ppm, typically starting at 20 ppm) provides selective pulmonary vasodilation without systemic hypotension. 3, 1, 2 This is particularly important when pulmonary hypertension contributes to RV failure.

• Monitor methemoglobin levels every 6 hours during inhaled nitric oxide therapy. 1, 2
• Avoid abrupt discontinuation of inhaled nitric oxide due to risk of rebound pulmonary hypertension. 3, 1
• When weaning inhaled nitric oxide, initiate sildenafil 20 mg three times daily to prevent rebound. 1, 2
• Inhaled prostacyclin (20-30 ng/kg/min) is an alternative with comparable efficacy to inhaled nitric oxide. 3

For chronic pulmonary arterial hypertension with RV failure, oral sildenafil 20 mg three times daily reduces pulmonary vascular resistance. 1

Respiratory Management: Minimizing Harm

Optimize ventilator settings to minimize increases in RV afterload and pulmonary vascular resistance. 3, 2

• Use tidal volumes of 6 mL/kg lean body weight to prevent lung overdistension. 3, 2
• Keep peak airway pressures <30 cmH2O to avoid pulmonary vascular compression. 2
• Limit PEEP to ≤10 cmH2O if oxygenation allows, as excessive PEEP worsens RV afterload through lung overdistension. 3, 2
• Maintain oxygen saturation ≥90% (target 94-98%) to prevent hypoxic pulmonary vasoconstriction. 1, 2
• Correct acidosis and avoid permissive hypercapnia, as both acutely increase pulmonary vascular resistance. 3, 2
• Minimize intrathoracic positive pressure ventilation when possible. 3, 2

The evidence shows that driving pressure ≥18 cmH2O and PaCO2 ≥48 mmHg are independent risk factors for RV failure in ARDS, with risk exceeding 60% when multiple factors are present. 3

Mechanical Circulatory Support: For Refractory Cases

Consider RV mechanical support (Impella RP or Protek Duo) for select patients with persistent isolated RV failure refractory to medical therapy. 3, 1

• The Protek Duo centrifugal pump allows splicing of an oxygenator for concomitant respiratory insufficiency. 3
• RV failure from progressive pulmonary hypertension is poorly treated with devices providing only RV support, as forced perfusion may precipitate pulmonary hemorrhage; veno-arterial ECMO may be preferred in these cases. 3
• Severe tricuspid regurgitation should be repaired at the time of LVAD implantation to prevent worsening RV failure. 3

Addressing Underlying Causes

Identify and treat specific etiologies, as distinct causes respond differently to therapies. 3

• Initiate anticoagulation immediately for pulmonary embolism unless contraindications exist. 5
• Treat infections, arrhythmias, or other precipitating factors. 6
• Evaluate for left-sided heart disease contributing to RV dysfunction. 1
• Correct hypoxia, acidosis, and electrolyte abnormalities that increase pulmonary vascular resistance. 2

Hemodynamic Monitoring

Pulmonary artery catheter placement is recommended for patients refractory to pharmacological treatment or with uncertain hemodynamics, as invasive assessment facilitates identification of shock phenotype and guides therapy. 3, 2

• Target cardiac index >2 L/min/m². 2
• Target pulmonary wedge pressure <20 mmHg. 2
• Direct Fick method remains the gold standard for cardiac output measurement, though thermodilution is superior to estimated Fick. 3

Critical Pitfalls to Avoid

• Aggressive fluid resuscitation worsens RV distension and compromises cardiac output through ventricular interdependence—this is the single most critical error. 1, 2
• Failing to maintain adequate systemic perfusion pressure when using inodilators. 3
• Abrupt discontinuation of inhaled nitric oxide causing rebound pulmonary hypertension. 3, 1
• Excessive PEEP and high driving pressures that increase RV afterload. 3, 2
• Using systemic vasodilators that drop systemic pressure below RV pressure, causing RV ischemia. 3