What is the treatment for right ventricle infarction?

Treatment of Right Ventricular Infarction

The cornerstone of treatment for right ventricular infarction is aggressive intravenous fluid administration to maintain elevated right-sided filling pressures, combined with early reperfusion therapy, while strictly avoiding nitrates, diuretics, and vasodilators that can precipitate catastrophic hypotension. 1

Immediate Diagnostic Confirmation

• Record right precordial lead V4R on ECG immediately, as ST-segment elevation ≥1 mm in this lead is the single most predictive finding for RV infarction, though it may resolve within 10 hours of symptom onset 1, 2
• Look for the clinical triad of hypotension, clear lung fields, and elevated jugular venous pressure in the setting of inferior MI, though this has sensitivity <25% 1
• Kussmaul's sign (paradoxical rise in jugular venous pressure with inspiration) is a key clinical indicator 1

Volume Resuscitation: First-Line Therapy

Administer intravenous normal saline aggressively—begin with a 500-2500 mL bolus, followed by 500 mL/hour—to maintain the elevated right-sided filling pressure necessary for cardiac output. 1

• Target right atrial pressure ≥10 mm Hg and >80% of pulmonary wedge pressure 1
• Optimal left ventricular diastolic filling pressure (pulmonary artery wedge pressure) should be maintained at 14-18 mm Hg 1
• Hemodynamic monitoring with pulmonary artery catheter is generally required to optimize volume administration and is Class I indication for hypotension not responding promptly to initial fluid administration 1

Critical Medications to AVOID

Never administer nitrates, diuretics, or ACE inhibitors in acute RV infarction, as these reduce preload and can cause severe, potentially fatal hypotension. 1, 2

• Morphine should also be used cautiously as it can worsen hypotension 3
• This is a common and dangerous pitfall in management 2

Reperfusion: Mortality Reduction

Early reperfusion with primary percutaneous coronary intervention (PCI) or thrombolytic therapy is essential, as it reduces mortality from >85% to approximately 60% in shock patients. 1

• RV infarction identifies a high-risk subgroup with 25-31% in-hospital mortality (versus 6% for inferior MI without RV involvement), making these patients high-priority candidates for reperfusion 1, 4
• Primary PCI is preferred when available; transfer to catheterization laboratory shortly after initial stabilization 1
• If PCI cannot be performed expeditiously, administer thrombolytic therapy 1
• The right ventricle is relatively resistant to permanent damage and usually recovers even after prolonged occlusion, with most patients showing return of normal RV function over weeks to months 1, 4, 5

Inotropic Support: Second-Line Therapy

If fluid administration fails to achieve hemodynamic improvement and stabilization, escalate to inotropic support: 1

• Dobutamine is the preferred inotropic agent for RV infarction when cardiac output fails to increase after adequate volume loading 1, 2
• If systolic blood pressure remains <80 mm Hg despite fluids, initiate dopamine at 5-15 µg/kg/min 1
• For marked hypotension, norepinephrine may be required initially until systolic pressure reaches at least 80 mm Hg, then transition to dopamine 1

Mechanical Support

Consider intra-aortic balloon counterpulsation for patients with refractory hypotension despite optimal medical therapy, particularly as a bridge to definitive intervention 1

Maintain Atrioventricular Synchrony

• AV sequential pacing is indicated for symptomatic high-degree heart block unresponsive to atropine, as loss of atrial contraction severely compromises RV filling and cardiac output 1, 2
• Prompt cardioversion for hemodynamically significant supraventricular tachycardia 1
• Atrial infarction (from proximal RCA occlusion) eliminates augmented atrial contractility and exacerbates hemodynamic compromise 4

Reduce RV Afterload (When LV Dysfunction Present)

If concomitant left ventricular dysfunction increases RV afterload: 1

• Consider arterial vasodilators (sodium nitroprusside, hydralazine) or ACE inhibitors only after adequate volume resuscitation and hemodynamic stabilization
• These agents are contraindicated in the acute hypotensive phase

Monitoring for Complications

• RV infarction carries significantly higher risk of life-threatening arrhythmias and sudden cardiac death 6, 5, 7
• Continuous cardiac monitoring is essential 2
• Watch for bradyarrhythmias requiring temporary pacing 6, 7

Key Pathophysiologic Principles

The hemodynamic derangements result from: 1

• Acute RV dilation causing increased intrapericardial pressure with pericardial restraint
• Reduced RV systolic pressure and output leading to decreased LV preload
• Interventricular septal shift toward the left ventricle
• The pressure gradient between right and left atria becomes the critical driving force for pulmonary perfusion
• LV-septal contraction via paradoxical septal motion becomes essential for maintaining RV output 4