What is the management of right ventricular myocardial infarction (RV MI)?

Management of Right Ventricular Myocardial Infarction

The cornerstone of RV MI management is aggressive IV fluid resuscitation with normal saline to maintain RV preload, combined with urgent reperfusion via primary PCI, while strictly avoiding all vasodilators including nitrates, diuretics, morphine, and ACE inhibitors that can precipitate catastrophic hypotension. 1, 2

Recognition and Diagnosis

Clinical Presentation

The classic triad consists of hypotension, clear lung fields, and elevated jugular venous pressure in the setting of inferior STEMI, though this triad has less than 25% sensitivity. 1, 2 Look specifically for:

• Distended neck veins or Kussmaul's sign (paradoxical rise in JVP with inspiration) 2
• Hypotension disproportionate to the extent of LV dysfunction 1, 3
• Clear lung fields despite hemodynamic compromise 1

Electrocardiographic Diagnosis

ST-segment elevation ≥1mm in right precordial lead V4R is the single most predictive ECG finding, with 88% sensitivity and 78% specificity. 2 This lead should be recorded routinely in all cases of inferior STEMI and shock, as ST elevation in V4R can resolve within 10 hours. 2

Additional ECG findings include:

• ST elevation of greatest magnitude in lead III compared to leads II and aVF 3
• Q-waves and ST-segment elevation in V1-3 1

Hemodynamic Confirmation

Right atrial pressure ≥10 mmHg and >80% of pulmonary capillary wedge pressure is both sensitive and specific for RV infarction. 2

Echocardiography confirms the diagnosis by demonstrating dilated, hypokinetic-to-akinetic right ventricle with dilated right atrium and low-velocity tricuspid regurgitation from annular dilatation. 1

Acute Management Algorithm

Step 1: Maintain RV Preload (First Priority)

Administer rapid IV fluid loading with normal saline initially to restore adequate RV filling pressures. 1, 2 Careful hemodynamic monitoring is required during fluid administration. 1

Critical caveat: Strictly avoid all medications that reduce preload:

• Nitrates (including sublingual and IV) 1, 2
• Diuretics 1, 2
• Morphine 3
• ACE inhibitors/ARBs 1, 2

These agents can cause profound, life-threatening hypotension by reducing the already compromised RV preload. 2

Step 2: Urgent Reperfusion (Highest Priority for Mortality Reduction)

Direct PCI should be performed as soon as possible as it may result in rapid hemodynamic improvement. 1 RV infarction with hemodynamic compromise identifies a high-risk subgroup with 25-30% in-hospital mortality (versus 6% for uncomplicated inferior MI), making these patients high-priority candidates for reperfusion. 1, 2

Fibrinolytic therapy is appropriate in the hypotensive patient if PCI is not available, though some question exists about its effectiveness specifically in RV infarction. 1

Step 3: Maintain AV Synchrony

Atrial contribution to RV filling is critical in this context. 1

• For atrial fibrillation: Prompt cardioversion 1
• For symptomatic high-degree heart block unresponsive to atropine: AV sequential (dual chamber) pacing 1, 2

Step 4: Inotropic Support if Needed

If cardiac output fails to increase after adequate volume loading, administer dobutamine. 2 Begin with dopamine at 5-15 µg/kg/min if marked hypotension is present (systolic BP <80 mmHg), then transition to dobutamine once pressure reaches ≥90 mmHg. 1

Step 5: Mechanical Circulatory Support for Refractory Shock

Consider intra-aortic balloon pump counterpulsation for persistent shock despite volume loading and inotropic support. 1, 2 In eligible patients with cardiogenic shock, timely use of mechanical circulatory support provides the RV time needed to recover from the ischemic insult. 4

Step 6: Reduce RV Afterload (Only if Concomitant LV Dysfunction Present)

If LV dysfunction coexists, use arterial vasodilators and ACE inhibitors cautiously to reduce RV afterload. 2 This is the only scenario where vasodilators may be considered in RV infarction.

Special Considerations

Conduction Disturbances

Sinus bradycardia is common in the first hour of inferior MI. 2 Administer IV atropine 0.3-0.5mg, repeated up to 1.5-2.0mg total, for bradycardia with hypotension. 2

Prognosis and Recovery

Most patients demonstrate return of normal RV function over weeks to months, suggesting RV "stunning" rather than irreversible necrosis has occurred. 1, 5 The RV appears more resistant to permanent infarction compared to the LV due to lower oxygen demand, dual systolic-diastolic coronary perfusion, and more extensive collateral flow. 1, 4

However, RV infarction significantly increases in-hospital mortality to 25-30% and remains a marker of worse outcome in acute coronary syndrome. 1, 2, 4

Critical Pitfalls to Avoid

The most dangerous error is administering nitrates to a patient with RV infarction, which can cause profound hypotension by reducing preload. 2 Volume depletion may mask signs of RV involvement, delaying diagnosis. 2

Early recording of lead V4R is essential, as ST elevation can resolve within 10 hours, potentially missing the diagnostic window. 2