Right Ventricular Infarction – Recognition, Diagnosis & Management

Right Ventricular Infarction – Recognition, Diagnosis & Management

Right ventricular (RV) infarction is a commonly overlooked but clinically significant subset of acute myocardial infarction (AMI). It most often occurs in association with inferior wall MI, especially when the culprit lesion involves the proximal right coronary artery (RCA). Early recognition is crucial because RV infarction behaves very differently from left-sided infarcts and requires unique management strategies.

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🔎 Pathophysiology

The RV is supplied primarily by the RCA in most individuals. An occlusion proximal to the RV marginal branches leads to ischemia of the RV free wall.

Key consequences include:

Reduced RV contractility

Decreased RV output → reduced LV preload

Systemic hypotension despite clear lungs

High sensitivity to nitrates/diuretics

RV function greatly depends on preload, so anything that reduces venous return can precipitate collapse.

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🧩 Clinical Presentation

The classic triad of RV infarction:

1. Hypotension

2. Jugular venous distension

3. Clear lung fields

Other findings:

Inferior wall MI symptoms (chest pain, diaphoresis)

Bradyarrhythmias (due to RCA sinoatrial or AV node involvement)

Kussmaul’s sign (JVP rise with inspiration)

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📌 ECG Findings

RV infarction should be suspected in all inferior MI cases.

Key ECG clues

Inferior MI pattern: STE in II, III, aVF

STE in V1 (unusual for pure inferior MI)

ST-segment elevation in right-sided leads, especially V4R (most specific):

≥1 mm STE in V4R is diagnostic of RV infarction

Always order a right-sided ECG if inferior MI + hypotension or JVD.

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📸 Echocardiography

Useful findings:

RV dilation

Hypokinesis or akinesis of RV free wall

Normal or near-normal LV function (important differentiator)

Septal bowing toward the LV

Echo is especially helpful for hemodynamically unstable patients.

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🧪 Hemodynamics

On right heart catheterization:

Elevated RA and RV pressures

Normal or low pulmonary capillary wedge pressure

RA pressure > LV end-diastolic pressure

“Dip and plateau” may be seen but less marked than in restrictive physiology

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💉 Management Principles

Management differs significantly from LV infarction.

1. Restore Coronary Flow

Primary PCI of the RCA is the definitive treatment.

Fibrinolysis if PCI unavailable.

2. Maintain RV Preload

The RV is preload-dependent.

✔ Give fluids (cautiously):

500–1000 mL bolus if hypotensive

Avoid overloading, especially if echo shows high filling pressures

❌ Avoid these in acute RV infarction:

Nitrates

Diuretics

Morphine These reduce preload and can cause severe hypotension.

3. Support Bradyarrhythmias

Temporary pacing for high-grade AV block.

Atropine may help in some cases, but pacing is often more reliable.

4. Inotropes (if needed)

If hypotension persists after adequate fluids:

Dobutamine is preferred.

Norepinephrine may be used if shock persists with poor systemic perfusion.

5. Mechanical Support

IABP is less effective because it mainly supports LV.

RV assist devices may be considered in refractory shock.

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📉 Complications

Cardiogenic shock (RV type)

Severe bradycardia/AV block

Atrial arrhythmias

Ventricular septal rupture (rare but catastrophic)

Right heart failure

Early recognition reduces mortality significantly.

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🧠 Key Takeaways

Always suspect RV infarction in inferior MI with hypotension or elevated JVP but clear lungs.

V4R is the most reliable ECG lead.

Treat with fluids first; avoid nitrates and diuretics.

Primary PCI of the proximal RCA is the definitive therapy.