What is the management of arrhythmia in a patient with an inferior wall myocardial infarction (MI) due to a right coronary artery (RCA) occlusion?

Management of Arrhythmias in Inferior Wall MI Due to RCA Occlusion

Initiate continuous electrocardiographic monitoring immediately and maintain it for at least 24-48 hours, prioritizing early reperfusion therapy as the single most important anti-arrhythmic intervention, while avoiding prophylactic antiarrhythmic drugs which may be harmful. 1, 2

Immediate Monitoring and Assessment

• Begin continuous ECG monitoring without delay upon suspicion of inferior MI, continuing uninterrupted for a minimum of 24-48 hours regardless of reperfusion status 1
• Obtain right-sided chest leads (V3R and V4R) immediately in all patients with inferior ST-elevation to detect right ventricular involvement, as proximal RCA occlusion frequently causes RV infarction 1
• The sinoatrial nodal artery typically arises from the proximal RCA, making atrial ischemia and supraventricular arrhythmias particularly common in this anatomic pattern 1, 3
• RV infarction occurs in 50% of inferior MI cases and creates unique hemodynamic vulnerabilities that predispose to arrhythmias 4

Priority: Early Reperfusion

Early reperfusion is the most effective anti-arrhythmic strategy and reduces both ventricular arrhythmias and cardiovascular death. 2

• Urgent angiography with revascularization should be performed if the patient has not received reperfusion therapy, as this addresses the underlying arrhythmogenic substrate 2
• The right ventricle demonstrates remarkable recovery potential even after prolonged occlusion, but reperfusion accelerates functional recovery and improves survival 4

Specific Arrhythmia Management

Bradyarrhythmias and Conduction Blocks

Sinus bradycardia is extremely common in the first hour of inferior MI (30-40% of patients) due to increased vagal tone and the Bezold-Jarisch reflex from RCA reperfusion 1, 2

• For asymptomatic bradycardia: No treatment required 2
• For symptomatic bradycardia with hypotension (SBP <80 mmHg): Administer atropine 0.5 mg IV increments up to 2.0 mg total, titrating to achieve heart rate ~60 bpm 1, 2
• Avoid atropine in infranodal AV block (associated with anterior MI and wide-complex escape rhythms), as it is ineffective and potentially harmful 1

Transcutaneous pacing patches should be applied prophylactically in high-risk patients, particularly those receiving thrombolytics to avoid vascular access complications 1

• Immediate transcutaneous pacing indicated for: Mobitz type II second-degree AV block, new bifascicular block with first-degree AV block, or symptomatic bradycardia unresponsive to atropine 1
• Transvenous pacing should be considered for persistent high-grade blocks, though pacing has not been definitively shown to reduce mortality (the benefit is obscured by extensive myocardial damage) 1

Supraventricular Arrhythmias

Atrial fibrillation occurs in 10-16% of acute MI patients overall, with higher rates in inferior MI with proximal RCA occlusion due to sinoatrial nodal artery involvement 1, 3

• AF typically develops within the first 24 hours and is usually transient 1
• Systemic embolization risk is highest on day 1, with >90% occurring by day 4, necessitating anticoagulation with heparin 1, 3

For hemodynamically unstable AF (severe hypotension or intractable ischemia): Immediate electrical cardioversion 1, 2

For AF with rapid ventricular rate but hemodynamic stability:

• First-line: IV beta-blockers (metoprolol 2.5-5.0 mg IV every 2-5 minutes up to 15 mg total, or atenolol 2.5-5.0 mg over 2 minutes up to 10 mg total) 1, 2
• Monitor blood pressure and heart rate continuously; stop if SBP falls below 100 mmHg or HR below 50 bpm 1
• Contraindications: Clinical LV dysfunction, bronchospastic disease, or AV block 1
• Alternative: Rapid digitalization if beta-blockers contraindicated 1

For well-tolerated AF with controlled rate: No specific treatment beyond anticoagulation required 2

Ventricular Arrhythmias

Isolated ventricular ectopic beats require no treatment, even when complex, as their predictive value for ventricular fibrillation is questionable 2

For sustained monomorphic VT without hemodynamic compromise (BP ≥90 mmHg, no angina or pulmonary edema):

• First-line: IV beta-blockers unless contraindicated 2
• Alternative pharmacologic options: 1
  • Lidocaine: 1.0-1.5 mg/kg bolus, supplemental boluses of 0.5-0.75 mg/kg every 5-10 minutes (max 3 mg/kg), then infusion 2-4 mg/min
  • Procainamide: 20-30 mg/min loading (up to 12-17 mg/kg), then 1-4 mg/min infusion
  • Amiodarone: 150 mg IV over 10 minutes, then 1.0 mg/min for 6 hours, then 0.5 mg/min maintenance (superior for recurrent sustained VT) 2, 5

For hemodynamically unstable VT: Immediate synchronized cardioversion (100 J for monomorphic VT >150 bpm) 1, 2

For ventricular fibrillation:

• Immediate unsynchronized defibrillation at 200 J (or 360 J per ACLS protocol) 1
• If resistant to defibrillation, follow ACLS hierarchy: epinephrine 1 mg IV push, then lidocaine 1.5 mg/kg, then bretylium 5-10 mg/kg, or amiodarone 150 mg bolus 1, 5
• VF occurs most commonly within the first 48 hours; rare case reports document VF with RV branch occlusion even in recessive RCA 6

Post-VF management:

• Correct electrolyte abnormalities (hypokalemia, hypomagnesemia) - this is mandatory 2
• Administer beta-blockers to inhibit sympathetic tone and prevent ischemia 1
• If antiarrhythmic infusion initiated (e.g., lidocaine 2 mg/min), maintain for only 6-24 hours then discontinue to reassess ongoing need 1

Critical Pitfalls to Avoid

Never administer prophylactic antiarrhythmic drugs - they are not indicated and may be harmful 2

Avoid vasodilators and diuretics in RV infarction, as the ischemic right ventricle is volume-dependent and these agents can precipitate severe hemodynamic collapse 4

Do not use atropine for infranodal AV block (wide-complex escape rhythm), as it is ineffective at this level 1

Reassess monitoring need every 24 hours based on clinical findings, absence of sustained VT/VF, high-degree AV block, electrical instability, or recurrent ischemia 1

Hemodynamic Considerations Specific to RCA Occlusion

• The ischemic right ventricle becomes stiff, dilated, and volume-dependent, with RV pressure generation dependent on LV-septal contractile contributions 4
• Proximal RCA occlusions (above RA branches) cause ischemic depression of RA contractility, further impairing RV filling and worsening hemodynamic compromise 4
• Bradyarrhythmias are particularly detrimental as they limit output from the rate-dependent noncompliant ventricles 4
• Volume resuscitation and restoration of physiological rhythm are often effective, with parenteral inotropic support reserved for refractory cases 4