What is the differential diagnosis and management for R on T (premature ventricular contraction) induced ventricular tachycardia?

R-on-T Induced Ventricular Tachycardia: Differential Diagnosis and Management

Key Clinical Context

R-on-T phenomenon itself is not a critical determinant of sustained ventricular tachyarrhythmias and represents a rare trigger for serious arrhythmias, even in acute myocardial infarction. 1, 2 The differential diagnosis focuses on identifying the underlying substrate and precipitating factors rather than the R-on-T pattern itself.

Differential Diagnosis

Primary Underlying Conditions

Acute myocardial ischemia/infarction is the most critical diagnosis to consider, as arrhythmias in this setting are manifestations of continuing ischemia, pump failure, altered autonomic tone, hypoxia, and electrolyte disturbances that require immediate correction. 3

• Acute STEMI with reperfusion: R-on-T VPCs occur more frequently during thrombolysis (8 VPCs/hour) than after completion (0.6 VPCs/hour), though they remain rare overall (1.8% of total VPCs). 2
• Non-reperfused infarction: Higher rates of R-on-T VPCs (15/hour vs 8/hour in reperfused patients) suggest failed reperfusion as a key substrate. 2

Metabolic and Electrolyte Derangements

• Hypokalemia is specifically highlighted as a correctable cause of ventricular arrhythmias in acute MI. 3
• Hypoxia and acid-base disturbances must be identified and corrected as they lower the threshold for ventricular arrhythmias. 3

Structural Heart Disease

• Left ventricular dysfunction and pump failure create the substrate for sustained ventricular arrhythmias. 3
• Papillary muscle dysfunction or rupture (particularly posteromedial papillary muscle in inferior MI) can cause hemodynamic instability that precipitates arrhythmias. 3

Iatrogenic Causes

• Epicardial pacemaker undersensing: PVCs may be undersensed despite appropriate sensing thresholds because pacemakers detect R waves using slew rate (voltage/time), making wide QRS complexes like PVCs prone to undersensing and triggering R-on-T stimulation. 4
• Proarrhythmic drug effects: Class I or III antiarrhythmic drugs carry inherent proarrhythmic risk. 5

Accessory Pathway-Mediated Arrhythmias

• Pre-excited atrial fibrillation (WPW syndrome): This presents as irregular wide-complex tachycardia that can degenerate into ventricular fibrillation if AV nodal blocking agents are administered. 3, 5

Management Algorithm

Step 1: Immediate Hemodynamic Assessment

If hemodynamically unstable (hypotension, heart failure, altered mental status), perform immediate synchronized cardioversion regardless of the underlying mechanism. 3

• Cardioversion avoids complications of antiarrhythmic drugs and should be considered early. 3
• Have defibrillation immediately available as VT can degenerate into ventricular fibrillation. 3

Step 2: Correct Underlying Precipitants (Hemodynamically Stable Patients)

Address reversible causes before initiating antiarrhythmic therapy:

• Restore coronary perfusion if acute ischemia is present—mechanical reperfusion of the infarct-related artery is the definitive treatment. 3
• Correct hypokalemia to therapeutic levels (>4.0 mEq/L in acute MI). 3
• Optimize oxygenation and acid-base status. 3
• Treat pump failure if present, as this is a major substrate for sustained arrhythmias. 3

Step 3: Pharmacologic Management for Sustained VT

Beta-blockers are first-line therapy unless contraindicated (e.g., severe heart failure, bronchospasm). 3

If high risk for recurrent ventricular fibrillation or beta-blockers are contraindicated:

• Intravenous amiodarone is superior to lidocaine, especially for recurrent sustained VT requiring cardioversion or ventricular fibrillation. 3

  • Loading: 5 mg/kg (approximately 300 mg) over 1 hour, followed by 900-1200 mg over 24 hours. 3
  • For breakthrough VT/VF: 150 mg supplemental infusions over 10 minutes. 6
  • Maintenance: 0.5 mg/min can continue for 2-3 weeks. 6

• Lidocaine as alternative: 1 mg/kg IV bolus, followed by 0.5 mg/kg every 8-10 minutes to maximum 4 mg/kg, or continuous infusion 1-3 mg/min. 3

Step 4: Management of Non-Sustained VT

Non-sustained VT that is well-tolerated does not necessarily require treatment. 3

• No specific therapy is required for isolated R-on-T VPCs or complex ventricular ectopy (multiform complexes, short runs) as their value as predictors of ventricular fibrillation is questionable. 3
• Beta-blockers remain appropriate for secondary prevention. 3

Step 5: Differentiate from Accelerated Idioventricular Rhythm

Accelerated idioventricular rhythm (ventricular rate <120 bpm) is a harmless consequence of reperfusion and requires no treatment. 3

• This is critical to avoid unnecessary antiarrhythmic therapy in post-reperfusion patients. 3

Critical Pitfalls to Avoid

Do NOT Administer AV Nodal Blocking Agents in Pre-Excited AF

Verapamil, diltiazem, beta-blockers, and digoxin are absolutely contraindicated in pre-excited atrial fibrillation (irregular wide-complex tachycardia with WPW), as they may accelerate conduction through the accessory pathway and precipitate ventricular fibrillation. 3, 5

• Use procainamide or ibutilide instead if hemodynamically stable. 3
• Perform immediate cardioversion if unstable. 3

Do NOT Delay Cardioversion in Unstable Patients

Hemodynamic instability mandates immediate cardioversion—do not delay for pharmacologic trials. 3, 5

Do NOT Overinterpret R-on-T as High-Risk

R-on-T VPCs and R-on-T-initiated VT are rare (1.8% of VPCs, 3.3% of VT episodes) and do not reliably predict severe ventricular tachyarrhythmias. 2

• Only 17.2% of VT episodes and 20% of VT runs are R-on-T initiated. 7, 8
• In one study, only 4 of 8 ventricular fibrillation episodes were R-on-T initiated. 7
• The absence of obvious precursors strengthens the argument for prophylactic treatment in acute MI, but R-on-T itself is not the critical determinant. 1

Epicardial Pacing Precautions

When epicardial pacing wires are in place, carefully monitor for undersensing, especially when PVCs occur frequently, as wide QRS complexes may be undersensed despite appropriate sensing thresholds. 4

• Consider adjusting pacing parameters or switching to demand mode cautiously. 4

Avoid High-Concentration Peripheral Infusions

Amiodarone concentrations >2 mg/mL cause high rates of peripheral vein phlebitis—use central venous access for concentrations >2 mg/mL. 6

• Rapid loading infusions at higher concentrations than recommended have caused hepatocellular necrosis and acute renal failure. 6