Pharmacotherapy: Ventricular Arrhythmias

Monomorphic VT

The pharmacologic management of both monomorphic and polymorphic VT aims to restore normal sinus rhythm and prevent recurrence. Here are the key interventions for each:

Monomorphic VT:

Management for Unstable Patients:

1. Electrical Cardioversion:
   • Administer sedation (etomidate or propofol preferred if conscious).
   • Initial synchronized shock at 100 J or higher; subsequent shocks can increase energy up to a maximum of 200 J if needed for conversion.
   • Consider higher energies if ventricular function is poor.
2. Amiodarone:
   • First-line for stable monomorphic VT along with procainamide.
   • IV/IO bolus of 150 mg (50 mg/min) over 10 minutes.
   • Follow with infusion of 1 mg/min for the first 6 hours, then 0.5 mg/min.
   • Oral maintenance dosing: 200-400 mg daily.
   • Monitor thyroid function, liver enzymes, and pulmonary toxicity.
   • Avoid in severe sinus node dysfunction due to bradycardia risk.
   • Be cautious about interactions with warfarin, statins, and antitubercular therapy.
3. Procainamide:
   • IV/IO bolus of 10-15 mg/kg (1,000-1,500 mg) over 30-60 minutes, max 100 mg/min.
   • Stop infusion for hypotension or if VT terminates.
   • Repeat bolus or start infusion at 1-4 mg/min if VT recurs.
   • Monitor ECG for QT prolongation and widening of QRS > 50% baseline.
   • Adjust dose for renal dysfunction; start at 7.5 mg/kg if creatinine clearance <60 mL/min.
   • Avoid in heart block, myocardial depression, and prolonged QT.
4. Lidocaine:
   • IV bolus 1-1.5 mg/kg (or 100 mg) over 2 minutes.
   • Repeat bolus every 5 minutes until a maximum of 3 mg/kg.
   • If VT recurs, start infusion at 1-4 mg/min.
   • Causes less negative inotropy compared to amiodarone or procainamide.
   • Monitor for CNS toxicity such as seizures and confusion.
   • Reduce dose in hepatic dysfunction.
   • Advantages over amiodarone and procainamide as it does not routinely cause hypotension.

Polymorphic VT
Management for Stable Polymorphic VT:

1. Magnesium Sulfate:
   • Preferred for torsades de pointes or polymorphic VT associated with a long QT interval.
   • Corrects hypokalemia if present and shortens QT regardless of magnesium level.
   • Dose: 2 g diluted in 10 mL D5W or normal saline IV over 5-20 minutes, repeatable up to 2 additional doses if needed.
   • Monitor for hypotension.
2. Amiodarone:
   • Can be used first-line if polymorphic VT is not known to be long QT-related.
   • Avoid if the QTc interval is markedly prolonged.
   • Administer a 150 mg IV bolus over 20-60 minutes, followed by an infusion.
   • Monitor QTc interval, hypotension, and AV block; stop amiodarone if QTc prolongs excessively.
3. Lidocaine:
   • An alternative to amiodarone, especially if QTc prolongation is present.
   • Administer an IV bolus followed by an infusion, titrated to suppress the arrhythmia.
   • Monitor for CNS toxicity symptoms.

Additional Measures:

• Overdrive Pacing: Temporary transvenous pacing to help suppress recurrent polymorphic VT episodes, targeting a pacing rate of 90-110 bpm. Avoid when QTc is markedly prolonged.
• Isoproterenol Infusion: Consider for polymorphic VT related to bradycardia or pauses, titrating the infusion to keep the heart rate >70 bpm. Use with caution if long QT is present.

In summary, the pharmacologic management of VT includes electrical cardioversion for unstable monomorphic VT, while stable monomorphic and polymorphic VT are managed with intravenous antiarrhythmics such as amiodarone, procainamide, lidocaine, and magnesium sulfate. The goal is to promptly terminate arrhythmia episodes and prevent deterioration into ventricular fibrillation.