What are the treatment differences between monomorphic and polymorphic ventricular tachycardia?

Treatment Differences Between Monomorphic and Polymorphic Ventricular Tachycardia

The fundamental treatment difference is that monomorphic VT responds to synchronized cardioversion and antiarrhythmic drugs, while polymorphic VT requires unsynchronized high-energy defibrillation (like VF) and treatment directed at the underlying cause rather than rhythm suppression. 1

Initial Assessment: Hemodynamic Stability Determines Everything

For both rhythm types, if the patient is hemodynamically unstable (hypotension, altered mental status, chest pain, acute heart failure, or shock), proceed immediately to electrical therapy without delay. 1, 2

• Unstable patients with either rhythm type should not receive antiarrhythmic drugs first—this wastes critical time 1
• Obtain a 12-lead ECG only in stable patients to confirm the rhythm and guide pharmacologic choices 1, 2

Monomorphic VT: Synchronized Cardioversion and Rhythm-Specific Drugs

Unstable Monomorphic VT

• Perform synchronized cardioversion starting at 100 J (monophasic or biphasic), escalating stepwise if the first shock fails 1
• Provide sedation if the patient is conscious but hypotensive before cardioversion 2

Stable Monomorphic VT

Procainamide is the preferred first-line agent with the highest efficacy for terminating stable monomorphic VT 2, 3:

• Dose: 10 mg/kg at 50-100 mg/min IV over 10-20 minutes 2
• Monitor blood pressure and ECG continuously during infusion 3
• Contraindications: severe heart failure or acute MI 2

Alternative agents if procainamide is contraindicated or unavailable:

• Amiodarone 150 mg IV over 10 minutes (can repeat to maximum 2.2 g/24 hours), though less effective than procainamide 1, 4
• Sotalol 1.5 mg/kg over 5 minutes (avoid if QT prolonged) 1
• Lidocaine 1-1.5 mg/kg IV bolus is second-line and less effective than the above agents 1, 3

Special case—LV fascicular VT (RBBB morphology with left axis deviation):

• Use IV verapamil or beta-blockers instead of the standard agents 2

Polymorphic VT: Treat Like VF and Address the Cause

Electrical Therapy

Polymorphic VT requires unsynchronized high-energy shocks (defibrillation doses) because synchronization is impossible with the constantly changing QRS morphology 1:

• The irregular rates and multiple QRS configurations prevent the defibrillator from identifying an R-wave for synchronization 1
• Use the same energy doses and strategy as for ventricular fibrillation 1

Pharmacologic Management: Depends on QT Interval

The critical distinction is whether the QT interval is prolonged during sinus rhythm (torsades de pointes) or normal (typically ischemic) 1, 5:

Polymorphic VT WITH Long QT (Torsades de Pointes)

• Stop all QT-prolonging medications immediately 1, 5
• Give IV magnesium sulfate 1-2 g regardless of serum levels 1, 5
• Correct electrolyte abnormalities (hypokalemia, hypomagnesemia) 1, 5
• Increase heart rate to prevent pauses that trigger the arrhythmia:
  • Temporary overdrive pacing at 90-110 bpm is preferred 5
  • IV isoproterenol if pacing unavailable 1, 5
• The mechanism: bradycardia and pauses prolong the QT interval maximally, creating the substrate for triggered activity 5

Polymorphic VT WITHOUT Long QT (Usually Ischemic)

• The most common cause is acute myocardial ischemia 1
• Give IV beta-blockers and consider amiodarone to reduce recurrence 1
• Do NOT use isoproterenol or pacing—these are appropriate only for torsades and would be harmful in ischemic polymorphic VT 5
• Pursue urgent revascularization if ischemia is confirmed 6

Common Pitfalls to Avoid

Never give adenosine for polymorphic or irregular wide-complex tachycardia—it is only relatively safe for regular, monomorphic wide-complex rhythms 1

Do not use AV nodal blockers (adenosine, calcium channel blockers, digoxin, beta-blockers) for irregular wide-complex tachycardia that might be pre-excited atrial fibrillation—these can paradoxically accelerate the ventricular response 1

Recognize the "short-long-short" sequence on telemetry that heralds torsades: a premature beat, compensatory pause (bradycardia), then another premature beat initiating polymorphic VT 5

In polymorphic VT, the underlying mechanism determines treatment—do not reflexively give magnesium and pacing for all polymorphic VT, only when QT is prolonged 1, 5

Long-Term Considerations After Acute Stabilization

• Monomorphic VT in structural heart disease warrants ICD placement and consideration of catheter ablation, particularly if recurrent 2
• Polymorphic VT requires identification and treatment of the underlying substrate (ischemia, channelopathy, electrolyte disorder) to prevent recurrence 7, 6
• Idiopathic monomorphic VT (structurally normal heart) does not increase sudden cardiac death risk and treatment focuses on symptom control 7