Management of Ventricular Tachycardia
Immediate Assessment: Hemodynamic Stability is the Critical Decision Point
The first and most crucial step is determining hemodynamic stability—this single assessment dictates whether you cardiovert immediately or have time for pharmacological intervention. 1, 2
Define Unstable VT (Any of These = Immediate Cardioversion):
- Systolic blood pressure ≤90 mmHg 2
- Altered mental status or syncope 1, 2
- Chest pain suggesting acute ischemia 2
- Signs of acute heart failure 2
- Heart rate ≥150 bpm increases likelihood of instability 2
Obtain 12-Lead ECG Only If Patient is Stable
- For hemodynamically stable patients, obtain a 12-lead ECG to characterize the VT morphology (monomorphic vs polymorphic) and guide pharmacological choices 1, 3
- Do not delay cardioversion in unstable patients to obtain an ECG 3, 2
Management Algorithm for UNSTABLE VT
Direct current cardioversion is the only appropriate treatment for hemodynamically unstable VT—do not attempt pharmacological conversion. 1, 2
Cardioversion Protocol:
- If patient is conscious but unstable: Provide immediate sedation before cardioversion 1, 2
- For monomorphic VT: Start with 100J synchronized shock, escalate to 200J, then 360J if unsuccessful 1, 2
- For polymorphic VT or uncertain rhythm: Treat as ventricular fibrillation with unsynchronized defibrillation at 200J 1
- For in-hospital cardiac arrest: Attempt immediate defibrillation at maximum output 1
- For out-of-hospital cardiac arrest: Begin CPR with chest compressions immediately until defibrillation is available 1
Post-Cardioversion Management:
- After successful cardioversion, administer antiarrhythmic drugs to prevent VT recurrence 2
- Intravenous amiodarone (150 mg over 10 minutes, then 1 mg/min infusion) may facilitate defibrillation and prevent recurrences 1, 4
Management Algorithm for STABLE Monomorphic VT
For hemodynamically stable monomorphic VT, procainamide is the first-line pharmacological agent due to superior efficacy, unless the patient has severe heart failure or acute MI. 2, 5
First-Line: Procainamide (If No Heart Failure or Acute MI)
- Dosing: 10 mg/kg IV at 50-100 mg/min over 10-20 minutes (maximum 10-20 mg/kg total) 1, 2
- Monitoring: Watch continuously for hypotension and QRS widening during administration 2
- Contraindications: Severe heart failure, acute myocardial infarction, renal dysfunction 1, 2
- Procainamide demonstrates the greatest efficacy among antiarrhythmics for stable monomorphic VT 2
Alternative: Amiodarone (If Heart Failure or Suspected Ischemia Present)
- Dosing: 150 mg (5 mg/kg) IV over 10 minutes, followed by 1 mg/min infusion for 6 hours, then 0.5 mg/min maintenance 1, 2, 4
- Amiodarone reduces life-threatening arrhythmias, required shocks, and symptomatic VT episodes 2, 5
- FDA-approved for hemodynamically unstable VT and frequently recurring VF 4
- Caution: Intravenous amiodarone at concentrations >2 mg/mL requires central venous access to avoid peripheral vein phlebitis 4
Third-Line: Sotalol
- May be considered for stable monomorphic VT, but exercise caution due to significant beta-blocking properties 2
Special Case: LV Fascicular VT (RBBB Morphology + Left Axis Deviation)
Critical Pitfall: Lidocaine is Only Moderately Effective
- Intravenous lidocaine is significantly less effective than procainamide, sotalol, or amiodarone 1, 5
- Consider lidocaine only as a second-line option when preferred agents are contraindicated 1
Management of STABLE Polymorphic VT
If Normal QT Interval (Likely Ischemia-Related):
- Treat underlying myocardial ischemia aggressively with revascularization and beta-blockade 1, 2
- Consider IV beta-blockers as first-line therapy 1
- Follow with IV procainamide or amiodarone 1
If Prolonged QT Interval (Torsades de Pointes):
- Magnesium sulfate: 8 mmol IV bolus followed by 2.5 mmol/hour infusion 2
- Correct electrolyte abnormalities (potassium to 4.5-5 mM/L, magnesium) 1, 2
- Consider temporary overdrive pacing for pause-dependent torsades 1
- Isoproterenol may be reasonable for recurrent pause-dependent torsades (except in congenital LQTS) 1
Critical Pitfalls to Avoid
Never Use Calcium Channel Blockers in Structural Heart Disease VT
- Verapamil and diltiazem are contraindicated in VT associated with structural heart disease—they may precipitate hemodynamic collapse and worsen outcomes. 3, 2
- Only use calcium channel blockers for specific VT subtypes like LV fascicular VT 1
When in Doubt, Treat as VT
- Never assume wide-complex tachycardia is supraventricular—when uncertain, treat as VT 2
- Electrical cardioversion is first-line for stable wide-complex tachycardia of uncertain etiology 1
Do Not Delay Cardioversion in Unstable Patients
- Attempting pharmacological conversion in hemodynamically unstable patients wastes critical time and worsens outcomes 3, 2
Post-Acute Management and Prevention
Pharmacological Prevention:
- Beta-blockers are the cornerstone of long-term VT prevention and significantly reduce recurrent VT/VF episodes (HR 0.48,95% CI 0.26-0.89) 3, 5
- Combination of amiodarone plus beta-blocker significantly reduces ICD shocks compared to beta-blocker alone (HR 0.27,95% CI 0.14-0.52) 3
- Optimize heart failure medications according to current guidelines in patients with LV dysfunction 3
Catheter Ablation Indications:
- Urgent catheter ablation is recommended for scar-related heart disease with incessant VT or electrical storm 1, 3, 2, 5
- Consider catheter ablation after first episode of sustained VT in ischemic heart disease patients with an ICD 3, 5
- For recurrent ICD shocks due to sustained VT, either amiodarone or catheter ablation is recommended 3
ICD Considerations:
- ICD implantation should be considered for secondary prevention in survivors of sustained VT 3
- Implant ICD in patients undergoing catheter ablation whenever they satisfy eligibility criteria 3