• Definitive diagnosis of VT may be difficult and time-consuming. In a hemodynamically unstable patient, emphasis should be placed on prompt treatment rather than diagnosis.
• History of MI, angina, or heart failure increases the likelihood of VT.
• ECG findings suggestive of VT
  • Wide QRS complex (>120 msec)
  • Atrioventricular dissociation: Visualization of P waves in or between QRS complexes. Only present <50% of the time
  • Fusion beats: Convergence of an action potential through both the normal pathway and the ectopic focus producing a QRS complex of mixed morphology.
  • Capture beat: Atrial impulse arriving at the AV node when the ventricular myocardium is available for depolarization; results in a QRS complex of normal morphology.
  • Precordial concordance: QRS complexes with the same polarity in V1–V6 have a 90% specificity for VT.
• Arterial line readings may demonstrate changes in BP that reflect variable atrial contribution to filling.
• Central and pulmonary catheter waveforms may demonstrate cannon "A" waves that reflect atrial contraction against a closed AV valve.

• Pulseless VT
  • CPR
  • Defibrillation (200 J biphasic, 360 J monophasic). DO NOT delay shock to determine if monomorphic or polymorphic VT.
  • Identify and treat the underlying cause
• Stable monomorphic VT
  • Procainamide: 20–50 mg/min IV until the arrhythmia is suppressed, hypotension occurs, or the QRS widens by 50%. The maximum cumulative dose is 17 mg/kg or 100 mg every 5 minutes. Avoid if a prolonged QT interval or significant LV dysfunction.
  • Amiodarone: 150 mg IV over 10 minutes (repeat if necessary), followed by 1 mg/min infusion for 6 hours.
  • Sotalol: 1.5 mg/kg IV over 5 minutes. Avoid if prolonged QT interval or significant LV dysfunction.
  • Lidocaine (second-line therapy): Less effective in terminating VT than procainamide, sotalol, or amiodarone.
  • Avoid verapamil and diltiazem in stable VT, associated with profound hypotension.
  • Elective synchronized cardioversion: 100 J (mono or biphasic), increase in stepwise fashion if no response.
  • Anti-tachycardia pacing: Internal pacemaker or external pacing (rarely).
• Polymorphic VT
  • Defibrillate immediately as patients have a tendency to degenerate into VF.
  • Assess the QT duration following defibrillation. In patients with a normal QT interval, ischemia is the most common cause of polymorphic VT. Treat with amiodarone and/or beta-blocker.
• Torsades de Pointes
  • Defibrillation (200 J biphasic, 360 J monophasic).
  • Avoid QT-prolonging agents
  • Avoid Class IA and III anti-arrhythmic agents (K⁺ blocking properties)
  • Correct electrolytes. Magnesium sulfate 1–2 grams IV over 15 minutes. Administer potassium if patient is hypokalemia (maintain a high-normal level of 4.5–5 mmol/L)
  • Increase heart rate: Atropine, isoproteronol, electrical pacing. Increasing the heart rate >90 bp, can suppress early after-depolarizations and shorten the QTc.
• Familial long QT syndrome
  • Avoid sympathetic stimulation
  • Consider beta-blockade
  • Thoracic epidural, left stellate ganglion block, left surgical cardiac sympathetic denervation.

Pediatric Considerations

Pregnancy Considerations

• Invasive monitoring and intensive care setting postoperatively.
• 12-lead EKG: Assess QT duration and indicators of myocardial ischemia.
• Labs: Electrolytes, Ca²⁺, Mg²⁺, ABG, cardiac enzymes, toxicology screen.
• Echocardiogram: Assess for structural heart disease and evidence of ischemia.
• Cardiology/electrophysiology consultation
  • Anti-arrhythmic therapy
  • Electrophysiology study, ablation, or ICD
  • Treatment/follow-up of coronary disease
• MRI is imaging test of choice for ARVC.
• Genetic screening for familial disorders

1. Neumar RW , Otto CW , Link MS , et al. Part VIII: Adult advanced cardiovascular life support: 2010 AHA Guidelines for CPR and Emergency Cardiovascular Care. Circulation. 2010;122: S729–S767.
2. Pellegrini CN , Scheinman MM. Clinical management of ventricular tachycardia. Curr Probl Cardiol. 2010;35:453–504.
3. Zipes DP , Camm AJ , Borggrefe M , et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: A report of the ACC/AHA Task force and the European Society of Cardiology Committee for Practice Guidelines. Circulation. 2006;114:e385–e484.

• Common etiologies of VT: Hypoxemia, hypomagnesemia, hypokalemia/hyperkalemia, myocardial ischemia, pulmonary embolism, and excess sympathetic stimulation.
• Unstable VT should be immediately defbrillated (200 J biphasic, 360 J monophasic).
• Stable VT can be treated with antiarrhythmic drugs or synchronized cardioversion (100 J).
• In patients with a history of VT, avoid anesthetic drugs that have been associated with it: succinylcholine (hyperkalemia); droperidol (QT prolongation and Torsades de Pointes); naloxone (sympathetic stimulation in opioid-dependent patient).