Ventricular Tachycardia



  • Ventricular tachycardia (VT) is a series of three or more repetitive beats originating from the ventricle at a rate faster than the upper limit of normal for age. The QRS complex is always different from sinus rhythm and is usually wide but can appear narrow in infants. VT may, but not always, have atrioventricular (AV) dissociation; nonsustained VT: >3 beats and <30 seconds
  • Sustained VT: lasts >30 seconds
  • VT may be monomorphic or polymorphic.
  • Torsades de pointes: a polymorphic variant
    • The QRS complexes gradually change shape and axis throughout the tachycardia.
    • Associated with congenital long QT syndrome (LQTS), acquired long QT, and Brugada syndrome


  • Metabolic disturbances (hypoxia, acidosis, hypo/hyperkalemia, hypomagnesemia, hypothermia)
  • Drug toxicity (e.g., digitalis toxicity, antiarrhythmic agents)
  • Substance abuse (cocaine, methamphetamine)
  • Myocardial ischemia (e.g., Kawasaki disease, congenital coronary anomalies)
  • Trauma
  • Invasive lines or catheters
  • Pericardial effusion


  • LQTS may be inherited in an autosomal recessive or autosomal dominant pattern. It is mostly commonly associated with potassium cardiac ion channel defects and may be associated with hearing loss and/or a family history of sudden death.
  • Brugada syndrome may be inherited in an autosomal dominant pattern. It is most commonly associated with a defect in the cardiac sodium channel (SCN5A) and appears to be inherited in an autosomal dominant pattern.


VT may result from a reentrant, triggered, or abnormal automaticity mechanism.


  • Diverse and often overlapping
  • LQTS
  • Brugada syndrome
  • Catecholaminergic polymorphic VT
  • Myocarditis
  • Dilated cardiomyopathy
  • Hypertrophic cardiomyopathy
  • Arrhythmogenic right ventricular cardiomyopathy
  • Before and after surgery for congenital heart disease (CHD) (e.g., tetralogy of Fallot, transposition of the great arteries, aortic stenosis, Ebstein anomaly, and pulmonary vascular occlusive disease)
  • Myocardial tumors
  • Heart failure
  • Idiopathic


Based on electrocardiogram (ECG), rhythm strip, Holter, or event monitor


  • Varies widely, ranging from asymptomatic to sudden cardiac arrest/death
  • Other symptoms include palpitations, presyncope or syncope, exercise intolerance, and dizziness.


  • Can be normal; occasional heart rhythm irregularity secondary to premature ventricular complexes (PVCs) may be auscultated.
  • Acute, sustained VT may have signs of hemodynamic compromise, including lack of palpable pulse.
  • Signs of underlying heart disease may be present.


Wide complex tachyarrhythmia

  • Suspect VT until proven otherwise.
  • Supraventricular tachycardia (SVT) with aberrancy
  • Antidromic tachycardia (antegrade conduction down an accessory pathway during an AV reciprocating tachycardia [e.g., Wolff-Parkinson-White syndrome]).
  • Atrial flutter or atrial fibrillation with rapid antegrade conduction over an accessory pathway
  • Sinus tachycardia or SVT with underlying bundle branch block



  • Serum electrolytes, including magnesium and potassium levels, blood gas, and serum drug levels as appropriate
  • Urine toxicology screen
  • ECG
    • AV dissociation during tachycardia is diagnostic but not always present or easily seen.
    • Bundle branch morphology (right or left) and QRS axis during tachycardia may help localize the site of origin.
    • Typically, repolarization (T wave) abnormalities are present.
    • A prolonged QTc interval during sinus rhythm may help establish a LQTS diagnosis.
    • Brugada pattern: right bundle branch block with coved-type ST elevation and T-wave inversion in leads V1 and V2 during sinus rhythm. Brugada pattern may be more obvious when the patient is febrile and/or with leads V1 and V2 placed one intercostal space higher than standard.
  • Echocardiogram
    • Rule out CHD, pericardial effusion, tumors, hypertrophic and dilated cardiomyopathy, myocarditis.
  • Ambulatory Holter monitor
    • Quantitative assessment of ventricular ectopy, and frequency, rate, and duration of VT
    • Less frequent episodes may need longer term monitoring with an event monitor or implantable loop recorder.
  • Exercise stress test (>5 years old)
    • Benign PVCs are characteristically suppressed with exercise and return in the immediate recovery period.
    • Exacerbation or worsening of ventricular arrhythmias is concerning.
  • Cardiac magnetic resonance imaging: assessment for arrhythmogenic right ventricular cardiomyopathy and abnormalities that are beyond the resolution of echocardiography


  • Cardiac catheterization: hemodynamic assessment, endomyocardial biopsy, and coronary artery angiography
  • Electrophysiologic study indications
    • Confirm diagnosis and mechanism of a wide complex rhythm.
    • Determine appropriate medical therapy in a patient with inducible VT.
    • Evaluate for suspected VT in the setting of structural or functional heart disease, syncope, or cardiac arrest.
    • Risk assessment of VT. Evaluate syncope in the setting of palpitations.
    • Characterize VT with consideration for catheter ablation.



  • If the patient is hemodynamically compromised, prompt synchronized direct-current (pediatric, 1 to 2 joules/kg; adult, 100 to 400 joules/kg) cardioversion is indicated.
  • Asynchronous defibrillation is needed for ventricular fibrillation or pulseless VT.
  • Cardiopulmonary resuscitation is needed for persistent hemodynamic compromise.


  • Acute
    • Some forms of VT in structurally normal hearts may respond to adenosine (pediatric, 0.1 to 0.3 mg/kg rapid push; adult 6 to 12 mg).
    • Esmolol IV (bolus, 0.5 mg/kg; infusion, 50 to 300 mcg/kg/min).
    • Procainamide IV (bolus, 5 to 15 mg/kg over 20 to 60 minutes; infusion, 20 to 100 mcg/kg/min).
    • Amiodarone IV (bolus, 2 to 5 mg/kg over 30 minutes; infusion, 5 to 10 mcg/kg/min).
    • Lidocaine IV (bolus,1 mg/kg over 1 minute; infusion, 20 to 50 mcg/kg/min).
    • MgSO4 is indicated for torsades de pointes.
    • Overdrive ventricular pacing may terminate the tachycardia but should be used cautiously as it may accelerate the VT or induce ventricular fibrillation.
  • Chronic
    • Class IB (mexiletine and phenytoin)
    • β-Blockers (propranolol, nadolol, metoprolol) are used in LQTS and may be effective in exercise-induced VT and postoperative CHD.
    • Class III agents (amiodarone and sotalol) should be avoided in patients with LQTS.
    • Class IC agents (flecainide) may be proarrhythmic and sudden death has been reported in patients with structural heart disease.
    • Verapamil is often effective for right ventricular outflow tract VT and left ventricular fascicular VT.


Cardiology consultation and close follow-up is needed.


  • An implantable cardioverter defibrillator is indicated for survivors of sudden cardiac arrest without a reversible cause and those at risk for sudden cardiac arrest.
  • Pacing may help suppress ectopy that causes VT.
  • Catheter ablation using radiofrequency energy or cryothermal energy


Patient with hemodynamically unstable forms of VT should be stabilized and admitted.

Ongoing Care



  • Monitoring in an intensive care unit is needed for transition to a stable chronic suppressive medical regimen.
  • Frequency of outpatient follow-up is dependent on the underlying cause and clinical severity.
  • ECG, Holter monitor, and exercise stress test are helpful in titrating and assessing efficacy of medical therapy.


Patients should be counseled about potential triggers of VT, which is dependent on the underlying etiology. Exercise-related VT should prompt exercise restrictions. LQTS patients should avoid QT prolonging medications. Brugada syndrome patients should receive antipyretics promptly during times of fever.


  • Generally, very good in patients with idiopathic VT and a structurally normal heart
  • Suppression of ventricular ectopy with exercise has a favorable prognosis.
  • In patients with heart disease (congenital or acquired) or LQTS and other channelopathies, VT may increase the risk of presyncope, syncope, and possibly sudden death.


  • Sudden cardiac arrest/sudden cardiac death
  • Acquired cardiomyopathy (from chronic, persistent VT and a lack of AV synchrony)

Additional Reading

  1. Ceresnak SR, Liberman L, Avasarala K, et al. Are wide complex tachycardia algorithms applicable in children and patients with congenital heart disease? J Electrocardiol. 2010;43(6):694–700. [PMID:20382398]
  2. Escudero C, Carr R, Sanatani S. The medical management of pediatric arrhythmias. Current Treat Options Cardiovasc Med. 2012;14(5):455–472. [PMID:22907424]
  3. Kleinman ME, Chameides L, Schexnayder SM, et al. Part 14: pediatric advanced life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18 Suppl 3):S876–S908. [PMID:20956230]
  4. McBride ME, Marino BS, Webster G, et al. Amiodarone versus lidocaine for pediatric cardiac arrest due to ventricular arrhythmias: a systematic review. Pediatr Crit Care Med. 2017;18(2):183–189. [PMID:28009655]
  5. Wang S, Zhu W, Hamilton RM, et al. Diagnosis-specific characteristics of ventricular tachycardia in children with structurally normal hearts. Heart Rhythm. 2010;7(12):1725–1731. [PMID:20691281]



  • 427.1 Paroxysmal ventricular tachycardia
  • 26.82 Long QT syndrome
  • 746.89 Other specified congenital anomalies of heart


  • I47.2 Ventricular tachycardia
  • I45.81 Long QT syndrome
  • Q24.8 Other specified congenital malformations of heart


  • 25569003 Ventricular tachycardia (disorder)
  • 9651007 Long QT syndrome (disorder)
  • 418818005 brugada syndrome (disorder)
  • 426525004 sustained ventricular tachycardia (disorder)
  • 444658006 Nonsustained ventricular tachycardia


  • Q: Should siblings of patients with LQTS be evaluated?
  • A: Yes. Siblings and parents (even if asymptomatic) should have an ECG, Holter monitor, and exercise stress test for evaluation of the QT interval. Commercial genetic testing is currently available to detect mutations in the most common genes that cause the LQTS. The test will positively identify ~75% of patients with the LQTS. Genetic testing may be considered in patients in whom there is a high suspicion of LQTS.
  • Q: Can patients with underlying substrates for VT be identified before onset of symptoms?
  • A: Family history suspicious for sudden cardiac death may prompt evaluation for inheritable forms of LQTS, cardiomyopathy, and CHD. Early identification of patients with underlying substrates for VT may lead to preventative therapy.
  • Q: Who should be screened for VT?
  • A: Children with syncope and palpitations should be screened for CHD and underlying substrates for VT. Families with a history of unexplained sudden death, frequent miscarriages, and sudden infant death syndrome may have an inheritable substrate for VT.


Walter L. Li, MD

© Wolters Kluwer Health Lippincott Williams & Wilkins