eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiology

Ventricular Tachycardia: Treatment & Medication

Author: Mark E Alexander, MD, Assistant Professor, Department of Pediatrics, Children's Hospital of Boston and Harvard Medical School
Coauthor(s): Charles I Berul, MD, Associate Professor of Pediatrics, Harvard Medical School; Senior Associate, Department of Cardiology, Children's Hospital of Boston
Contributor Information and Disclosures

Updated: Feb 3, 2009

Treatment

Medical Care

  • Therapy may not be needed in asymptomatic patients whose ventricular tachycardia (VT) patterns suggest a low risk of sudden death. Symptoms or a clinically significant short-term risk of sudden cardiac death (SCD) frequently warrants admission for evaluation and consideration of therapeutic options.
  • Initial therapy for ventricular fibrillation is immediate, unsynchronized direct current (DC) defibrillation. Data suggest that a brief (ie, 90 s) period of chest compressions may improve survival when ventricular fibrillation is witnessed, but immediate defibrillation is the therapy of choice. Do not waste time on other aspects of resuscitation before initial defibrillation, unless defibrillation is unavailable.
  • Identify and target potential substrates for arrhythmia-specific therapy.
  • Optimal inpatient management is performed with secure vascular access and continuous cardiac monitoring. In the ideal case, cardiac monitoring systems are connected to a central monitoring station in a cardiac care unit or ICU. Simple bedside monitors with high-rate and low-rate alarms are inadequate to monitor patients with the potential for unstable ventricular arrhythmia (VA).
  • For unstable patients, conduct simultaneous evaluation and therapy.
  • For hemodynamically stable patients, evaluation is followed by serial drug therapy. Diagnostic or therapeutic catheterization also may be performed.

Surgical Care

Selected patients require highly individualized interventional procedures, such as the following:

  • Excisional biopsy: Incessant VT is sometimes secondary to focal lipoid cardiomyopathy, isolated fibromas, or hamartomas. In selected patients, surgical excision may be both diagnostic and therapeutic.
  • Implantable cardioverter/defibrillators (ICDs): ICDs have revolutionized the care of adults with high-risk VT after myocardial infarction. ICDs are increasingly used in high-risk pediatric patients.24,25 Transvenous systems have been used in patients who weigh as little as 20 kg. In highly selective situations, toddlers and large infants have received epicardial systems implanted through a sternotomy.26 Creative, hybrid approaches are further increasing clinicians' willingness to use ICDs in young patients (see Media file 3).
  • Radiofrequency catheter ablation or cryoablation: Both catheter-directed radiofrequency ablation and intraoperative resection or cryoablation of VT foci have been successful with monomorphic VTs; however, their use is unproved for patients with polymorphic VT. Unlike supraventricular arrhythmias, for which catheter ablation has a more than 95% success rate, VT ablation in pediatric patients and in patients with congenital heart disease (CHD) has a success rate of about 60%.27,28 Both a lack of arrhythmia and proximity to the bundle of His limit the ability to provide effective therapy.
  • Left cervical sympathectomy: For many years, this procedure was performed for refractory long QT syndrome (LQTS). Although it may still have a role when performed by skilled surgeons, many groups now choose a combination of pharmacologic alpha-blockade and beta-blockade, often with ICD placement.

Consultations

  • Patients should be referred to a cardiologist.
  • Primary care physicians may certainly observe infrequent asymptomatic premature ventricular contractions (PVCs), often with a 24-hour Holter evaluation, to confirm the frequency and severity of arrhythmia. For most other patients with VA more complex than this, prompt referral and direct communication with a pediatric cardiologist is indicated. Referral facilitates appropriate testing and decision making about evaluating the patient on an inpatient or outpatient basis.
  • The patterns and relative risks of arrhythmia in adult and pediatric patients differ substantially. Whenever feasible, a cardiologist with specific training and expertise in pediatric heart disease should evaluate the patient. Expedite referral when any of the following indications are present:
    • Symptoms of syncope or apparent heart failure
    • Family history of premature death or seizures
    • History or physical suggesting structural heart disease or heart failure
    • Arrhythmia triggered by medications
    • Arrhythmia triggered by recreational drugs
    • Nonsustained or sustained VT
    • History of cardiac surgery or known heart disease, even if it is apparently repaired

Diet

  • Diet is rarely is a factor in VA.
  • Diuretic use or abuse, anorexia, or chronic diarrhea can induce hypokalemia, which exacerbates VA.
  • Primary or dietary rickets rarely produces sufficient hypocalcemia to cause QT prolongation and a risk of arrhythmia.

Activity

  • The updated 2005 Bethesda conference offers useful initial set of recommendations for patients with ventricular ectopy.29
    • In the absence of detailed investigations and referral, the activity of patients with PVCs that are more than isolated is typically restricted to low-static or low-dynamic activities.
    • Similar restrictions are recommended for those with clinically significant ectopy and most forms of heart disease or symptoms.
    • Patients whose findings on subsequent investigation suggest benign VT often may resume their full activities.
    • Detailed recommendations for both patients with inherited heart disease and those with CHD have been updated in the 36th Bethesda Conference.30
  • Exercise represents a paradox because its long-term health benefits may lower the overall incidence of cardiac events, but the instantaneous risk of cardiac events appears to increase during or immediately after exertion. Some patients with prolonged-QT syndrome have drowned, particularly after diving into cold water, presumably because they developed ventricular fibrillation.
  • Elite athletes, particularly males, may have an athletic heart syndrome that can include mildly increased left ventricular mass with normal left ventricular cavity dimensions. One third of these patients have more than 100 premature ventricular beats per 24 hours with other higher grade ectopy, including couplets and nonsustained VT.

Medication

Although antiarrhythmic drug therapy can suppress spontaneous arrhythmia and although it may help individual patients, some of these medications have increased mortality rates in selected adult and pediatric patients. Mortality rates typically increase when the overall risk is less than the risk of proarrhythmia. Although digoxin is approved for use in infants, it lacks specific antiarrhythmic properties that aid in the control of most ventricular arrhythmias. All other agents, despite the current use, are not approved for use in young children.

Antiarrhythmic drug therapy is further complicated because no single drug is ideal in all settings. Beta-blockade, with intravenous (IV) esmolol or any of the oral (PO) preparations, is a good initial choice for nearly all forms of ventricular arrhythmia (VA). In addition, it has few absolute contraindications in the treatment of serious arrhythmia.

Other medications have important limitations. Use of verapamil in children younger than 1 year is associated with infrequent episodes of cardiovascular collapse and death. Procainamide is an excellent choice for incessant reentrant VA in many settings, but it may exacerbate long QT syndrome (LQTS). PO agents in Vaughn-Williams class I-A (eg, quinidine, procainamide), class I-C (eg, flecainide, propafenone), or class III (eg, sotalol, amiodarone) can cause ventricular proarrhythmia and suppress clinical arrhythmia while increasing mortality rates in selected populations. Both IV and PO amiodarone may have important noncardiac adverse effects. Make therapeutic decisions carefully after consulting with an experienced pediatric cardiologist (electrophysiologist).

Intravenous amiodarone in infants and young children deserves particular attention. The medications broad efficacy and ready availability has increased in popularity in managing sustained arrhythmias in the ICU and emergency setting. A prospective tiered dose pediatric trial showed good efficacy but a nearly 50% incidence of major adverse events.31

Neonates may have relatively frequent episodes of nonsustained ventricular tachycardia or, more precisely, accelerated idioventricular rhythm (AIVR). Although thorough noninvasive evaluation with monitoring and echocardiography is warranted, the risk of mortality is probably zero. Similarly, the risks associated with many forms of VA are quite low in the patient without cardiomyopathy or a probable ion-channel defect. In both of these settings, avoiding therapy with potentially risky drugs and then choosing an agent that is more effective at decreasing arrhythmias on ambulatory monitoring may be important.

Beta-blockers

Propranolol, atenolol, nadolol, and esmolol are the beta-blockers most frequently used to manage VA. They appear to be particularly effective in treating patients with VA, LQTS, or HCM. Other agents may be useful; sotalol, propafenone, and amiodarone have beta-blocking properties. Beta-blockers have not been associated with ventricular proarrhythmia; this is a major advantage of this class compared with other agents, particularly class I and III agents. Base the choice between beta-blockers on the duration of action, selectivity, and preparation.


Propranolol (Inderal)

Nonselective beta-blocker with long record of use and relative safety. Generally short acting, but long-acting preparations available. Stable liquid preparation can be used to treat infants. Significant efficacy data available.

Adult

80-240 mg/d PO divided q6-8h; or qd as SR preparation

Pediatric

PO: 1-4 mg/kg/d divided q6-8h
IV: Not recommended; however, for arrhythmias, 0.01-0.1 mg/kg, not to exceed 1 mg/dose slow bolus recommended; change to PO as soon as possible

Coadministration with aluminum salts, barbiturates, nonsteroidal anti-inflammatory drugs (NSAIDs), penicillins, calcium salts, cholestyramine, and rifampin may decrease effects; calcium channel blockers, cimetidine, loop diuretics, and monoamine oxidase inhibitors (MAOIs) may increase toxicity; may increase toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines

Documented hypersensitivity; uncompensated congestive heart failure (CHF), bradycardia, cardiogenic shock, AV conduction abnormalities, severe ventricular dysfunction; severe asthma; diabetes

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Asthma and bronchospasm; AV conduction disturbance; depression; bradycardia; hypoglycemia in infants; beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw slowly and monitor closely; infants may have clinically important hypoglycemia, particularly when PO intake impaired


Atenolol (Tenormin)

Cardioselective beta1-blocker. Compared with propranolol, may have better tolerability and pharmacokinetics, and frequently has equivalent efficacy.

Adult

25-100 mg/d PO qd; divided q12h in some settings, particularly in adolescents

Pediatric

0.1-0.3 mg/kg/d PO qd or divided q12h

Coadministration with Al salts, barbiturates, Ca salts, cholestyramine, NSAIDs, penicillins, and rifampin may decrease effects; haloperidol, hydralazine, loop diuretics, and MAOIs may increase toxicity

Documented hypersensitivity; uncompensated CHF, bradycardia, cardiogenic shock, AV conduction abnormalities, severe ventricular dysfunction; severe asthma; diabetes

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Asthma and bronchospasm; AV conduction disturbance; depression; bradycardia; hypoglycemia in infants; beta-adrenergic blockade may reduce symptoms of acute hypoglycemia and mask signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism and cause thyroid storm; monitor patients closely and withdraw drug slowly


Nadolol (Corgard)

Nonselective beta-blocker that has more favorable pharmacokinetics than propranolol, which may increase efficacy in some settings.

Adult

40-240 mg/d PO qd or divided q12h in some settings

Pediatric

1-2 mg/kg/d PO qd or divided q12h

Exogenous catecholamines; antihypertensive agents; calcium channel blockers exaggerate negative inotropic and chronotropic effects

Documented hypersensitivity; uncompensated CHF, bradycardia, cardiogenic shock; AV conduction abnormalities, severe ventricular dysfunction; severe asthma; diabetes

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Asthma and bronchospasm; AV conduction disturbance; depression; bradycardia; hypoglycemia in infants; beta-adrenergic blockade may reduce symptoms of acute hypoglycemia and mask signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism and cause thyroid storm; monitor patients closely and withdraw drug slowly


Esmolol (Brevibloc)

Short-acting, IV, beta1-blocker useful in acute care settings.

Adult

Loading dose: 0.5 mg/kg/min IV; then IV infusion 50-200 mcg/kg/min, increase q5-10min until maximum acceptable dose or efficacy

Pediatric

Loading dose: 0.5 mg/kg IV; then IV infusion 100-500 mcg/kg/min IV, increase q5-10min until maximum acceptable dose or efficacy; if significant ventricular dysfunction, consider test dose of 0.25 mg/kg IV and observe effects

Cardiotoxicity may increase with concurrent sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; concurrent digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents increase toxicity

Documented hypersensitivity; uncompensated CHF, bradycardia, cardiogenic shock; AV conduction abnormalities, severe ventricular dysfunction; severe asthma; diabetes

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Asthma and bronchospasm; AV conduction disturbance; depression; bradycardia; hypoglycemia in infants; beta-adrenergic blockade may reduce symptoms of acute hypoglycemia and mask signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism and cause thyroid storm


Betaxolol (Kerlone)

Long-acting, PO, highly selective beta1-blocker that decreases automaticity of cardiac contractions. Potential adverse effects same as those of other beta-blockers, but high beta1-selectivity of drug (or bisoprolol) may permit low doses that avoid adverse effects.

Adult

10 mg PO qd initially; may increase to 40 mg/d
Severe renal impairment: 5 mg PO qd initially; may increase by 5-mg increments q2wk, not to exceed 20 mg/d

Pediatric

Not established

Cardiotoxicity may increase with concurrent sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; concurrent digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents increase toxicity

Documented hypersensitivity; uncompensated CHF, bradycardia, cardiogenic shock; AV conduction abnormalities, severe ventricular dysfunction; severe asthma; diabetes

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Asthma, bronchospasm, AV conduction disturbance, depression; bradycardia; hypoglycemia in infants; beta-adrenergic blockade may reduce symptoms of acute hypoglycemia and mask signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism and cause thyroid storm; decrease dose in renal impairment

Class I antiarrhythmics

This class of agents has complex actions. The drugs primarily block sodium channels, decreasing conduction velocity (QRS widening). Only IV procainamide and lidocaine are presented here. Quinidine, the initial drug in this class, is associated with excessive ventricular proarrhythmia in most patient groups. Propafenone, disopyramide, flecainide, and other agents may have a role in long-term therapy in some patients. Some children and adults with ischemic heart disease have increased mortality rates while taking these medications despite apparent control of their arrhythmia.


Procainamide (Procanbid, Pronestyl)

Once mainstay of PO therapy, long-term use associated with lupuslike syndrome. With important exception of LQTS, torsadelike polymorphic VT, and related disorders, controls both ventricular and supraventricular arrhythmias. Hypotension and reflex increase in AV conduction important adverse effects to consider. Therapeutic levels of procainamide and N -acetyl-procainamide (NAPA; major, active metabolite), can be monitored.

Adult

Loading dose: 500-1000 mg IV over 20-60 min
Maintenance infusion: 2-6 mg/min IV

Pediatric

Loading dose: 5-10 mg/kg IV over 20-60 min
Maintenance infusion: 20-40 mcg/kg/min IV; infants may need up to 80 mcg/kg/min

Increases levels of NAPA in patients taking cimetidine, ranitidine, beta-blockers, amiodarone, trimethoprim, and quinidine; may increase effects of skeletal muscle relaxants, quinidine, lidocaine, and neuromuscular blockers; ofloxacin inhibits tubular secretion and may increase bioavailability; may increase risk of cardiotoxicity with concurrent sparfloxacin

Documented hypersensitivity; LQTS, second- or third-degree heart block, complete heart block, torsade de pointes; systemic lupus erythematosus (SLE)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor for hypotension; plasma concentrations of procainamide and NAPA may increase in renal failure; high or toxic concentrations may induce AV block or abnormal automaticity; caution in complete AV block, digitalis intoxication, organic heart disease, renal disease, and hepatic insufficiency


Lidocaine (Xylocaine IV for Cardiac Arrhythmias)

Class I-B antiarrhythmic. Mainstay in IV suppression of VA in adults with ischemic heart disease; less clearly effective in children, though has advantage of general safety. Generally tolerated by patients with poor ventricular function and potentially effective in virtually every setting of serious VA.

Adult

Loading dose: 50 mg IV; repeat q3-5min not to exceed cumulative dose of 200 mg
Maintenance infusion: 1-4 mg/min IV

Pediatric

Loading dose: 1 mg/kg IV; repeat in 10-15 min for 2 doses
Maintenance infusion: 20-50 mcg/kg/min IV

Coadministration with cimetidine or beta-blockers increases toxicity; coadministration with procainamide and tocainide may result in additive cardiodepressant action; may increase effects of succinylcholine

Documented hypersensitivity to amide-type local anesthetics; avoid in Adams-Stokes syndrome and Wolff-Parkinson-White syndrome; avoid in severe sinoatrial, AV, or intraventricular block, if artificial pacemaker not in place

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Use solution without preservatives; caution in heart failure, hepatic disease, hypoxia, hypovolemia or shock, respiratory-depression, and bradycardia; may increase risk of CNS and cardiac adverse effects in older patients; high plasma concentrations can cause seizures, heart block, and AV conduction abnormalities

Class III antiarrhythmics

Amiodarone is generally reserved for potentially life-threatening VA. It elicits potassium channel blockade and prolongs repolarization.


Amiodarone (Cordarone)

Complex and potent antiarrhythmic agent with several actions on cardiac action potential, exceedingly complex pharmacokinetics, and extracardiac pharmacodynamics. May inhibit AV conduction and sinus-node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation.
PO efficacy may take weeks. With exception of disorders of prolonged repolarization (eg, LQTS), may be drug of choice (DOC) for life-threatening VA refractory to beta-blockade and initial therapy with other agents.

Adult

Loading dose: 800-1600 mg/d PO divided in 1-2 doses/d for 1-3 wk, then 600-800 mg/d divided in 1-2 doses/d for 1 mo
Maintenance dose: 400 mg/d PO
Alternative IV loading dose: 150 mg IV over first 10 min, then 360 mg over next 6 h, then 540 mg over next 18 h; IV must be further diluted before administration

Pediatric

Loading dose: 10-15 mg/kg/d PO divided in 1-2 doses/d for 1-3 wk, then 2-6 mg/kg/d divided in 1-2 doses/d for 1 mo
Alternative IV loading dose: 2-3 mg/kg IV over 5-10 min, repeat bolus q10-30min; not to exceed cumulative dose of 10-15 mg/kg/d

Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; protease inhibitors (eg, indinavir, ritonavir, amprenavir, nelfinavir) inhibit amiodarone metabolism resulting in increased serum levels and may prolong the QT interval; cardiotoxicity increased by sparfloxacin, and disopyramide; coadministration with calcium channel blockers may cause additive effect and further decrease myocardial contractility; cimetidine may increase amiodarone levels; drugs that prolong QTc (eg, dofetilide, sotalol) likely to have additive effect

Documented hypersensitivity; complete AV block, intraventricular conduction defects; patients taking ritonavir or sparfloxacin

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

IV preparation may induce hypotension (Ca may reverse); carefully monitor pulmonary function, corneal staining, thyroid function; caution in thyroid or liver disease; caution in electrolyte imbalance (ie, hypokalemia, hypomagnesemia); in infants and young children, incidence of serious adverse events significant, and patients may require pacing or other support

Calcium channel blockers (Vaughn-Williams class IV)

Verapamil is primarily marketed to control hypertension or heart rate during atrial tachycardia.


Verapamil (Calan, Verelan)

Can diminish PVCs associated with perfusion therapy and decrease risk of ventricular fibrillation and VT. By interrupting reentry at AV node, can restore normal sinus rhythm in patients with paroxysmal SVTs (PSVTs). IV and PO. Some automatic VTs and RBBB reentrant VT in normal hearts often sensitive. Fatal cardiovascular collapse reported in infants and neonates given IV form. PO preparations include short-acting (q6h) and sustained-release (SR) preparations for qd dosing.

Adult

IV: 2.5-10 mg; 5 mg typical
PO: 180-320 mg/d divided q6h; extended-release (ER) form may be administered qd

Pediatric

IV: 0.1-0.3 mg/kg/dose, not to exceed 5 mg/dose; use with extreme caution in infants (severe apnea, bradycardia, hypotensive reactions, and cardiac arrest have occurred)
PO: 3-7 mg/kg/d divided q6h; ER form may be administered qd in older patients

May increase carbamazepine, digoxin, and cyclosporine levels; coadministration with amiodarone can cause bradycardia and decrease cardiac output; with concurrent beta-blockers, may increase cardiac depression; cimetidine may increase levels; may increase theophylline levels

Documented hypersensitivity; severe CHF, sick sinus syndrome, second- or third-degree AV block; hypotension (<90 mm Hg systolic); infants

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

AV conduction disturbance and bradycardia may occur, monitor ECG and blood pressure closely; monitor liver function

More on Ventricular Tachycardia

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Differential Diagnoses & Workup: Ventricular Tachycardia
Treatment & Medication: Ventricular Tachycardia
Follow-up: Ventricular Tachycardia
Multimedia: Ventricular Tachycardia
References
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References

  1. Brodsky M, Wu D, Denes P, et al. Arrhythmias documented by 24 hour continuous electrocardiographic monitoring in 50 male medical students without apparent heart disease. Am J Cardiol. Mar 1977;39(3):390-5. [Medline].

  2. Sobotka PA, Mayer JH, Bauernfeind RA, et al. Arrhythmias documented by 24-hour continuous ambulatory electrocardiographic monitoring in young women without apparent heart disease. Am Heart J. Jun 1981;101(6):753-9. [Medline].

  3. Jacobsen JR, Garson A Jr, Gillette PC, McNamara DG. Premature ventricular contractions in normal children. J Pediatr. Jan 1978;92(1):36-8. [Medline].

  4. Nagashima M, Matsushima M, Ogawa A, et al. Cardiac arrhythmias in healthy children revealed by 24-hour ambulatory ECG monitoring. Pediatr Cardiol. 1987;8(2):103-8. [Medline].

  5. Roggen A, Pavlovic M, Pfammatter JP. Frequency of spontaneous ventricular tachycardia in a pediatric population. Am J Cardiol. Mar 15 2008;101(6):852-4. [Medline].

  6. [Best Evidence] Colan SD, Lipshultz SE, Lowe AM, et al. Epidemiology and cause-specific outcome of hypertrophic cardiomyopathy in children: findings from the Pediatric Cardiomyopathy Registry. Circulation. Feb 13 2007;115(6):773-81. [Medline].

  7. [Best Evidence] De Rosa G, Butera G, Chessa M, et al. Outcome of newborns with asymptomatic monomorphic ventricular arrhythmia. Arch Dis Child Fetal Neonatal Ed. Nov 2006;91(6):F419-22. [Medline].

  8. Davis AM, Gow RM, McCrindle BW, Hamilton RM. Clinical spectrum, therapeutic management, and follow-up of ventricular tachycardia in infants and young children. Am Heart J. Jan 1996;131(1):186-91. [Medline].

  9. Pfammatter JP, Paul T. Idiopathic ventricular tachycardia in infancy and childhood: a multicenter study on clinical profile and outcome. Working Group on Dysrhythmias and Electrophysiology of the Association for European Pediatric Cardiology. J Am Coll Cardiol. Jun 1999;33(7):2067-72. [Medline].

  10. Van Hare GF, Stanger P. Ventricular tachycardia and accelerated ventricular rhythm presenting in the first month of life. Am J Cardiol. Jan 1 1991;67(1):42-5. [Medline].

  11. Harris KC, Potts JE, Fournier A, Gross GJ, Kantoch MJ, Cote JM. Right ventricular outflow tract tachycardia in children. J Pediatr. Dec 2006;149(6):822-826. [Medline].

  12. Charron P, Dubourg O, Desnos M, et al. Diagnostic value of electrocardiography and echocardiography for familial hypertrophic cardiomyopathy in genotyped children. Eur Heart J. Sep 1998;19(9):1377-82. [Medline].

  13. Southall DP, Richards J, Mitchell P, et al. Study of cardiac rhythm in healthy newborn infants. Br Heart J. Jan 1980;43(1):14-20. [Medline].

  14. Bomma C, Rutberg J, Tandri H, et al. Misdiagnosis of arrhythmogenic right ventricular dysplasia/cardiomyopathy. J Cardiovasc Electrophysiol. Mar 2004;15(3):300-6. [Medline].

  15. Tandri H, Calkins H, Nasir K, et al. Magnetic resonance imaging findings in patients meeting task force criteria for arrhythmogenic right ventricular dysplasia. J Cardiovasc Electrophysiol. May 2003;14(5):476-82. [Medline].

  16. Tandri H, Bluemke DA, Ferrari VA, et al. Findings on magnetic resonance imaging of idiopathic right ventricular outflow tachycardia. Am J Cardiol. Dec 1 2004;94(11):1441-5. [Medline].

  17. Silka MJ, Hardy BG, Menashe VD, Morris CD. A population-based prospective evaluation of risk of sudden cardiac death after operation for common congenital heart defects. J Am Coll Cardiol. Jul 1998;32(1):245-51. [Medline].

  18. Frangini PA, Cecchin F, Jordao L, et al. How revealing are insertable loop recorders in pediatrics?. Pacing Clin Electrophysiol. Mar 2008;31(3):338-43. [Medline].

  19. Kothari DS, Riddell F, Smith W, Voss J, Skinner JR. Digital implantable loop recorders in the investigation of syncope in children: benefits and limitations. Heart Rhythm. Nov 2006;3(11):1306-12. [Medline].

  20. Saarel EV, Doratotaj S, Sterba R. Initial experience with novel mobile cardiac outpatient telemetry for children and adolescents with suspected arrhythmia. Congenit Heart Dis. Jan 2008;3(1):33-8. [Medline].

  21. Alexander ME, Cecchin F, Huang KP, Berul CI. Microvolt t-wave alternans with exercise in pediatrics and congenital heart disease: limitations and predictive value. Pacing Clin Electrophysiol. Jul 2006;29(7):733-41. [Medline].

  22. Alexander ME, Walsh EP, Saul JP, et al. Value of programmed ventricular stimulation in patients with congenital heart disease. J Cardiovasc Electrophysiol. Aug 1999;10(8):1033-44. [Medline].

  23. Khairy P, Landzberg MJ, Gatzoulis MA, et al. Value of programmed ventricular stimulation after tetralogy of fallot repair: a multicenter study. Circulation. Apr 27 2004;109(16):1994-2000. [Medline].

  24. Alexander ME, Cecchin F, Walsh EP, et al. Implications of implantable cardioverter defibrillator therapy in congenital heart disease and pediatrics. J Cardiovasc Electrophysiol. Jan 2004;15(1):72-6. [Medline].

  25. Berul CI, Van Hare GF, Kertesz NJ, et al. Results of a multicenter retrospective implantable cardioverter-defibrillator registry of pediatric and congenital heart disease patients. J Am Coll Cardiol. Apr 29 2008;51(17):1685-91. [Medline].

  26. Stephenson EA, Batra AS, Knilans TK, et al. A multicenter experience with novel implantable cardioverter defibrillator configurations in the pediatric and congenital heart disease population. J Cardiovasc Electrophysiol. Jan 2006;17(1):41-6. [Medline].

  27. Morwood JG, Triedman JK, Berul CI, et al. Radiofrequency catheter ablation of ventricular tachycardia in children and young adults with congenital heart disease. Heart Rhythm. Sep 2004;1(3):301-8. [Medline].

  28. Laohakunakorn P, Paul T, Knick B, et al. Ventricular tachycardia in nonpostoperative pediatric patients: role of radiofrequency catheter ablation. Pediatr Cardiol. Mar-Apr 2003;24(2):154-60. [Medline].

  29. Zipes DP, Ackerman MJ, Estes NA, et al. Task force 7: arrhythmias. J Am Coll Cardiol. Apr 19 2005;45(8):1354-63. [Medline].

  30. Maron BJ, Chaitman BR, Ackerman MJ, et al. Recommendations for physical activity and recreational sports participation for young patients with genetic cardiovascular diseases. Circulation. Jun 8 2004;109(22):2807-16. [Medline].

  31. [Best Evidence] Saul JP, Scott WA, Brown S, et al. Intravenous amiodarone for incessant tachyarrhythmias in children: a randomized, double-blind, antiarrhythmic drug trial. Circulation. Nov 29 2005;112(22):3470-7. [Medline].

  32. Antzelevitch C, Brugada P, Borggrefe M, et al. Brugada syndrome: report of the second consensus conference: endorsed by the Heart Rhythm Society and the European Heart Rhythm Association. Circulation. Feb 8 2005;111(5):659-70. [Medline].

  33. Atkins DL, Scott WA, Blaufox AD, et al. Sensitivity and specificity of an automated external defibrillator algorithm designed for pediatric patients. Resuscitation. Feb 2008;76(2):168-74. [Medline].

  34. Berul CI, Hill SL, Geggel RL, et al. Electrocardiographic markers of late sudden death risk in postoperative tetralogy of Fallot children. J Cardiovasc Electrophysiol. Dec 1997;8(12):1349-56. [Medline].

  35. Corrado D, Basso C, Rizzoli G, et al. Does sports activity enhance the risk of sudden death in adolescents and young adults?. J Am Coll Cardiol. Dec 3 2003;42(11):1959-63. [Medline].

  36. Cullen S, Celermajer DS, Franklin RC, et al. Prognostic significance of ventricular arrhythmia after repair of tetralogy of Fallot: a 12-year prospective study. J Am Coll Cardiol. Apr 1994;23(5):1151-5. [Medline].

  37. Deal BJ, Miller SM, Scagliotti D, et al. Ventricular tachycardia in a young population without overt heart disease. Circulation. Jun 1986;73(6):1111-8. [Medline].

  38. Denfield SW, Kearney DL, Michael L, et al. Developmental differences in canine cardiac surgical scars. Am Heart J. Aug 1993;126(2):382-9. [Medline].

  39. Driscoll DJ, Edwards WD. Sudden unexpected death in children and adolescents. J Am Coll Cardiol. Jun 1985;5(6 Suppl):118B-121B. [Medline].

  40. Dungan WT, Garson A Jr, Gillette PC. Arrhythmogenic right ventricular dysplasia: a cause of ventricular tachycardia in children with apparently normal hearts. Am Heart J. Oct 1981;102(4):745-50. [Medline].

  41. Fazio G, Corrado G, Zachara E, et al. Ventricular tachycardia in non-compaction of left ventricle: is this a frequent complication?. Pacing Clin Electrophysiol. Apr 2007;30(4):544-6. [Medline].

  42. Fish FA, Gillette PC, Benson DW Jr. Proarrhythmia, cardiac arrest and death in young patients receiving encainide and flecainide. The Pediatric Electrophysiology Group. J Am Coll Cardiol. Aug 1991;18(2):356-65. [Medline].

  43. Fishberger SB, Colan SD, Saul JP, et al. Myocardial mechanics before and after ablation of chronic tachycardia. Pacing Clin Electrophysiol. Jan 1996;19(1):42-9. [Medline].

  44. Fogel MA, Weinberg PM, Harris M, Rhodes L. Usefulness of magnetic resonance imaging for the diagnosis of right ventricular dysplasia in children. Am J Cardiol. Apr 15 2006;97(8):1232-7. [Medline].

  45. Francis J, Sankar V, Nair VK, Priori SG. Catecholaminergic polymorphic ventricular tachycardia. Heart Rhythm. May 2005;2(5):550-4. [Medline].

  46. Friedman RA, Moak JP, Garson A Jr. Clinical course of idiopathic dilated cardiomyopathy in children. J Am Coll Cardiol. Jul 1991;18(1):152-6. [Medline].

  47. Garson A. Ventricular arrhythmias after repair of congenital heart disease: who needs treatment?. Cardiol Young. 1991;1:177-81.

  48. Garson A Jr, Smith RT, Moak JP, et al. Ventricular arrhythmias and sudden death in children. J Am Coll Cardiol. Jun 1985;5(6 Suppl):130B-133B. [Medline].

  49. Gelatt M, Hamilton RM, McCrindle BW, et al. Arrhythmia and mortality after the Mustard procedure: a 30-year single- center experience. J Am Coll Cardiol. Jan 1997;29(1):194-201. [Medline].

  50. Gutgesell H, Atkins D, Barst R, et al. Cardiovascular Monitoring of Children and Adolescents Receiving Psychotropic Drugs: A Statement for Healthcare Professionals From the Committee on Congenital Cardiac Defects, Council on Cardiovascular Disease in the Young, American Heart Association. Circulation. Feb 23 1999;99(7):979-982. [Medline].

  51. Harrison DA, Harris L, Siu SC, et al. Sustained ventricular tachycardia in adult patients late after repair of tetralogy of Fallot. J Am Coll Cardiol. Nov 1 1997;30(5):1368-73. [Medline].

  52. Hill SL, Evangelista JK, Pizzi AM, et al. Proarrhythmia associated with cisapride in children. Pediatrics. Jun 1998;101(6):1053-6. [Medline].

  53. Kennedy HL, Whitlock JA, Sprague MK. Long-term follow-up of asymptomatic healthy subjects with frequent and complex ventricular ectopy. N Engl J Med. Jan 24 1985;312(4):193-7. [Medline].

  54. Knauth AL, Gauvreau K, Powell AJ, et al. Ventricular size and function assessed by cardiac MRI predict major adverse clinical outcomes late after tetralogy of Fallot repair. Heart. Feb 2008;94(2):211-6. [Medline].

  55. Liberthson RR. Sudden death from cardiac causes in children and young adults. N Engl J Med. Apr 18 1996;334(16):1039-44. [Medline].

  56. Maron BJ, Gardin JM, Flack JM. HCM in the general population [comment]. Circulation. Aug 1 1996;94(3):588-9. [Medline].

  57. Maron BJ, Thompson PD, Puffer JC, et al. Cardiovascular preparticipation screening of competitive athletes. A statement for health professionals from the Sudden Death Committee (clinical cardiology) and Congenital Cardiac Defects Committee (cardiovascular disease in the young), American Heart. Circulation. Aug 15 1996;94(4):850-6. [Medline].

  58. Maron BJ, Zipes DP. Introduction: eligibility recommendations for competitive athletes with cardiovascular abnormalities-general considerations. J Am Coll Cardiol. Apr 19 2005;45(8):1318-21. [Medline].

  59. Matitiau A, Perez-Atayde A, Sanders SP, et al. Infantile dilated cardiomyopathy. Relation of outcome to left ventricular mechanics, hemodynamics, and histology at the time of presentation. Circulation. Sep 1994;90(3):1310-8. [Medline].

  60. Moss AJ, Schwartz PJ, Crampton RS, et al. The long QT syndrome. Prospective longitudinal study of 328 families. Circulation. Sep 1991;84(3):1136-44. [Medline].

  61. Neuspiel DR, Kuller LH. Sudden and unexpected natural death in childhood and adolescence. JAMA. Sep 13 1985;254(10):1321-5. [Medline].

  62. Nollert G, Fischlein T, Bouterwek S, et al. Long-term survival in patients with repair of tetralogy of Fallot: 36- year follow-up of 490 survivors of the first year after surgical repair. J Am Coll Cardiol. Nov 1 1997;30(5):1374-83. [Medline].

  63. Ovadia M, Duque KS. Sporadic isolated left ventricular noncompaction: dread disease or not?. Pacing Clin Electrophysiol. Apr 2007;30(4):455-7. [Medline].

  64. Paul T, Marchal C, Garson A Jr. Ventricular couplets in the young: prognosis related to underlying substrate. Am Heart J. Mar 1990;119(3 Pt 1):577-82. [Medline].

  65. Pedersen DH, Zipes DP, Foster PR, Troup PJ. Ventricular tachycardia and ventricular fibrillation in a young population. Circulation. - Foster PR;60(5):988-97. [Medline].

  66. Perry JC, Garson A. Encainide and flecainide in children: separating the wheat from the chaff. J Am Coll Cardiol. Aug 1991;18(2):366-7. [Medline].

  67. Polderman KH. Hypothermia and neurological outcome after cardiac arrest: state of the art. Eur J Anaesthesiol Suppl. 2008;42:23-30. [Medline].

  68. Rocchini AP, Chun PO, Dick M. Ventricular tachycardia in children. Am J Cardiol. May 1981;47(5):1091-7. [Medline].

  69. Schwartz PJ, Moss AJ, Vincent GM, Crampton RS. Diagnostic criteria for the long QT syndrome. An update. Circulation. Aug 1993;88(2):782-4. [Medline].

  70. Shah M, Akar FG, Tomaselli GF. Molecular basis of arrhythmias. Circulation. Oct 18 2005;112(16):2517-29. [Medline].

  71. Shapiro F, Sethna N, Colan S, et al. Spinal fusion in Duchenne muscular dystrophy: a multidisciplinary approach. Muscle Nerve. May 1992;15(5):604-14. [Medline].

  72. Sharma JR, Sathanandam S, Rao SP, Acharya S, Flood V. Ventricular tachycardia in acute fulminant myocarditis: medical management and follow-up. Pediatr Cardiol. Mar 2008;29(2):416-9. [Medline].

  73. Skinner JR, Chung SK, Nel CA, et al. Brugada syndrome masquerading as febrile seizures. Pediatrics. May 2007;119(5):e1206-11. [Medline].

  74. Sumitomo N, Sakurada H, Taniguchi K, et al. Association of atrial arrhythmia and sinus node dysfunction in patients with catecholaminergic polymorphic ventricular tachycardia. Circ J. Oct 2007;71(10):1606-9. [Medline].

  75. Tandri H, Macedo R, Calkins H, et al. Role of magnetic resonance imaging in arrhythmogenic right ventricular dysplasia: insights from the North American arrhythmogenic right ventricular dysplasia (ARVD/C) study. Am Heart J. Jan 2008;155(1):147-53. [Medline].

  76. Walsh EP, Rockenmacher S, Keane JF, et al. Late results in patients with tetralogy of Fallot repaired during infancy. Circulation. May 1988;77(5):1062-7. [Medline].

  77. Zareba W, Moss AJ, Schwartz PJ, et al. Influence of genotype on the clinical course of the long-QT syndrome. International Long-QT Syndrome Registry Research Group. N Engl J Med. Oct 1 1998;339(14):960-5. [Medline].

  78. Zipes DP, Ackerman MJ, Estes NA 3rd, Grant AO, Myerburg RJ, Van Hare G. Task Force 7: arrhythmias. J Am Coll Cardiol. Apr 19 2005;45(8):1354-63. [Medline].

  79. Zipes DP, Foster PR, Troup PJ. Atrial induction of ventricular tachycardia: reentry versus triggered automaticity. Am J Cardiol. Jul 1979;44(1):1-8. [Medline].

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Further Reading

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Keywords

ventricular tachycardia, nonsustained ventricular tachycardia, accelerated ventricular rhythms, premature ventricular contractions, PVC, repetitive monomorphic ventricular tachycardia, sustained monomorphic ventricular tachycardia, torsade de pointes, ventricular ectopic activity, VEA, ventricular ectopy, ventricular fibrillation, V fib, ventricular flutter, V flutter, ventricular premature beats, ventricular arrhythmia, VA, VT, V tach, sudden cardiac death, syncope, congenital heart disease, long QT syndrome, LQTS, tetralogy of Fallot, ventricular fibrillation, aortic stenosis, hypertrophic cardiomyopathy, HCM, ventricular septal defects, Chagas disease, trypanosomiasis, Brugada syndrome, cocaine, tricyclic antidepressant use, Kawasaki disease, right bundle-branch block, RBBB, right ventricular outflow tract ventricular tachycardia, left bundle-branch block, LBBB

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Contributor Information and Disclosures

Author

Mark E Alexander, MD, Assistant Professor, Department of Pediatrics, Children's Hospital of Boston and Harvard Medical School
Mark E Alexander, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, Heart Rhythm Society, and Pediatric Electrophysiology Society
Disclosure: Nothing to disclose.

Coauthor(s)

Charles I Berul, MD, Associate Professor of Pediatrics, Harvard Medical School; Senior Associate, Department of Cardiology, Children's Hospital of Boston
Charles I Berul, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Heart Rhythm Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Medical Editor

Christopher Johnsrude, MD, Associate Professor of Pediatrics, Director of Electrophysiology, University of Louisville School of Medicine; Consulting Staff, Pediatric Cardiology Associates, PSC
Christopher Johnsrude, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Cardiology
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Hugh D Allen, MD, Professor, Department of Pediatrics, Division of Pediatric Cardiology and Department of Internal Medicine, Ohio State University College of Medicine
Hugh D Allen, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, American Society of Echocardiography, Society for Pediatric Research, Society of Pediatric Echocardiography, and Western Society for Pediatric Research
Disclosure: Nothing to disclose.

CME Editor

Gilbert Herzberg, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College
Gilbert Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD, Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital of Wisconsin
Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

 
 
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