Junctional Ectopic Tachycardia Treatment & Management

  • Author: M Silvana Horenstein, MD; Chief Editor: Stuart Berger, MD   more...
 
Updated: Nov 28, 2011
 

Medical Care

Congenital junctional ectopic tachycardia (JET) is usually initially treated with antiarrhythmic therapy, with the choice of medication guided by the degree of coexisting ventricular dysfunction. The most appropriate management of asymptomatic infants with "slow" JET (ie, 150 beats per minute [bpm]) is debatable. However, these asymptomatic patients should have close monitoring.

Numerous therapeutic options have been used for the treatment of postoperative JET, including the following:

  • Some propose that management of symptomatic infants with slow JET should consist of digoxin to control symptoms of cardiac failure and antiarrhythmic drugs to control the ventricular rate of the arrhythmia. However, caution should be used because development of ventricular fibrillation or faster tachycardia (≤ 400 bpm) during progressive digoxin loading has been described in patients with congenital JET and severe cardiac failure.
  • Propafenone has also been effective in preventing or controlling JET in some neonates, especially neonates with slower ventricular rates (approximately 170 bpm).
  • Amiodarone may successfully control ventricular rate. Furthermore, the combination of amiodarone and a class Ic antiarrhythmic drug can be used to reduce the dose of amiodarone.
  • A multicenter study reported that success of intravenous amiodarone is dose-related.[7] However, so are its side effects. Therefore, the dose-related risks should be taken into account when treating children with incessant arrhythmias.
  • True drug-refractory JET is very rare. Therefore, in patients who fail to respond to a single drug regimen, a second antiarrhythmic agent with different electrophysiological effects may be added.
  • Controlled hypothermia has been relatively effective in reducing JET rate in patients in the immediate postoperative period.[8, 9] These patients are often intubated and can be effectively paralyzed, sedated, and cooled. For refractory cases, adding procainamide has been effective.[10] Other traditional approaches include increase of ventricular preload and reduction of inotropic agents (which are also usually chronotropic) as much as possible.
  • The use of atrial or AV sequential pacing can help to restore AV sequence and cardiac output once the JET rate is reduced.
  • Multiple antiarrhythmic agents have been used and are considered somewhat effective in postoperative JET.
  • Occasionally, atrial high-rate pacing to the point of 2:1 AV block can provide a controlled ventricular response while continuing to suppress the JET focus. This finding suggests a relatively high insertion site of the JET focus into the AV conduction system.
  • Ventricular paired pacing, with or without additional atrial pacing, has been used in rare cases when patients have not responded to other therapies. This technique is potentially dangerous and requires essentially constant monitoring and adjustment by personnel who are extremely familiar with electrophysiologic procedures. During ventricular paired pacing, electrolytes and antiarrhythmic medications should be administered by constant infusions only.
  • A small-case series advocates for radiofrequency catheter ablation for JET if antiarrhythmic drug therapy has failed.[11] Success was safely achieved by plotting the entire His-bundle using a modern navigation system that would permit marking the spot of earliest retrograde conduction during tachycardia, and, later, empirically ablating that spot during sinus rhythm.
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Surgical Care

The primary functions of surgical care in postoperative JET are to correct major residual defects that may be contributing to morbidity, to ensure that atrial-based pacing can be achieved, and to provide extracorporeal life support (ie, extracorporeal membrane oxygenation [ECMO]) if required.

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Contributor Information and Disclosures
Author

M Silvana Horenstein, MD  Assistant Professor, Department of Pediatrics, University of Texas Medical School at Houston; Medical Doctor Consultant, Legacy Department, Best Doctors, Inc

M Silvana Horenstein, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and American Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Robert Murray Hamilton, MD, MSc, FRCPC  Section Head, Electrophysiology, Senior Associate Scientist, Physiology and Experimental Medicine, Labatt Family Heart Centre; Professor, Department of Pediatrics, University of Toronto Faculty of Medicine

Robert Murray Hamilton, MD, MSc, FRCPC is a member of the following medical societies: American Heart Association, Canadian Cardiovascular Society, Canadian Medical Association, Canadian Medical Protective Association, Cardiac Electrophysiology Society, Heart Rhythm Society, Ontario Medical Association, Pediatric Electrophysiology Society, Royal College of Physicians and Surgeons of Canada, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Specialty Editor Board

Charles I Berul, MD  Professor of Pediatrics and Integrative Systems Biology, George Washington University School of Medicine; Chief, Division of Cardiology, Children's National Medical Center

Charles I Berul, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, Pediatric and Congenital Electrophysiology Society, and Society for Pediatric Research

Disclosure: Johnson & Johnson Consulting fee Consulting

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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.

Gilbert Z Herzberg, MD  Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College; Consulting Staff, Department of Pediatrics, Sound Shore Medical Center

Gilbert Z 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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Lead II rhythm strip of a surface ECG from a patient with postoperative JET. Atrial activity (P) is marked with blue lines and ventricular depolarization (QRS) is marked in red. Note the narrow QRS complexes due to their origin at the AV junction. Also note the dissociation between atrial and ventricular depolarizations where some of the QRS complexes seem to "follow" the P waves. However, this is not possible because the PR intervals are exceedingly short to allow conduction. In addition, some of the P waves fall after the QRS.
 
 
 
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