Junctional Ectopic Tachycardia Guideline

Publication: 21/04/2021  
Next review: 21/04/2024  
Clinical Guideline
ID: 6938 
Approved By: Trust Clinical Guidelines Group 
Copyright© Leeds Teaching Hospitals NHS Trust 2021  


This Clinical Guideline is intended for use by healthcare professionals within Leeds unless otherwise stated.
For healthcare professionals in other trusts, please ensure that you consult relevant local and national guidance.

Junctional Ectopic Tachycardia Guideline


Junctional Ectopic Tachycardia (JET) occurs in 5 – 10% of post-operative congenital cardiac patients. It is self-limiting but can be life-threatening as it occurs at a vulnerable phase of a patient’s post-operative course and may last days. It compromises cardiac output as it reduces ventricular filling by i) a loss of the ‘atrial kick’ and ii) a reduction in filling time secondary to the tachycardia.

Risk Factors for the Development of JET

  • Infant < 6 months old
  • Within 72 hours of surgery
  • Long cardiopulmonary bypass or X-clamp time
  • Transient AV block after weaning off cardiopulmonary bypass
  • Post-operative Inotropes - Especially Dopamine and Adrenaline
  • Type of Operation, including but not exclusively Tetralogy of Fallot, VSD, AVSD, TAPVD.

Figure 1: Risk factors for development of JET. This is not an exhaustive list and any surgery that is close to the bundle of His may increase the risk.

If any of these risk factors are present, we would strongly recommend that the cardiothoracic surgeon performing the operation ensures that both atrial and ventricular wires are inserted.

Good intra-operative and post-operative intensive care are essential in reducing the chances of a patient developing JET. Key components of this care include maintaining normothermia (target 36.0-37.0C), ensuring the patient is adequately filled, and that electrolytes are in normal range. 

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A formal ECG is essential to diagnose JET and it should not be diagnosed on the basis of bedside telemetry alone. An atrial wire study is performed by attaching the V1 lead to one, or both, of the atrial pacing wires.

The features on an ECG and Atrial wire study include:

  • A usually normal QRS complex but there may be incomplete or complete bundle branch block.
  • Ventricular Rate > Atrial Rate
  • AV dissociation; Often P-waves cannot be identified or are inverted following a QRS complex but will be very evident on an atrial wire study.
  • It can be mistaken for SVT but will not respond to Adenosine.
  • At lower rates can demonstrate 1:1 retrograde ventricular atrial conduction

(Erickson 2006, Miall 2015)

Example of a 12-lead ECG of a patient in JET. Note the p-waves are intermittently visible, an atrial wire study would show that they are ‘walking through’ the QRS complexes.


Example of Atrial Wire Study 12-lead ECG and rhythm strip of a patient with JET & retrograde 1:1 conduction:


JET occurs at a critical post-operative phase for the patient; they are likely to be already compromised following a significant insult from surgery and cardiopulmonary bypass. JET then results in an increased myocardial oxygen demand that can result in an insidious deterioration. Treatment must therefore be aggressive when required. This guideline is based on a staged approach, but these stages must be progressed along if there is haemodynamic compromise from JET without improvement.

Given the nature of JET it is resistant to cardioversion; either electrical or pharmacological. Therefore, treatment is aimed at:

  1. reducing the rate.
  2. restoration of AV synchrony.
  3. reducing the metabolic demand and optimising cardiac output.

(Miall 2015, Ali et al. 2010, Kidson, Lafferty 2020)

The management of JET should begin with prevention; usual good post-operative care of the cardiac patient remains important. It may avoid the initiation of JET and increases the chance of quick resolution.

Analgesia and Sedation

Ensuring optimal analgesia and sedation is important, as it will reduce tachycardia and endogenous catecholamines. It will reduce metabolic workload and therefore myocardial oxygen demand. Paralysis is not usually part of this but is needed if significant hypothermia is to be used or the patient is very unstable.


Electrolyte optimisation is important in both the prevention and treatment of JET, so in the post-operative phase these should be monitored closely and corrected if suboptimal. If JET is confirmed we recommend correcting to achieve levels of Magnesium >1.5mmol/l, Potassium >4mmol/L and Calcium (ionised on blood gas) >1.2mmo/L. Corrections should be administered as per the PICU Electrolyte guideline. Even if Magnesium levels are optimal it can be beneficial to give a further correction dose as it has also been shown to successfully revert patients to a sinus rhythm.

Anaemia, Acidosis and Hypovolaemia

Haemoglobin should be within appropriate levels as this will improve oxygen delivery to tissues. Hypovolaemia should be treated if present. Acidosis should be treated but this should be balanced against the side-effects and likely increase in CO2 production that will result from the use of bicarbonate.


Inotropes are often necessary in the post-operative phase of cardiac surgery, but they may worsen JET. If possible, consideration should be made to reduce these. Dopamine and Adrenaline are particularly arrhythmogenic and have been associated with an increased risk of JET so should be reduced where possible (Hoffman et al. 2002).


If the rate of JET is relatively controlled (we suggest < 170 bpm) it may be possible to achieve AV synchrony using pacing. This is achieved by atrially pacing slightly above the JET rate which may restore AV synchrony and thereby improve ventricular filling and cardiac output. The pacing should be initiated in the atrium and therefore ideally be AAI (this may require setting the pacing box to ‘DDD’ mode without any Ventricular output). If there are underlying conduction defects or anti-arrhythmics present, then DDD mode (i.e. atrial and ventricular pacing) may be required, but this is likely to result in ventricular dysynchrony.


Amiodarone has shown to be effective in controlling the JET rate and reverting the rhythm back to sinus. It may also slow the rate enough to allow the use of pacing to restore synchrony. It slows the repolarisation period and refractory period of the SA and AV nodes, and the ventricles. It also inhibits the effects of adrenergics.

Our guideline suggests when the rate is over 170 bpm, and it is deemed necessary to treat, Amiodarone should be the first line treatment, rather than pacing or hypothermia.

Although the currently available evidence suggests giving a loading dose of Amiodarone 5mg/kg over 30 minutes is safe and not associated with haemodynamic compromise, we also accept that many clinicians working in the Paediatric Cardiac Intensive Care environment have personal experience of patients acutely deteriorating when a loading dose is given this quickly, and even to the point of having a cardiac arrest. We therefore advise that the rate of administration should be decided jointly, on a case-by-case basis, by the PICU Consultant and Cardiothoracic Surgeon on call. They may also seek the opinion of the Consultant Paediatric Cardiologist if needed. If a decision is made not to give the loading dose over 30 minutes and instead just start the infusion, we recommend that if the patient remains haemodynamically stable the team should consider increasing this rate as tolerated until 5mg/kg has infused and then reduce back to the standard infusion rate of between 10-20 micrograms/kg/minute. In special circumstances it may be appropriate to use even higher maintenance infusion rates of up to of 40micrograms/kg/minute e.g. children on ECMO.

As stated above there is often anxiety around the use of Amiodarone, but it is probably the most effective pharmacological agent we have for JET currently. Hypotension and bradycardia can occur, and the clinician should be prepared to treat these effects before its administration which would include connecting the pacing wires to a pacing box and setting it for back-up pacing if required. It is important to have corrected electrolyte imbalances where possible to help minimise adverse effects. Administration should ideally be via a central line and please note that pharmacy guidelines should be consulted when prescribing and administering Amiodarone – see http://www.leedsformulary.nhs.uk/docs/PICU%20amiodarone%20monograph.pdf?UNLID=6938595272020819151155
(Kovacikova et al. 2009, Perry et al. 1996) 


It is important to achieve normothermia in these patients. Pyrexia will increase tachycardia and metabolic demand and should be controlled. The use of hypothermia should further reduce the heart rate and metabolic demand but does so at the expense of recognised side-effects. These include reduced coagulation, reduced immunological function and healing ability, reduced cardiac contractility and increased systemic vascular resistance. Its use should be balanced against these side-effects on a case by case basis, but it is thought to improve JET both independently and when in combination with medication, such as amiodarone; though evidence for this is limited (Pfammatter et al. 1995).

It is suggested that cooling is to a core temperature of 33-35°C; this will require paralysis to achieve. Simple use of cold packs in an awake patient is of no benefit, cooling should be achieved using a cooling blanket. There is no evidence that a temperature of 32-33°C is more effective and may just increase side-effects but if there is resistant JET with haemodynamic instability it may be considered.


ECMO is the last but important option in the management of this condition. Given its complexities the use of ECMO should be considered early, but only once Amiodarone therapy has failed. The decision to put a patient on ECMO should only be done followed a full MDT discussion and explanation of the potential risks and benefits to the family.

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Record: 6938

The aim of this guideline is to improve understanding and early recognition of junctional ectopic tachycardia in children who have undergone congenital cardiac surgery, and to standardise its management in our hospital.

Clinical condition:

Junctional Ectopic Tachycardia

Target patient group:
Target professional group(s): Secondary Care Doctors
Adapted from:

Evidence base

ALI, T., MORRIS, K. and BARRY, P., 2010. Paediatric Intensive Care (Oxford Specialist Handbooks in Paediatrics). Oxford University.
ERICKSON, S.J., 2006. Guidelines for the management of junctional ectopic tachycardia following cardiac surgery in children. Current Paediatrics, vol. 16, no. 4, pp. 275-278.
HOFFMAN, T.M., BUSH, D.M., WERNOVSKY, G., COHEN, M.I., WIEAND, T.S., GAYNOR, J.W., SPRAY, T.L. and RHODES, L.A., 2002. Postoperative junctional ectopic tachycardia in children: incidence, risk factors, and treatment. The Annals of Thoracic Surgery, vol. 74, no. 5, pp. 1607-1611.
KIDSON, C. and LAFFERTY, N., 2020. Paediatric Intensive Care Unit (PICU), 14th January. Available from: https://www.clinicalguidelines.scot.nhs.uk/ggc-paediatric-guidelines/ggc-guidelines/cardiovascular-diseases/junctional-ectopic-tachycardia-jet-post-operative/
KOVACIKOVA, L., HAKACOVA, N., DOBOS, D., SKRAK, P. and ZAHOREC, M., 2009. Amiodarone as a first-line therapy for postoperative junctional ectopic tachycardia. The Annals of Thoracic Surgery, vol. 88, no. 2, pp. 616-622.
MIALL, L. Park’s The Pediatric Cardiology Handbook, Anonymous Seminars in Fetal and Neonatal Medicine, 2015.
PERRY, J.C., FENRICH, A.L., HULSE, J.E., TRIENMAN, J.K., FRIEDMAN, R.A. and LAMBERTI, J.J., 1996. Pediatric use of intravenous amiodarone: Efficacy and safety in critically III patients from a multicenter protocol. Journal of the American College of Cardiology, vol. 27, no. 5, pp. 1246-1250.
PFAMMATTER, J., PAUL, T., ZIEMER, G. and KALLFELZ, H.C., 1995. Successful management of junctional tachycardia by hypothermia after cardiac operations in infants. The Annals of Thoracic Surgery, vol. 60, no. 3, pp. 556-560.

Approved By

Trust Clinical Guidelines Group

Document history

LHP version 1.0

Related information

Consent was obtained from the parent of the child seen in the photographs in this guideline and this has been documented in that patient’s record.

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