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Tachyarrythmia originating from atrioventricular (AV) node, AV junction or proximal bundle of His is known as junctional tachycardia (JT) or junctional ectopic tachycardia (JET) which commonly occurs in infancy and childhood [1]. Broadly JT can be congenital or acquired. Post-operative JET is the most common acquired cause: hypoxia, dyselectronemia, digoxin toxicity are rare causes of junctional ectopic tachycardia. We report a rare case of JET where polyionotropes increased AV junction automaticity resulting in incessant JET.      

A 11-year-old male child with Ewing sarcoma and structurally normal heart was admitted with septic shock and desaturation to the pediatric intensive care unit. He was mechanically ventilated and started with ionotropes (dopamine and nor-adrenaline and adrenaline) along with empirical injectable antibiotics after obtaining blood culture. Next day, patient developed narrow complex regular tachycardia suggestive of junctional ectopic tachycardia (JET). Child developed acute kidney injury with serum creatinine of 1.6 mg/dL with normal serum Na+ and K+ level. Rapid bolus adenosine injection did not terminate the tachycardia. Patient was started with amiodarone infusion which reverted the rhythm after 6 hours of infusion. JET are sometimes incessant and also demonstrate even delayed response to broad spectrum anti-arrhythmic like amiodarone.  

Junctional ectopic tachycardia is a focal automatic tachycardia arising from AV node, AV junction or proximal His bundle. It occurs most commonly in infancy and childhood. Congenital form is rare, difficult to treat and associated with significant mortality [2]. Most common acquired JET is post-operative and occurs in 1 to 15% of pediatric cardiac surgery patients within 72 hours. Age less than 6 months, post-operative use of dopamine or milrinone, prolonged use of aortic cross-clamp and cardiopulmonary bypass, total surgical time, fever and dyselectronemia are the risk factors behind generation of JET [3-5]. It occurs more commonly in cardiac surgery that involves the crux of the heart including tetralogy of Fallot, AV canal, and ventricular septal defect repair, as well as repair of anomalous pulmonary venous return, arterial switch operation, Norwood procedure, and interrupted aortic arch repair. Fluid and electrolyte shifts, trauma, stretch, local edema, or ischemia in the region of the AV node or bundle of His are the proposed mechanism for post-operative JET. 

Beside all those proposed mechanisms, we report a rare case of incessant JET that developed after polyionotrope infusion suggesting the fact that ionotropes can also rarely increase automaticity of AV junction resulting in this incessant JET.

We report a rare case of polyionotrope induced junctional ectopic tachycardia in an adolescent child reminding us the fact that judicious use of multiple ionotropes in children may save a child from developing this incessant rhythm. Usually associated with hemodynamic deterioration, early reversal of this rhythm improves the hemodynamics and clinical outcome. 

Contributors: DA, DS: manuscript writing, patient management; JDG, SP: manuscript editing, patient management. DA will act as a study guarantor. All authors approved the final version of this manuscript and are responsible for all aspects of this study.

Funding: None; Competing interests: None stated.