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Table of Contents
Year : 2012  |  Volume : 15  |  Issue : 3  |  Page : 224-228
Dexmedetomidine controls junctional ectopic tachycardia during Tetralogy of Fallot repair in an infant

1 Department of Anesthesiology, Nationwide Children's Hospital, 700 Children's Drive, Columbus, OH 43105, USA
2 Department of Cardiothoracic Surgery and The Heart Center, Nationwide Children's Hospital, 700 Children's Drive, Columbus, OH 43105, USA
3 Department of Anesthesiology and Pediatrics, Nationwide Children's Hospital, 700 Children's Drive, Columbus, OH 43105, USA

Click here for correspondence address and email

Date of Submission17-Jan-2012
Date of Acceptance14-Apr-2012
Date of Web Publication4-Jul-2012


Dexmedetomidine is a highly selective α2 -adrenergic agonist approved for short-term sedation and monitored anesthesia care in adults. Although not approved for use in the pediatric population, an increasing number of reports describe its use in pediatric patients during the intraoperative period and in the intensive care unit. Dexmedetomidine can potentially have an adverse impact on the cardiovascular system secondary to its negative chronotropic and dromotropic effects. However, it is these cardiac effects that are currently being explored as a therapeutic option for the treatment of perioperative tachyarrhythmias in pediatric patients with congenital heart disease (CHD). We report the use of dexmedetomidine to treat junctional ectopic tachycardia (JET), which developed following cardiopulmonary bypass for surgical correction of Tetralogy of Fallot in a 6-week-old infant. Within 15 min of increasing the dexmedetomidine infusion from 0.5 to 3 μg/kg/h, JET converted to normal sinus rhythm. This case report provides additional anecdotal evidence that dexmedetomidine may have a therapeutic role in the treatment of perioperative tachyarrhythmias in pediatric patients with CHD. The specific effects of dexmedetomidine on the cardiac conduction system are reviewed followed by a summary of previous reports describing its use as a therapeutic agent to treat perioperative arrhythmias.

Keywords: Congenital heart disease, Dexmedetomidine, Junctional ectopic tachycardia

How to cite this article:
LeRiger M, Naguib A, Gallantowicz M, Tobias JD. Dexmedetomidine controls junctional ectopic tachycardia during Tetralogy of Fallot repair in an infant. Ann Card Anaesth 2012;15:224-8

How to cite this URL:
LeRiger M, Naguib A, Gallantowicz M, Tobias JD. Dexmedetomidine controls junctional ectopic tachycardia during Tetralogy of Fallot repair in an infant. Ann Card Anaesth [serial online] 2012 [cited 2021 Nov 27];15:224-8. Available from:

   Introduction Top

Postoperative tachyarrhythmias, including junctional ectopic tachycardia (JET), are often encountered after surgery for congenital heart disease (CHD) and may be associated with significant morbidity and even mortality. [1],[2],[3],[4] JET can be one of the most resistant and life-threatening arrhythmias. In a prospective analysis, the incidence of JET after surgery for CHD was 8%, with an increased risk in younger patients, in patients with longer ischemic times and in patients with higher inotropic scores. [1] Postoperative arrhythmias can lead to rapid hemodynamic instability, requiring urgent treatment.

Unfortunately, junctional tachyarrhythmias can be difficult to treat. The current first-line pharmacologic agents may be ineffective or may have significant adverse effects. [5],[6] Nonpharmacologic measures that have been reported include therapeutic hypothermia or the use of mechanical support, which may in themselves have serious consequences. [7],[8] As such, alternative and novel therapeutic interventions may offer benefits in the treatment of this potentially refractory postoperative arrhythmia.

Dexmedetomidine is a highly selective α2 -adrenergic agonist. Although not currently Food and Drug Administration (FDA) approved for the pediatric population, it has been shown to be effective in various clinical scenarios in CHD patients. Uses include sedation during mechanical ventilation, prevention of procedure-related anxiety, emergence delirium and shivering after anesthesia, and the treatment of withdrawal. [9] We describe the use of dexmedetomidine for the treatment of intraoperative JET in a 6-week-old infant following CPB for Tetralogy of Fallot (TOF) repair. The specific effects of dexmedetomidine on the cardiac conduction system are reviewed followed by a summary of previous reports describing the use of dexmedetomidine as a therapeutic agent to treat perioperative arrhythmias.

   Case Report Top

A 6-week-old, 4 kg infant presented for TOF repair. The patient's past medical history was significant for DiGeorge Syndrome, myelomeningocele (repaired), Arnold- Chiari malformation More Details status post ventriculoperitoneal shunt placement, a right-sided aortic arch and agenesis of the right kidney. Additionally, there was dysplasia of the pulmonary valve resulting in a dilated main pulmonary artery causing bronchial compression with respiratory compromise in the supine position. Preoperative computed tomography scan revealed marked enlargement of the pulmonary arteries with moderate narrowing (50%) of the left mainstem bronchus in the expiratory phase in both the supine and the prone positions. Because of these issues, the infant had been hospitalized since birth. There was a baseline oxygen requirement of 2 L/min via a high-flow nasal cannula to maintain an oxygen saturation greater than 90%. Preoperatively, the patient's hemodynamic status was stable with a normal sinus rhythm (NSR), a heart rate (HR) of 159 bpm and a blood pressure (BP) of 86/40 mmHg. The preoperative hemoglobin was 11.1 g/dL.

The patient was held nil per os for 4 h and transported to the operating room where routine American Society of Anesthesiologists' monitors were placed. Anesthetic induction was carried out with fentanyl (5 μg/kg) administered via a preexisting 24-gauge peripheral intravenous cannula and inhaled sevoflurane. Tracheal intubation was facilitated with pancuronium (0.25 mg/ kg). The patient's trachea was intubated with a cuffed 3.0 mm endotracheal tube. Following tracheal intubation, two 22-gauge peripheral intravenous cannulae and a 22-gauge right radial arterial cannula were placed. Maintenance anesthesia included isoflurane, fentanyl (25 μg/kg administered prior to CPB) and a dexmedetomidine infusion of 0.5 μg/kg/h. During prebypass period, the patient's hemodynamic status was stable with a NSR, a HR of 152 bpm and a BP of 56/24 mmHg. During the initiation of CPB, phenylephrine was administered for a BP of 30-40/20-30 mmHg. CPB was carried out at a temperature of 28°C. Two units of packed red blood cells were administered during CPB. The TOF was repaired with a transannular patch, augmentation of the right ventricular outflow tract, patch closure of the VSD and primary closure of the patent foramen ovale during a total CPB time of 117 min and an aortic cross-clamp time of 78 min. After release of the aortic cross-clamp, a loading dose of magnesium sulfate and of milrinone was administered.

Within several minutes of releasing the aortic cross-clamp, the rhythm changed from NSR to JET, with an increase of the HR to 190-200 bpm and a decrease of the mean arterial pressure (MAP) to 27 mmHg. Dampening of both the arterial and the pulse oximetry waveforms was noted. Because the patient was still on CPB support, no adenosine was administered and cardioversion was not attempted. Instead, the dexmedetomidine infusion was increased from its baseline of 0.5 to 3 μg/kg/h. Within 15 min, the rhythm converted to a NSR, the HR decreased to 152 bpm while the MAP increased to 43 mmHg. With the return of a NSR, the arterial and pulse oximetry waveforms improved. The dexmedetomidine infusion was decreased to 1 μg/kg/min and the patient was weaned from CPB without the need for additional inotropic support. The dexmedetomidine infusion was then titrated down to 0.5 μg/kg/min.

After CPB, a milrinone infusion was started at 0.25 μg/ kg/ min. A 10 mL/kg fluid bolus was administered for a low BP and postoperative coagulation dysfunction was treated with cryoprecipitate and platelets. The remainder of the intraoperative course was uneventful. Postoperatively, the infant was transported to the cardiothoracic intensive care unit (CTICU) with the dexmedetomidine infusion at 0.5 μg/kg/h and milrinone at 0.25 μg/kg/min. Hemodynamic function was stable upon arrival to the CTICU, with a NSR, a HR of 149 bpm and a BP of 70/51 mmHg. The dexmedetomidine infusion was discontinued the next morning. On postoperative Day (POD) #2, vasopressin was started to treat a low systolic BP. By POD #3, all inotropic medications had been discontinued and the patient's trachea was extubated on POD #4. The remainder of the postoperative course was uneventful.

   Discussion Top

When considering the adverse effect profile of dexmedetomidine, its effects on HR and BP have generally been the focal point. The incidence of bradycardia is increased when dexmedetomidine is administered with other medications that possess negative chronotropic effects (propofol, B-blockers, succinylcholine, digoxin, pyridostigmine), in scenarios when the negative chronotropic effects of a drug may be exaggerated (hypothermia or during vagotonic procedures such as laryngoscopy) and following large or rapid bolus doses. [9] Although generally of limited concern in the pediatric population, the potential impact of these negative chronotropic effects is illustrated by anecdotal reports of mortality in adult patients with co-morbid cardiovascular conditions and asystole unresponsive to therapy in a pediatric patient during lung transplant. [10],[11],[12] However, the exact role that dexmedetomidine played in these adverse outcomes remains controversial and anecdotal.

The negative chronotropic effects of dexmedetomidine have been used as a therapeutic maneuver in various clinical scenarios. Anecdotally, the negative chronotropic effects of dexmedetomidine have been used to treat tachycardia during off-pump coronary artery bypass surgery or in a preemptive fashion to decrease the incidence of postoperative tachyarrhythmias. [13],[14] In our patient, who developed JET following CPB for TOF repair, an increase of the dexmedetomidine infusion from 0.5 to 3 μg/kg/h was temporally associated with a conversion to NSR within 15 min and the resolution of the hypotension. Previous data support the potential use of dexmedetomidine as a therapeutic agent to treat perioperative arrhythmias in the pediatric population [Table 1]. [15],[16],[17],[18],[19] Chrysostomou et al. were the first to suggest the potential therapeutic role of dexmedetomidine in their retrospective review of the use of dexmedetomidine to treat 14 pediatric patients with tachyarrhythmias. [15] Dexmedetomidine was used as a primary drug in nine patients and as a rescue drug in five others when primary treatment had failed (amiodarone or amiodarone and hypothermia). Arrhythmias included JET, junctional accelerated rhythm, atrial ectopic tachycardia and supraventricular tachycardia (SVT) and atrial flutter (AF). Dexmedetomidine was administered as a continuous infusion starting at 0.5-2 μg/kg/h unless an immediate effect was considered necessary, in which case a loading dose of 0.5-1 μg/kg was administered. The end points of the study were conversion to NSR within 3 min for SVT, within 2 h for all other arrhythmias or a decrease in HR significant enough to improve hemodynamic function. Dexmedetomidine was effective in all six patients with JET, with a decrease of the mean HR from 197 ± 22 to 165 ± 17 bpm. Five of these patients received dexmedetomidine as a first-line agent and one as a rescue treatment. All four patients with SVT converted to NSR. One patient with AF who failed amiodarone received a bolus dose of dexmedetomidine, but did not respond and required electrical cardioversion. Overall, the primary outcome was achieved in 13 of 14 patients. Adverse effects were seen in four patients, three with hypotension responding to the administration of fluid and one with a brief episode of complete AV block. Nine patients were transiently paced during the administration of dexmedetomidine to improve AV synchrony.
Table 1: Anecdotal experience with dexmedetomidine to treat perioperarive tachyarrhythmias

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The same investigators evaluated the preemptive potential of dexmedetomidine in preventing postoperative arrhythmias in a cohort of 32 pediatric patients undergoing surgery for CHD and compared the outcomes to 20 patients who did not receive dexmedetomidine. [17] Dexmedetomidine was started after the induction of anesthesia, continued intraoperatively and postoperatively for 38 ± 4 h at an average dose of 0.76 ± 0.04 μg/kg/h. Sustained postoperative arrhythmias occurred in 10 control patients compared with two patients who received dexmedetomidine (P = 0.001). This included a 25% versus 0% (P = 0.01) incidence of ventricular tachycardia and a 25% versus 6% (P = 0.05) incidence of supraventricular arrhythmias. Transient complete heart block occurred in two control patients and in one patient who received dexmedetomidine. Control patients had a higher heart rate (141 ± 5 versus 127 ± 3 bpm, P = 0.03), more episodes of sinus tachycardia (40% versus 6%; P = 0.008), required more postoperative fentanyl (39 ± 8 versus 19 ± 3 μg/kg; P = 0.005) and greater doses of antihypertensive agents, including nitroprusside (20 ± 7 versus 4 ± 1 μg/kg; P = 0.004) and nicardipine (13 ± 5 versus 2 ± 1 μg/kg; P = 0.02).

Anecdotal success in isolated case reports has also been described with the use of dexmedetomidine to treat stable ventricular tachycardia and postoperative SVT. [16],[18],[19] One of these patients had required extracorporeal life support (ECLS) related to the postoperative arrhythmia following total cavopulmonary anastomosis. [19] While on ECLS, dexmedetomidine was administered, resulting in the conversion to NSR and the ability to wean from ECLS.

Additional information and somewhat conflicting reports regarding the chronotropic and dromotropic effects of dexmedetomidine have been provided by two different groups of investigators. [20],[21] Hammer et al. evaluated hemodynamic and electrophysiologic variables before and after the administration of dexmedetomidine in 12 children. [20] Dexmedetomidine was administered as a loading dose of 1 μg/kg followed by a continuous infusion at 0.7 μg/kg/h. In addition to a decrease in HR, dexmedetomidine depressed sinus and AV node function with a prolongation of sinus node recovery time and a lengthening of AV node block cycle and the PR interval. No change was noted in atrial or ventricular muscle refractory times. The authors cautioned against the use of dexmedetomidine during electrophysiologic studies, given that it may cause undesirable and misleading measurements as well as interfere with the ability to induce arrhythmias. They also cautioned against its use in patients at risk for bradycardia or with underlying AV or sinus node dysfunction.

A broader picture of the effect of dexmedetomidine on the cardiac conduction system is provided by a subsequent study that investigated changes noted on the surface electrocardiogram. [21] ECGs obtained on a cohort of 51 pediatric patients who received dexmedetomidine for sedation were compared with a retrospective cohort of patients who had not received dexmedetomidine. Neonates and infants had a greater decrease in the HR compared with older children, while other parameters were similar. Although changes were noted in various electrophysiologic parameters, including the PR interval, PRc, PR index and the QRS interval, these changes were determined to be related to changes in HR and not related to a direct effect of dexmedetomidine on cardiac conduction. When the changes in the ECG intervals and HR were compared with the control group who had not received dexmedetomidine, there were no differences. Therefore, the authors speculated that the changes likely reflected the normal postoperative course following cardiothoracic surgery and CPB. The authors speculated that their findings were different from those of Hammer et al., as the previous study had a much smaller cohort, did not consider the impact of HR changes on the ECG intervals and had baseline anesthesia with propofol and ketamine, which may have impacted the findings.

The precise mechanism for its antiarrhythmic properties has not been fully elucidated. Dexmedetomidine administration results in activation of central presynaptic α2A -adrenergic receptors in the locus cereleus leading to activation of G proteins. This causes a decrease in adenylate cyclase activity, which decreases cyclic adenosine monophosphate and ultimately decreases norepinephrine release. The decrease in heart rate seen with dexmedetomidine administration may be a combination of the decrease in the sympathetic outflow from the central nervous system and a reflex response at the sinus node to peripheral vasoconstriction. It is unknown whether the cardiac effects are related to the α2A -adrenergic receptors in the central nervous system and α2B -adrenergic receptors in the peripheral vasculature or whether direct interaction with receptors in the heart are involved. The antiarrhythmic properties of dexmedetomidine may be secondary to stimulation of α2A -adrenergic receptors in the dorsal motor nucleus in the vagus nerve thereby increasing vagal efferent output to the myocardium. [22] Enhanced vagal output prolongs the effective refractory period of myocardial cells, inhibits ventricular automaticity and provides an anti-arrhythmic effect. [22],[23]

In summary, we provide additional anecdotal evidence of the potential efficacy of dexmedetomidine as a therapeutic agent for the control of arrhythmias in the perioperative period in pediatric patients with CHD. In our patient, JET occurred following CPB and repair of Tetralogy of Fallot. Conversion to NSR occurred within 15 min of increasing the dexmedetomidine infusion from 0.5 to 3 μg/kg/h. According to the manufacturer's recommendations for procedural and ICU sedation, a loading infusion of 0.5-1 μg/kg should be administered over 10 min followed by a maintenance infusion of 0.2-1 μg/kg/h guided by the desired clinical effect. For use as an anti-arrhythmic agent, Chrysostomou et al. used an infusion of 0.5-2 μg/kg/h unless an immediate effect was needed, in which case they gave a loading dose of 0.5-1 μg/kg. In our patient, by increasing the infusion to 3 μg/kg/h for 15 min, an effective bolus of 0.75 μg/kg was administered over the 15-min time period. Although anecdotal, the accumulating evidence suggests the potential utility of dexmedetomidine in both preventing and treating arrhythmias following surgery for CHD. Future controlled trials are needed to better address its utility in these scenarios.

   References Top

1.Batra AS, Chun DS, Johnson TR, Maldonado EM, Kashyap BA, Maiers J, et al. A prospective analysis of the incidence and risk factors associated with junctional ectopic tachycardia following surgery for congenital heart disease. Pediatr Cardiol 2006;27:51-5.  Back to cited text no. 1
2.Andreasen JB, Johnsen SP, Ravn HB. Junctional ectopic tachycardia after surgery for congenital heart disease in children. Intensive Care Med 2008;34:895-902.  Back to cited text no. 2
3.Pfammatter JP, Bachmann DC, Wagner BP, Pavlovic M, Berdat P, Carrel T, et al. Early postoperative arrhythmias after open-heart procedures in children with congenital heart disease. Pediatr Crit Care Med 2001;2:217-22.  Back to cited text no. 3
4.Mildh L, Hiippala A, Rautiainen P, Pettilä V, Sairanen H, Happonen JM. Junctional ectopic tachycardia after surgery for congenital heart disease: incidence, risk factors and outcome. Eur J Cardiothorac Surg 2011;39:75-80.  Back to cited text no. 4
5.Karacan M, Olgun H, Becit N. Successful use of intravenous amiodarone in a child with combined postoperative junctional and ectopic tachycardias. Cardiol Young 2009;19:407-9.  Back to cited text no. 5
6.Bronzetti G, Formigari R, Giardini A, Frascaroli G, Gargiulo G, Picchio FM. Intravenous flecainide for the treatment of junctional ectopic tachycardia after surgery for congenital heart disease. Ann Thorac Surg 2003;76:148-51; discussion 151.  Back to cited text no. 6
7.Jhang WK, Lee SC, Seo DM, Park JJ. Mechanical circulatory support to control medically intractable arrhythmias in pediatric patients after cardiac surgery. Korean Circ J 2010;40:471-4.  Back to cited text no. 7
8.Kelly BP, Gajarski RJ, Ohye RG, Charpie JR. Intravenous induction of therapeutic hypothermia in the management of junctional ectopic tachycardia: a pilot study. Pediatr Cardiol 2010;31:11-7.  Back to cited text no. 8
9.Tobias JD, Gupta P, Naguib A, Yates AR. Dexmedetomidine: Applications in the pediatric patient with congenital heart disease. Pediatr Cardiol 2011;32:1075-87.  Back to cited text no. 9
10.Ingersoll-Weng E, Manecke GR Jr, Thistlethwaite PA. Dexmedetomidine and cardiac arrest. Anesthesiology 2004;100:738-9.  Back to cited text no. 10
11.Sichrovsky TC, Mittal S, Steinberg JS. Dexmedetomidine sedation leading to refractory cardiogenic shock. Anesth Analg 2008;106:1784-6.  Back to cited text no. 11
12.Zhang X, Schmidt U, Wain JC, Bigatello L. Bradycardia leading to asystole during dexmedetomidine infusion in an 18 year-old double-lung transplant recipient. J Clin Anesth 2010;22:45-9.  Back to cited text no. 12
13.Ruesch S, Levy JH. Treatment of persistent tachycardia with dexmedetomidine during off-pump cardiac surgery. Anesth Analg 2002;95:316-8.  Back to cited text no. 13
14.Jalonen J, Hynynen M, Kuitunen A, Heikkilä H, Perttilä J, Salmenperä M, et al. Dexmedetomidine as an anesthetic adjunct in coronary artery bypass grafting. Anesthesiology 1997;86:331-45.  Back to cited text no. 14
15.Chrysostomou C, Beerman L, Shiderly D, Berry D, Morell VO, Munoz R. Dexmedetomidine: a novel drug for the treatment of atrial and junctional tachyarrhythmias during the perioperative period for congenital cardiac surgery: a preliminary study. Anesth Analg 2008;107:1514-22.  Back to cited text no. 15
16.Parent BA, Munoz R, Shiderly D, Chrysostomou C. Use of dexmedetomidine in sustained ventricular tachycardia. Anaesth Intensive Care 2010;38:781.  Back to cited text no. 16
17.Chrysostomou C, Sanchez-de-Toledo J, Wearden P, Jooste EH, Lichtenstein SE, Callahan PM, et al. Perioperative use of dexmedetomidine is associated with decreased incidence of ventricular and supraventricular tachyarrhythmias after congenital cardiac operations. Ann Thorac Surg 2011;92:964-72; discussion 972.  Back to cited text no. 17
18.Ohsugi E, Nagamine Y, Ohtsuka M. The effect of dexmedetomidine in a child with intractable supraventricular tachyarrhythmias after total cavopulmonary connection. Masui 2011;60:493-5.  Back to cited text no. 18
19.Delwadia S, Naguib A, Tobias J. Dexmedetomidine controls supraventricular tachycardia following cardiac surgery in a child. World J Pediatr Cong Heart Surg. [In Press].  Back to cited text no. 19
20.Hammer GB, Drover DR, Cao H, Jackson E, Williams GD, Ramamoorthy C, et al. The effects of dexmedetomidine on cardiac electrophysiology in children. Anesth Analg 2008;106:79-83.  Back to cited text no. 20
21.Chrysostomou C, Komarlus R, Lichtenstein S, Shiderly D, Arora G, Orr R, et al. Electrocardiographic effects of dexmedetomidine in patients with congenital heart disease. Intensive Care Med 2010;36:836-42.   Back to cited text no. 21
22.Kamibayashi T, Hayashi Y, Mammoto T, Yamatodani A, Sumikawa K, Yoshiya I. Role of the vagus nerve in the antidysrhythmic effect of dexmedetomidine on halothane/epinephrine dysrhythmias in dogs. Anesthesiology 1995;83:992-9.  Back to cited text no. 22
23.Hayashi Y, Sumikawa K, Maze M, Yamatodani A, Kamibayashi T, Kuro M, et al. Dexmedetomidine prevents epinephrine induced arrhythmias through stimulation of central alpha two adrenoreceptors in halothane anesthestized dogs. Anesthesiology 1991;75:113-7.  Back to cited text no. 23

Correspondence Address:
Michelle LeRiger
Department of Anesthesiology and Pain Medicine, Nationwide Children's Hospital, 700 Children's Drive, Columbus, OH 43105
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-9784.97978

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