PEDIATRICS Volume 141, number s5, April 2018:e20163792CASE REPORT

Within the pediatric population, ventricular tachycardia (VT) is a rare clinical entity, with an incidence of only 1.1 per 100 000 childhood years.1 In the absence of structural heart disease, the reentrant pathways typically responsible for VT in adults are uncommon in children. More commonly, focal areas of triggered automaticity and transmission are acquired during embryologic development and are believed to induce these nonreentrant VTs.2 The most common source of focal VT is in the right ventricular outflow tract (RVOT), and it accounts for ∼70% of cases.3

A variety of pharmacologic antiarrhythmic agents may be used to treat polymorphic VT. However, in cases of monomorphic VT originating from the RVOT, the successful use of adenosine and radiofrequency catheter ablation have both been described.4, 5 We describe our experience with an 11-year-old patient found to have right ventricular outflow tract ventricular tachycardia (RVOT-VT) who was successfully converted to sinus rhythm by using vagal maneuvers.

CASE PRESENTATION

An 11-year-old girl with a history of poorly controlled moderate persistent

asthma presented to the emergency department (ED) with respiratory distress and a rash. One day before presentation, the patient was seen in the same ED for a fever of 102°F and severe right-sided abdominal pain. She was discharged from the hospital in stable condition with a radiographic diagnosis of community-acquired pneumonia to be treated with oral antibiotics. Six hours after receiving her initial dose of azithromycin, the child developed an erythematous, lacy rash on her chest, combined with periorbital swelling and significant dyspnea. Despite receiving diphenhydramine, acetaminophen, and an albuterol nebulizer, the patient had only mild improvement in her symptoms. Persistence of symptoms prompted her return to the ED for further management.

On arrival to the ED, the patient was noted to have significant respiratory distress and hypoxia to 84% on room air. She received an albuterol-ipratropium nebulizer, which resulted in significant improvement in her respiratory distress and dyspnea. After the administration of albuterol, her heart rate initially rose to 170 beats per minute. It was later noted that the patient’s heart rate reached 220 beats per minute. Neither rhythm type nor

Vagal Termination of Ventricular Tachycardia in a Pediatric PatientKasey J. Chaszczewski, MD, Cyndi Sosnowski, MD, Rani Ganesan, MD

Ventricular tachycardia is a rare clinical entity in pediatric patients and typically requires chemical and/or electrical intervention to convert into a sustained sinus rhythm. However, for certain forms originating from the right ventricular outflow tract, conversion with adenosine and vagal maneuvers has been demonstrated in adult patients. In this case, we suggest that pediatric patients with right ventricular outflow tract ventricular tachycardia who are hemodynamically stable may benefit from a trial of vagal maneuvers.

abstract

To cite: Chaszczewski KJ, Sosnowski C, Ganesan R. Vagal Termination of Ventricular Tachycardia in a Pediatric Patient. Pediatrics. 2018;141(s5): e20163792

Department of Pediatrics, Rush University Medical Center, Chicago, Illinois

Dr Chaszczewski aided in the care of the clinical case and drafted the initial manuscript; Dr Sosnowski provided in-depth electrocardiographic review of the patient and reviewed and revised the manuscript; Dr Ganesan aided in the care of the clinical case and reviewed and revised the manuscript; and all authors approved the final manuscript as submitted.

DOI: https:// doi. org/ 10. 1542/ peds. 2016- 3792

Accepted for publication Oct 3, 2017

Address correspondence to Kasey J. Chaszczewski, MD, Department of Pediatrics, Rush University Medical Center, 1620 W Congress Pkwy, 457A Pavilion Building, Chicago, IL 60612. E-mail: kasey.j.chaszczewski@gmail.com

PEDIATRICS (ISSN Numbers: Print, 0031-4005; Online, 1098-4275).

Copyright © 2018 by the American Academy of Pediatrics

FINANCIAL DISCLOSURE: The authors have indicated they have no financial relationships relevant to this article to disclose.

FUNDING: No external funding.

POTENTIAL CONFLICT OF INTEREST: The authors have indicated they have no potential conflicts of interest to disclose.

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PEDIATRICS Volume 141, number s5, April 2018 S413

blood pressure during this heart rate were documented or reported. The child’s heart rate was later noted to be 130 beats per minute without documentation of any intervention. With persistence of hypoxia, the patient was transferred to our PICU for further management.

On arrival to the PICU, the child was noted to be afebrile with mild nasal flaring. Her lung examination revealed diminished breath sounds over the right lower lung fields without wheezing or a prolonged expiratory phase. Approximately 90 minutes after arrival, she became febrile to 104°F and had significantly worsened respiratory distress associated with diffuse inspiratory and expiratory wheezing. The patient received intravenous (IV) solumedrol and inhaled albuterol; this resulted in significant improvement in her respiratory status. Soon after, the patient abruptly developed a fixed tachycardia to 220 beats per minute. Bedside cardiac monitor tracings (Fig 1) were consistent with a nonsinus tachyarrhythmia with occasional fusion beats (Fig 2). The patient maintained normal blood pressure values and appropriate mentation. Additional and prolonged vagal maneuvers were attempted, including ice to the face, Valsalva maneuvers, coughing, and retching, which briefly

resulted in an unsustained sinus rhythm but quickly reverted back to a nonsinus tachyarrhythmia. Rapid IV adenosine bolus followed by a normal saline flush through a peripheral hand IV was attempted without effect. Ultimately, after the patient blew against her closed mouth while kicking against resistance, she converted and remained in sinus rhythm. The 12-lead electrocardiogram (ECG) obtained during the event (Fig 3) demonstrated wide QRS complexes consistent with VT.

The patient was kept relatively normothermic, and the use of inhaled β agonists was minimized. The patient experienced a second episode of wide, complex tachycardia, which again resolved with a significant coughing spell. First-line β blockade was avoided because of the patient’s history of poorly controlled asthma. Instead, verapamil was initiated for treatment. No structural abnormalities were identified on the echocardiogram, and VT was not reproduced on the stress testing after the initiation of verapamil. Before discharge, the patient tolerated test doses of inhaled levalbuterol without incident. She was discharged on hospital day 2, with scheduled pediatric cardiology and allergy and immunology visits for ongoing management. On follow-up evaluation

in the pediatric cardiology clinic at 2 weeks, the patient denied reports of any palpitations. The decision was made to continue to monitor her on medical therapy, with follow-up in 6 months or sooner if symptomatic.

DISCUSSION

The initial challenge of this case was the correct identification of the child’s tachyarrhythmia. Albuterol-induced supraventricular tachycardia (SVT) has been well described, 6 and intermittent conversion to sinus rhythm with vagal maneuvers is clinically consistent with this diagnosis. However, a few features of our patient’s ECG are not indicative of SVT and are consistent with RVOT-VT. First, SVT displays a rapid depolarization demonstrated by a rapid initial upstroke in the QRS complex. Alternatively, this upstroke is not as steep in VT and is more consistent with our patient’s dysrhythmia (Fig 3). Second, the presence of a fusion beat strongly supports the diagnosis of VT. A fusion beat occurs when a supraventricular impulse is conducted in an anterograde fashion through the atrioventricular (A-V) node and “fuses” with an impulse that has originated from the ventricles. Depolarization occurring from

FIGURE 1At the time the patient developed a fixed tachycardia to 220 beats per minute, the bedside cardiac monitoring strip revealed a wide complex tachyarrhythmia.

FIGURE 2While the patient’s wide complex tachycardia persisted, the bedside cardiac monitoring strip revealed intermittent fusion beats (arrow) consistent with VT.

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simultaneous supraventricular and ventricular beats yields a QRS complex with an intermediate duration (Fig 2) and implies A-V dissociation.

Although it is a cornerstone of abortive therapy for SVT, adenosine is rarely used or effective in VT. However, adenosine’s ability to abort RVOT-VT has been demonstrated in multiple human and animal models.5, 7, 8 In supraventricular tissue, adenosine directly activates G-protein–coupled potassium influx channels. In turn, these channels hyperpolarize sinoatrial nodal cells and decrease action potential duration in A-V nodal tissue, yielding negative chronotropic and dromotropic effects, respectively.9 However, these G-protein–coupled potassium channels are not expressed in the ventricular myocardium. As a result, adenosine does not have a direct effect on the resting membrane potential or action potential duration in ventricular myocardium. Adenosine’s clinical efficacy in

RVOT-VT is presumed to be a result of its indirect role in antagonizing the stimulatory effects of cyclic adenosine monophosphate on the calcium current and β-adrenergy on potassium and chloride channels.10, 11 This adrenergic mechanism is further supported in electrophysiologic studies in which researchers were able to induce VT with catecholamine facilitation and then abort it using adenosine therapy.8 Our patient’s presentation of VT is consistent with the previously mentioned electrophysiologic studies because her arrhythmia occurred after albuterol administration. Considering adenosine’s action on RVOT-VT, our patient’s arrhythmia would have been expected to respond to IV adenosine. However, given its exceptionally short half-life, it is likely that her peripheral IV catheter was too distal to permit adequate drug action at the myocardial level. Alternatively, the use of adenosine at higher doses through a centrally placed IV line may have

converted our patient’s arrhythmia to a normal sinus rhythm.

In addition to increased sympathetic stimulation, an elevated temperature has also been demonstrated to induce VT in pediatric patients with a history of RVOT-VT.12 In the case of a 7-year-old child with a history of RVOT-VT during a febrile illness, isoproterenol infusion alone resulted in a sinus tachycardia to 190 beats per minute. While the child was afebrile, the rhythm remained sinus. It was postulated that in addition to increased adrenergic activity, the patient’s fever also produced a surge of inflammatory cytokines that contributed to increased RVOT automaticity. In our case, the patient was febrile during her episode of VT, which is consistent with the previously mentioned case report’s hypothesis of a significant role for inflammatory cytokines.12 Lerman13 has also described the utility of vagal maneuvers in adult patients with RVOT-VT. The mechanism

FIGURE 312-lead ECG obtained during the acute event reveals a wide complex tachycardia with intermittent sinus beats (solid arrow) that occurred during vagal maneuvers, followed by PVCs (dotted arrow) and then progression to VT. PVC, premature ventricular contraction.

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of these maneuvers is mediated by acetylcholine release, which serves to decrease cyclic adenosine monophosphate and β-adrenergic stimulation of the ventricular myocardium, similar to adenosine.14 Our patient represents the first described case of vagal termination of RVOT-VT in the pediatric literature.

CONCLUSIONS

We report the first documented case of vagal termination of VT in the pediatric population. Although the use of adenosine and radiofrequency catheter ablation has been detailed for the treatment of pediatric patients with RVOT-VT, pediatric patients who are hemodynamically stable with intact mental status may benefit from trials of vagal maneuvers in suspected RVOT-VT.

REFERENCES

1. Roggen A, Pavlovic M, Pfammatter JP. Frequency of spontaneous ventricular tachycardia in a pediatric population. Am J Cardiol. 2008;101(6):852–854

2. Markowitz SM, Weinsaft JW, Waldman L, et al. Reappraisal of cardiac magnetic resonance imaging in idiopathic outflow tract arrhythmias. J Cardiovasc Electrophysiol. 2014;25(12):1328–1335

3. 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. 1999;33(7):2067–2072

4. Millane T, Hawker RE, Lau KC. Radiofrequency catheter ablation of right ventricular outflow tract tachycardia in a preschooler. Pediatr Cardiol. 1999;20(2):143–146

5. Lerman BB, Belardinelli L, West GA, Berne RM, DiMarco JP. Adenosine-sensitive ventricular tachycardia: evidence suggesting cyclic AMP-mediated triggered activity. Circulation. 1986;74(2):270–280

6. Cook P, Scarfone RJ, Cook RT. Adenosine in the termination of albuterol-induced supraventricular tachycardia [published correction appears in Ann Emerg Med. 1995;25(1):119]. Ann Emerg Med. 1994;24(2):316–319

7. Griffith MJ, Garratt CJ, Rowland E, Ward DE, Camm AJ. Effects of intravenous adenosine on verapamil-sensitive “idiopathic”

ventricular tachycardia. Am J Cardiol. 1994;73(11):759–764

8. Lerman BB, Ip JE, Shah BK, et al. Mechanism-specific effects of adenosine on ventricular tachycardia. J Cardiovasc Electrophysiol. 2014;25(12):1350–1358

9. Wieland T, Lutz S, Chidiac P. Regulators of G protein signalling: a spotlight on emerging functions in the cardiovascular system. Curr Opin Pharmacol. 2007;7(2):201–207

10. Isenberg G, Belardinelli L. Ionic basis for the antagonism between adenosine and isoproterenol on isolated mammalian ventricular myocytes. Circ Res. 1984;55(3):309–325

11. Belardinelli L, Shryock JC, Song Y, Wang D, Srinivas M. Ionic basis of the electrophysiological actions of adenosine on cardiomyocytes. FASEB J. 1995;9(5):359–365

12. Fujita S, Nakayama Y, Usuda K, Hanaoka R, Yamada K, Hatasaki K. Catheter ablation for right ventricular outflow tract ventricular tachycardia induced by fever in a 7-year-old girl. Pediatr Cardiol. 2010;31(1):128–131

13. Lerman BB. Response of nonreentrant catecholamine-mediated ventricular tachycardia to endogenous adenosine and acetylcholine. Evidence for myocardial receptor-mediated effects. Circulation. 1993;87(2):382–390

14. Linden J, Hollen CE, Patel A. The mechanism by which adenosine and cholinergic agents reduce contractility in rat myocardium. Correlation with cyclic adenosine monophosphate and receptor densities. Circ Res. 1985;56(5):728–735

ABBREVIATIONS

A-V:  atrioventricularECG:  electrocardiogramED:  emergency departmentIV:  intravenousRVOT:  right ventricular outflow

tractRVOT-VT:  right ventricular

outflow tract ventricu-lar tachycardia

SVT:  supraventricular tachycardia

VT:  ventricular tachycardia

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DOI: 10.1542/peds.2016-37922018;141;S412Pediatrics 

Kasey J. Chaszczewski, Cyndi Sosnowski and Rani GanesanVagal Termination of Ventricular Tachycardia in a Pediatric Patient

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Kasey J. Chaszczewski, Cyndi Sosnowski and Rani GanesanVagal Termination of Ventricular Tachycardia in a Pediatric Patient

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