ILLUSTRATIVE CASE

Reentry Tachycardia in Children

Adenosine Can Make It Worse
Maximilian D. Hien, MD,*† Fernando Benito Castro, MD,† Philippe Fournier, MD,†
Anne Filleron, MD,† and Tu-Anh Tran, PhD†
presence of a delta wave. Echocardiography was normal and a
Objectives: We report on a rare but severe complication of adenosine use treatment with flecainide was introduced to prevent recurrence
in a child with reentry tachycardia. of atrial fibrillation (AF).
Methods and Results: Treatment with adenosine, which is the standard
medical therapy of atrioventricular reentry tachycardia, led to the develop-
Patient History
ment of an irregular wide complex tachycardia, caused by rapid ventricular
response to atrial fibrillation. The girl was finally stabilized with electrical The girl had been diagnosed with a Wolff-Parkinson-White
cardioversion. We analyze the pathomechanism and discuss possible (WPW) syndrome in 2011 after a first episode of SVT, terminated
treatment options. by vagal stimulation. Treatment with acebutolol had been initi-
Conclusions: Atrial fibrillation, as well as its conduction to the ventri- ated. Similar incidents of tachycardia had occurred roughly once
cles, can be caused by adenosine. Rapid ventricular response in children per month, lasting 1 to 2 minutes and ended spontaneously or with
with Wolff-Parkinson-White syndrome is more frequent than previously vagal maneuvers. Electrophysiological ablation had been sched-
believed. A patient history of atrial fibrillation is a contraindication for car- uled at the age of 15 years.
dioversion with adenosine and needs to be assessed in children with reentry
tachycardia. High-risk patients may potentially profit from prophylactic DISCUSSION
comedication with antiarrhythmic agents, such as flecainide, ibutilide, or Supraventricular reentry tachycardia is the most common
vernakalant, before adenosine administration. rhythm disturbance in children, with AVRT accounting for two
Key Words: irregular wide complex tachycardia, Wolff-Parkinson-White,
thirds of these cases.3 Atrioventricular reentry tachycardia is most
atrial fibrillation, rapid ventricular response, adenosine
commonly associated with the WPW syndrome, which is esti-
mated to develop in 35% of the children who present a WPW pat-
(Pediatr Emer Care 2016;00: 00–00) tern.4 The WPW pattern is a condition of ventricular preexcitation
via an accessory conduction pathway (AP) bypassing the atrioven-
CASE tricular (AV) node. It is expected to be present in 0.07% to 0.25%
A 12-year-old girl was taken to our pediatric emergency of the general population.5,6 Most children with WPW syndrome
department presenting with palpitations due to tachycardia at are diagnosed after a first episode of AVRT.
245 bpm. She was conscious and did not present clinical signs of Mortality rates of WPW syndrome are reported at 0.02% to
hemodynamic instability with a blood pressure of 105/60 mm Hg. 0.6% per year,7 with pediatric data being scarce. The vital risk is
The initial electrocardiogram (ECG) (Fig. 1) revealed sup- determined by degradation of AVRT to AF and immediate con-
raventricular reentry tachycardia (SVT) with the typical features duction to the ventricles by the AP in anterograde direction, caus-
of atrioventricular reentry tachycardia (AVRT). Several at- ing rapid ventricular response at rates of 150 to 300 bpm, risking
tempts of converting AVRT to normal sinus rhythm by vagal ventricular fibrillation and heart failure.8–10
maneuvers failed. Chemical cardioversion1 with a bolus of aden- Although most published cases of AVRT degenerating to AF
osine 0.05 mg/kg was ineffective and was repeated with in children are reports from electrophysiological studies where ar-
0.1 mg/kg. Instead of terminating SVT, the patient rhythm turned rhythmia is induced artificially,11 we report on a child with WPW
abruptly into an irregular wide complex tachycardia of approxi- AVRT, which developed AF and rapid ventricular response after
mately 240 bpm (Fig. 2). The patient's clinical state permitted a adenosine treatment in the emergency department, leading to
second line pharmacological treatment. Amiodarone 5 mg/kg signs of hemodynamic decompensation.
was administered slowly under monitoring,1 without effect. Adenosine is the agent of choice to differentiate SVT patho-
The patient now reported chest pain and showed signs of de- mechanisms.1 Although adenosine is effective in 93% to 99% of
compensation with persisting tachycardia and a blood pressure of the cases,12 the clinician in the emergency department needs to
79/52 mm Hg. Electric cardioversion after sedation was per- be aware of the risk that wide-complex tachycardia may develop
formed at 1 J/kg, instantaneously converting the irregular wide instead of a temporary block of AV nodal activity.
complex tachycardia into sinus rhythm at 90 bpm (Fig. 3), with Two mechanisms have to be outlined in this context:
Activation of adenosine A1-receptors induces AV nodal hy-
perpolarization for several seconds. A similar effect exists on
From the *Department of Pediatrics, Heidelberg University Children's Hospital,
Heidelberg, Germany; and †Department of Pediatrics, Nîmes University Hospi-
atrial and AP tissue, causing shortening of the action potential
tal, Nîmes, France and refractory period of atrial cells, thus inducing the develop-
Disclosure: The authors declare no conflict of interest. ment of AF.13,14 Atrial fibrillation of this origin should normally
All authors have contributed to the conception of this illustrative case, drafting be quickly self-limiting and without clinical impact. However, the
of the manuscript, reviewing and revising the manuscript and have
approved the submitted final version.
presence of an AP with bidirectional conduction capacity com-
Written informed consent was obtained from the parents of the patient involved bined with the pharmacological effect of adenosine blocking
in this case report. (or slowing) AV nodal conduction will provoke anterograde con-
Reprints: Maximilian D. Hien, MD, Pediatric Intensive Care Im Neuenheimer duction of the fibrillations to the ventricles, thereby causing rapid
Feld 430 69120 Heidelberg, Germany (e‐mail: maximilian.hien@med.uni-
heidelberg.de; hienimax@yahoo.de).
ventricular response of up to 300 bpm.
Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved. Second, a patient can present in AF from the start. If adeno-
ISSN: 0749-5161 sine is given, it will stabilize the fibrillations through the same

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Hien et al Pediatric Emergency Care • Volume 00, Number 00, Month 2016

FIGURE 1. Initial ECG of AVRT. ECG at admission with typical ECG features of AVRT: Narrow complex tachycardia at 228 bpm, no P-waves
preceding the narrow QRS complexes, retrograde P-waves hidden in ST (arrows). The average RP interval of 100 to 120 ms is significantly
shorter than the average PR interval of 160 to 180 ms. Downsloping ST segments in V6, ST depression is present in I, II, V4-V5, with a
monomorphic aspect of the ECG in all derivations.

mechanism.13,14 In addition, by blocking AV conduction, it will 12%.12,15 Laboratory findings for the incidence of AF differ from
enhance conduction of these fibrillations to the ventricles, also 10% to 51%. Up to two thirds of these children develop rapid
causing rapid ventricular response. ventricular response under electrophysiological stimulation.11,16
In our case, there was no interruption of conduction in the AV These findings suggest that the risk of encountering wide com-
node (Fig. 2). Adenosine failed to refractorize the AV nodal tissue. plex tachycardia leading to heart failure after adenosine adminis-
Instead, it slowed down AV nodal conduction with the second dose, tration is still uncertain and probably underestimated. The
enough to permit anterograde conduction of AF to the ventricles. existence of this complication is not yet widely appreciated by
Despite several reports of AF related to adenosine adminis- the clinicians who use the drug.17
tration, cause and effect have not been well documented. The in- Atrial fibrillation can be difficult—if not impossible—to diag-
cidence of AF induced by adenosine lies between 2.7% and nose on an ECG when AVRT is present, due to the superposition

FIGURE 2. Rhythm transformation from AVRT to irregular wide complex tachycardia after administration of adenosine. Initial narrow complex
AVRT of about 250 bpm, followed by an abrupt change (dark grey shading) initiated by a completely deformed wide QRS complex which
reappears several times (straight arrows). The predominant rhythm turns into a relatively monomorphic but irregular tachycardia of the same
heart rate (250 bpm), with deformed wide QRS complexes (asterisks). Two oblique arrows point out capture beats. Clues for the presence of
WPW AF2: (1) irregularity of the rhythm; (2) rapid ventricular response >200 bpm; (3) Delta wave of preexcitation in sinus rhythm; (4) wide,
bizarre QRS complex.

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Pediatric Emergency Care • Volume 00, Number 00, Month 2016 Adverse Effects of Adenosine in Children

FIGURE 3. Sinus ECG with delta wave after cardioversion. ECG after cardioversion, showing the electrocardiographic triad for WPW
syndrome2: (1) PR interval less than 120 ms; (2) Delta wave (zoom image) with a slow rise of the rising branch of R (triangle); a widened QRS
complex and repolarization changes reflected as ST segment or T wave changes.

with the rapid reentry circuits which conceal atrial activity. Be- Amiodarone and procainamide are listed in the 2010 guide-
cause, in most cases, when a child arrives in AVRT, there are lines of pediatric life support.1 These medications slow ventricular
no prior ECG readings or electrophysiological examination re- conduction, but need to be administered over 30 to 60 minutes.
sults available, it is recommended to try adenosine for interruption Cardioversion is then delayed 8 to 24 hours after administration. Ami-
of the reentrant tachycardia if vagal maneuvers fail. However, the odarone additionally slows AV nodal conduction, thus supporting AF
clinician should bear in mind that the WPW patient has a predis- conduction similar to adenosine. It can cause acceleration of the ven-
position to develop AF11,12 and that more WPW children than tricular rate and degeneration to ventricular fibrillation.21 There is
previously believed may develop rapid ventricular response. very limited data to the use of procainamide in children.1 Later re-
Circumstances permitting, it may be valuable to check if pre- ports rather recommend the use of ibutilide,2 which significantly pro-
vious ECG recordings or rhythm stripes of the patient are avail- longs the refractory period of APs and decreases the ventricular
able to identify patients with a history of AF. Familial AF, wide response in patients with WPW AF. Because most WPW pa-
complex tachycardia, or Ebstein anomaly may indicate a predispo- tients presenting AF are young individuals, the side effects of
sition for complications of adenosine treatment. Further risk fac- ibutilide (torsade de pointes, QT prolongation) are unlikely, and
tors for the development of ventricular fibrillation are male sex the blood pressure profile is better than with procainamide.
or elevated stress levels (eg, competitive athletes). Intermittent Flecainide is effective in treating acute-onset AF with an ef-
preexcitation is associated with a lower risk of rapid ventricular re- fect after 1 to 2 hours. Pagis et al22 used flecainide in a pediatric
sponse and fibrillation.18 case of rapid ventricular response and succeeded in terminating
Additional examinations can be carried out if SVT has been AF. There is, however, an underrecognized risk of developing
successfully terminated. For patients with persistent preexcitation, atrial flutter, which may be life-threatening if conducted 1:1.23
a stress ECG is recommended. Disappearance of the preexcitation Propafenone, digoxin, and verapamil have previously been
under stress is a sign of lower risk for sudden cardiac death. Per- proposed, but their use is now generally discouraged due to severe
sistent preexcitation should lead to an invasive (electrophysiolog- side effects.20,24
ical) examination which can improve risk stratification: A short Vernakalant is a fairly new drug, selectively affecting atrial
anterior refractory period of the AP (<270 ms), a minimum RR in- tissue, which is supposed to be superior in efficacy and takes ef-
fect within 8 to 14 minutes.25 However, no studies have been pub-
terval < 250 ms and right anterior location of the AP or multiple
lished to its use in children yet.
pathways are positive predicting factors for the risk of developing
AF with rapid ventricular response11,18,19 and should lead to
catheter ablation. CONCLUSIONS
Children with known AF, positive family history, and possi- In cases of hemodynamic compromise, there are currently no
bly male athletes with WPW may be considered to be high-risk feasible alternatives to the use of adenosine and/or electrical car-
patients, where the use of adenosine should be reevaluated. These dioversion for hemodynamically unstable patients with AVRT.
and further risk factors still need to be defined. The AVRT epi- The association of WPW with AF is still not well known in chil-
sodes are often well tolerated by children: hemodynamic impair- dren, but it is probably more common than previously recognized.
ment is rare, episodes frequently cease spontaneously, 60% are It is thus important to keep in mind that treatment with adenosine
successful in interrupting SVT with vagal maneuvers.20 In con- can cause AF and lead to rapid ventricular response, fibrillation,
trast, rapid ventricular response to AF is the most important cause and heart failure. The existence of this complication is not yet
of cardiac death in patients with WPW syndrome, occurring at a widely appreciated by the clinicians who use adenosine. This
rate of up to 0.6% per year.2,7 Furthermore, hemodynamic en- case illustrates the need to assess the risk of AF before the use
durance of wide complex tachycardia is limited in time and di- of adenosine when possible and to define high-risk constella-
minishes with growing age of the pediatric patient, eventually tions. For high-risk patients, future testing of prophylactic
leading to heart failure. comedication with antiarrhythmic agents such as ibutilide,
Recommendations for a second-line pharmacological ap- flecainide or vernakalant may be warranted to prevent this severe
proach are heterogeneous: complication of treatment with adenosine.

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Hien et al Pediatric Emergency Care • Volume 00, Number 00, Month 2016

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