Creative Commons Open Access Journal No author-side fee 
  • Users Online: 94
  • Print this page
  • Email this page
Submit article

Table of Contents
Year : 2021  |  Volume : 3  |  Issue : 1  |  Page : 39-41

An intriguing case of neonatal arrhythmia: An experience with antiarrhythmics and direct current cardioversion

1 Department of Neonatology, Government Medical College and Hospital, Chandigarh, India
2 Department of Cardiology, Government Medical College and Hospital, Chandigarh, India

Date of Submission24-Apr-2021
Date of Acceptance07-May-2021
Date of Web Publication24-May-2021

Correspondence Address:
Anam Siddiqui
D Block, Level IV, Department of Neonatology, Government Medical College and Hospital, Sector 32, Chandigarh
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ACCJ.ACCJ_6_21

Rights and Permissions

In the fetal and early neonatal period, clinically significant arrhythmias are remarkably rare whose medical management has been an area of dilemma in terms of safety and efficacy. We present a case of a hemodynamically stable female neonate presenting to us with atrial tachycardia with morphology of atrial fibrillation (AF) and atrial flutter (AFl). After a poor response to multiple antiarrhythmics, direct current cardioversion (DCC) was the final solution. Short-term maintenance therapy with oral propranolol was given with no recurrence. Hence, stepwise approach to infants with AFl can lead to an excellent prognosis with a low risk of recurrence.

Keywords: Antiarrhythmic drugs, atrial fibrillation, atrial flutter, cardioversion, neonatal arrhythmias

How to cite this article:
Jain S, Siddiqui A, Rao K R, Chawla D. An intriguing case of neonatal arrhythmia: An experience with antiarrhythmics and direct current cardioversion. Ann Clin Cardiol 2021;3:39-41

How to cite this URL:
Jain S, Siddiqui A, Rao K R, Chawla D. An intriguing case of neonatal arrhythmia: An experience with antiarrhythmics and direct current cardioversion. Ann Clin Cardiol [serial online] 2021 [cited 2021 Nov 27];3:39-41. Available from:

  Introduction Top

The incidence of arrhythmias is roughly 1%–2% in the late fetal period and around 1% in the neonatal period.[1] The most common tachycardia is sinus tachycardia and supraventricular tachycardia (SVT). SVT in neonates is typically caused by reentry, with the most common variant being atrioventricular (AV) reentrant tachycardia. Atrial flutter (AFl) is a rarer type of SVT accounting for up to one-third of clinically relevant cases of fetal tachyarrhythmias.[2] Atrial fibrillation (AF) is an uncommon arrhythmia in newborns, with few cases being reported.[3] In hemodynamically unstable cases, cardioversion is the treatment of choice. However, in stable cases, antiarrhythmic drugs are suggested.[4]

  Clinical Summary Top

A female baby was born to a 28-year-old third gravida previously healthy woman with a history of one abortion and one live child (G3P1L1A1). The baby was born at 36 weeks of gestation with a birth weight of 3.2 kg, had no congenital malformation on antenatal scans, and had no family history of cardiovascular disease. Owing to the history of previous cesarean section and persistent fetal tachycardia with no anatomical defects on fetal echo, the woman underwent urgent cesarean section. The baby had an Apgar score of 9 and 9 at 1 and 5 min, respectively, with no visible congenital malformation. At 2 h of life, heart rate (HR) of the baby was noted to be 300 beats per minute (bpm) with a regular rhythm. She received three incremental doses of adenosine starting at 0.05 mg/kg/dose at 4 h of life, with no effect following which amiodarone intravenous (IV) bolus was given at 5 mg/kg decreasing the HR to 200 bpm at 6 h of life. IV amiodarone maintenance was initiated at 5 μg/kg/min, and the baby was referred to our center for further management.

She was admitted at 54 h of life with an HR of 210 bpm with electrocardiogram (ECG) showing the morphology of atrial tachycardia [Figure 1]. She had a respiratory rate of 62 breaths per minute with no intercostal retractions and a normal chest X-ray. Oxygen saturation was above 94% with oxygen therapy using a hood box. She was hemodynamically stable with no murmur or significant hepatomegaly. Blood investigations were noncontributory. Repeat ECG done at 58 h of life showed a ventricular rate of 210 bpm, morphologically AF [Figure 2]. After the cardiology consultation, the baby was put on oral propranolol at 0.5 mg/kg/day in addition to maintenance IV amiodarone infusion at 5 μg/kg/min. Repeat ECG showed slowing of the HR to 70 bpm. Propranolol was stopped in view of extreme drop in HR, and amiodarone was tapered over the next 24 h.
Figure 1: Regular, long RP, narrow QRS tachycardia with a rate of 214 beats per minute, likely atrial tachycardia

Click here to view
Figure 2: Irregularly irregular, narrow complex tachycardia, with a ventricular rate of approximately 210 beats per minute, likely atrial fibrillation

Click here to view

After stopping antiarrhythmics, repeat ECG showed AFl with fast ventricular rate. The baby was further planned for a trial of three doses of oral sotalol therapy after consultation with an electrophysiologist. After the first dose of oral sotalol at 1 mg/kg/dose, ECG revealed bradycardia with an HR of 70 bpm, likely AFl with slow ventricular rate [Figure 3]. Further doses of sotalol were withheld in view of bradycardia. In view of refractory nature of the SVT and inability to tolerate the antiarrhythmics, the baby underwent direct current cardioversion (DCC) with dose of 1 J/kg, which reverted the rhythm back to normal sinus rhythm [Figure 4]. The baby remained hemodynamically stable after the cardioversion, and subsequent ECG showed normal sinus rhythm with HR varying 120–140 bpm. Two-dimensional ECHO was done after normalization of HR that revealed 4 mm ostium secundum atrial septal defect with left-to-right shunt with mild tricuspid regurgitation and normal biventricular function.
Figure 3: Bradycardia with a rate of around 70 beats per minute, likely atrial flutter with slow ventricular rate (after first dose of sotalol), saw tooth waves (black arrows)

Click here to view
Figure 4: Normal sinus rhythm and rate after direct current cardioversion

Click here to view

Further stay remained uneventful, and the baby was discharged on day 13 of life on oral propranolol at 2 mg/kg/day. Maintenance therapy was stopped at 1 year of age, with no recurrence on follow-up.

  Discussion Top

In the fetal and early neonatal period, transient and asymptomatic rhythm disturbances are common, but clinically significant arrhythmias are remarkably rare. Intrauterine intervention is needed for fetal arrhythmia if it is sustained and accompanied by major structural heart disease, hydrops fetalis, or fetal heart failure, none of which was present in the index case, and hence, no intrauterine intervention was called for. Reentrant SVT is the most common type of tachyarrhythmia observed in the neonatal period, and adenosine is the first drug of choice. If there is no response, the second-line antiarrhythmics belonging to class IA (procainamide or quinidine), class IC (flecainide), or class III (amiodarone or sotalol) can be considered.[2] The index case also received adenosine as first line followed by amiodarone from previous center on these lines. AF is highly uncommon in newborns. Potential risk factors for the occurrence of AF are low birth weight, prematurity at birth, low Apgar score, hypovolemia, anemia, and malpositioned central venous catheters.[3] None of these risk factors were present in the index case. AFl, although uncommon in the pediatric population, has been well described in the fetal and neonatal period.[5] In an infant with structurally normal heart, initial goal of medical management is termination of AFl because of its infrequent recurrence.[6] As the mechanism of AFl is macro-reentry within the atrial wall and not the AV node, adenosine cannot terminate AFl but can unmask the flutter wave by causing AV block and helps establish the diagnosis.[7],[8] In the index case also, adenosine made the morphology of the arrhythmia clearer rather than terminating it. Neonatal AFl has various treatment options, which include medical cardioversion, synchronized DCC, and transesophageal pacing.[5] AFl in neonates might be resistant to the first-line therapies such as beta-blockers (esmolol, propranolol) or digoxin and the second-line agents such as flecainide, amiodarone, or sotalol, and cardioversion may be required.[4]

In the index case, adenosine failed to revert the SVT following which amiodarone was used. Amiodarone has multipronged action as class I (blocks INa), class II (antiadrenergic), and class IV (blocks ICaL) agents in addition to its class III effects (blocks IK).[9] Due to the nonresponsiveness to amiodarone infusion, propranolol was started to control the fast ventricular rate. However, in view of the abrupt decrease in HR, propranolol was stopped, and amiodarone was gradually tapered. As the main goal of medical management was to achieve normal sinus rhythm, oral sotalol was added. Sotalol is a noncardioselective beta-blocker with additional class III antiarrhythmic properties (action potential duration prolongation) and has reverse use dependence. Oral or IV preparations can be used with frequent QTc monitoring.[10] However, in our case, the administration of oral sotalol resulted in AFl with slow ventricular rate (70 bpm) hence was discontinued and DCC was planned. DCC is highly effective, in terminating tachycardia related to reentry, such as AFl and many cases of AF. DCC depolarizes all excitable myocardium and possibly by prolonging refractoriness, interrupts reentrant circuits, and establishes electrical homogeneity, which terminates reentry. Interruption of the tachyarrhythmia for only the brief time produced by the shock may prevent its return for long periods, despite the persistence of the anatomic and electrophysiologic substrates.[9] Maintenance therapy with antiarrhythmics is usually advised to prevent recurrence. Follow-up is needed to check for arrhythmia recurrence and possible side effects of the antiarrhythmic therapy.[7] Infants with AFl generally have an excellent prognosis once in sinus rhythm with a low risk of recurrence, rarely needing long-term antiarrhythmics.[4]

  Conclusion Top

Our case represents a refractory neonatal arrhythmia, which first appeared to be typical SVT, but post adenosine came out to be atrial flutter that failed to respond to medical therapy (adenosine, amiodarone, propranolol, and sotalol) but was successfully managed with DCC. Our case highlights the importance of serial ECGs and a stepwise approach to a neonatal SVT. As in our case, infants with AFl generally have an excellent prognosis once in sinus rhythm with a low risk of recurrence, rarely needing long-term antiarrhythmics.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient's parent has given consent for her images and other clinical information to be reported in the journal. The patient's parent understands that the names and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Badrawi N, Hegazy RA, Tokovic E, Lotfy W, Mahmoud F, Aly H. Arrhythmia in the neonatal intensive care unit. Pediatr Cardiol 2009;30:325-30.  Back to cited text no. 1
Yuan SM. Fetal arrhythmias: Diagnosis and treatment. J Matern Fetal Neonatal Med 2020;33:2671-8.  Back to cited text no. 2
Bassareo PP, Marras AR, Marras M, Marras S, Mercuro G. Atrial fibrillation in a preterm newborn with structurally normal heart. Oxf Med Case Reports 2017;2017:omx010.  Back to cited text no. 3
Woo J, Khan O, Caldarelli L, Williams P. Tachycardia in the neonate. Pediatr Ann 2015;44:e247-50.  Back to cited text no. 4
Aljohani OA, Perry JC, Williams MR. Intravenous sotalol for conversion of atrial flutter in infants. HeartRhythm Case Rep 2018;4:117-20.  Back to cited text no. 5
Dick M. Clinical Cardiac Electrophysiology in the Young. 2nd ed. New York: Springer; 2006.  Back to cited text no. 6
Kothari DS, Skinner JR. Neonatal tachycardias: An update. Arch Dis Child Fetal Neonatal Ed 2006;91:F136-44.  Back to cited text no. 7
Ban JE. Neonatal arrhythmias: Diagnosis, treatment, and clinical outcome. Korean J Pediatr 2017;60:344-52.  Back to cited text no. 8
Zipes D, Libby P, Bonow R, Mann DL, Tomaselli GF, Braunwald E, editors. In: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 11th ed. Philadelphia, PA: WB Saunders; 2019.  Back to cited text no. 9
Pfammatter JP, Paul T. New antiarrhythmic drug in pediatric use: Sotalol. Pediatr Cardiol 1997;18:28-34.  Back to cited text no. 10


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

This article has been cited by
1 Antiarrhythmics
Reactions Weekly. 2021; 1867(1): 37
[Pubmed] | [DOI]


    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

  In this article
Clinical Summary
Article Figures

 Article Access Statistics
    PDF Downloaded74    
    Comments [Add]    
    Cited by others 1    

Recommend this journal