Published online: 2020-09-28

72 Case Report

Development of Antiarrhythmic Therapy-Resistant

Ventricular Tachycardia, Ventricular Fibrillation, and
Premature Ventricular Contractions in a 15-Year-Old
Patient
Can Yilmaz Yozgat1 Osman Yesilbas2 Akin Iscan3 Ismail Yurtsever4 Hafize Otcu Temur4
Nigar Bayramova5 Gokce Ergun5 Nur Tekin5 Yilmaz Yozgat6

1 Faculty of Medicine, Bezmialem Vakif University, Istanbul, Turkey Address for correspondence Can Yilmaz Yozgat, MD, Faculty of
2 Department of Pediatric Critical Care Medicine, Bezmialem Vakif Medicine, Adnan Menderes Bulvari, Vatan Caddesi, Bezmialem Vakif

This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited.
University, Istanbul, Turkey University, Istanbul 34093, Turkey (e-mail: yozgatyilmaz@gmail.com).
3 Department of Pediatric Neurology, Bezmialem Vakif University,
Istanbul, Turkey
4 Department of Radiology, Bezmialem Vakif University, Istanbul, Turkey
5 Department of Pediatrics, Bezmialem Vakif University, Istanbul, Turkey
6 Department of Pediatric Cardiology, Bezmialem Vakif University,
Istanbul, Turkey
J Pediatr Intensive Care 2022;11:72–76.

Abstract Sudden cardiac arrest (SCA) is the sudden cessation of regular cardiac activity so that the
victim becomes unresponsive, with no signs of circulation and no normal breathing. Asystole,
ventricular tachycardia (VT), ventricular fibrillation (VF), and pulseless electrical activity are
the underlying rhythm disturbances in the pediatric age group. If appropriate interventions
(cardiopulmonary resuscitation-CPR and/or defibrillation or cardioversion) are not performed
rapidly, this condition progresses to sudden death. There have not been many reported cases
of the approach and treatment of cardiac arrhythmias after SCA. Herein, we would like to
report a case of a 15-year-old female patient with dilated cardiomyopathy (DCM) who was
admitted to our clinic a year ago, and while her left ventricular systolic functions were
improved, SCA suddenly occurred. Since the SCA event occurred in another city, intravenous
treatment of amiodarone was done immediately and was switch to continuous infusion dose
of amiodarone until the patient arrived at our institution’s pediatric intensive care unit (PICU)
3 hours later. During the patient’s 20-day PICU hospitalization, she developed pulseless VT and
VF from time to time. The patient’s pulseless VT and VFattacks were brought under control by
the use of a defibrillator and added antiarrhythmic drugs (amiodarone, flecainide, esmolol,
Keywords and propafenone). Intriguingly, therapy-resistance bigeminy with premature ventricular
► bigeminy premature contractions (PVCs) continued despite all these treatments. The patient did not have
ventricular adequate blood pressure measured by invasive arterial blood pressure monitoring while
contractions having bigeminy PVCs. The intermittent bigeminy PVCs ameliorated rapidly after intermittent
► pediatric intensive boluses of lidocaine. In the end, multiple antiarrhythmic therapies and intermittent bolus
care unit lidocaine doses were enough to bring her cardiac arrhythmias after SCA under control. This
► lidocaine case illustrates that malign PVC’s should be taken very seriously, since they may predispose to
► ventricular the development of VT or VF. Also, this case highlights the importance of close vigilance of
tachycardia arterial pressure tracings of patients with bigeminy PVCs which develop after SCA and should
► ventricular fibrillation not be accepted as normal.

received © 2020. Thieme. All rights reserved. DOI https://doi.org/

May 9, 2020 Georg Thieme Verlag KG, 10.1055/s-0040-1715851.
accepted Rüdigerstraße 14, ISSN 2146-4618.
July 4, 2020 70469 Stuttgart, Germany
published online
September 28, 2020
 PVC and Development of VT and VF in an Adolescent
Introduction
Sudden cardiac arrest (SCA) is the sudden cessation of regular
cardiac activity so that the victim becomes unresponsive, with
no signs of circulation and no normal breathing. Asystole,
ventricular tachycardia (VT), ventricular fibrillation (VF), and
pulseless electrical activity are the underlying rhythm distur-
bances in the pediatric age group. If appropriate interventions
(cardiopulmonary resuscitation-CPR and/or defibrillation or
cardioversion) are not performed rapidly, this condition pro-
gresses to sudden death. The event is called SCA if an interven-
tion (e.g., defibrillation) or spontaneous reversion restores
circulation, though SCD is named if the patient dies. However,
SCD is used to describe both fatal and nonfatal cardiac arrests,
which is persisted by convention.1 The most prevalent reason
of SCA is an unexpected sustained VT or VF as a result of
preexisting cardiovascular problems. A wide range of cardio-
vascular problems, such as congenital and inherited cardiac
disorders, may cause SCA in young people.2–5 A 15-year-old
female patient with dilated cardiomyopathy (DCM) was ex-
amined in our clinic a year ago and found to have preserved left
ventricular systolic function. Despite this, SCA occurred soon
after. There have not been many reported cases to the approach
and treatment of cardiac arrhythmias after SCA. Herein, we
would like to report a case of development of therapy-resis-
tance VT, VF, and bigeminy premature ventricular contractions
(PVCs) despite antiarrhythmic treatment due to SCA in a 15-
year-old pediatric patient.
Case Report
A 15-year-old teen female patient had already been hospital-
ized in our institution’s pediatric intensive care unit (PICU) for a
month with the diagnosis of DCM and atrial fibrillation accom-
panied by severe systolic dysfunction. Cardiac magnetic reso-
nance imaging (MRI) was performed during the first
admission, a year ago. MRI results showed a resemblance of
acute myocarditis due to the existence of T2-weighted edema.
When the patient was discharged from the hospital, a trans-
thoracic echocardiographic examination demonstrated that
the left ventricle was dilated with second-degree mitral regur-
gitation and mild systolic dysfunction (ejection fraction [EF]:
52%, shorting fraction [SF]: 26%). The patient’s Holter electro-
cardiogram (ECG) recording was in sinus rhythm and had rare
ventricular ectopic beats. The patient’s home was in another
city. The patient was put under the medical treatment of
amiodarone 100-mg twice a day and propranolol 40-mg twice
a day for 8 months after she was discharged from the hospital.
Fig. 1 ECG strip showing the return of spontaneous circulation with right bundle branch block (RBBB) after 15 minutes of CPR. CPR,
cardiopulmonary resuscitation; ECG, electrocardiogram; VT, ventricular tachycardia.
Journal of Pediatric Intensive Care
Yozgat et al. 73
For her heart insufficiency, the patient was prescribed with
enalapril 50 mg, carnitine 50 mg/kg twice a day, digoxin 5 þ 5
drops þ multivitamin þ the treatment of intramuscular ben-
zathine penicillin of 1.2  units/kg IM was started on a half-
month basis. The patient was first followed-up in 3 months
intervals and then at 2-month intervals. During the follow-up
at 5 months, the digoxin drip was terminated due to the return
of normal systolic functions. Also, rare ventricular ectopic beats
were detected in the patient’s Holter ECG. In the follow-up at
8 months, amiodarone treatment was slowly reduced and the
propranolol treatment was increased. Weekly Holter record-
ings were taken. During the period of amiodarone reduction,
the patient was observed in the same city. PVCs infrequently
continued in the Holter recordings, though bigeminy couplets
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or VT attacks were not detected. The patient was sent to her
home in another city on the 7th day of the termination of
amiodarone treatment. The patient was asked to send her ECG
records at 10-day intervals. ECG recordings were normal. After
1.5 months, the patient had an SCA and The patient had return
of spontaneous circulation with right bundle branch block
(RBBB) after 15 minutes of CPR (►Fig. 1). Intravenous treat-
ment of amiodarone was done immediately and was switch to a
continuous infusion until the patient arrived at our institu-
tion’s PICU.
The patient was intubated and arrived at our PICU 3 hours
later. The pupils of the patient were equal and showed a
bilateral light response. The last echocardiographic exami-
nation of the patient was the same as the transthoracic
echocardiographic examination before the PICU admission.
The patient’s blood pressure was 100/70 mm Hg. No cardiac
changes due to hypoxia, which could develop after CPR, were
detected in the patient. The patient continued to receive
amiodarone. An implantable cardioverter defibrillator (ICD)
was planned when the patient’s hemodynamic status and the
neurological state were stable. There had not been any notable
changes in the patient’s cardiac arrhythmias for 2 days. On
day 3 of PICU admission, the patient developed bigeminal
PVCs, and the patient’s invasive arterial blood pressure moni-
toring showed hypotension during her PVCs (►Video 1;
available in the online version). Since bigeminy PVCs could
cause hemodynamic distortion, it was decided that the pa-
tient should not stay in the bigeminy PVCs rhythm for a long
time. Lidocaine was administered to the patient when the
patient had PVCs. The patient’s bigeminy PVCs were improved
whenever lidocaine was administrated (►Video 2; available in
the online version). On day 4 of PICU admission, the patient’s
PVCs continued briefly at 2- to 3-hour intervals three times a
day and only stopped after the administration of lidocaine.
Vol. 11 No. 1/2022 © 2020. Thieme. All rights reserved.
74 PVC and Development of VT and VF in an Adolescent
There was only one time that three beats of VT were observed
with bigeminy PVCs. The intermittent bolus administration of
intravenous lidocaine was 1 mg/kg. Thereupon, a lidocaine
infusion was added to the current amiodarone treatment that
the patient was receiving. This ameliorated the bigeminy PVCs
for 24 hours but then on day 5 of PICU admission the patient
started to develop bigeminy PVCs with a widened QRS again.
While the patient was continuing to receive a lidocaine
infusion, bigeminy PVCs responded and ameliorated well to
additional intermittent bolus administrations of intravenous
lidocaine. Noradrenaline was promptly initiated due to the
patient’s mild blood pressure. The patient’s bigeminy PVCs
persisted despite both infusions of amiodarone and lidocaine;
therefore, an esmolol infusion was added to her current
medical regimen. On day 6 of PICU admission, the lidocaine
infusion, which she had been taking for 2 days, was discon-
tinued by slowly decreasing its dosage within 7 to 10 days
after starting flecainide. During days 7 and 9 of PICU admis-
sion, esmolol and amiodarone infusions and oral flecainide
treatment worked very well, and she did not have any cardiac
arrhythmias for 48 hours.
Video 1
The patient’s intra-arterial blood pressure monitor
showing adequate blood pressure perfusion was not
observed in the patient during her bigeminy PVCs. PVC,
premature ventricular contraction. Online content
including video sequences viewable at: https://www.
thieme-connect.com/products/ejournals/html/
10.1055/s-0040-1715851.
Video 2
Video showing the spontaneous resolution of the
patient’s bigeminy PVCs after the administration of
lidocaine. Online content including video sequences
viewable at: https://www.thieme-connect.com/
products/ejournals/html/10.1055/s-0040-1715851.
On day 10 of PICU admission, the patient developed a
sudden pulseless VT that improved after defibrillation and
CPR (►Video 3; available in the online version). The patient’s
condition repeated three times. On day 11 of PICU admission,
the patient was again observed with bigeminy PVCs, and her
bigeminy PVCs could only stop by the bolus administration of
intravenous lidocaine. Therefore, since the patient had an
excellent response to lidocaine, the oral flecainide dose that
she received was increased to three doses. The other infusions
of esmolol and amiodarone were reduced by 20%. On day 13 of
PICU admission, the patient’s treatment was switched to oral
Journal of Pediatric Intensive Care Vol. 11 No. 1/2022 © 2020. Thieme. All rights reserved.
Yozgat et al.
metoprolol instead of the intravenous administration of esmo-
lol. On the same day while the patient was receiving metopro-
lol 50 mg, an amiodarone infusion, and oral flecainide, she
suddenly developed bigeminy PVCs followed by VT, again. The
patient underwent cardioversion twice. On day 14 of PICU
admission, the patient’s treatment of flecainide was replaced
with propafenone. On day 15 of PICU admission, the patient did
not have any bilateral light response. Also, she showed no
response to painful stimuli, and all brain stem reflexes were
absent. Therefore, the sedative and analgesics medications
were discontinued. There had not been any notable improve-
ment of the patient’s condition for 3 days. On day 18 of PICU
admission, the patient’s blood pressure decreased significantly
despite the noradrenaline and dopamine and adrenalin infu-
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sions. At the end of the same day, the patient had an SCA and
after 30 minutes of CPR, the patient lost her life.
Video 3
Video showing the sudden development of pulseless
VT followed by VF and the patient’s ECG improved after
doing defibrillation. ECG, electrocardiogram; PVC,
premature ventricular contraction; VF, ventricular
fibrillation; VT, ventricular tachycardia. Online
content including video sequences viewable at:
https://www.thieme-connect.com/ products/
ejournals/html/10.1055/s-0040-1715851.
Discussion
The definition of SCD is unanticipated death due to cardiovas-
cular reasons, which happens within 1 hour in an individual.1
SCA and/or SCD is a critical clinical obstacle that modern
cardiology has to face, mainly because SCA has mortality
between 350,000 and 400,000 in the adult population in the
United States, and most of these cases already have preexisting
cardiac problems.6 The most prevalent cause of SCA is an
unexpected sustained VT or VF as a result of preexisting
cardiovascular problems. These arrhythmias provide a solid
grounding for the electrical precariousness of the heart.6,7 A
wide range of cardiovascular problems, such as congenital and
inherited cardiac disorders, may cause SCA in young people.2–5
In our case, the patient had preexisting DCM and secondary to
myocarditis and a propensity for VF which likely caused SCA.
Dimas et al reported a clinical retrospective study of all
pediatric patients who had DCM at a single institution from
1990 to 2004. A total of 85 patients participated in the study.
Their study aimed to detect the frequency of cardiac arrhyth-
mias in pediatric patients with DCM. At the beginning of the
hospitalization, six pediatric patients developed nonsus-
tained VT. One pediatric patient had sustained VT or fibrilla-
tion. Six patients had supraventricular arrhythmias. During a
subsequent hospitalization or outpatient follow-up, seven
patients had the following arrhythmias: supraventricular
arrhythmias in two, nonsustained VT in four, and both atrial
 PVC and Development of VT and VF in an Adolescent
and ventricular arrhythmias in one. One single episode of
SCA occurred in one patient without a history of sustained
arrhythmias.8 In our case, SCA occurred without a history of
sustained arrhythmias similar to the findings of this report.
Another study9 that investigated the incidences of arrhyth-
mias of DCM was done by Abd El Mohsen et al. The authors
conducted a study on 29 pediatric patients with DCM at a
single institution between January 2012 and December 2014.
The mean age of patients was approximately 7 years. Six
patients had ventricular arrhythmias that represented a rate
of 20.7%. These were more commonly detected among the
female pediatric patients. Only one patient experienced a
life-threatening arrhythmia supra-ventricular tachycardia
representing a rate of 3.4%.9
The definition of VF is rapid, irregular, and erratic electri-
cal activity of the heart due to erratic alteration in the
electrocardiographic waveform. The ventricles of the heart
cannot contract harmoniously, which causes a reduction in
cardiac output. This is the most prevalent reason for SCA. VF
can also happen in patients who are unacquainted with their
condition. The only chance of survival for these patients
entirely hinges on both CPR and defibrillation.10 There have
been several reported studies which demonstrated that
resuscitation efforts are not sufficient (survival less than
10%) if these are delayed, though acts like bystander chest
compression and early use of defibrillation that can double or
even triple the chance of survival.10 Amiodarone treatment
is accepted as medical cardioversion because amiodarone
includes properties of all antiarrhythmic classes from I to IV
(14). In our case, we initially bolused amiodarone, followed
by maintenance therapy which was continued in order to
prevent possible cardiac arrhythmias due to cardiac arrest.
Scar-related reentry, anisotropic interventricular conduc-
tion, spatial dispersion of ventricular repolarization, or
functional bundle branch/interfascicular macroreentry can
result in grievous VTs such as VF and polymorphic VT.11–13 In
our case, we believe that the reason behind SCA was the
patient’s condition of myocarditis, secondary to a scar-relat-
ed reentry mechanism.
The most crucial factor in determining the prognosis of a
patient after SCA is how much the brain was exposed to
hypoxia during SCA. The synchronized contraction of myo-
cardium must be continued after SCA to prevent the notable
loss in cardiac output.
The direct arterial pressure monitoring of patients under
anesthesia has been going on for more than 50 years. Physi-
cians could benefit from the analysis of the morphology and
detail of the arterial pressure waveform, but most physicians
do not put much prominence into them.15 The shape of the
arterial waveform can provide vital information about the
alterations in the circulation, such as malign dysrhythmias,
that could be formed when the myocardial function is
disturbed. Also, modern arterial pressure traces waveforms
provide an approximation of alterations in the circulation.
The area under the curve is affected by peripheral vascular
resistance, myocardial performance, and stroke volume.16
Typically, the fact that there were frequent PVCs already
demonstrated electrical instability, even if the PVCs would
Journal of Pediatric Intensive Care
Yozgat et al. 75
have had adequate output on the arterial pressure tracing.
However, during the period of bigeminy PVCs in our case, there
was a notable deterioration of arterial pressure tracing, and
that sufficient blood pressures could not be maintained for
proper tissue perfusion. Also, despite the use of flecainide, β-
blocker triple therapy, and amiodarone, the rhythm of bigemi-
nal PVCs developed again in our case. We observed that every
time a bolus lidocaine was administered, the patient’s cardiac
rhythm immediately returned to the sinus rhythm. Patients
with the preexisting conditions of arrhythmic cardiac arrest,
sustained VT, or arrhythmic syncope have the highest indica-
tions of ICD implantation.17 In our case, there was not any
indication for ICD placement before the occurrence of SCA.
Automated external defibrillator (AEDs) are extremely neces-
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sary for out-of-hospital cardiac arrests; 60 to 80% of these
cardiac arrests occur at patients’ homes.18,19
Conclusion
In conclusion, the cardiac rhythm should be carefully exam-
ined after SCA, and any changes that may occur in a patient’s
arterial blood pressure tracing should carefully be moni-
tored. Bigeminy PVCs should not be considered innocent. A
high index of vigilance should be raised on arterial pulse
tracing during bigeminy PVCs and if the blood pressure
cannot provide adequate perfusion, intravenous lidocaine
may ameliorate the abnormal rhythm. This case shows that
automated external defibrillators (AEDs) are extremely nec-
essary for out-of-hospital cardiac arrests. The importance of
AEDs training with family members of at-risk cardiac
patients could have significantly increased the patients’
chances of survival from SCA.
Authors’ Contributions
All authors participated in creating content for the manu-
script, editing, and provided final approval for submission.
No undisclosed authors contributed to the manuscript.
Funding
None.
Conflict of Interest
None declared.
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