Abstract: A 75 year old woman with atrial fibrillation-related tachycardia-induced cardiomyopathy suffered ventricular fibrillation induced by dobutamine and was successfully defibrillated into atrial fibrillation in hospital. During the following 7 days, she suffered a cardiac electrical storm with 55 episodes of ventricular tachycardia rapidly degenerating to ventricular fibrillation and was converted with a total of 51 defibrillations and 4 chest compressions. Sinus rhythm was restored by electric cardioversion in the second episode of ventricular fibrillation. There was no response to the use of any recommended anti arrhythmic drugs. However, the use of chlorpromazine and promethazine surprisingly stabilized her heart rhythm. During a two-year follow-up period, the patient has remained free of ventricular fibrillation episodes and maintained sinus rhythm. [Guo YL, Zhang HY, Han YF, Zhang SL. Successful resuscitation of a patient With electrical storm over 7 days: a case report. Life Sci J 2012;9(2

Hai-Ying Zhang

Shu-Lin Zhang

Wei Zhang

Yue-Ling Guo

Yun-Feng Han

CiteSeerX

Life Science Journal 2012;9(2)                               http://www.lifesciencesite.com 
 
1011 
 
Successful resuscitation of a patient With electrical storm over 7 days: a case report 
 
Yue-Ling Guo1, Hai-ying Zhang2, Wei Zhang2, Yun-Feng Han2, Shu-Lin Zhang2 
 
1. Department of Medical Engineering, The Military General Hospital of Beijing PLA, Beijing 100070, China; 
2. Department of Geriatrics, The Military General Hospital of Beijing PLA, Beijing 100070, China; 
Correspondence author: Yun-Feng Han (hanyf001@126.com) 
(The first two authors contributed equally to this work) 
 
Abstract: A 75 year old woman with atrial fibrillation-related tachycardia-induced cardiomyopathy suffered 
ventricular fibrillation induced by dobutamine and was successfully defibrillated into atrial fibrillation in hospital. 
During the following 7 days, she suffered a cardiac electrical storm with 55 episodes of ventricular tachycardia 
rapidly degenerating to ventricular fibrillation and was converted with a total of 51 defibrillations and 4 chest 
compressions. Sinus rhythm was restored by electric cardioversion in the second episode of ventricular fibrillation. 
There was no response to the use of any recommended anti arrhythmic drugs. However, the use of chlorpromazine 
and promethazine surprisingly stabilized her heart rhythm. During a two-year follow-up period, the patient has 
remained free of  ventricular fibrillation episodes and maintained sinus rhythm. 
[Guo YL, Zhang HY, Han YF, Zhang SL. Successful resuscitation of a patient With electrical storm over 7 days: 
a case report. Life Sci J 2012;9(2):1011-1014] (ISSN:1097-8135). http://www.lifesciencesite.com. 150 
 
Key Words: electrical storm;  tachycardia-induced cardiomyopathy;  dobutamine  
 
Introduction   
The term tachycardia-induced cardiomyopathy 
(TIC) or tachycardiomyopathy refers to impairment 
in left ventricular function secondary to chronic 
tachycardia, which is partially or completely 
reversible once the tachyarrhythmia is controlled. 
The incidence of TIC is unknown, but in selected 
studies of patients with atrial fibrillation, 
approximately 25% to 50% of those with left 
ventricular dysfunction had some degree of TIC[1,2]. 
Data on the prognostic significance of electrical 
storm strongly suggest that these patients have a poor 
outcome. Electrical storm might be an independent 
risk factor for cardiac death. In the AVID trial[3], 
patients with electrical storm had an increased risk of 
nonsudden cardiac death (risk ratio, 2.4). In the 
MADIT –II substudy, patients with electrical storm 
had a 7.4-fold higher risk of death than patients 
without electricalstorm[4].  
The term electrical storm (ES) was introduced in 
the 1990s to describe a state of electrical instability of 
the heart characterized by a series of malignant 
ventricular arrhythmias in a short period of time[5]. 
This condition has been described in patients with 
post-infarction coronary artery disease, as well as in 
patients with various forms of cardiomyopathy, 
valvular disease, surgically corrected congenital heart 
disease, and genetically determined cardiac diseases 
without any apparent underlying structural disease, 
such as Brugada syndrome[6]. They need immediate 
resuscitative treatment, identification of the 
underlying cause and strategies for long term 
prevention of recurrence. We present a case of 
electrical storm when a woman with TIC was 
defibrillated 51 times over 7days but went on to make 
a good recovery.  
 
CASE REPORT  
A 75-year-old woman was admitted to our 
hospital due to worsening palpitation and dyspnoea. 
She had had hypertension for twenty years and atrial 
fibrillation for six month. The patient had no history 
of ischaemic heart disease, type 2 diabetes, 
hyperlipidaemia, chest pain, syncopal episode, or 
alcohol and drug abuse. She did not smoke and did 
not report any family history of syncope and sudden 
death. Blood pressure (BP) was 136/82 mmHg. 
Physical examination was unremarkable aside from a 
fast irregular pulse. Thyroid function tests were 
normal. Laboratory data were within normal limits. 
An electrocardiogram revealed atrial fibrillation with 
a ventricular rate of 107 beats per minute.  The QT 
interval was 0.358s and no significant ST change was 
observed. The chest X-ray showed cardiomegaly 
(cardiothoracic ratio, 60%). The echocardiography 
revealed a dilated left ventricle with a diastolic 
diameter of 6.0cm and a reduced ejection fraction of 
45%. A diagnosis of dilated cardiomyopathy was 
made. The patient was commenced on digoxin, 
valsartan, furosemide, spironolactone and metoprolol.  
On the 5th hospital day, when dobutamine was 
infused at a rate of 1ug/kg/min for 3 hours, ECG 
monitoring revealed ventricular tachycardia (VT) 
rapidly degenerating to ventricular fibrillation (VF). 
Immediate chest compressions were started.  Bolus 
infusion of 1 mg of adrenaline was given. Atrial 
fibrillation was restored by 3 electric cardioversion 
(200, 300, 360 Joule ). Serum level of potassium was 
Life Science Journal 2012;9(2)                               http://www.lifesciencesite.com 
 
1012 
 
in the normal range (4.1mmol/L). Initial laboratory 
findings revealed  no significant abnormalities 
including electrolyte disturbance, troponin and 
CPK-MB enzymes. After 75mg of amiodarone was 
administered intravenously over 10 minutes, 
continuous intravenous administration (60mg per 
hour) was given.     
Ten hours later after her first VF in the Ward, 
she suffered a new event of  VT rapidly 
degenerating to VF and successfully defibrillated 
(200J) into sinus rhythm(70 times per minute). After 
intravenous bolus of 40mg of lidocaine and 75mg of 
amiodarone, continuous intravenous lidocaine 
(120mg per hour) and  amiodarone (60mg per hour) 
was given. She suffered 2 episodes of VF and 
successfully defibrillated (200J) into sinus rhythm in 
next 4 hours. A diagnosis of ES was made. 
Immediately, metoprolol was administered 
intravenously 3 times (5mg/times) in one hour. Oral 
metoprolol was added to 50mg per day. The serum 
potassium level was kept at 4.0 mmol/L or higher. 
    The electrical storm persisted, despite the 
continuous infusion of lidocaine,  amiodarone and 
repeated doses of metoprolol, magnesium and 
potassium. Her hemodynamic condition was stable 
and serum electrolytes were normal. She suffered 
15-20 episodes of VT and 5--10 episodes of VF each 
day in the next 5 days. Each event triggered 
immediate chest compressions for 20-30s while 
charging the defibrillator. Sinus rhythm was restored 
by electric cardioversion(150-200J, total 51 times) or 
chest compressions(4 times) in each shock. The 
QT/QTc interval was 0.428s/0.426s and no 
significant ST change was observed, but she never 
suffered the event of torsade de pointes (TdP). Five 
days later after her first VF in the Ward, she was 
sedated by intramuscular chlorpromazine and 
promethazine. Surprisingly, the occurrence of VF was 
markedly decreased to 1--2 episodes of VF each day. 
After two days the occurrence of VT and VF 
terminated. 
Ten days later after her first VF, sedation was 
discontinued and she regained consciousness with 
intact cerebral function. Coronary angiography 
showed normal coronary arteries. There was only a 
slight increase in cardiac enzymes (Troponin I: 0.2 
ng/mL) during ES. The echocardiography revealed a 
dilated left ventricle with a diastolic diameter of 
5.5cm and a reduced ejection fraction of 50%. Chest 
x-ray showed cardiomegaly  (cardiothoracic ratio, 
60%) and Cardiac MR showed dilated 
cardiomyopathy. No premature ventricular 
contractions were detected by 24-hour Holter 
monitoring. An implantable cardioverter defibrillator 
was not implanted due to economic reason.  
Interestingly, upon discharge from the hospital 
the patient had no ventricular arrhythmias. At follow 
up six months later, a repeat echocardiogram 
confirmed that the left ventricular dimensions had 
returned to normal(diastolic diameter of 5.0cm) and 
the estimated ejection fraction was 70%. A diagnosis 
of atrial fibrillation-related TIC was made. During a 
two-year follow-up period, the patient has remained 
free of ventricular fibrillation episodes and 
maintained sinus rhythm. She has continued 
long-term treatment with metoprolol and amiodarone. 
At present, she is in excellent condition. 
  
Discussion 
    ES is defined as the recurrence of 
hemodynamically unstable VT and/or VF, twice or 
more in 24 hours, requiring electrical cardioversion 
or defibrillation[7,8]. With the arrival of the ICD 
(implantable cardioverter defibrillator) this definition 
was broadened, and ES is also defined as the 
occurrence of three or more distinct episodes of 
ventricular tachycardia (VT) or ventricular 
fibrillation (VF) in 24 hours, requiring the 
intervention of the defibrillator [9]. It should be noted 
that this latter definition does not include the 
presence of hemodynamic instability. This condition 
has been described in patients with post-infarction 
coronary artery disease, as well as in patients with 
various forms of cardiomyopathy, valvular disease, 
surgically corrected congenital heart disease, and 
genetically determined cardiac diseases without any 
apparent underlying structural disease, such as 
Brugada syndrome[6]. 
The patient reported to have atrial fibrillation six 
month prior to admission. The echocardiography 
revealed a dilated left ventricle with a diastolic 
diameter of 6.0cm and a reduced ejection fraction of 
45% after admission. Six month after sinus rhythm 
was restored by electric cardioversion, a repeat 
echocardiogram confirmed that the left ventricular 
dimensions had returned to normal and the estimated 
ejection fraction was 70%. So, a diagnosis of atrial 
fibrillation-related TIC was made. Clinically, the 
most common cause of TIC is believed to be atrial 
fibrillation (AF), which is increasing in incidence 
with the aging of society. AF causes TIC via 2 
distinct mechanisms: inadequate diastolic filling and 
tachycardia-induced systolic dysfunction. When AF 
develops, the active atrial contraction disappears in 
end-diastole, leading to a reduction in the cardiac 
output by 15–20%[10]. This insufficient diastolic 
filling is augmented by the shortening of diastolic 
filling time. Furthermore, sustained tachycardia 
results in impaired systolic function through a 
mechanism represented by TIC, which leads to a 
greater reduction in the cardiac output[10,11]. A recent 
report  has suggested a risk of sudden death in this 
Life Science Journal 2012;9(2)                               http://www.lifesciencesite.com 
 
1013 
 
particular group[12]. Our report is the first to 
document one patient with fibrillation-related TIC 
who suffered ES and has a good recovery. 
    It is noteworthy that, in spite of a detailed 
analysis of the electrocardiogram, haematological 
and biochemical examinations, and the 
patients’clinical symptoms, in only 36% was any 
triggering mechanism found that could provoke 
electrical storm. Those factors were acute ischemia, 
worsening heart failure, hypokalemia, 
hypomagnesemia, arrhythmogenic drug therapy, 
hyperthyroidism, and infection or fever. In this case, 
we found, CHF secondary to atrial fibrillation-related 
TIC, who developed ES during low-dose dobutamine 
infuse. Dobutamine is an inotropic pharmaceutical 
that improves the hemodynamic and clinical status of 
patients suffering from congestive heart failure (CHF) 
refractory to standard treatment[13]. The 
proarrhythmic effects of dobutamine are supported by 
several observations. It increases the dispersion of 
action potential duration in adjacent areas of ischemic 
and non-ischemic myocardium in experimental 
animals[14], and increases the incidence of VT in 
patients[15]. 
    Electrical storm activates the sympathetic 
nervous system. β-Blockers play a key role in the 
management of ES. In a canine study[16], β-blockers 
increased the fibrillation threshold (that is, made the 
animals less susceptible 
to fibrillation) 6-fold under ischemic and 
nonischemic conditions. Amiodarone is widely used 
in the treatment of electrical storm[6]. In acute 
amiodarone therapy, rapid intravenous administration 
blocks fast sodium channels in a use-dependent 
fashion (producing more channel blockade at faster 
heart rates), inhibits norepinephrine release, and 
blocks L-type calcium channels but does not prolong 
ventricular refractoriness. Conversely, in oral 
amiodarone therapy, prolonged ventricular refractory 
periods are seen over periods ranging from days to 
weeks[17]. Amiodarone has few negative inotropic 
effects and is safe in patients who have depressed 
systolic function. Amiodarone or β-blockers are 
generally accepted as the best available drugs for 
prevention of arrhythmic storm[18]. Class I 
antiarrhythmic drugs are used widely, with variable 
success rates, and can play a role in polymorphic 
ventricular arrhythmias[19]. But in our report, there 
was no response to the use of any above drugs in the 
patient.      
    The physical and emotional stress that patients 
experience in association with electrical storm and 
multiple electrical cardioversions often perpetuates 
arrhythmias. All patients who have electrical storm 
should be sedated. Short-acting anesthetics such as 
propofol, benzodiazepines, and some agents of 
general anesthesia have been associated with the 
conversion and suppression of VT[20]. Left stellate 
ganglion blockade and thoracic epidural anesthesia 
have also reportedly suppressed electrical storms that 
were refractory to multiple antiarrhythmic agents and 
β-blockade[21]. These therapeutic approaches directly 
target nerve fibers that innervate the myocardium, 
and a reduced adrenergic tone is most likely 
responsible for the reported efficacy[22]. In this article, 
we found, there was no response to the use of any 
recommended anti arrhythmic drugs. However, the 
use of chlorpromazine and promethazine surprisingly 
stabilized her heart rhythm. 
The good neurological outcome in the patient 
was probably due to a number of positive factors. 
This case illustrates that immediate and high quality 
chest compressions is necessary. Each episode of VF 
initiated immediate manual chest compressions while 
charging the defibrillator, thus hands-off time was 
reduced to a minimum. 
This case illustrates the importance of 
defibrillation, multiple anti-arrhythmic agents and 
sedation in management of electrical storm. Despite 
repeated defibrillations, she went on to make a good 
recovery. Every possible attempt should be made to 
reduce as far as possible the number of patients who 
undergo it.  
 
Correspondence author:  
Yun-Feng Han 
Department of Medical Engineering,  
The Military General Hospital of Beijing PLA,  
Beijing 100070, China;  
hanyf001@126.com. 
 
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5/20/2012 


Successful resuscitation of a patient With electrical storm over 7 days: a case report

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Successful resuscitation of a patient With electrical storm over 7 days: a case report

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