European Heart Journal: Acute Cardiovascular Care (2023) 12, 69–73
https://doi.org/10.1093/ehjacc/zuac160
Management of patients with electrical storm:
an educational review
Borislav Dinov*, Angeliki Darma, Sotirios Nedios, and Gerhard Hindricks
Department for Electrophysiology, Heart Center of Leipzig, Struempellstrasse 39, 04289 Leipzig, Germany
Online publish-ahead-of-print 27 December 2022
The introduction of implantable cardioverter-defibrillators (ICDs) for
termination of ventricular tachycardia (VT) changed dramatically the
outcomes of patients with malignant ventricular arrhythmias (VAs).
ICDs reduced the all-cause mortality not only in survivals of cardiac ar­
rest but also in patients with higher risk of sudden cardiac death (SCD).
Importantly, several randomized studies and registries demonstrated
that a significant proportion of the ICD recipients received appropriate
therapies. After 1 year, 17% of the patients in MADIT II study had an
arrhythmic even successfully terminated by the ICD, and in 2 years
this number increased to 21%.1 ICD utilization improved the survival
of patients with ischaemic heart disease (IHD), heart failure (HF) but
also allowed for more patients to survive to an end-stage HF. Many
of them require frequent hospitalizations for HF worsening, recurrent
ICD therapies, or treatment of serious comorbidities, which imposes
great pressure and costs on health care providers. Finally, some patients
experience multiple appropriate ICD shocks in a short period of time
that can jeopardize their life. This medical condition received the
name electrical storm (ES) in order to stress on the urgent, life-
threatening nature of this entity in analogy with the thunderstorms.
Definition of electrical storm and
clinical presentation
Electrical storm is usually defined as >3 VT/VF episodes in 24 h sepa­
rated by 5 min and requiring either ATP or shocks to terminate.2
Although this definition is arbitrary, it is commonly used in clinical trials
and in scientific publications to define a subset of patients with high VA
burden and increased risk for poorer outcomes. Patients with ES ex­
perience significant morbidity, frequent hospitalizations for VTs, HF
worsening and increased mortality.3–5 Therefore, an appropriate ES
management must be initiated promptly and performed by trained pro­
fessionals in specialized clinics.
ES can present as almost asymptomatic VT episodes terminated by
ATPs only, or as multiple VTs causing series of painful ICD shocks
and syncope. Importantly, the ICD recipients suffer more often from
depression and anxiety disorders that can be very severe in patients
with ES. ES can also cause a life-threatening electrical instability in result
of incessant VT or cardiogenic shock requiring advanced life support. In
a recent study or 253 patients hospitalized for ES, 37% presented with
haemodynamic instability. Older age, reduced ejection fraction (EF),
haemoglobin level, and use of catecholamines were associated with
an increased 1-year mortality.6 Although recurrent ES is a risk factor
The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal: Acute Cardiovascular Care or of the European Society of Cardiology.
* Corresponding author. Tel: +49 341 865 252 134, Fax: +49 341 865 1460, Email: dinovbobi@yahoo.com
© The Author(s) 2022. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please email: journals.permissions@oup.com.
EDITORIAL
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for worsening of HF, the deterioration of the heart function may pre­
cipitate the occurrence of VA through multiple neurohumoral, haemo­
dynamical, and electrophysiological alterations. Therefore, optimization
of the HF therapy to alleviate the haemodynamic derangements and
correction of the acute triggers are important part of the management
of patients with ES.
Although inappropriate ICD shocks are not classified as ES, the
symptoms and the consequences are similar to those of a real ES trig­
gered by VTs. Patients with non-ischaemic cardiomyopathies and pri­
mary electrical diseases are at increased risk for inappropriate ICD
shocks due to higher prevalence of atrial fibrillation, normal AV conduc­
tion and younger age.7–9 In addition to poor discrimination of atrial ar­
rhythmias, inappropriate ICD therapies can occur in result of T-wave
oversensing, noise detection, and rarely electromagnetic interference.
Precipitating factors and predictors
for occurrence of electrical storm
Recognizing the most frequent precipitating factors for occurrence of
ES is crucial for interrupting it. In patients with IHD, acute myocardial
ischaemia can trigger ES, mostly due to fast VTs and ventricular fibrilla­
tion. In HF patients, increased wall-stress, electrolyte disturbances, in­
creased sympathetic tone, or side-effects of drugs such as
catecholamines, antiarrhythmics, or over-the-counter drugs can also
elicit ES. Furthermore, decompensated metabolic conditions such
hypo- or hyperkalaemia, acidosis, or hyperthyroidism can provoke re­
current VTs.
Certain clinical characteristics such as monomorphic VT as a trigger
of ICD shocks, use of Class I antiarrhythmic drugs (AADs) and lower EF
were associated with ES. In a retrospective study of 330 ICD recipients
with ischaemic and non-ischaemic cardiomyopathy, ICD for secondary
prevention, as well as previous appropriate and inappropriate shocks
were independent predictors for occurrence of ES.10
Management of patients with
electrical storm
The appropriate management of patients with an ES is complex and
consists of several steps (Figure 1). Although ES is associated with
high early mortality, most patients survive the ES episodes without ma­
jor complications. Nevertheless, ES is regarded as a medical emergency
70
Figure 1 Flowchart for stepwise approach to ES.
and should trigger a clinical visit, generally within a week, to confirm the
appropriateness of the therapy, to exclude device malfunction and to
handle the ES. ICD devices with home-monitoring play important
role for remote and timely detection of ES which can be a harbinger
of imminent clinical worsening.
Step 1: Acute termination of
electrical storm
In its most severe forms, ES can cause a cardiogenic shock due to myo­
cardial stunning caused by incessant or recurrent VT triggering ICD dis­
charge. Patients’ sedation, and in severe cases intubation, mechanical
ventilation, and haemodynamical support are recommended to reduce
the sympathetic tone and stabilize the haemodynamics. Importantly,
the ICD shocks can be temporarily withheld by placing a magnet
over the device which can be executed from paramedics or trained
non-medical stuff. Infrequently, an incessant VT can cause a depletion
of all shocks that requires an external cardioversion or defibrillation.
Correction of the predisposing factors
Myocardial infarction is the most frequent cause of scar-related VTs.
Acute myocardial ischaemia can provoke VTs by changing the local rest­
ing membrane potential, and the properties of the action potential caus­
ing increased automaticity or early depolarizations. If acute myocardial
ischaemia is suspected, a coronary angiography must be performed;
however, in most patients with monomorphic VTs after myocardial in­
farction the leading mechanism is a re-entry that is dependent on older
scars. In a retrospective study, coronary revascularization prior to abla­
tion of monomorphic VT was necessary in 11% only, and coronary angi­
ography was not associated with post-ablation outcomes.11 Therefore,
coronary angiography must be reserved only for patients with ES, who
presented with chest pain, ST elevation, and/or significantly elevated
B. Dinov et al.
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troponin levels. However, minor or moderately elevated hsTnT levels
are frequently observed in patients with VT and ICD shocks and is not
associated with acute coronary syndrome.
Besides acute ischaemia, other triggers of ES such as electrolyte dis­
turbances; metabolic acidosis, hyperthyroidism or acute HF must be
corrected. Importantly, some drugs that are commonly used to treat
HF such as catecholamines or digitalis may be proarrhythmic and, if pos­
sible, should be discontinued.
Antiarrhythmic drugs to interrupt the
electrical storm
Antiarrhythmic drugs are indispensable part of the management of the
ES; however, they are more efficient to terminate the VT than to sup­
press future arrhythmias. Unfortunately, class IA and class IC AAD are
contraindicated in patients with myocardial infarction and depressed
EF, and only selective beta-blockers, lidocaine, and amiodaron are ap­
proved for patients with HF. The ability of amiodarone to suppress VA
and to reduce arrhythmic deaths against placebo were demonstrated
in patients with myocardial infarction in two older randomized studies
(EMIAT, CAMIAT), although the use of amiodarone was not associated
with overall mortality benefit. Amiodarone is recommended as a first-
choice therapy for VT in all types of substrates due to its potency and
less pronounced negative inotropism. Despite its noticeable effect on
the QT interval, it has a lower potential for TdP and pro-arrhythmia in
comparison to sotalol and Class I AAD, owing to its ability to prolong
the repolarization uniformly. In severe, refractory cases, combination
of amiodarone and intravenous lidocaine is acceptable, although high-
doses lidocaine must be avoided and limited to <48 h, due to severe
neurological side-effects, sinus arrest, and suppression of myocardial con­
tractility. Amiodarone can slow a VT below the detection threshold of
the ICD causing a haemodynamic deterioration; therefore three zone
programming should be considered in patients on amiodarone.
Management of electrical storm
Procainamide is a Class IA drug that was more effective than amiodar­
one intravenously to terminate monomorphic VT in a randomized study.12
Although, the use of procainamide was also associated with less acute ma­
jor adverse events than amiodarone, it must be used with caution especially
in patients with low EF and significantly impaired renal function.
Some rare diseases may require specific AADs to interrupt the ES
such as short acting beta-blockers and flecainide in catecholaminergic
VT, isoproterenol or quinidine in Brugada syndrome or mexiletine
in LQTS Type 3 syndrome. In combination with amiodarone, the non-
selective lipophilic beta-blocker propranolol was superior than metro­
prolol to interrupt the ES in patients with ICD and HF, based on
evidences from a small randomized study.13 However, the use of non-
selective beta-blockers in HF patients is not adherent to the current HF
guidelines, and its long-term use must be discouraged.
Step 2: Prevention of recurrence of
electrical storm
Optimization of the ICD programming
A paramount step in the management of patients with ES is the optimal
programming of the ICD device to reduce the number of inappropriate
and unnecessary ICD shocks. Inappropriate ICD therapy is reported in
8–40% of the ICD recipients depending on the patients’ characteristics
and the underlying disease. Appropriate device programming using onset,
stability, and morphology recognition as criteria may help to improve the
discrimination of supraventricular from VT. Furthermore, certain manu­
facturer specific algorithms may help to discriminate between SVT and
VT, as well as to avoid T-waves oversensing and to recognize noise.
Data from earlier ICD studies suggested high rates of unnecessary
therapy elicited by VTs that otherwise would terminate spontaneously.
Strategies to avoid unnecessary ICD shocks such as implementation of
high-rate therapy (> 200 bpm), use of monitor zone, longer detection
times, and preference to anti-tachycardia (ATP) has been found effect­
ive to reduce the rate of inappropriate therapy, appropriate shocks and
mortality.14 ATPs can effectively terminate even faster VTs and only
rarely accelerate a slower VT into faster ones or VF. In ADVANCE
III trial, extending the number of intervals to detect from 18/24 to
30/40 did not affect negatively the incidence of syncope or mortality,
although the number of ICD therapies was significantly reduced.15
Therefore, the most recent ESC/EHRA/HRS guidelines also support
this programming giving it level of evidence IA.16
Antiarrhythmic drugs for prevention of ES
In emergency settings AAD can terminate VT but in the long run they
are less effective for preventing ES. Data on the effectiveness of amio­
daron to prevent ICD shocks and ES are controversial. In a randomized
comparison, combination of amiodarone and beta-blocker was super­
ior to beta-blockers alone and sotalol in reducing the burden of ICD
shocks.17 However, the rates of drug discontinuation after 1 year
were 18% for amiodarone, 23.5% for sotalol, and only 5% for beta-
blockers. On the other hand, in a cohort of almost 4500 recipients of
ICD in the German DEVICE-registry, the combined therapy of amio­
daron and beta-blockers was associated with a 2-fold increased risk
of death after 1 year of follow-up in comparison to beta-blocker
only. However, the rates of ICD shocks, ES, and hospitalizations for
VT ablation was comparable between the groups.18
Mexiletine is an old Class IB drug that is considered as an alterna­
tive option to lidocaine in patients with VTs refractory to amiodar­
one. In a small group of patients from the cohort of the VANISH
trial, treated with mexiletine after amiodarone failure, over 90% of
the patients experienced the primary end-point including ICD
shocks after 9 months follow-up.19 Combined with other data
71
from older studies, it appears that mexiletine had limited efficacy
to suppress VT in IHD.
Radiofrequency catheter ablation for
terminating of ES
Patients with ES or incessant VTs are frequently referred for RFCA which
is also recommended by the recently updated HRS and ESC guide­
lines.2,16 When referring a patient with a VT for RFCA, several factors
such as patients’ symptoms, emergency, type of cardiomyopathy, and co­
morbidities must be careful evaluated. In patients with IHD and ES, RFCA
was highly successful to terminate ES, preventing the inducibility of any
VT in 89% of the ablated patients.20,21 Two main strategies for mapping
and ablation exist that are effective to terminate the VT (Figure 2).
Activation mapping during VT is very effective to terminate the arrhyth­
mia, but requires inducible VT and longer mapping times which can jeop­
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ardize the patient. Substrate mapping and ablation in sinus rhythm can be
performed even in patients with non-inducible and hemodynamically un­
stable VTs. Substrate ablation of late potentials and homogenization of
low-voltage areas has been shown to be more effective to prevent VT
recurrences, than tailored ablation of the mappable VT only.22 The effect­
iveness of RFCA for treatment of ES was also confirmed in patients with
non-ischaemic dilated cardiomyopathy, although, it was less successful
than in patients with IHD with reported acute success rates of 70%.23
However, in population of patients with arrhythmogenic right ventricular
cardiomyopathy and ES, RFCA was shown to be less effective and pre­
vented the inducibility of VT in <50%.24 Importantly, in patients with
ES a successful RFCA of all monomorphic VTs was independently asso­
ciated with lower rates of VT recurrence and higher survival rates.20,21
In spite of the undoubted progress, RFCA of VT remains a highly com­
plex procedure that carries a risk for complications, especially in emergency
settings or in low volume centres with little experience in the care of crit­
ically ill patients.25 Data from a big registry including more than 670 patients
with ES showed that patients who were referred for RFCA of ES were old­
er and sicker as compared to those without ES, and had lower EF, more
advanced HF, higher prevalence of cardiovascular comorbidities, and re­
quired longer ablation times.26 Mechanical circulatory support may be use­
ful in high-risk patients with ES and advanced HF to support adequate
blood pressure, coronary and end-organ perfusion in the settings of inces­
sant VT and long-lasting procedures (Figure 3).27
Data from registries and previous randomized studies consistently
showed that catheter ablation is superior to antiarrhythmic drugs to
terminate VT and to prevent VT recurrences. In the randomized
VANISH trial, RFCA was associated with longer times to ICD shock,
less hospitalizations for HF, and death in comparison to AAD therapy
escalation.28 These outcomes are in line with more recently published
results from the randomized SURVIVE-VT study, showing that endo­
cardial RFCA for VT was associated with significant reduction of inces­
sant VTs, ES and cardiac hospitalizations in comparison to AAD
therapy, mainly amiodaron and sotalol.29
Even though the RFCA of scar-related VT has been proved to be
highly effective for acute control of the arrhythmias, the long-term out­
comes are less satisfactory and ES is recognized as an unfavourable pre­
dictor of in-hospital death and recurrences after VT ablation. The
recurrences of VT in patients with ischaemic and non-ischaemic cardio­
myopathy can be explained by the properties of the underlying sub­
strate, the progression of the underlying heart disease or target sites
which remain out of reach for ablation.
Bail out strategies and experimental
therapies
In patients with ES in whom AAD and RFCA failed to suppress the VA,
several bail out options like alcoholic septal ablation, surgical endocardial
resection, infusion needle, cryoablation, or bipolar ablation can be
72
Figure 2 Activation map (A) of a slow re-entry VT in a patient with an inferior myocardial infarction. The VT and the highly fractionated local elec­
trogram at the exit site are shown (B). Isochronal map (C) showing an incomplete figure-of-eight re-entry, also seen in the magnified square (D). An
example of substrate map with a large low-voltage area in a patient with LV apical aneurysm (E).
Figure 3 Fluoroscopic image (AP view) of the heart showing abla­
tion catheter inserted into the left ventricle through a steerable trans-
septal sheet and retrogradely inserted Impella Device.
considered. However, due to lack of strong data favouring one strategy
or another, the management of refractory ES must be adapted to the pa­
tient’s health status, the local conditions and the operator’s experience.
Autonomic sympathetic system is an important precipitating factor
for ES and several non-randomized studies demonstrated promising re­
sults of cardiac sympathetic denervation in patients with refractory VT.
Video-assisted thoracoscopic cardiac denervation with extirpation of
stellate ganglion or the less invasive stellate ganglion block using local
anaesthesia with bupivacaine can reduce significantly the burden of
VTs and the ICD shocks in patients with ES.30,31
B. Dinov et al.
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More recently, an existing non-invasive technique for treatment of
malignant tumours was adopted in the electrophysiology as a promising
tool to control refractory, scar-related VT. By applying high-dose gam­
ma radiation at scar areas in myocardium responsible for VT, an impres­
sive reduction of the VT burden can be achieved.32,33 However, in spite
of the encouraging initial results and acute safety, there are rising con­
cerns about late adverse events associated with the high-dose irradi­
ation. Finally, if the VT is deemed untreatable, in patients with
end-stage HF or severe cardiomyopathies, an evaluation for heart
transplantation or mechanical assist device as a destination therapy
should be considered.
End-of-life issues and ES
The introduction of ICD therapy was a major step in the prevention of
SCD and many trials consistently showed that ICD prolonged life in dif­
ferent population groups, including HF patients. With protection of the
ICD devices, many ICD recipients survive to advanced stage HF which is
accompanied by profound myocardial and neurohumoral derange­
ments leading to higher vulnerability to malignant arrhythmias. In these
patients, ES is a major cause of hospitalization, a symptom of failing
heart and often a harbinger of imminent death. In the same time, pa­
tients with advanced HF NYHA ≥ III are underrepresented in the
ICD trials, leaving serious doubts about the appropriateness of ICD
therapy in these particular group. In the SCD-HefT study, the survival
benefit was observed after 1 year of ICD implantation and only in pa­
tients with NYHA Class II, whereas no significant benefit was observed
in those with NYHA III symptoms.34
As the HF get worse, there is an increased risk for VT and appropriate
shocks, and in the same time, higher likelihood of death due to non-
arrythmia causes. Therefore, the benefits and the implications of ICD im­
plantation must be assessed according to the patients’ needs prior the ICD
implantation and thereafter. In a big European survey, an increasing trend
for ICD therapy deactivation in patients with uncurable conditions such as
end-stage HF, malignancies, sepsis, stroke from 2006 to 2015 was ob­
served, although, ICD remained active in almost 50% of the patients,
and in 34% in the last 24 h before the death.35 If death is obvious and inev­
itable, deactivation of the device therapy should be considered to prevent
Management of electrical storm
causing a distressing death. Importantly, the option of deactivation of the
ICD therapy should be carefully discussed with the patients and their family
members and should follow robust local protocols.
Summary
(1) ES is associated with significant distress, morbidity, and mortality.
Patients with ES have high risk for hospitalization, HF decompensation,
and in-hospital death.
(2) Acute management of ES requires sedation, antiarrhythmic drugs and
correction of precipitating factors. In severe refractory cases, intub­
ation, mechanical ventilation, and circulatory support are necessary.
(3) Radiofrequency catheter ablation is also frequently required to ter­
minate the ES and to achieve acute and long-term freedom of VT.
Catheter ablation is superior than antiarrhythmic drugs to suppress
the ES and can be performed as a first-step procedure
(4) Optimization of the ICD programming is crucial to spare the anxiety
and the distress from further appropriate and inappropriate shocks.
Use of appropriate discrimination criteria and algorithms, ATPs and
extending the detection times are important measures to reduce
the burden of ES
(5) In patients with end-stage HF, deactivation of the ICD therapy should
be considered and discussed with patients and their caregivers. In suit­
able patients, heart transplantation or mechanical assist device im­
plantation as a destination therapy may be considered.
Conflict of interest: None declared.
Funding
None declared.
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