Article, Cardiology

Electrical storm: A focused review for the emergency physician

a b s t r a c t

Background: Electrical storm is a dangerous condition presenting to the Emergency Department that requires rapid diagnosis and management.

Objective: This article provides a review of the diagnosis and management of electrical storm for the emergency clinician.

Discussion: Electrical storm is defined as >=3 episodes of sustained ventricular tachycardia, ventricular fibrillation, or shocks from an implantable cardioverter defibrillator within 24 h. Patients may present with a wide array of symptoms. Initial evaluation should include an electrocardiogram with a rhythm strip and continuous cardiac monitoring, a medication history, assessment of hemodynamic stability, and identification of potential triggers. Management includes an antiarrhythmic and a beta blocker. Refractory patients may benefit from double- sequential defibrillation or more invasive procedures such as intra-aortic balloon pumps, Catheter ablation and extracorporeal membrane oxygenation for critically ill patients. These patients will typically require admission to an intensive care unit.

Conclusion: Electrical storm is a condition associated with significant morbidity and mortality. It is important for clinicians to be aware of the current evidence regarding the evaluation and management of these patients.

(C) 2020


Although there is no uniformly accepted definition of electrical storm (ES; also known as Arrhythmic storm or ventricular tachycar- dia/fibrillation storm), the most commonly referenced criteria consists of a period of cardiac instability defined by >=3 episodes of sustained ven- tricular tachycardia (VT), ventricular fibrillation (VF), or the receipt of Appropriate shocks from an Implantable cardioverter defibrillator within 24 h [1]. Some experts include incessant VF/VT episodes that return after successful defibrillation and those that are refractory to commonly used interventions [2,3]. Studies have found that ES occurs in 4% to 40% of patients with ICDs with a median of two episodes per person and they are at increased risk during the first couple days follow- ing implantation of the device [4-10]. Electrical storm is more common in patients with low ejection fraction, chronic renal failure, and prior myocardial infarction [8,11].

Electrical storm is associated with significant morbidity and mortal- ity, with a mortality rate of up to 14% in the first 48 h [12]. Studies have consistently demonstrated increased mortality among patients with ES when compared with control patients that have ICDs [5,6,10]. One study found that the risk of death with ES was 2.4-fold higher than with

* Corresponding author.

E-mail addresses: [email protected] (S. Dyer), [email protected] (B. Mogni).

isolated VT/VF and that this risk increased to 5.4-fold in the first three months [11]. Therefore, it is essential for Emergency Medicine (EM) cli- nicians to be familiar with the diagnosis and management of this condition.


The authors searched PubMed and Google Scholar for articles using the keyword “electrical storm”. Authors included case reports and se- ries, retrospective and prospective studies, systematic reviews and meta-analyses, clinical guidelines, and other narrative reviews. The lit- erature search was restricted to studies published in English. Emergency Medicine physicians with experience in critical appraisal of the litera- ture reviewed all of the articles and decided which studies to include via consensus, with a focus on EM-relevant articles. A total of 84 re- sources were selected for inclusion in this review.


Anatomy and pathophysiology

Most ES events are due to underlying structural heart disease [13]. Common causes of structural heart disease associated with ES include nonischemic cardiomyopathy, arrhythmogenic right ventricular cardio- myopathy, sarcoidosis, amyloidosis, Chagas disease, Brugada syndrome,

0735-6757/(C) 2020

and post-surgical resection [14-17]. These conditions lead to scarring or fibrosis, thus establishing a zone of remaining myocytes that create a slow area of conduction. When combined with an anatomic or func- tional conduction block, these create a re-entry circuit [13,14,18,19].

Between 4% and 40% of patients with an ICD experience ES [4-10]. Among these cases, patients with low left ventricular ejection fractions, chronic renal failure, ventricular tachycardia as their primary indication for ICD placement, and patients taking a class 1A antiarrhythmic were more likely to experience ES events [20]. In comparison, patients with ICD placement for primary prevention had a lower incidence [20]. Re- versible etiologies of ES include drug toxicity, heart failure exacerbation, acute myocardial ischemia, thyrotoxicosis, hypokalemia, hypomagnese- mia, infection, fever, and QT prolongation [4,6,8,10,13,22-24]. Impor- tantly, while antiarrhythmic medications are intended to reduce dysrhythmias, they may also increase the risk of ES in some cases [21]. Unfortunately, identifiable causes are only discovered in 10% to 25%

of cases as most episodes of ES are idiopathic in nature [4,6,9,24]. One

study found that 61% of episodes occurred between 8:00 am to

Table 1

Criteria for differentiating SVT with aberrant conduction from VT [30-36].

Brugada criteria 1. Absence of an RS complex in all precordial leads

R-to-S interval N100 ms in one precordial lead
  • Atrioventricular dissociation
  • Morphology criteria for VT present both in precordial leads V1/V2 and V6

    For LBBB:

    R wave N30 ms in V1

  • RS interval N60 ms in V1
  • Notched S wave in V1
  • QS complex in V6
  • qR wave in V6
  • For RBB:

    Monophasic R wave in V1

  • Notched downslope to R wave in V1
  • qR wave in V1
  • QS complex in V6
  • R/S ratio b1 in V6

    4:00 pm on Monday through Friday, suggesting that there may also be a circadian pattern to ES [25]. Electrical storm episodes were also more frequent in months with a wide temperature range, which has

    been hypothesized to be due to increased activation of the sympathetic nervous system and renin-angiotensin system, combined with greater

    aVR Vereckei algorithm

    Initial R wave in aVR

  • Initial r or q wave N40 ms in aVR
  • Presence of a notch in the descending limb or a pre- dominantly negative QRS complex in aVR
  • Ratio of initial to terminal ventricular activation veloc- ity <=1

    potential for dehydration [25,26].

    Pava criteria 1. R-wave peak time in lead II >=50 ms

    History and physical examination

    Electrical storm can present with a variety of symptoms, which can include palpitations, chest pain, syncope, hypotension, and cardiac ar- rest [20,27]. As such, the initial presentation can be vague, so clinicians

    The ventricular tachycardia score

    (>=3 points to diagnose VT)

    Initial R wave in V1 (1 point)

  • Initial r N40 ms in V1/V2 (1 point)
  • Notched S in V1 (1 point)
  • Initial R in aVR (1 point)
  • Lead II R wave peak time >=50 ms (1 point)
  • No RS in V1-V6 (1 point)
  • Atrioventricular dissociation (2 points)

    should maintain a high index of suspicion and ensure patients are placed on a cardiac monitor.

    After initial assessment of hemodynamic stability, a more thorough history can be obtained to identify the precipitating event. Medications are a common cause of ES, so it is important to obtain a good medication history. As many patients may already be taking an antiarrhythmic, it is important to determine which medications they are taking. For exam- ple, class 1A antiarrhythmics, are a known cause of ES even at therapeu- tic levels [21,28]. Clinicians should also ask about recent medication changes (particularly the addition or modification of medications with QT prolonging effects).

    Diarrhea leading to hypokalemia was found to cause up to 20% of ES events in one study, while infections in general are also a known risk factor [24]. Patients should also be asked about recent use of alcohol or drugs of abuse [17,23,24]. Another study found that binge drinking of alcohol was a contributing factor in 8% of cases [23].

    If the patient has an ICD, they should be asked about the number of discharges and the device should be interrogated in the ED. Approxi- mately 10% to 20% of patients with ICDs will experience recurrent ven- tricular tachyarrhythmias [2,11,24,29].

    Diagnostic testing

    Patients with suspected ES should have an electrocardiogram (ECG) performed immediately with a rhythm strip performed. These patients should also be placed on continuous cardiac monitoring. It can be diffi- cult to distinguish a supraventricular tachycardia with aberrant conduction from ventricular tachycardia [30-33,41]. Table 1 presents a few criteria available for differentiating SVT with aberrancy versus ven- tricular tachycardia (Table 1). However, in the critically ill patient, clini- cians should treat this as VT until proven otherwise [20].

    For patients who have received an ICD, a device interrogation should be performed for evaluation of the shock delivery and arrhythmic pa- rameters (e.g., heart rate, time of onset, morphology). Sometimes the ICD will need to be reprogrammed to stop the recurrent firing [15,20,37,38,40].

    SVT, supraventricular tachycardia; VT, ventricular tachycardia.

    A complete blood count with differential, complete metabolic panel, troponin, thyroid stimulating hormone, magnesium, and brain natri- uretic peptide are all appropriate labs to seek out potential precipitating causes [4,6,8,10,13,15,22-24]. A chest radiograph should be obtained to assess for alternate etiologies and to determine if any lead displacement has occurred in patients with an ICD [39].


    The standard approach recommended for VT/VF by the Advanced cardiac life support guidelines typically fail to stabilize these pa- tients, therefore it is important to tailor the resuscitation to the unique features of ES [29]. Potentially Reversible etiologies (e.g., electrolyte ab- normalities, prolonged QT interval) should be sought and treated. For Hemodynamically stable patients, medications should be discussed with a cardiologist when possible as they may influence the ability to perform subsequent electrophysiologic testing. The 2017 ACLS guide- lines initially recommend intravenous antiarrhythmics and Beta blockers along with catheter ablation, sympathetic denervation, and se- dation for refractory VT/VF [1].

    Patients experiencing ES have an increase in their baseline sympa- thetic tone which can be further compounded by repeated ICD shocks, exogenous epinephrine given through ACLS, and the psychological stress that is caused by this disease state [43]. This intense surge in cat- echolamines and activation of the sympathetics makes the heart more susceptible to ischemia, further arrhythmias, and potentiates the ES state. The use of exogenous epinephrine increases the likelihood of VF, myocardial dysfunction, and oxygen demand through activation of the beta receptors. For this reason, repeated doses of epinephrine are not recommended for these patients as it is believed that it may worsen ES [20]. Similarly, suppression of this sympathetic tone through the use of beta blockade plays a key role in treating ES.

    One trial looking at post-myocardial infarction patients with ES demonstrated that beta blockade decreased the incidence of sudden

    death and VF [29]. In animal studies, non-selective beta blockade helps balance out the myocardial oxygen demand and delivery of oxygen through the coronaries, thereby decreasing Ischemic injury, increasing the VF threshold, improving the capability of restoring a perfusing rhythm through less Electrical shocks, and improving post- resuscitation cardiac function and survival [44,45]. The first human trial to look at beta blockade in ES was Nademanee et al. in 2000, where they showed beta blockers helped patients’ short and long term survival [29]. An increasing amount of data suggests beta blockade has been associated with improved outcomes in ES patients with an in- creased rate of sustained ROSC and survival to discharge with a favor- able neurological outcome [46]. Previous studies have predominantly used metoprolol and propranolol for beta-blockade with propranolol being superior to metoprolol at suppressing ES, likely secondary to its non-selective beta blockade and lipophilic nature leading to increased effect on the central nervous system [47]. There is evidence that esmolol successfully treats patients with ES, but there is a need for studies to di- rectly compare esmolol to other more commonly studied beta blockers in ES such as metoprolol or propranolol [42,48]. Studies using esmolol for ES administered a loading dose of esmolol at 500 ug/kg and then an infusion started from 0-100 ug/kg/min if there was no ROSC after 10 min of CPR including at least 3 defibrillation attempts, 300 mg of amiodarone, and 3 mg of epinephrine [42]. Additionally several studies have suggested the efficacy of the stellate ganglion block to terminate ES. Excessive sympathetic innervation to the heart can be mitigated by blocking the stellate ganglion nerve using an ultrasound-guided paratracheal approach [29,49-51].

    Amiodarone is one of the most effective drugs in treating this patient

    population and has widely been used for the acute treatment of ES [22]. In patients with shock-resistant VF, amiodarone was associated with decreased rates of Ventricular tachyarrhythmias [52], decreased risk of further ICD shocks (when used in conjunction with beta blockers) [53], and higher rates of Survival to hospital admission [54]. In the acute setting, intravenous amiodarone should be given to both hemody- namically stable ES patients for prevention of further dysrhythmias and unstable ES patients with refractory shockable arrhythmias as a part of ACLS and prior to other interventions. Azimilide and dofetilide have

    also been described as potential anti-arrhythmic agents to treat ES [2] (Fig. 1).

    While other antiarrhythmics have been described for ES, amioda- rone remains the first-line agent. Other agents, such as the class I antiar- rhythmics (e.g., lidocaine, procainamide) are not recommended as first- line therapies for ES as they have variable efficacy in this population. While lidocaine can be effective in treating ventricular arrhythmias due to ischemia [55], it is inferior to amiodarone in patients with shock-resistant VF [54]. Outside of ischemia, lidocaine is an ineffective anti-arrhythmic and only converts ventricular tachycardia in 8-30% of cases [20,56].

    Patients experiencing ES undergo a substantial amount of physical and emotional stress. This can further increase the sympathetic nervous system activity, a known precipitant for ES, thereby perpetuating ven- tricular arrhythmias [20]. Studies have suggested that reducing the sympathetic nervous system output through boluses of sedation, such as propofol and thoracic Epidural anesthesia, may be effective treat- ments for ES. A case report describes boluses of propofol leading to the resolution of persistent VT [57]. Propofol has little known effects on the cardiac Conduction system but can influence Cardiac activity due to its suppression of the sympathetic nervous system [57]. Alterna- tively, a case series suggests thoracic epidural anesthesia is an alterna- tive therapy to directly inhibiting the cardiac sympathetic innervation without the potential side effects of sedation [58] (Fig. 2).

    There are two situations in which the treatment of ES should deviate from the interventions discussed thus far. The first are patients with a history of Brugada syndrome or concern for Brugada syndrome based upon prior ECGs. Although the exact incidence of ES in Brugada syn- drome patients is not known, these patients are at higher risk of experiencing a Life-threatening arrhythmia [59]. Many of the pharmaco- logical interventions traditionally used in ES will have no effect or can further perpetuate ES in patients with Brugada syndrome. Isoprotere- nol, a beta agonist, should be the first-line therapy in this population as it decreases the ST elevation and suppresses VT by acting on the car- diac Calcium channels [59,60]. In addition, isoproterenol can be effective in treating patients with short QT syndrome in ES [1,61]. The second sit- uation is when the presenting rhythm is polymorphic VT, which



    Propranolol Metoprolol

    Class III agents


    Bolus: 300 to 500 mcg/kg IV for 1 min

    Infusion: 25 to 50 mcg/kg/min IV up to 250 mcg/kg/min (titrate q 5-10 mins)

    Bolus: 0.15mg/kg Iv over 10 min

    Bolus: 2-5mg IV every 5 min, up to 3 doses in 15 min

    Bolus: 150mg IV over 10 min

    Infusion: 1mg/min IV for 6 h, then 0.5mg/min for 18 h

    Class I agents


    Bolus: 10mg/kg IV over 10 min Infusion: max of 2-3g/24h


    Bolus: 1.0 to 1.5mg/kg IV, repeat dose 0.5 to

    0.75 mg/kg IV max dose 3 mg/kg



    Bolus: 1 to 2 mcg IV

    Infusion: 0.15mcg/minute IV and titrate to 0.3mcg/min as needed

    Fig. 1. Antiarrhythmic medications for treatment of electrical storm.

    Fig. 2. Management of electrical storm algorithm.

    accounts for 7% of ES cases and can be the first sign of ischemia [3,20]. Recurrent episodes of polymorphic VT should trigger an investigation into an acquired prolonged QT as the treatment requires a unique approach to prevent degeneration into Torsades de pointes. Most commonly, polypharmacy with or without an electrolyte imbalance, such hypokalemia and hypomagnesemia, is the cause of an acquired prolonged QT [3]. If there is a suggestion of a prolonged QT/torsades de pointes, then the medications discussed earlier should all be avoided as many will further prolong the QT. Instead, magnesium and potassium should be aggressively repleted when hypokalemia or hypomagnesemia are suspected as the cause [3,20]. Empiric treat- ment with magnesium for all ES patients does not seem to improve ROSC or survival to hospital discharge and therefore should be re- served for those cases where a prolonged QT interval or torsades de pointes are suspected [62].

    The use of Double sequential defibrillation for patients with refractory ventricular arrhythmias has recently become popularized by Prehospital providers [63,64]. The concept involves using two set of defibrillator pads on the same patient which are fired simultaneously or sequentially. Initial canine studies suggested that two sequential shocks lowered the defibrillation threshold energy needed to terminate the arrhythmia, which is thought to be from the second vector of elec- tricity reaching the myocardium [64]. While case reports and case series show promise for DSD as a potential resuscitative treatment for patients with ES, multiple recent literature reviews and a matched case-control study have not shown any statistically significant difference in patient survival or neurological outcomes compared to standard defibrillation [64,66-71]. However, it has been suggested that DSD may be associated with improved outcomes when used earlier on in the resuscitation (typ- ically between the fourth and eighth defibrillation attempts) [72]. In ad- dition to the unclear benefit of DSD, there has been the suggestion of

    potential harm. One case report describes damage sustained to a defi- brillator that was used in DSD, leaving it nonfunctional and suggests that this could affect patient safety as well as void any manufacturer’s warranty [73]. Fortunately, more recent evidence suggests that placing the sets of pads in two near-orthogonal vectors prevents damage to ei- ther defibrillator by decreasing the exposure of a defibrillator to the high voltage from the other (Fig. 3) [74]. This same study suggests that firing the two defibrillators either simultaneously, b10 ms, or at least 100 ms apart has the greatest potential to terminate the arrhyth- mia [74].

    If patients remain in ES despite the above interventions, the patient may benefit from more invasive options. Intra-aortic balloon pumps and catheter ablation can be effective therapies in the acute setting as well as to decrease the recurrence of the arrhythmia and increase long term survival [75-77]. The use of extracorporeal cardiopulmonary re- suscitation has also shown promise as an effective therapy with an in- crease in survival and improved neurological outcomes compared to those receiving conventional cardiopulmonary resuscitation [78-80]. Other invasive devices including left ventricular assist devices have been reported to effectively manage ES [81-84]. If these services are at your disposal, have them involved early when treating patients with ES.


    All patients presenting to the Emergency Department with ES should be admitted to a closely monitored setting, preferably an inten- sive care unit. If a hospital does not have electrophysiology services or a cardiologist who is able to manage ES, it may be reasonable to transfer to a higher level of care.

    Fig. 3. a. Anterior position of orthogonal defibrillator pad placement. b. Posterior position of orthogonal defibrillator pad placement.


    Electrical storm is a dangerous condition that requires rapid diag- nosis and management. Electrical storm is defined as >=3 episodes of sustained VT, VF, or shocks from an ICD within 24 h. Patients may present with a variety of symptoms. An ECG with a rhythm strip should be performed and patients should be placed on continuous cardiac monitoring. A medication history should also be obtained. Initial management includes an antiarrhythmic and a beta blocker. Refractory patients may benefit from DSD, with intra-aortic balloon pumps and extracorporeal membrane oxygenation reserved for crit- ically ill patients that do not respond to the above measures. These patients will generally require admission to an intensive care unit. Knowledge of ES is essential to ensure appropriate evaluation and management.

    Prior presentations



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