Electrical Storm and Incessant Ventricular Tachycardia: A Practical, Step-by-Step Clinical Guide

Introduction

Electrical storm and incessant ventricular tachycardia are life-threatening ventricular arrhythmias that require rapid, structured, and mechanism-based management. This practical clinical guide outlines a step-by-step approach to the assessment and treatment of electrical storm and incessant VT, based on current ESC, EHRA and AHA/ACC/HRS recommendations and real-world critical care experience.

The article is written in collaboration with Dr Njord Nordstrand, Consultant Cardiologist at the Cardiac Intensive Care Unit, Oslo University Hospital Rikshospitalet, and is intended for clinicians managing complex ventricular arrhythmias in acute and intensive care settings.

Scope and clinical framework

Given the severity of electrical storm and incessant VT, patients should be considered early for transfer to centres with access to mechanical circulatory support and catheter ablation when required. This article provides an updated, practical framework for managing these conditions in the emergency department, on medical wards, and in intensive care units, where decisions often need to be made rapidly and under uncertainty.

The SCAI classification (Society for Cardiovascular Angiography and Interventions) is used to grade the severity of cardiogenic shock and circulatory failure and is recommended to support clinical assessment (see figure). Patients are categorised into five stages, from A (At risk) to E (Extremis), reflecting a continuum from risk without shock to advanced shock and circulatory collapse. The classification offers a shared clinical language and supports risk stratification and escalation of care.

SCAI classification

Understanding the Conditions

Electrical storm is defined as three or more episodes of ventricular arrhythmia or ICD therapy within 24 hours. It is often driven by heightened sympathetic activity and may be triggered by infection, stress, ischaemia, or worsening heart failure.

Incessant VT differs in that the arrhythmia is continuous or recurs immediately after termination, usually due to a stable re-entry substrate. While electrical storm often requires rapid sympathetic control, incessant VT typically necessitates early consideration of catheter ablation.

Initial Assessment and Early Decisions

On admission, it is crucial to distinguish between:

• Patients in cardiogenic shock with cerebral compromise (SCAI class C), who should be rapidly sedated and treated with cardioversion and/or antiarrhythmic therapy before further diagnostics

• Patients with residual haemodynamic reserve (SCAI class B), who tolerate the arrhythmia and allow more extensive evaluation

  
  

In ventricular arrhythmias, acute myocardial ischaemia must be considered early. If clinical presentation and troponin dynamics suggest acute coronary syndrome, urgent coronary angiography is indicated. If ischaemia is unlikely, stabilising measures should be prioritized. Assessment should include looking for known structural heart disease such as ischaemic or dilated cardiomyopathy, and potential triggers including infection, thyrotoxicosis, electrolyte disturbances, or dehydration.

Haemodynamic assessment is central. Rapid evaluation of perfusion, blood pressure, level of consciousness, pulmonary congestion, and peripheral temperature is required. Monitoring should ideally include echocardiography, arterial line, and central venous access. Many patients with slow VT may appear deceptively stable but often have limited reserve and may deteriorate abruptly. Continuous invasive blood pressure monitoring and central venous access should therefore be established early.

Helpful indicators of “stability” include arrhythmia burden, patient stress response, clinical tolerance during VT, and whether central venous oxygen saturation (SvO₂) falls during episodes. These parameters are difficult to assess clinically alone and should be closely monitored, preferably using invasive measures when available.

In patients with an ICD or CRT-D, it is essential to determine whether the arrhythmia falls below the detection threshold. This is particularly relevant in patients treated with amiodarone or high-dose beta-blockers, where VT may be slow and misinterpreted as supraventricular tachycardia. Early device interrogation, ig available, is therefore recommended. While pacemakers do not terminate tachyarrhythmias, they may provide valuable diagnostic information and can be useful when overdrive pacing is required.

Reversible Causes and Laboratory Assessment

Investigation and correction of reversible factors must proceed in parallel with treatment. Potassium and magnesium should be corrected towards the upper normal range. Renal function, inflammatory markers, and acid–base status provide important information regarding triggers and prognosis. Thyroid function tests should be obtained early, particularly in patients treated with amiodarone

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Common clinical triggers include infection, dehydration, thyrotoxicosis, anaemia, and medication changes. In heart failure patients, even minor shifts in fluid balance or electrolytes may destabilise electrical stability. Temperature control is equally important; patients with sepsis-related electrical instability often respond favourably to intravenous paracetamol.

Acute Stabilization and Priority Interventions

Sedation is one of the most effective interventions in electrical storm. Suppression of sympathetic tone often results in an immediate reduction in trigger activity and myocardial irritability. Light sedation may be attempted in stable patients (SCAI class B), but in the presence of frequent episodes or pronounced autonomic activation, deeper sedation and intubation are frequently required. Ideally, this should be undertaken before haemodynamic compromise develops.

Agents suitable for lighter sedation prior to intubation include dexmedetomidine (Dexdor), morphine, midazolam, or diazepam. For example, diazepam 2.5 mg may be administered and titrated until the patient is calm or lightly sedated, with morphine added if needed. Oral sedatives may be considered in awake patients during a more stable phase (SCAI class B).

Beta-blockers are a cornerstone of therapy in ventricular tachyarrhythmias. Metoprolol is often sufficient in relatively stable patients (SCAI class A or B), while short-acting agents such as esmolol or landiolol may offer better control in borderline cases. Their short half-life allows rapid dose reduction if haemodynamic tolerance is poor. Consensus documents and ESC guidelines highlight landiolol as a preferred option; it is the most beta-1 selective agent available and has minimal blood pressure–lowering effects. This can be critical both for tolerance and when sedation is planned, as it may reduce the need for volume resuscitation and catecholamine support during intubation.

Amiodarone should be administered in parallel but should not be relied upon as monotherapy, as its acute efficacy may be limited.

Electrolyte therapy plays a clear role in polymorphic VT and torsades de pointes, where intravenous magnesium is first-line treatment. In monomorphic VT, magnesium has no proven benefit but may be used adjunctively in hypokalaemia. Both potassium and magnesium should be maintained in the upper normal range. Magnesium is also indicated in digoxin toxicity and in bidirectional VT caused by digoxin intoxication, but not in bidirectional VT of other aetiologies.

Calcium or sodium bicarbonate have narrow indications and should be reserved for hyperkalaemia or intoxication with calcium channel or sodium channel blockers.

Third Antiarrhythmic Agent and Timing

Electrical storm requires rapid escalation if arrhythmias persist despite treatment. If new episodes occur within one hour of initiating beta-blocker and amiodarone therapy, a third agent (a sodium channel blocker) should be considered. In incessant VT, escalation should occur earlier, typically within 10 to 20 minutes, as the goal is stabilization while preparing for ablation.

If arrhythmias persist after 30 to 60 minutes of beta-blocker and amiodarone therapy, a third antiarrhythmic should be added, guided by the underlying mechanism.

Mexiletine is the sodium channel blocker with the best documented efficacy as add-on therapy in refractory VT and electrical storm. It can be safely combined with beta-blockers and amiodarone when first-line therapy is insufficient and has been shown to reduce VT/VF episodes and ICD therapies in patients with structural heart disease. Its effect is moderate and best documented as adjunctive therapy rather than monotherapy; catheter ablation still remains more effective when feasible. Typical dosing is 200–400 mg orally two to three times daily. Gastrointestinal and neurological adverse effects are common and require monitoring.

Lidocaine has extensive clinical experience and is administered intravenously for acute VT/VF. ACC, AHA, and HRS guidelines describe lidocaine as an option in acute unstable arrhythmias, though it is less effective than amiodarone for incessant VT and does not improve survival to discharge compared with placebo or amiodarone. Some studies suggest modest improvements in ROSC, 24-hour survival, and survival to discharge compared with amiodarone in in-hospital VT/VF arrest, but differences are limited. Lidocaine has minimal efficacy in preventing VT recurrence during electrical storm and is primarily an acute termination agent rather than a maintenance therapy.

Overall, lidocaine is a useful intravenous agent for acute episodes, while mexiletine represents a relevant oral adjunct for persistent or recurrent VT in patients for whom ablation is not feasible or has failed. Both have established but clearly defined roles in electrical storm and refractory VT associated with structural heart disease.

Flecainide is generally not recommended in structural heart disease due to proarrhythmic risk related to slowed conduction and enhanced re-entry in scar tissue. It may be considered in idiopathic arrhythmias or catecholaminergic polymorphic VT (CPVT). In clinical practice, however, flecainide is still used relatively frequently in ischaemic cardiomyopathy because it is more readily available than mexiletine and often easier to administer than lidocaine.

Procainamide has demonstrated good efficacy in clinical trials but is unfortunately not available in Norway.

Quinidine is a specialised agent typically reserved for channelopathies such as Brugada syndrome and early repolarisation syndrome. In practice, it may be used when other strategies fail and is associated with relatively few acute adverse effects.

Table 1: Vasoactive agents in electrical storm and incessant VT

Drug	When to use	Clinical effect / rationale	Limitations / warnings
Noradrenaline (norepinephrine)	• Hypotension in electrical storm or incessant VT • Cardiogenic shock	• Potent vasoconstrictor • Improves MAP and end-organ perfusion • Lower arrhythmic risk than dopamine/adrenaline	• Higher doses may increase ventricular arrhythmia propensity, especially in severe heart failure • Titrate to the lowest effective dose
Dobutamine	• Persistently low cardiac output despite vasopressor support • When additional inotropy is required	• Increases contractility and cardiac output • Reduces systemic vascular resistance	• Can trigger ventricular arrhythmias (dose-dependent; higher risk with arrhythmogenic substrate) • Requires close haemodynamic monitoring
Sodium nitroprusside	• Hypertension and/or high afterload • When elevated afterload contributes to arrhythmia and decompensation	• Reduces preload and afterload • Unloads the left ventricle • May reduce myocardial oxygen demand	• Not routine in electrical storm • Risk of hypotension • Avoid in low blood pressure
Vasopressin	• Hypotension refractory to noradrenaline (can also be considered early/first-line in selected cases)  • When additional vasoconstriction is desired without increasing heart rate	• Potent vasoconstrictor without direct chronotropy; typically less pro-arrhythmic than catecholamines • Useful as first agent or add-on	• Hyponatraemia can occur • No direct inotropic effect
Phenylephrine	• Selected situations such as dynamic LVOT obstruction	• Increases SVR without increasing heart rate	• May reduce cardiac output in poor LV function
Adrenaline (epinephrine)	• Selected emergency situations only • VT/VF during cardiac arrest (ACLS)	• Strong inotropy and vasoconstriction	• High arrhythmic risk • Often unsuitable or contraindicated in electrical storm
Dopamine	• Rarely: bradycardia with hypotension	• Can increase heart rate and cardiac output	• High arrhythmic risk • Less favourable safety profile than noradrenaline

Use of Vasoactive Agents in Electrical Storm and Incessant VT

In patients with electrical storm or incessant VT, particularly in the context of ischaemic cardiomyopathy, arrhythmias frequently coexist with haemodynamic instability. Vasoactive agents may therefore be required to maintain organ perfusion and adequate blood pressure while antiarrhythmic therapy and definitive interventions are planned.

Nitroprusside may be useful in selected patients with concomitant hypertension or marked afterload. By reducing both venous and arterial resistance, it can improve left ventricular performance and reduce myocardial oxygen demand, occasionally contributing to stabilization. It is not used routinely but may be considered when increased afterload is a contributing factor.

In hypotension, vasopressors are required, and noradrenaline is generally recommended as first-line therapy. It provides predictable blood pressure support and carries a lower arrhythmic risk than dopamine or adrenaline. However, increasing attention has been directed towards potential adverse effects of high-dose noradrenaline. At higher doses, or in patients with severe heart failure, noradrenaline may increase the risk of ventricular arrhythmias. Dosing should therefore always be titrated to the lowest effective level that ensures adequate organ perfusion.

Mean arterial pressure (MAP) targets must be individualized. Patients following cardiac arrest (post-ROSC) often require higher MAP targets to ensure adequate cerebral perfusion. In contrast, patients with electrical storm or incessant VT who are deeply sedated, often intubated, and have reduced metabolic and oxygen demands may tolerate lower blood pressure levels, provided organ perfusion is adequate, for example demonstrated by sufficient urine output and stable central venous oxygen saturation and lactate.

If escalating doses of noradrenaline are required, typically exceeding 0.25 μg/kg/min, the addition of vasopressin  is recommended to limit further catecholamine exposure. In our clinical practice, we often initiate vasopressin (0.01 - 0.03U/min) early and escalate noradrenaline only if adequate blood pressure is not achieved In the presence of sepsis with concomitant electrical instability, noradrenaline should nevertheless remain first-line therapy in accordance with established recommendations.

Phenylephrine is not routinely recommended but may be considered in selected situations, such as dynamic left ventricular outflow tract obstruction.

Dobutamine is indicated when low cardiac output persists despite vasopressor therapy. It increases contractility and reduces systemic vascular resistance but may provoke ventricular arrhythmias, particularly at higher doses or in patients with a pronounced arrhythmogenic substrate. Its use therefore requires close haemodynamic monitoring.

There is limited randomized evidence to guide the optimal choice of vasoactive agent in arrhythmic storm, and therapy must be individualized based on haemodynamic response and arrhythmia burden. Vasoactive drugs should be viewed as a bridge to definitive therapies, including antiarrhythmic optimization, catheter ablation, and mechanical circulatory support.

Sympathetic Modulation as a Specialized Intervention

In patients who do not respond adequately to pharmacological therapy and sedation, sympathetic blockade is an important therapeutic option. Left-sided stellate ganglion block has documented efficacy and can be performed bilaterally. It is often feasible at the bedside under ultrasound guidance, has rapid onset, and a low complication rate. Beta-1 receptors within the stellate ganglion may contribute to its antiarrhythmic effects.A commonly used preparation consists of 100 IU botulinum toxin diluted in 2 ml lidocaine and 8 ml sodium chloride, giving a total volume of 10 ml, with 5 ml administered per side when bilateral injection is performed.

An alternative approach is epidural sympathetic blockade, which may provide a broader effect but requires greater expertise and resources. Both strategies can be used as a bridge to ablation or for temporary stabilisation.

Device Programming and Pacing Strategies

Optimization of ICD or CRT-D programming is a key component of management. VT occurring just below the detection threshold can often be better controlled by adjusting detection zones and allowing additional ATP (Anti-tachycardia pacing) attempts. ATP can terminate the majority of monomorphic VT episodes and should be prioritised over shocks whenever safe.

Overdrive pacing, preferably atrial pacing without ventricular pacing, may be used in patients with or without implanted devices. In CRT patients, comparing QRS duration during pacing with intrinsic conduction is informative; a narrower paced QRS often reflects improved haemodynamics and may serve as a surrogate for more effective cardiac output.

In patients without an implanted device, a temporary atrial pacing lead may be inserted. Its effectiveness is often limited by a low Wenckebach point*, particularly in the presence of beta-blockers and sodium channel blockers.

The haemodynamic impact of pacing can be assessed using central venous oxygen saturation or by measuring LVOT-VTI on echocardiography.

*The Wenckebach point represents the highest atrial pacing rate that still allows 1:1 AV conduction, thereby limiting the maximum effective pacing rate.

Haemodynamic Support

Mechanical circulatory support has become central in the management of severe ventricular arrhythmias. An intra-aortic balloon pump (IABP) can improve perfusion, reduce afterload, and alleviate secondary mitral regurgitation. Establishing IABP support before deep sedation may be prudent in patients with impaired left ventricular function.

Improving cardiac output is critical in this population, as reduced peripheral organ perfusion can lead to multiorgan failure and secondary systemic inflammatory response syndrome, which is itself proarrhythmic and may reinforce a vicious cycle.

Impella and ECMO are used in refractory electrical storm and cardiogenic shock and play a key role as bridges to ablation. Impella, positioned within the left ventricle, may itself provoke arrhythmias due to mechanical irritation but is often justified as a bridge to rapid ablation. ECMO is used less frequently, although some international centres employ smaller cannulae and lower flow rates in this patient group.

Evidence suggests improved survival when mechanical support is initiated proactively, before the development of multiorgan failure. The PAINESD risk score may aid decision-making but should not be the sole determinant of mechanical support.

PAINESD Score: Risk Stratification in Electrical Storm and VT Ablation

The PAINESD score identifies patients at high risk of haemodynamic collapse during electrical storm or VT ablation. Points are assigned to the following variables:

• P Pulmonary disease (COPD) – 5 points

• A Age > 60 years – 3 points

• I Ischaemic cardiomyopathy – 6 points

• N NYHA class III–IV – 6 points

• E Ejection fraction < 25% – 3 points

• S VT storm at presentation – 5 points

• D Diabetes mellitus – 3 points

  
  

Interpretation

• Low risk: < 8–10 points. Usually haemodynamically stable; mechanical support considered only in selected cases.

  
  

• Moderate risk: 10–15 points. Increased risk of decompensation during sedation or ablation; low threshold for mechanical support or intensive monitoring.

  
  

• High risk: ≥ 15–17 points. Substantial risk of haemodynamic collapse. These patients have demonstrated improved outcomes with proactive mechanical circulatory support (IABP, Impella, or ECMO) prior to ablation or deep sedation.

  
  

Clinical relevance: The PAINESD score is primarily a decision-support tool to identify patients who may benefit from early haemodynamic support. It should not dictate management in isolation but helps identify the most vulnerable patients in whom aggressive intervention may improve outcomes.

When Should Cardioversion Be Performed?

Electrical cardioversion is life-saving in polymorphic VT, ventricular fibrillation, or haemodynamic collapse. In slow monomorphic VT, where the patient is relatively stable, and in incessant VT with rapid recurrence after termination, it may be reasonable in selected cases to defer shocks if ongoing measures are expected to be effective, the arrhythmia is haemodynamically tolerated, and close monitoring is ensured.

ATP (Anti-tachycardia pacing) should be attempted whenever feasible. If clinical deterioration occurs, cardioversion must not be delayed. Repeated shocks should prompt consideration of sedation and intubation, as escalation can occur rapidly.

Isoprenaline: When Indicated and When to Avoid

Isoprenaline has a very specific role in the management of ventricular arrhythmias. It is recommended only in torsades de pointes or electrical storm in patients with congenital or acquired long QT syndrome, when arrhythmias are pause- or bradycardia-dependent, and when electrolyte correction or pacing is insufficient.

By increasing heart rate and shortening the QT interval, isoprenaline can suppress pause-dependent polymorphic arrhythmias. Outside this indication, isoprenaline should not be used. It is contraindicated in idiopathic VT, Brugada syndrome, arrhythmogenic right ventricular cardiomyopathy, and structural heart disease, where it may exacerbate arrhythmias and cause harm. In such cases, standard therapy with beta-blockers, amiodarone, sotalol, and catheter ablation should be followed.

Catheter Ablation

Catheter ablation is the definitive treatment for incessant VT and should be considered early. Indications include monomorphic VT in structural heart disease, failure of pharmacological therapy, frequent recurrences, and haemodynamic instability. Early contact with an electrophysiology centre is essential to plan timing and interim management.

A 12-lead ECG during ongoing arrhythmia should be obtained whenever possible to facilitate procedural planning. Patients who require intubation should generally be considered candidates for ablation unless the arrhythmia is expected to resolve once a transient trigger is treated.

Central Venous Catheter

A central venous catheter (CVC) is useful for advanced haemodynamic monitoring, administration of vasoactive agents, and assessment of pacing strategies and other ongoing interventions. In patients with pacemakers or ICDs, particular attention must be paid to infection risk, as device-related infection can have severe consequences and may necessitate complete system extraction.

If a CVC is deemed necessary, insertion should be performed with meticulous sterile technique. Although robust evidence is lacking, we recommend a low threshold for prophylactic antibiotics in clinical practice, for example cefazolin or cefalotin (1 g four times daily), analogous to the approach used for temporary pacing leads.

Table 2: Treatment strategy when there is inadequate respons

Clinical step / scenario	Intervention	Rationale / comments
1. Initiate therapy	Beta-blocker + amiodarone	Foundation for both electrical storm and incessant VT. Reduces sympathetic drive and stabilises myocardial electrophysiology.
2. Reassess response	• Electrical storm: reassess after 30–60 min • Incessant VT: reassess after 10–20 min	Early reassessment is crucial. VT that does not terminate promptly → high risk of haemodynamic decompensation.
3. New episodes / inadequate control	Add a third antiarrhythmic based on mechanism	See drug-specific options below.
3A. Acute, unstable VT / ischaemic component	Lidocaine (IV)	Rapid onset; generally safe in structural heart disease. Less effective for incessant VT, but useful acutely.
3B. Refractory VT in structural heart disease	Mexiletine (oral)	Best documented add-on therapy. Reduces recurrence and ICD therapies. Useful when ablation is unavailable/contraindicated or has failed.
3C. Idiopathic VT or CPVT	Flecainide	Effective in non-structural arrhythmias. Avoid in ischaemic/dilated cardiomyopathy due to pro-arrhythmia.
3D. Channelopathy (Brugada, early repolarisation, idiopathic VF)	Quinidine	Mechanism-specific (Ito block). Rarely used in structural heart disease.
4. After adding a third agent	Reassess haemodynamics, recurrence, and tolerance	If still unstable: escalate to sedation, intubation, and mechanical circulatory support.
5. Early ablation	• Always consider in incessant VT  • Consider in electrical storm with recurrent monomorphic VT on structural substrate	Ablation is definitive therapy for incessant VT. Do not delay unnecessarily.
6. Continuous re-evaluation	Optimize pacemaker/ICD/CRT programming, correct electrolytes, address triggers	Optimizing reversible factors and device settings may be decisive for stabilization.

Practical Decision Support

When the clinical situation is unclear, the following steps may help establish direction. These principles apply to all haemodynamically unstable patients, not only those with electrical storm:

1. Identify the primary mechanism triggering the arrhythmia.

2. Formulate a plan to address this mechanism.

3. Implement the interventions deemed appropriate.

4. Reassess and repeat from step 1 if the strategy fails.

   
   

Key questions in this patient population include:

1. What SCAI class is the patient in?

2. Is this electrical storm or incessant VT?

3. Have reversible causes been corrected and baseline therapy optimised?

   
   

If episodes persist, escalation should include sedation, intensified beta-blockade, amiodarone, lidocaine, mexiletine, and consideration of intubation and early mechanical support. In incessant VT, overdrive pacing, lidocaine, mexiletine, IABP, and early ablation are central interventions.

Summary

Management of electrical storm and incessant VT requires a systematic approach combining sympathetic suppression, appropriate antiarrhythmic therapy, optimal device programming, haemodynamic support, and early consideration of catheter ablation. This article presents a practical framework intended to support clinicians in high-pressure clinical scenarios and to facilitate safer and more predictable management.

References

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2. Lenarczyk R, Zeppenfeld K, Tfelt-Hansen J, et al. Management of patients with an electrical storm or clustered ventricular arrhythmias: EHRA clinical consensus statement. Europace. 2024;26:euae049.

3. Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS Guideline for management of patients with ventricular arrhythmias. Circulation. 2018;138:e272–e391.

4. Sapp JL, Wells GA, Parkash R, et al. Ventricular tachycardia ablation versus escalation of antiarrhythmic drugs. N Engl J Med. 2016;375:111–121.

5. Savastano S, Baldi E, Compagnoni S, et al. Electrical storm treatment by stellate ganglion block (STAR study). Eur Heart J. 2024;45:823–833.

6. Mariani S, Napp LC, Lo Coco V, et al. Mechanical circulatory support for life-threatening arrhythmia. Int J Cardiol. 2020;308:42–49.

7. Jentzer JC, Noseworthy PA, Kashou AH, et al. Multidisciplinary Critical Care Management of Electrical Storm: JACC State-of-the-Art Review. J Am Coll Cardiol. 2023;81(22):2189–2206. doi:10.1016/j.jacc.2023.03.424.