Management of Ventricular Electrical Storm: A Contemporary Appraisal

Gurukripa N. Kowlgi; Yong-Mei Cha


Europace. 2020;22(12):1768-1780. 

In This Article

Clinical Presentations and Diagnosis

Ventricular electrical storm can have diverse clinical presentations, depending on multiple factors. The rate of VA, underlying LV function, and the presence of ICD determine how patients present. Patients with significant LV dysfunction usually are unable to tolerate VES and may present with syncope and sudden cardiac death as the first symptom. Patients who are relatively more compensated, especially those with slower VA, may present with symptoms of palpitations, and lightheadedness before developing syncope. Patients with incessant VA with slower rates (100–120 beats/min), may also develop symptoms representative of worsening congestive heart failure.[27]

Individuals with ICDs can have a wide range of presentations—from being completely asymptomatic with VA episodes treated with ATP to recurrent ICD shocks.[28] Patients with frequent ICD shocks are at risk for developing psychological disorders, particularly severe anxiety, and depression.[29]

Prompt identification of VES is critical as it warrants rapid management. The approach depends on whether or not the patient has an ICD implanted. In those patients without an ICD, the clinician must scrutinize the twelve-lead electrocardiogram of the presenting rhythm. The majority of VES present with monomorphic VT, which is a re-entrant arrhythmia generated by non-homogenous myocardial scarring. Polymorphic VT and VF, on the other hand, are seen in acute ischaemia, electrolytes disarrangement, prolonged QT intervals, and genetic channelopathies. Often times, differentiating monomorphic VT vs. supraventricular tachycardia (SVT) with aberrancy can be challenging.[30] Several algorithms have been published to aid in the differential of VT from SVT.[31–33] In cases of ambiguity, especially in the setting of structural heart disease, a wide-complex tachycardia should be treated as VA unless proved otherwise.[34,35] If the situation permits, an astute clinician should make a mental checklist to rule-out the following conditions in all wide complex tachycardias:

  1. SVT with a pre-existing bundle branch block: Thus, comparison to a prior electrocardiogram is paramount.

  2. SVT with rate-related aberrant conduction: Right bundle branch aberrancy more common but can present with left bundle branch block as well.[36]

  3. Antidromic atrioventricular reciprocating tachycardia: By extension, any SVT that conducts antegrade over an accessory pathway can produce a wide QRS complex. Pre-excitation with a delta wave can be recognized by careful review of QRS morphology.

  4. Electrolyte disorders such as hyperkalaemia.

  5. Drugs: The list predominantly includes sodium channel blockers such as the Vaughan Williams Class I antiarrhythmic drugs (Quinidine, Procainamide, Flecainide, among others). If time permits, a thorough history should be obtained to exclude the use of recreational drugs such as cocaine and amphetamines that can have similar QRS complex widening effects.

  6. Paced rhythms: Certain specific causes such as pacemaker-mediated tachycardia, and normal upper-rate behaviour must be considered in patients with ICDs.

In patients with ICDs who experience device therapies, the first step must be to verify if the therapies were indeed appropriate. Shocks for reasons other than VA are termed inappropriate shocks and can occur in as high as 40% of ICD recipients despite novel discriminating device algorithms.[37–39] Some of the established reasons for inappropriate therapies include SVT with rates in the VT/VF zone, oversensing in the ventricular lead: such as T-wave oversensing and lead malfunction with noise detection associated with lead fracture, or loss of lead insulation.[37,40]