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THE MORNING REPORT

The Best in FOAM Education

Drew Nguyen, MD

Monomorphic VT Storm

Definition

  • The occurrence of three or more hemodynamically stable ventricular tachyarrhythmias within 24 hours​

  • VT recurring soon after (within five minutes) termination of another VT episode​

  • Sustained and non-sustained VT resulting in a total number of ventricular ectopic beats greater than sinus beats in a 24-hour period​

  • In patients with an ICD, the most widely accepted definition of electrical storm is three or more appropriate therapies for ventricular tachyarrhythmias, including antitachycardia pacing or shocks, within 24 hours

Pathophysiology

  • VT/VF increases intracellular calcium levels, which may be pro-arrhythmic.​

  • Shocks and episodes of cardiac arrest (e.g. treated with epinephrine) may cause myocardial injury.​

  • Myocardial injury and pain stimulate an outpouring of endogenous catecholamines, promoting recurrent arrhythmia.

Medical antiarrhythmic therapy

Amiodarone ​(1st line)

  • 300 mg bolus (over 10 minutes), then 1 mg/min x6 hours, then 0.5 mg/min.​

  • Additional boluses can be given for recurrence (up to a total of ~900 mg in boluses).​

  • Avoid >2.2 grams total dose within 24 hours (i.e., >900 mg in bolus doses).​

  • Patients on chronic oral amiodarone should still be reloaded with IV amiodarone

propranolol ​(2nd line)

  • Loading bolus 0.15 mg/kg IV over 10 minutes (~10 mg). Follow heart rate and hold the infusion if the heart rate falls <45 b/m.​

  • Maintenance: 3-5 mg IV Q6hr.​

OR​

esmolol infusion ​(2nd line)

  • Loading dose is 0.5 mg/kg IV (~30 mg) over one minute.​

  • Start infusion at 0.050 mg/kg/min (~3 mg/min).​

  • May re-load & up-titrate infusion in increments of 0.05 mg/kg/min every 10 minutes, up to a maximal dose of 0.3 mg/kg/min (~20 mg/min).

Lidocaine​ (3rd line)

  • Bolus with 1-1.5 mg/kg and then infuse at a rate of 0.02 mg/kg/min (~1.5 mg/min)​

  • May re-bolus with 0.5-0.75 mg/kg IV, up to a total dose of 3 mg/kg.​

  • May titrate up to ~4 mg/min.​

  • modestly effective in scar-related monomorphic VT, but it may be more useful in the context of acute ischemia

Consider Reversible Triggers

  • Drug toxicity​

  • Electrolyte disturbances (ie, hypokalemia and hypomagnesemia)​

  • New or worsened heart failure​

  • Acute myocardial ischemia​

  • Thyrotoxicosis​

  • QT prolongation (which may be related to drug toxicity, electrolyte imbalance, or an underlying syndrome such as long QT syndrome)

Intubation and sedation

  • Intubation is often required for a true VT storm as patients may lose airway control during episodes of VT/VF​

  • Deep sedation itself is therapeutic.​

    • Propofol seems to work particularly well here but may cause hypotension due to vasodilation​

    • Dexmedetomidine may also reduce sympathetic tone, however, has some drawbacks which make it 2nd line​

      • Dexmedetomidine is sluggish to titrate.​

      • Dexmedetomidine can't achieve the same depth of deep sedation that propofol can.​

    • Benzodiazepine may be used if the patient is unable to tolerate propofol/dexmedetomidine due to severe hypotension.​

  • Analgesia is important for any intubated patient, but it's especially important in VT storm because untreated pain can drive sympathetic tone and promote recurrent arrhythmia.

Management of refractory cases

  • Catheter ablation​

  • Thoracic epidural anesthesia and/or general anesthesia​

  • Insertion of an intraaortic balloon pump or a temporary ventricular assist device​

  • Stellate ganglion block



References

  • Farkas, J. (2023, March 21). Monomorphic VT storm. EMCrit Project. https://emcrit.org/ibcc/storm/#definition ​

  • Passman, R. (n.d.). Electrical storm and incessant ventricular tachycardia. UpToDate. https://www.uptodate.com/contents/electrical-storm-and-incessant-ventricular-tachycardia

Drew Nguyen, MD

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