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Refractory Ventricular Tachycardia: Approach to Management

Author: Laryssa Patti (EM Chief Resident, Rutgers – RWJMS) // Edited by: Alex Koyfman, MD (EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital, @EMHighAK) and Brit Long, MD (@long_brit, EM Chief Resident at SAUSHEC, USAF)

A 66-year-old male presents complaining of persistent “nausea” that’s been ongoing for the last 12 hours. The patient’s presenting vitals are T 96F, HR 140, RR 18, BP 65/35, and pulse ox 99% on room air.  An ECG is performed and shows monomorphic ventricular tachycardia (VT). With that blood pressure, the patient is unstable, making this one of the easier decisions in emergency medicine. Unstable patient plus shockable rhythm means apply electricity, right? So what happens when cardioversion doesn’t work?

Refractory ventricular tachycardia, also known as “electrical storm,” is defined as at least two or more separate ventricular tachycardia (VT) or fibrillation (VF) episodes requiring intervention in a 24-hour period (1, 2, 3).

So what to do?

  1. ABCs

Start with the basics. Assemble your team. Manage the airway, if necessary. Establish multiple and reliable vascular access sites. An IO is acceptable if IV access is unobtainable and the patient is in extremis.

  1. Search for causes

The reasons for refractory VT/VF are extensive: cardiac ischemia, heart failure, medication changes, systemic illness, renal failure, hypokalemia, hypomagnesemia, hyperthyroidism, increased catecholamine levels, etc. Hohnloser et al. (4) found that up to 25% of patients with refractory VT had reversible causes, so if there’s something in the history that points to one of these, address it. Consider giving magnesium and/or potassium empirically if indicated.

  1. Start with ACLS

If pulseless, give epinephrine as per the ACLS algorithm, with the caveat that catecholamines can increase myocardial susceptibility to arrhythmia. Consider amiodarone and lidocaine after epinephrine.

Administration of amiodarone leads to fast sodium channel blockade in a use-dependent mechanism, in which greater sodium channel blockade exists when the channel is being used more (e.g., at higher heart rates). It also blocks L-type calcium channels, but it does not change myocardial refractory time. Although amiodarone has a risk for prolongation of the QT, the episodes of torsades des pointes secondary to its use are minimal (7).

During cardiac arrest, amiodarone is given as 300 mg IV bolus, with a second bolus of 150 mg. For more stable rhythms, amiodarone is given as 150 mg in 100 mL of D5W over 10 minutes, followed by an infusion of 1 mg/min for 6 hrs.

Similar to amiodarone, lidocaine binds to fast sodium channels in a use-dependent mechanism and is more effective on ischemic tissue than amiodarone (8). However, it is not as effective at converting VT or VF in a non-ischemic patient (9).

Lidocaine is administered as a bolus at 1 to 1.5 mg/kg IV/IO (70 -100 mg in a 70 kg person). Subsequent doses can be given at 0.50-0.75 mg/kg IV/IO (35-50 mg in a 70 kg person) every 5-10 minutes, and can be given as an infusion at 1 to 4 mg/min, with a maximum total dose of 3 mg/kg (210 mg in a 70 kg person) over 1 hour.

  1. Beta-blockers

Recurrent episodes of VT can elevate the sympathetic tone, increasing frequency of future episodes. Nademanee et al. in 2000 showed that administration of beta blockers can increase the fibrillation threshold and decrease risk for sudden cardiac death in patients presenting with recurrent VT after myocardial infarction, hypothesizing that the damaged myocardial cells are more sensitive to sympathetic tone (6).

Driver et al. (11) performed a small study in which esmolol infusions were started in patients in refractory VF after multiple electrical cardioversions and administration of at least 3 mg epinephrine and 300 mg amiodarone. More patients who received esmolol obtained and sustained return of spontaneous circulation (ROSC), survived to intensive care unit admission, survived to hospital discharge, and survived with a favorable neurologic outcome, in comparison to patients who did not receive esmolol.

Esmolol is administered as a continuous infusion at 50-300 mcg/kg/min.

  1. Consider procedures to reduce the sympathetic drive

Ultrasound-guided stellate ganglion blockade has been shown in case studies (15, 16, 17) and one small randomized trial (18) to reduce mortality. The stellate ganglion is located at the level of C7, below the subclavian artery, and is the sympathetic ganglion that conducts sympathetic activity to the heart. By blocking the stellate ganglion, the amount of sympathetic outflow to the heart is decreased, which may in turn decrease the sensitivity of the myocardium to arrhythmias.

  1. Consider increasing the amount of energy given during defibrillation

High-energy defibrillation (also known as “double down” defibrillation or “double sequential” defibrillation) was initially suggested by Hoch et al. (13), in which the investigators administered sequential shocks from two defibrillators in less than 5 seconds. Defibrillator pads were placed adjacent to one another in an anterior-posterior manner, in order to maximize the amount of energy travelling through the heart. In their study, patients resuscitated with two defibrillators were able to regain spontaneous circulation. Walcott et al. (14) showed that although there was no significant change in survival following high-energy defibrillation, there was no increased risk to patients undergoing biphasic 360 joule shocks in comparison to 150 joule shocks.

  1. Special consideration for patients with Brugada syndrome

Isoproterenol, a beta-receptor agonist with positive inotropic and cardiotropic effects, should be considered in patients in refractory VT/VF secondary to Brugada syndrome. Isoproterenol works by increasing the level of intracellular calcium, increasing the stability of the myocardium. In a small study by Ohgo et al. (10), isoproterenol infusion normalized ST segment elevation in patients with electrical storm.

Isoproterenol is administered as an infusion at 0.1 to 1.3 mcg/min.

8.   Consider sedation

The stress of multiple defibrillations and the physical sensation of VT/VF can lead to an increase in sympathetic tone, releasing more catecholamines and making VF/VT harder to control. Sedation using propofol or benzodiazepines in the emergency department should be considered (5).

  1. Consider cardiac catheterization post-ROSC

Always speak to cardiology about catheterization in the patient with ROSC. A culprit lesion in the coronary vasculature can be the cause for VF/VT.

Although the idea of VF or VT that is resistant to electricity is the stuff that emergency physicians’ nightmares are made of, there are concrete steps and medications to administer in order to increase the likelihood of returning to a normal perfusion pattern.

 

References / Further Reading:

  1. Gao and Sapp. Electrical storm: definitions, clinical importance, and treatment. Curr Opin Cardiol. 2013 Jan;28(1):72-9
  2. European Heart Rhythm Association; Heart Rhythm Society, Zipes DP, Camm AJ, Borggrefe M, Buxton AE, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death). J Am Coll Cardiol 2006;48(5): e247–346.
  3. Exner et al. Electrical storm presages nonsudden death: the antiarrhythmics versus implantable defibrillations (AVID) trial. Circulation. 2001 Apr 24;103(16):2066-71
  4. Hohnloser et al. Electrical storm in patients with an implantable defibrillator: incidence, features, and preventative therapy: insights from a randomized trial. Eur Heart J. 2006 Dec;27(24):3027-32. Epub 2006 Oct 18.
  5. Eifling M, Razavi M, and Massumi A. The evaluation and management of electrical storm. Tex Heart Inst J. 2011; 38(2): 111–121.
  6. Nademanee K, Taylor R, Bailey WE, et al. Treating electrical storm: sympathetic blockade versus advanced cardiac life support-guided therapy. Circulation 2000; 102:742–747.
  7. Du XJ, Esler MD, Dart AM. Sympatholytic action of intravenous amiodarone in the rat heart. Circulation 1995;91(2):462–70.
  8. Nasir N Jr, Taylor A, Doyle TK, Pacifico A. Evaluation of intravenous lidocaine for the termination of sustained monomorphic ventricular tachycardia in patients with coronary artery disease with or without healed myocardial infarction. Am J Cardiol 1994;74(12):1183–6
  9. Dorian P, Cass D, Schwartz B, Cooper R, Gelaznikas R, Barr A. Amiodarone as compared with lidocaine for shock-resistant ventricular fibrillation [published erratum appears in N Engl J Med 2002;347(12):955]. N Engl J Med 2002;346(12):884–90.
  10. Ohgo T, Okamura H, Noda T, Satomi K, Suyama K, Kurita T, et al. Acute and chronic management in patients with Brugada syndrome associated with electrical storm of ventricular fibrillation. Heart Rhythm 2007;4(6):695–700.
  11. http://www.ncbi.nlm.nih.gov/pubmed/25033747Driver BE, Debaly G, Plummer DW, Smith SW. Use of esmolol after failure of standard cardiopulmonary resuscitation to treat patients with refractory ventricular fibrillation. Resuscitation, 2014 Oct;85(10):1337-41. doi: 10.1016/j.resuscitation.2014.06.032. Epub 2014 Jul 14
  12. Maury P, Hocini M, and Haissaguerre M. Electrical storms in Brugada syndrome: a review of pharmacologic and ablative therapeutic options. Indian Pacing Electrophysiol J. 2005 Jan 1;5(1):25-34.
  13. Hoch DH et al. Double sequential external shocks for refractory ventricular fibrillation. J Am Coll Cardiol. 1994;23(5):1141-1145
  14. Walcott GP, Melnick SB, Killingsworth CR, Ideker RE. Comparison of low energy versus high energy biphasic defibrillation shocks following prolonged ventricular tachycardia. Prehosp Emerg Care. 2010 Jan-Mar; 14(1): 62-70.
  15. Loyalka P et al. Left stellate ganglion block for continuous ventricular arrhythmias during percutaneous left ventricular assist device support. Tex Heart Inst J. 2011; 38(4): 409–411.
  16. Boe BA et al. Percutaneous ultrasound guided stellate ganglion nerve block suppresses recurrent ventricular fibrillation in an infant awaiting heart transplant. Circulation: Arrhythmia and Electrophysiology.2012; 5: e93-e94
  17. Hayase J et al. Percutaneous stellate ganglion block suppressing VT and VF in a patient refractory to VT ablation. Journal of Cardiovascular Electrophysiology. 2013 Aug; 24(8): 926-928.
  18. Nademanee et al. Treating electrical storm: Sympathetic blockade versus advanced cardiac life support-guided therapy. Circulation. 2000; 102: 742-747.

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