Is This Tattoo Compatible With Life?
Written by: Kent Li, MD. Edited by: Sunny Elagandhala.
Ventricular Tachycardia : Features, Approaches, and Considerations in Chemical Cardioversion
A 84-year-old nursing home patient is sent in for evaluation with the chief complaint of “AMS.” As you run through your impressively broad differential, zebras and horses alike, the patient deteriorates from AOx2 and answering questions, to babbling incomprehensible nonsense. Great differential, but let’s focus on the ABCs of resuscitation. He has a pulse. He is spontaneously breathing and maintaining his airway. You get a blood pressure of 80/45 and a heart rate of 140. You finally slap the pads on his diaphoretic chest and see this on the rhythm strip:
Is this VT or SVT with aberrancy?
Recognizing ventricular tachycardia:
Broad complex tachycardia, QRS >120 (3 boxes)
Regular
A-V dissociation is present — P-waves hidden throughout rhythm.
RSR’ with left notch greater than right
Presence of fusion and capture complexes
So you’ve diagnosed VT, what now?
The approach to management comes down to the patient’s hemodynamic stability, in essence 3 variations:
Pulseless
Unstable — IE hypotension or signs of end organ hypo-perfusion
Stable — mentating at baseline, stable VS
Your Toolbox to address each scenario:
1. ACLS — if patient is pulseless
2. Electrical cardioversion — if patient is unstable
3. Chemical or electrical cardioversion — in stable patient.
To simplify your thinking, if you treat all wide complex tachycardias as ventricular tachycardia, you will not mismanage the patient.
With ONE HUGE caveat — QRS> 200, or HR < 120, strongly consider toxicologic causes or hyperkalemia.
Dosages:
Lidocaine - Class 1B antiarrhythmic
Bolus: 1.0-1.5 mg/kg (repeat 0.5 – 0.75 mg/kg up to total of 3 mg/kg)
Infusion: 1-4 mg/min
Procainamide - Class 1A antiarrhythmic
Dose: 30-50 mg/min IV until dysrhythmia terminated (max of 18 mg/kg)
Infusion: 1 to 4 mg/minute, to be started after termination of arrhythmia.
Amiodarone - Class III antiarrhythmic
Bolus: 150 mg IV over 10 min
Infusion: 1 mg/min IV X 6 hours then 0.5 mg/min X 18 hours
An aside on the use of amiodarone:
Amiodarone rose to popularity despite a paucity of evidence during 60’s to 80’s, where it was touted as a wonder drug with minimal adverse effects. At the height of its use, thousands of patients were on amiodarone without FDA approval. During the early 2000’s its use was cemented in ACLS with the ALIVE trial, where it showed increased survival to hospital admission when compared to Lidocaine1, however failed to show benefit in survival to hospital discharge. [1]
It is now thoroughly documented all the adverse side effects of amiodarone including liver disease, thyroid dysfunction and pulmonary fibrosis. Additionally, amiodarone is now known to exhibit effects at not only potassium channels, as once thought, but also both sodium and calcium channels. Recently, there is emerging evidence that amiodarone is no longer the preferred antiarrhythmic — particularly in VT.
The PROCAMIO trial:
This trial featured a head to head comparison of IV amiodarone to procainamide in hemodynamically stable patients with wide-complex tachycardias. In sum — patients treated with procainamide had not only fewer adverse events, but also greater success in termination of arrhythmia within 40 minutes (67% vs 38% with amio) with an NNT of 3.3. [2]
However, still keep in mind that electrical cardioversion is superior to chemical cardioversion in the management of VT. If electing to attempt chemical cardioversion, all patients should be placed on pads.
Back to the case
This patient had an unstable ventricular tachycardia. Given the patients hypotension and decline in his mental status, we elected to electrically cardiovert the patient. We charged to 200 joules. Shock. The patient was now in respiratory arrest with thready pulses. VT was on the monitor. Charge, and shock. VT still. Charge — shock. Again, a wide complex tachycardia. At this point, the patient was in refractory VTach.
We decided to load the patient with amiodarone, and start a drip before again attempting cardioversion — this time successfully. An airway was secured, and the patient did not lose pulses at any point in time
Electrical defibrillation or cardioversion is always an option for patients with ventricular tachycardia, but I would like to focus this discussion on our chemical options.
Chemical therapies center upon sodium channel blockade and include class I antiarrhythmics — procainamide and lidocaine, and the class III drug amiodarone.
A slight nuance in management of refractory VTach:
Despite evidence for procainamide over amiodarone in stable VT, amiodarone still serves a role as the first line therapy in VT storm. There is evidence that higher doses of amiodarone — up to 1 gram over the first 24 hours, decreases the likelihood of recurrent VT [3]. Moreover, in sustained unstable ventricular tachycardias that are refractory to lidocaine or procainamide, evidence suggests response to amiodarone and decreased recurrence of unstable ventricular dysrhythmias over the following 24 hours [4].
The sympathetic adrenergic system is also thought to play a contributing role in VT storm. One small study found that patients treated with sympathetic blockade have decreased mortality rate at 1 week, and much higher survival to 1 year after refractory VT [5]. Typically non-selective beta blockers are preferred.
In all, the management of ventricular tachycardia is algorithmic. This case, however, highlights some special considerations when treating a patient in refractory VT. It is important to highlight that while more providers are shying away from amiodarone in stable VT, there remains a role for amiodarone in refractory VT. In the future, perhaps instead of multiple additional attempts of electical cardioversion – reach earlier for amiodarone and consider non-selective beta-blockade in a refractory case of VT.
[1] Dorian, P., Cass, D., Schwartz, B. et al, Amiodarone as compared with lidocaine for shock-resistant ventricular fibrillation. N Engl J Med. 2002;346:884–890. https://www.nejm.org/doi/full/10.1056/NEJMoa013029
[2] Ortiz M, Martín A, Arribas F, Coll-Vinent B, Del Arco C, Peinado R, et al. Randomized comparison of intravenous procainamide vs. intravenous amiodarone for the acute treatment of tolerated wide QRS tachycardia: the PROCAMIO study. Eur Heart J. 2017;38(17):1329–35. https://www.ncbi.nlm.nih.gov/pubmed/27354046
[3] Scheinman MM, Levine JH, Cannom DS, et al. Dose-ranging study of intravenous amiodarone HCl in patients with life-threatening ventricular tachyarrhythmias. The Intravenous Amiodarone HCl Multicenter Investigators Group. Circulation 1995;92:3264–72. https://www.ncbi.nlm.nih.gov/pubmed/7586313
[4] Levine J.H., Massumi A., Scheinman M.M., Winkle R.A., Platia E.V., Chilson D.A. Intravenous amiodarone for recurrent sustained hypotensive ventricular tachyarrhythmias. Intravenous amiodarone multicenter trial group. J Am Coll Cardiol. 1996;27:67–75. https://www.ncbi.nlm.nih.gov/pubmed?term=8522712
[5] Nademanee K, Taylor R, Bailey WE, Rieders DE, Kosar EM. Treating electrical storm : sympathetic blockade versus advanced cardiac life support-guided therapy. Circulation. 2000;102(7):742–747. doi:10.1161/01.cir.102.7.742 https://www.ncbi.nlm.nih.gov/pubmed?term=10942741
