Procainamide vs Amiodarone for Ventricular Tachycardia

...or you could just shock him...

I sent the following to Dr. Mattu:
38 yo M c h/o HTN and an unknown heart defect s/p repair as an infant p/w acute onset CP, dyspnea, and diaphoresis.  Pt had a similar episode at OSH 1 month prior that resolved after "some medication."  Pt denies drug use.

The first EKG is the one from triage - shows monomorphic vtach (looks like no RS complex in precordial leads, so definitely vtach per Brugada criteria).  BP was nl, pt was A&Ox4, and speaking in full sentences although dyspneic with RR in lower 20s and O2 sat 98% on RA.  Given his stability, I thought we'd give procainamide a try.  We opted for the 'push 100 mg every 5 minutes' option.  We got 3 doses in, and the pt became hypotensive with MAPs in the 40s.  So, we then elected for synchronized cardioversion.  We used 360J biphasic, which converted him w/o difficulty.  Immediately prior to conversion, the cards fellow showed up and felt it necessary to critique my use of procainamide, and instead demanded amiodarone be started prior to conversion.  So, we waited for the amio bolus and then initiated a ggt, followed by cardioversion.

 The second EKG is after synchronized cardioversion.  On my read, there is STE in aVR with reciprocal changes in lateral leads (which the cards fellow initially dismissed).  This prompted some consideration of immediate LHC, but ultimately decided to wait until the following day.

I obtained a third EKG about 30 min later to look for dynamic changes, only to find the ischemic changes resolved.  Meanwhile, the pt became bradycardic to the 40s and more diaphoretic, so I stopped the amio and HR improved.  His trop T was elevated prior to cardioversion (0.02), which trended up to 0.26 the following day (which I understand may have been a result of the electricity).  Turns out, dude used cocaine and meth and probably had corrective pulmonary stenosis surgery as an infant.  Probably a bad trifecta...

I have two questions, in particular, that I would love your insight on:
(1) I seem to remember an EMRAP discussion where you stated your preference for procainamide.  I downloaded (and attached here) the AHA guidelines that you referenced giving procainamide a class IIa recommendation, and amiodarone a class IIb.  Understanding that cardiology would have critiqued whatever I did, could you elaborate on your preference for procainamide?  Is there evidence proving its efficacy  and/or safety over amiodarone?

(2) What are your thoughts on the transient ST changes on the 2nd EKG?  Should we expect transient ischemia in such a focal distribution s/p electricity?  And, should we wait to activate the cath lab in pt's s/p electricity for serial EKGs if STE can be transient?

Here's an excerpt from his reply:

My preference for proc is based on that article you sent, and also 2 recent studies that show that amio is not very good at all for converting VT, contrary to what we were led to believe when it was introduced and pushed by the drug company. AHA finally caught up with the literature and even in the ACLS guidelines give proc a higher class rating than amio. 

Here's an excerpt from a handout of a lecture I do on this, which has some of the references:

• Marill, et al (Ann Emerg Med, 2006) — Conversion rates of amiodarone for stable VT only 29%
• Cummins, et al editorial (Ann Emerg Med, 2006) — most prior studies only indicated success rate 40-60%
• Tomlinson, et al (Emerg Med J, 2008) — Conversion rates of amiodarone for stable VT only 29%
• Only 15% success rate within 20 minutes
• ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and Prevention of Sudden Cardiac Death — Executive Summary, Circulation, Sept. 5, 2006
• “Intravenous amiodarone is not ideal for early conversion of stable monomorphic VT. Intravenous procainamide is more appropriate when early slowing of the VT rate and termination of monomorphic VT are desired.”
• “IV amiodarone is reasonable for patients with sustained monomorphic VT that is hemodynamically unstable, refractory to conversion with countershock, or recurrent despite procainamide or other agents.”
• AHA 2010 Guidelines for ACLS
• Procainamide Class IIa, amiodarone now Class IIb

Regarding the second question, it's true that ischemic changes can occur after shocks and also after EPI, but shouldn't last more than 10-15 min. I would treat the patient based on symptoms + ischemic findings. 

 References:

1. Zipes DP, Camm AJ, Borggrefe M, Buxton AE, Chaitman B, Fromer M, Gregoratos G, Klein G, Moss AJ, Myerburg RJ, 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): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Circulation 2006;114:e385–e484. 
2. Marill KA, et al. Amiodarone is poorly effective for the acute termination of ventricular tachycardia. Ann Emerg Med. 2006 Mar;47(3):217-24.
3. Cummins RO, Hazinski MF. The Quest for a Terminator. Ann Emerg Med. 2066 Mar;47(3):227-9.
4. Tomlinson DR, et al. Intravenous amiodarone for the pharmacological termination of haemodynamically-tolerated sustained ventricular tachycardia: is bolus dose amiodarone an appropriate first-line treatment? Emerg Med J. 2008 Jan;25(1):15-8.