Amiodarone vs Procainamide for Stable VT

Case Scenario:
A 38-year-old male with a history of hypertension and an unknown heart defect status post repair in infancy presents to the Emergency Department with acute onset chest pain, dyspnea, and diaphoresis.  He had a similar episode at another hospital 1 month prior that resolved after “some medication.”  He denies drug use.

An EKG is obtained in triage, and is shown below.

The patient’s blood pressure is 120/70.  He is alert and oriented, and speaking in full sentences although dyspneic with respiratory rate in lower 20s and O2 saturation 98% on RA.

Clinical Question: Which pharmacologic agent is most effective for termination of monomorphic ventricular tachycardia?

In the United States, there are 5 readily available options in every hospital’s formulary – amiodarone, procainamide, lidocaine, adenosine, and propofol (i.e. electricity).  Sotalol is another option, but the IV formulation is not readily available in many Emergency Departments in the US.

Amiodarone has emerged as a popular go-to anti-dysrhythmic for all things… dysrhythmic.  If syphilis is the great imitator, and hyperkalemia is the syphilis of EKGs (as Amal Mattu likes to say), then amiodarone is the syphilis of antiarrhythmics.  It is a Class I, II, III, and IV drug – meaning it acts indiscriminately on sodium channels, beta adrenergic receptors, potassium channels, and calcium channels.  It is administered by a loading dose of 150 mg IV over 10 minutes, followed by an infusion.  Currently, the AHA has it riding shotgun (with procainamide driving) with a Class IIb recommendation (1).

Procainamide is a Class Ia antiarrhythmic agent.  It is an older drug that tends to be less well-known.  I suspect it is only the popularity of amiodarone that has stunted procainamide’s use as a first-line agent in the minds of many emergency physicians and/or cardiologists.  It is usually administered one of two different ways – 17 mg/kg given at a max rate of 50 mg/min, or 100 mg over 2 minutes every 5 minutes until conversion.  For now, it sits a little uncomfortably in the driver’s seat with a Class IIa recommendation from the AHA (1).

Lidocaine is a Class Ib antiarrhythmic agent that has largely fallen out of favor.  It fell off of the simplified pulseless arrest ACLS algorithm in 2010; although, it is still considered reasonable for the initial treatment of sustained monomorphic ventricular tachycardia (Class IIb recommendation) (2).  Its biggest advantage is its relatively safe pharmacologic profile, and its ability to be administered quickly as an IV push.  The dose is 1 to 1.5 mg/kg IV push.  It’s sitting in the backseat, recommended as a second-line agent in monomorphic ventricular tachycardia (1).

It’s worth briefly mentioning adenosine as an option for stable, monomorphic wide-complex tachycardias.  The ACLS guidelines support the use of adenosine only for stable, monomorphic ventricular tachycardia for diagnostic and therapeutic purposes (1).  The rationale being that if the rhythm is actually SVT with aberrancy, then one would expect successful cardioversion with adenosine.  See Amal Mattu’s video post here for an explanation as to why the ACLS guidelines are wrong about this.  Suffice it to say, adenosine can convert SVT with aberrancy or ventricular tachycardia.  It is typically administered as a rapid 6 mg IV push, followed by a rapid 12 mg IV push (twice if refractory).

When in doubt, there is no debate that reaching for propofol and electrically cardioverting is the safest, most efficacious option.  This is probably the one option the cardiologist will not critique (rest assured your pharmacologic selection will be critiqued).

The main focus of this post is to malign the myth that amiodarone is superior to procainamide for stable ventricular tachycardia.  So, let’s get to it.

Unfortunately, there are no prospective, randomized, head-to-head trials comparing amiodarone to procainamide.  There are, however, two retrospective case series’ suggesting that the success rate of amiodarone for conversion within 20 minutes is 29% (5,7).  There is one retrospective cohort comparing amiodarone to procainamide that found success rates for conversion within 20 minutes to be 25% and 30%, respectively (not statistically significant) (8).  However, when looking at only those that were given amiodarone or procainamide as the initial antidysrhythmic treatment, the success rates were 25%, and 57%, respectively (again, not statistically significant).  Prior studies comparing the efficacy of procainamide to lidocaine suggest that the success rate of procainamide is closer to 80% (3, 4).  What I conclude from the evidence is that successful conversion when administering amiodarone is around 30%, and when administering procainamide, 50% to 80%.  This is all summarized in a nice systematic review by de Souza, et al (9).

It’s worth noting that all pharmacologic agents mentioned above can cause hypotension, and you should have a low threshold for synchronized cardioversion if and when that happens.  Post-conversion, it’s worth considering administration of a beta-blocker to reduce the adrenergic surge associated with ventricular tachycardia (also why this may be one time Ketamine should not be used as the sedative agent, as it is a sympathomimetic) (2).  A continuous infusion of the antiarrhythmic post conversion is standard practice, but does not have any evidence to support it.

Based on my understanding of the evidence, I propose the following therapeutic algorithm for stable, monomorphic ventricular tachycardia.

References // Further Reading