β-Blockade for the treatment of recurrent VF arrest

Maybe! In this post, I’ll be looking back at a couple papers that I came across over the last year. One of the more interesting developments in medicine over the last decade in my eyes has been the increasing focus on vagal tone in treating various diseases such as epilepsy and treatment-refractory depression, mostly via the use of implantable devices such as the vagal nerve stimulator (VNS). The mechanisms of action of the VNS in these somewhat-nebulous and poorly-understood pathologies is a murky thing, but the simplified way that I understand it is that you’re calming the body down– putting the foot on the sympathetic nervous system’s proverbial brake, in other words, and this has some beneficial effect. On my ICU rotation, I decided to look into work that has been done on the use of beta-blockade in septic shock patients (coming soon), and during that same month, a few clinicians I had worked with on my away rotation in emergency medicine published a chart review showing the use of beta-blockade in refractory VF cardiac arrest.

The paper on cardiac arrest comes out of Hennepin Co. medical center, and is the work of their new research director, a really cool and smart doc named Brian Driver and some of his colleagues who are very well-known in the emergency cardiology field. They present a retrospective review of 25 patients with refractory VF arrest, all of whom received at least 300 mg of amiodarone and 3 mg of epinephrine and three or more defibrillation attempts (why these numbers?)

Shortcomings of this include the retrospective nature, the sample size, which was small and therefore makes comparisons between these groups useful primarily for hypothesis generation (which is what the authors state), and the use of only one reviewer (presumably unblinded, but this was not addressed). That said, the question itself is a creative one to ask and the neurologic outcomes in the admittedly-small intervention group were excellent– very unusual for something with as high of associated morbidity/mortality as RVF.

Interestingly, the authors provide some historical information reflecting the use of beta blockade to treat cardiac arrest as early as in the 1960s, when the use of propanolol was a second-line agent after lidocaine or procainamide. They also discuss the use of beta-blockade in septic shock patients (as mentioned above– check back in the next couple days for a discussion of those papers) and the idea that dampening the non-beneficial hyperadrenergic state that exists in many critical illnesses may be the reason these studies have shown possible benefit. If any institution is equipped to do this study, it’s Hennepin, and I hope to see more from them regarding this soon.

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