Ventricular electrical storm

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

epidural man

Full Member
15+ Year Member
Joined
Jun 3, 2007
Messages
4,880
Reaction score
3,287
Over this last turkey holiday - my brother (an ICU/anesthesiologist) - was telling me about a case were he had some one with ventricular electrical storm - and to fix it (or control it at least) - he used isoproterenol to overdrive the ventricle. He said it worked well.

I had never heard of that and thought the idea was pretty brilliant.

Does this sort of thing happen a lot in ICUs? And is a beta-agonist commonly used?

My pea-brain would have used a beta-blocker instead of a beta agonist to INCREASE heart rate.
 
Last edited:
Hmm do not see that a lot. Only time I’ve really overdrive paced is in post cardiac surgery pts with external pacemakers, but I suppose isoprotrenol is the same thing.
Personally I like lidocaine for when too many PVCs/VT
 

Can do it pharmacologically or by pacing electrically.
I was going to mention overdrive pacing. Even that is relatively infrequently used, even by EP doctors. I can’t imagine using isoproterenol to do this. I’m amazed it worked, pure beta agonists are very arrythmogenic. Also can’t imagine ovwrdriving a heart to go faster than typical VT.
 
Over this last turkey holiday - my brother (an ICU/anesthesiologist) - was telling me about a case were he had some one with ventricular electrical storm - and to fix it (or control it at least) - he used isoproterenol to overdrive the ventricle. He said it worked well.

I had never heard of that and thought the idea was pretty brilliant.

Does this sort of thing happen a lot in ICUs? And is a beta-agonist commonly used?

My pea-brain would have used a beta-blocker instead of a beta agonist to INCREASE heart rate.

No this doesn't happen a lot in ICUs... Of course if your hospital has a big heart failure program / ICD population then yeah you'll see it more, but this is the first I've heard of this technique. Cool
 
Were a reasonably big cardiac centre. 8 cardiac ors daily. Its about a weekly occurrence maybe fortnightly in our csicu. Lido, mag, amio, stellate, overdrive, cath lab, Emerg cabg, ecpr. In that order is how we do it.

Don't do chemical overdrive much
Its almost always ischemic in origin for us anyway and needs revascularization
 
Last edited by a moderator:
Interestingly enough, we just used an isoproterenol today for an ep study/ablation to drive up the heart rate into overdrive pacing, then cardiovert once they mapped the atria. Hadn't done that before.
 
I thought one of the absolute contraindications to isoprenaline was exactly what was described in OP? Ventricular tachycardia +/- ventricular arrhythmia? (with exception of Brugada/early repol. where you're trying to promote APs getting killed off in the refractory period)

I thought refractory VF/VT is normally treated with lignocaine, esmolol, amiodarone infusions +/- electricity? Can someone explain why I'm wrong?
 
I remember my buddy at UCSD said they did a stellate ganglion block for refractory V-tach and it worked. Not sure how long it lasted though.
 
I’ve done a handful of Stellate ganglion blocks for this (left). They work well. So do lidocaine drips. Even sent one patient for an ablation of the ganglion and it pretty much resolved.
 
I’ve done a handful of Stellate ganglion blocks for this (left). They work well. So do lidocaine drips. Even sent one patient for an ablation of the ganglion and it pretty much resolved.

Are you a pain guy?
 
Ive never read of pharmacologic overdrive pacing for ES and can't get behind the idea physiologically. Every therapy I'm familiar with for ES is sympatholytic, antiarrythmic, or electric. Would love a good article discussing this
 
That's so funny. I was literally talking about this with the EP guys the other day. This is totally legit. He also said that it doesn't really matter if we get them out with pharm or transvenous pacing. The goal is to stabilize and then get them to EP for ablation.

It is somewhat conter-intuitive that one would use a arrhythmogenic drug to get out of an arrhythmia. But remember that the mechanism of the vent arrhythmia is early depol during repol. So if you shorten repol (faster heart rate) and have another source of depol (pacing or SA node from pharm) it should theoretically get the heart out of it.

This originally topic began in the context of prolonged QT syndrome which is more anesthesia relevant... The mechanism of Torsades and Vtach 2ndary to torsades is also early depol during repol. So if the patient didn't go into V fib (obv you would just cardiovert) but you keep seeing Torsades and the pt isn't in V Fib you can also use isoproterenol to pharm overpace or tranvenous overpace (but i would prob just give **** ton of mag first). The idea of sympathectomy from blocks or epidurals is also very interesting. It is suppose to lower the amount of circulating epi to lower arrhythmogenicity.

Really good discussion indeed. However, in real practice, if i see sustained VT, I would bolus esmolol just like @epidural man, mixed with all the lidocaine I could find and then call EP after the pt is stable. But if I run out of esmolol and lidocaine during stable VT I assume transvenous pacing would still work, where isoproterenol would not, given that beta blockade probably competitively inhibits the beta agonist so you can't pharm over pace as easily. The reason why i wouldn't straight jump to the pacing or increasing HR is that at a certain point a increase in HR doesn't equate to increased Cardiac Output. So even if i get the patient out of the bad rhythm, they still may become unstable due to low CO. Also in the patient population I deal with they usually have pretty bad coronaries, flirting with MI to get out of a perfusing rhythm is just not justified imo.

Nonetheless, EP is some really cool ****!!!
 
Last edited:
That's so funny. I was literally talking about this with the EP guys the other day. This is totally legit. He also said that it doesn't really matter if we get them out with pharm or transvenous pacing. The goal is to stabilize and then get them to EP for ablation.

It is somewhat conter-intuitive that one would use a arrhythmogenic drug to get out of an arrhythmia. But remember that the mechanism of the vent arrhythmia is early depol during repol. So if you shorten repol (faster heart rate) and have another source of depol (pacing or SA node from pharm) it should theoretically get the heart out of it.

This originally topic began in the context of prolonged QT syndrome which is more anesthesia relevant... The mechanism of Torsades and Vtach 2ndary to torsades is also early depol during repol. So if the patient didn't go into V fib (obv you would just cardiovert) but you keep seeing Torsades and the pt isn't in V Fib you can also use isoproterenol to pharm overpace or tranvenous overpace (but i would prob just give **** ton of mag first). The idea of sympathectomy from blocks or epidurals is also very interesting. It is suppose to lower the amount of circulating epi to lower arrhythmogenicity.

Really good discussion indeed. However, in real practice, if i see sustained VT, I would bolus esmolol just like @epidural man, mixed with all the lidocaine I could find and then call EP after the pt is stable. But if I run out of esmolol and lidocaine during stable VT I assume transvenous pacing would still work, where isoproterenol would not, given that beta blockade probably competitively inhibits the beta agonist so you can't pharm over pace as easily.

EP is some really cool ****!!!

If you're not actively having an arrhythmia, there's no such thing as overdrive pacing. I mean, there is, but youre just overdrive pacing the sinus rate, and you're only doing that electrically because the pharmacologic signal is transmitted through the sa node. The rationale for isuprel in torsades prevention is qt interval shortening by pushing the heart rate to 90 - 110. Repeated epi doses are a risk factor for electrical storm and the rationale for beta antagonists in this setting. My understanding anyway. Id still love to read something literature based on this, I couldn't find any

@Instatewaiter
 
Last edited:
I didn't read the thread so forgive me if this isn't close to what you're asking. There are a few types of overdrive pacing. First antitachycardia pacing (atp). It is the first mode most icds use before defibrillation. It will try and ventricular pace people out of prediminantly monomorphic VT. Very commonly this will cause VF and the defibrillator will have to shock.

We also use overdrive pacing for TdP because you decrease the likelihood an after depolarization will hit on the T wave and cause r on T. Same idea with isoproterenol in torsade.

Not sure I've ever heard anyone claim to use adrenergic agents to prevent other types of ventricular arrythmias. We use them (ie isoproterenol) in the EP lab to CAUSE VT. This is literally the opposite of most VT treatment as well. Beta blockers, sympathatectomy, even deep sedation all decrease beta activity to decrease VT. Perhaps there is some data I don't know about but I don't thing so...
 
Top