300mg slow-push Amiodarone post-ROSC, regardless of cardiac rhythm.

[RoadRat]

What is the physiologic reasoning behind amiodarone post-ROSC?

On the scene of a recent full-arrest, two of my firemedics were caught in a disagreement of the drug's use.

One argued amiodarone is only to be used post-ROSC on pts who were previously in v-fib or v-tach.
The other firemedic argued it is to be used on all post-ROSC pts, regardless of cardiac rhythm.

Our protocol states amiodarone IS to be used on all post-ROSC pts, but I was never educated of this while in school.

What's the point?



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[DrParasite]

IIRC (and someone can probably answer this better than me), amiodarone is an anti-arrhythmic, so the thinking is getting them into a stable rhythm and keeping them away from said bad arrhythmia are the purpose you give it. I am also going to guess that the most common rhythms to get a ROSC from are v fib and v tach, so the assumption is, if they were in those rhytyms prior, give the anti arrhythmic.

 

[WolfmanHarris]

Amiodarone works along 4 pathways to prolong Phase 3 of the cardiac action potential:
- Na+ channel blocker
- Ca+ channel blocker
- Beta-blocker
- K+ channel blocker

It's not currently in my medical directives for ROSC patient's and in fact we carry lidocaine over amio for some reason.

I have trouble seeing the rationale for pushing this drug during a ROSC as a matter of course. What rhythm are they presenting in and what benefit are you hoping to achieve with the amiodarone?

 

[Summit]

I have trouble seeing the rationale for pushing this drug during a ROSC as a matter of course. What rhythm are they presenting in and what benefit are you hoping to achieve with the amiodarone?

Agree here.

Amio is not without side effects, particularly common is hypotension which we want to avoid like the ****ing plague post ROSC among other goals. I've never heard of "everyone gets amio." I sure would think of a normal 150mg loading dose, when warranted, if it wasn't done intra-arrest.

 

[VFlutter]

You should only be giving Amio 300mg IV push in pulseless patients, not after ROSC. It can cause circulatory collapse.

So if the patient had a PEA or bradycardic arrest you are bolusing Amio post ROSC? That probably isn't the best idea...

 

[EpiEMS]

So if the patient had a PEA or bradycardic arrest you are bolusing Amio post ROSC? That probably isn't the best idea...

He did say *fire*medics...

(I couldn't resist.)

In all seriousness, wait, why are they giving amio for all post-ROSC patients?

 

[NomadicMedic]

We only give 150 of amio (over 10 minutes) post ROSC if they converted from VF/VT.

I've not seen it as a blanket post ROSC treatment.

 

[RoadRat]

I'm unable to edit my original post for an unknown reason. I continue to attempt to edit it, but for now I'll try to do it here:

The arrest pt was found to be in PEA of normal sinus rhythm.

We administered 2 rounds of epinephrine. Once we achieved ROSC, his rate increased to 112. By the time I finally consulted protocol and drew up the drug, the pt's heart rate was 156 with an abbreviated PR-interval, as confirmed by a 12-lead.

Again, our county's medical director specifies through written protocol that we are to give 300mg of amiodarone once ROSC is achieved *unless* lidocaine has already been used during the arrest.

The order to administer 300mg slow-push amiodarone to post-ROSC pts includes those who were previously in v-tach, v-fib, asystole, and PEA.


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[RoadRat]

I have trouble seeing the rationale for pushing this drug during a ROSC as a matter of course. What rhythm are they presenting in and what benefit are you hoping to achieve with the amiodarone?

I'm an inexperienced medic with only 4 months rural experience under my belt, so I'm not wise enough to argue against this particular protocol especially on-scene in the midst of treating an arrest.

Since my firemedics argued over it, I figured consulting protocol would resolve the argument and potentially give the pt better care.

The pt initially presented in PEA of normal sinus rhythm. Post-ROSC, his rate increased to 112 sinus tach with an abbreviated PR-interval as confirmed by a 12-lead prior to going enroute to the ER. Pt's initial blood pressure was also approx 86/64.

After consulting protocol and drawing up the drug, the pt's heart rate and blood pressure had increased to 156bpm and 208/182 (the blood pressure is, again, approximate. The pt was also on his second 1000ml bolus at the time of the elevated BP reading.)

After noticing the abbreviated PR-interval and the elevated HR of 156, I felt more confident about administering admiodarone.

At the point of drawing up the drug in the syringe, my purpose was to follow protocol because I recognize I'm not educated enough to confidently argue against an MD. I didn't have a truly medical rationale other than trusting protocol.

At the point which I hooked up the syringe to the INT and slow-pushed, my purpose for giving it was to decrease the HR back into what I feel are acceptable ranges, and potentially decrease the BP into acceptable ranges as well.

I recognize hypotension is a hazard in post-ROSC, but 208/182 seemed excessive.





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[VentMonkey]

I'm an inexperienced medic with only 4 months rural experience under my belt, so I'm not wise enough to argue against this particular protocol especially on-scene in the midst of treating an arrest.

Since my firemedics argued over it, I figured consulting protocol would resolve the argument and potentially give the pt better care.

The pt initially presented in PEA of normal sinus rhythm. Post-ROSC, his rate increased to 112 sinus tach with an abbreviated PR-interval as confirmed by a 12-lead prior to going enroute to the ER. Pt's initial blood pressure was also approx 86/64.

After consulting protocol and drawing up the drug, the pt's heart rate and blood pressure had increased to 156bpm and 208/182 (the blood pressure is, again, approximate. The pt was also on his second 1000ml bolus at the time of the elevated BP reading.)

After noticing the abbreviated PR-interval and the elevated HR of 156, I felt more confident about administering admiodarone.

At the point of drawing up the drug in the syringe, my purpose was to follow protocol because I recognize I'm not educated enough to confidently argue against an MD. I didn't have a truly medical rationale other than trusting protocol.

At the point which I hooked up the syringe to the INT and slow-pushed, my purpose for giving it was to decrease the HR back into what I feel are acceptable ranges, and potentially decrease the BP into acceptable ranges as well.

I recognize hypotension is a hazard in post-ROSC, but 208/182 seemed excessive.

Let us not forget the 2 Epi's that the patient received, alongside the liberal fluid challenge. What was the patients approximate down time?

All in all it doesn't sound like you did anything terribly wrong. It's merely a peculiar sounding protocol. Can you post a copy of your county's arrest/ ROSC protocols?

 

[RoadRat]

Let us not forget the 2 Epi's that the patient received, alongside the liberal fluid challenge. What was the patients approximate down time?

All in all it doesn't sound like you did anything terribly wrong. It's merely a peculiar sounding protocol. Can you post a copy of your county's arrest/ ROSC protocols?

Pt's down time was approx 20minutes to first CPR, 30minutes to ROSC.

I'll post the protocol next workday. We sadly don't have an app for them.


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[Summit]

I think your protocol is nuts and am not aware of any evidence to support blanked post ROSC amio, much less in a 300mg SIVP.

Ventmonkey I think is being cautious. I'll be blunt. Frankly, that is just nuts. I can think of tons of reasons not to do that and no reasons to do that, especially post PEA. But, there is plenty I don't know and hope to be corrected with some evidence... for your service's patients' sakes.

HR 156 and Systolic of 200 immediate ROSC after 2mg epi and 2L sounds perfectly reasonable as that epi finally actually comes back and hits they system (what is that ultra narrow pulse pressure telling you if it is in fact real?). The thing is, it won't last, even if you don't give anything to treat the pressure (and you shouldn't... I sure wouldn't treat a systolic of 200 prehospital).

You've got to be careful about provider induced BP oscillation... you make a hemodynamic state, then start chasing it with more pharm... you are liable to have it blow up in your face (patient crumps).

I've seen more than a few codes with a novice lead who is shocked, shocked, that the epi wears off and now the patient is brady/hypotensive/PEA again. I actually consider a PEA arrest where ROSC is achieved with nothing but CPR, epi, and fluid as a glaring sign in the sky that this patient will likely probably need a vasopressor drip and more fluid (especially if it wasn't primarily a respiratory arrest).

I invite my fellow posters to poke holes in these assertions.

 

[VentMonkey]

I think your protocol is nuts and am not aware of any evidence to support blanked post ROSC amio, much less in a 300mg SIVP.

Ventmonkey I think is being cautious. I'll be blunt. Frankly, that is just nuts. I can think of tons of reasons not to do that and no reasons to do that, especially post PEA. But, there is plenty I don't know and hope to be corrected with some evidence... for your service's patients' sakes.

HR 156 and Systolic of 200 immediate ROSC after 2mg epi and 2L sounds perfectly reasonable as that epi finally actually comes back and hits they system (what is that ultra narrow pulse pressure telling you if it is in fact real?). The thing is, it won't last, even if you don't give anything to treat the pressure (and you shouldn't... I sure wouldn't treat a systolic of 200 prehospital).

You've got to be careful about provider induced BP oscillation... you make a hemodynamic state, then start chasing it with more pharm... you are liable to have it blow up in your face (patient crumps).

I've seen more than a few codes with a novice lead who is shocked, shocked, that the epi wears off and now the patient is brady/hypotensive/PEA again. I actually consider a PEA arrest where ROSC is achieved with nothing but CPR, epi, and fluid as a glaring sign in the sky that this patient will likely probably need a vasopressor drip and more fluid (especially if it wasn't primarily a respiratory arrest).

I invite my fellow posters to poke holes in these assertions.

I concur, though your post is much more articulate. I too would like to know if the OP stuck around the ED long enough to see the temporary effects of the Epi wear off, and/ or trend up of down.

Amio for us in the arrest setting is pretty much what @DEmedic stated was in his protocols as well---post-ROSC---150 mg Amio gtt in the VF/ VT patient who'd received the initial 300 IVP assuming they've converted directly out of a ventricular arrest.

 

[VFlutter]

I would not treat tachycardia nor hypertension immediately post ROSC, it is likely a result of the Epi as Summit stated or compensatory for their shock state. And as stated they will likely crash soon after. I have a hard time believing that blood pressure, no offense. Systolic of 200 may be correct.

You have patient in a PEA, Amio will do nothing to help fix or prevent any of the conditions that likely cased them to arrest and if anything is more likely harmful. H's and T's

 

[zzyzx]

The AHA no longer recommends routinely giving amiodarone (or lidocaine) to patients after cardiac arrest even if they were shocked out of VT/VF. The reason for this is that is no evidence that this improves outcomes, and anti-arrhythmia drugs can cause harm. (Up to Date doesn't recommend this practice either.)

That said, this used to be standard of care for a long time, and, as we all know, in medicine old practices often take a long time to change.

(To the OP: are you sure that giving 300 mg IVP even for an asystole/PEA arrest post resuscitation is really in your protocols?)

As some of you may know, a long time ago it used to be standard of care to give lidocaine prophylactically to all patients who were diagnosed with MI's. There was a logical explanation for how this could benefit such patients--to keep them from developing lethal dysrhythmias. However, clinical trials showed that this practice was actually causing patient harm.