What to do after max dose of Amiodarone?

jwk said:
I guess it can't hurt, since they're "dead" anyway. But this is anecdotal evidence at best, hardly something to hang your hat on.

Old farts like me remember some of the old giant ER LifePak debrillators that could go to 500 joules. There's a reason everything has been dialed back down. Not everything functions along the lines of "if a little is good a lot must be better".
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I've has a medical director instruct me to get another lifepack and shock at 720, however the patient converted into asystole befor the second lifepack arrived.
 
WTEngel said:
If after your second dose of amiodarone (which should be given early after the shock to allow for 2 minutes of circulation with good CPR) at the next rhythm check you see a rhythm that could produce a pulse, you check for a pulse and go immediately into post resuscitation care if a pulse is in fact present. If a pulse is not present, you transition to the PEA/Asystole algorithm.
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Assuming that they are now in an organized rhythm.

My post was based entirely on the presumption that we are staying within a pulseless VT/V-Fib rhythm the entire time. Obviously is this is a megacode and we are getting organized rhythms without pulses then we weill go PEA/Asystole route.
 
sirengirl said:
I have been taught that if ROSC after your 2 boluses of Ami, you will want to do 1 more round of CPR (per new AHA ACLS standards) then hypothermia protocol (that is a local standard) and then consider hanging a maintenence infusion of the AMI (as here I was taught that the 2 boluses would "count" as the loading dose).
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I am not sure I understand what you are trying to say. The way I read your post, it sounds like you are saying there needs to be another 2 minutes of CPR after ROSC has been achieved. Is this what you are saying, or is something getting lost in communication?

If I misread, then I apologize.
 
TomB said:
I think there's already lots of eye opening data. Drugs don't work. Early CPR, defibrillation, and expert post-resuscitation care are key, including early identification of STEMI, PCI, therapeutic hypothermia, and CABG or ICD placement if necessary.
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I completely agree with everything you are saying.

Implementing changes based on these results could have a direct impact on how we view the effect (or lack thereof) of various treatments which have been considered the mainstay of ACLS care of the past 25 years.

I fully buy into the idea that there is little evidence to support or not support various medication therapies...however with the knowledge that our fundamentals (good strong BLS, v/q matching, etc.) have been so poor for so long, it is hard to determine how much we really want to trust data obtained previous to this new big push for the things you mentioned in your post.

I will be very interested to see what changes come around the bend based solely on the fact that we can now analyze the effect of interventions and there influence on outcome with the knowledge that the basic fundamentals are being performed effectively.

Until we reach that point however, any study that does not ensure good strong BLS is in place during resuscitative care is borderline futile based solely on the fact that it is nearly impossible to guarantee with any consistency whether it is the BLS or the new interventions which are harming or helping our patients.
 
abckidsmom said:
Most recently my ROSCs have been detected by EtCO2 changes. It's fairly unmistakable.
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WTEngel said:
Yes...excellent point that I forgot to mention. EtCO2 changes are reliable enough to be considered a "sign of life."

Generally we look at a sudden increase of 20-25 mmHg or more in order to be considered remarkable.

Be careful to consider what medications you have just pushed also. Bicarb administration (not routinely recommended anymore) can lead to variances in EtCO2, perfusion status not withstanding.
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Alright so I'm not crazy. We check for pulses if we get a large jump in EtCO2. Just had a total "oh :censored::censored::censored::censored: I've been doing it wrong this whole time!? How'd I misunderstand that?" moment. :D

WT, other than bicarb what would cause a change in EtCO2 besides ROSC? Changing blood chemistry with bicarb seems like a no brainer but now that I'm thinking about it I can't think of anything off the top of my head that would do it as well.

We carry mag but only for TDP, I suppose we could call for it if the pt was in refractory VF and we had maxed out on ami boluses. Only other antidysrhythmic we carry is lido.
 
Bicarb is the big one that sticks out in my head. That is the only one I routinely mention when I teach anyway...

Mag can be used for VF or VT, but it seems like the only condition where the evidence indicates it is truly superior to any other drug is in polymorphic VT (TDP). As far as having to call for orders to give it for VF but not for TDP, in the heat of battle, those squiggly lines can get awfully difficult to interpret sometimes...

The thing that I don't like about mag is that most people tend to push it too fast. It is supposed to be given over 3-5 minutes during arrest. How often do you think that actually happens, especially in the field? My reasoning on this is that we should push slowly until conversion, then stop and hang a drip. The lower the amount necessary for conversion the better.

Pushing too fast leads to the risk of conversion with dramatic bottoming out of blood pressure, meaning they will effectively be in PEA until you either start pressors/inotropes or the mag wears off to the point that there SVR increases enough to begin producing a pulse again.

This is my thoughts on the matter anyway. To be honest I really rank lido and amio about the same on effectiveness scales, although I use amio nearly 100% of the time, because it is what we have, and it seems to work well enough...nothing better or worse available.

I think there is a lot to be studied regarding the effectiveness of epi as a vasopressor as pH decreases in the patient who is in arrest. In fact, some studies have shown that the effects of vasopressin appear to be unaltered in the acidic patient, where the effects of epi tend to decrease dramatically. This could lead one to think that instead of considering vasopressin early in the code, perhaps we should be considering it later?
 
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WTEngel said:
I am not sure I understand what you are trying to say. The way I read your post, it sounds like you are saying there needs to be another 2 minutes of CPR after ROSC has been achieved. Is this what you are saying, or is something getting lost in communication?

If I misread, then I apologize.
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That is the impression that I was given by my instructors, however the extent I the conversation on it was right before our ACLS certification exam as a, "oh hey we also do this, to prime the pump with ATP, so remember that." I always thought a full 5 to be excessive but it seemed to be what they expected in our scenarios. I'd like to do some research on it and ask around with other medics in the area.

Also, agreed on the point with vasopressin later on in the sequence. I tink the problem with that is knowing how far down the sequence to use it- it does, after all, take the place of 2 epis.... (an as an aside, does anyone know why the heck it comes packaged 20units in 1mL?!)
 
Your instructors were wrong, or you misunderstood them regarding the ROSC and continuation of CPR.

Vasopressin only takes the place of one epi, either the first or second dose, but not both.

Might want to read up in the book or the journal article I mentioned earlier. It is packed full of useful info.
 
WTEngel said:
Your instructors were wrong, or you misunderstood them regarding the ROSC and continuation of CPR.

Vasopressin only takes the place of one epi, either the first or second dose, but not both.

Might want to read up in the book or the journal article I mentioned earlier. It is packed full of useful info.
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Vividly remember the "1st and 2nd" bit. Clarified it as such with my preceptor during ride time. However I agree with you and in fact all the literature says "first or second" which is why I have discussed it with numerous medics. Either it is a local thing here where I am at, or we are all illiterate. Which may well be the case.
 
Illiterate FTW!

I am giving you a hard time of course, but here it is, from the horse's mouth.

From the AHA Circulation Journal article published in November 2010:

"1 dose of vasopressin 40 units IV/IO may replace either the first or second dose of epinephrine in the treatment of cardiac arrest"
 
Our protocol is Epi q3-5 OR Vasopressin 40 IU IV or 80 IU ETT once, not as a replacement does.

I've given mag once for TDP and I know I pushed it too fast, somewhere in the realm of 60-90 seconds. I'm almost wondering if that's what happened seeing as she went from TDP to PEA at the next rhythm check then to asystole. In the big scheme of things we started in asystole -> PEA -> TDP with a long downtime ~20 minutes until ALS. Had an engine crew with an AED at around 10 minutes.

As far as ami vs. lido I've never given lido. The only time we give it is if we can't get access then we give it down the tube or we give it for R-on-T PVCs so I can't comment on how well it works.

Thank you!
 
mgaska84 said:
Ive always had this question with no clear answer. When working a code and you've reached the max dose, and you're still working the code, do you switch to Lidocaine or do you do an amio infusion? Thoughts?
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Bretylium Tosylate!

Just kidding. Mostly.

Anyone ever use it before it left our boxes? (Yes, I'm that old.)

abckidsmom said:
Most recently my ROSCs have been detected by EtCO2 changes. It's fairly unmistakable.
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Same here. Worked a traumatic cardiac arrest last year where the closest facility (by far) was not a trauma center. Intubated, good lines, and as we were pulling into a parking spot, ETCO2 went from about 30 to over 100. Let me tell you, they were less than happy when we walked in with a recently resuscitated trauma arrest.

WTEngel said:
Mag can be used for VF or VT, but it seems like the only condition where the evidence indicates it is truly superior to any other drug is in polymorphic VT (TDP). As far as having to call for orders to give it for VF but not for TDP, in the heat of battle, those squiggly lines can get awfully difficult to interpret sometimes...
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Our protocols state that we can use mag in cardiac arrest for "any suspected hypomagnesemic state". Our medical director says that you can suspect that on any refractory VF/VT arrest. Our EMS physicians give a fair amount of leeway if you're trying to reason your way through it with a little common sense.

This is my thoughts on the matter anyway. To be honest I really rank lido and amio about the same on effectiveness scales, although I use amio nearly 100% of the time, because it is what we have, and it seems to work well enough...nothing better or worse available.
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We still carry both, but amio is our first line always. Except when the guy with the AICD said "I'm in V tach, and it's too slow to trigger my AICD. It's happened before. Lidocaine always converts me." While I was pulling out my lidocaine, I was calling.

I think there is a lot to be studied regarding the effectiveness of epi as a vasopressor as pH decreases in the patient who is in arrest. In fact, some studies have shown that the effects of vasopressin appear to be unaltered in the acidic patient, where the effects of epi tend to decrease dramatically. This could lead one to think that instead of considering vasopressin early in the code, perhaps we should be considering it later?
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Excellent point. They took our vasopressin out; one of the opinions our medical director has (which I don't necessarily agree with) is that a simpler drug box with less drugs is always better. I think he's the best thing to happen to our system since, well, ever, but I just don't agree with that.
 
NVRob said:
Our protocol is Epi q3-5 OR Vasopressin 40 IU IV or 80 IU ETT once, not as a replacement does.

I've given mag once for TDP and I know I pushed it too fast, somewhere in the realm of 60-90 seconds. I'm almost wondering if that's what happened seeing as she went from TDP to PEA at the next rhythm check then to asystole. In the big scheme of things we started in asystole -> PEA -> TDP with a long downtime ~20 minutes until ALS. Had an engine crew with an AED at around 10 minutes.

As far as ami vs. lido I've never given lido. The only time we give it is if we can't get access then we give it down the tube or we give it for R-on-T PVCs so I can't comment on how well it works.

Thank you!
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I've given it for multifocal PVC's in a guy with a REALLY low BP due to internal bleeding to prevent a worse arrythmia while we were setting up a walking transfusion. Worked like a charm.
 
I am 50/50 on your medical director's opinion that less drugs are better in some cases.

With the current evidence being what it is, there doesn't seem to be any compelling reason to keep it. Will that change in the coming years? Perhaps.

Most of the time when teaching ACLS, we will tell the students about the vasopressin consideration, and then tell them to shelf that information, because they will not be required to reproduce it, and most likely will not be using it during a code.

Regarding the walking blood bank, the results from studies being done with military are pretty impressive. Wish we could implement something like that on the civilian side...
 
WTEngel said:
Regarding the walking blood bank, the results from studies being done with military are pretty impressive. Wish we could implement something like that on the civilian side...
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I think it would be great.

But logisitically impossible.

I am still hoping the British attempt to use DNA technology to reproduce unlimited quantities of typed blood in a lab works out, but I haven't heard anything about it since the project was funded.
 
Well, remember that we had

A: a roster of blood types, and kits to confirm.
B: the donors were soldiers, who go through pretty comprehensive blood work before deploying
C: a seven hour evac time.

It's a pretty extreme thing to do outside of a level III or IV facility, but we had no choice.

Also, I think systems should still carry lido, for other reasons as well.

One of them is that renal failure and amiodarone don't mix. It has the half life of gamma radiation.
 
I agree...logistically impossible...

We still have mismatches and incorrect type being administered in the hospital (rarely) with all the safeguards in place...I could reasonably assume the risk would rise with a walking blood bank.

With the walking blood bank in the military, is the product ever stored, or is it direct from donor to lab to patient? What is the turnaround time from donation to administration?

I am familiar with the concept, not with the process though...
 
There's kits that Chinook makes, complete with typing kits, donor bag, Y tubing, etc.

There's preservatives in the bag, but its meant to be taken from one table to the other. (I.e donor to patient.)

Did a little over a half dozen last year. The last one was from a 30 tablet salicylate O.D, and the transfusions had to be topped off with a vasopressin drip.
 
Fascinating.

The advances in trauma care over the next 10 years will be remarkable. Unfortunately they had to be learned in such a hostile manner.
 
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