why was atropine removed from acls?

[runswithneedles]

Do I shoot myself in the foot when I say this but how can their be evidence a drug does or does not work when the patient is in a rhythm that carries a high morbidity and mortality rate to begin with. A drug cant work if theirs nothing viable for the drug to act on or if the underlying condition which caused the cardiac arrest (medical or trauma) is still present.

[systemet]

Do I shoot myself in the foot when I say this but how can their be evidence a drug does or does not work when the patient is in a rhythm that carries a high morbidity and mortality rate to begin with. A drug cant work if theirs nothing viable for the drug to act on or if the underlying condition which caused the cardiac arrest (medical or trauma) is still present.

You missed your foot.

And identified a problem in cardiac arrest research. There's only a small percentage of people who are going to survive an asystolic arrest (the survival is much better for PEA). Part of this is that asystole often represents someone who has been in arrest for a long time period, and hasn't had bystander CPR, and it's not immediately treatable by one of our best therapies, defibrillation.

If you take 200 people in asystolic arrest (which would be quite large for a cardiac arrest study), and randomise them to atropine or saline, even with good inclusion / exclusion criteria, you're looking at perhaps 0 - 6 survivors. Perhaps less if you start looking at good neurologic outcomes, or at 6 months or at 1 year.

It's really hard to get decent statistics. So then you don't know if any difference you see is just chance, that one group just happened to get one more survivor than the others because of how they were randomly assigned. And then it becomes tempting to look at the large number of asystolic arrests and suggest that, maybe the statistics aren't great, but if there's a real difference it would benefit a large number of people. There was a fair controversy about this with vasopressin in asystole 5-10 years ago. There was a big article published in NEJM. It showed a small improvement in survival in asystole with vasopressin over epinephrine (I think), and urged immediate changes to the ILCOR guidelines. But if you look at confidence intervals, the 95% range included the possibility that the patient got better with vasopressin, that it had no effect, or that it killed people. [This still represents better epidemiological data that anything motivating for atropine.]

So, historically, we've tended to use things because "it seemed like a good idea", because we could think of a plausible physiological reason as to why they might help, and there was maybe some animal data. This included things like high-dose epinephrine, calcium or isoproterenol. Things we now know are harmful, or neutral at best.

Right now the best data suggests that drugs in cardiac arrest may not make a difference at all. With the trend toward evaluating current practice based on the available evidence, a lot of therapies are being removed. The problem right now, is you can make an argument for using atropine, in that some asystolic arrests might represent the consequence of excessive vagal tone. But I can make an argument that high dose glucagon might be good as an inotrope and adjunct to epinephrine. We just don't have good data to support either position. [There's even reasonable arguments for giving beta-blockers instead of epinephrine in VF/VT]. So what do you do? The current trend is towards removing things that lack a good evidence base.

[runswithneedles]

Glad to hear I missed my foot. So was ACLS started on "it seemed good on paper" kind of deal and as time progressed/EMS became a recognized health field that required its own research and Data collecting they began removing alot of therapies?

[JakeEMTP]

There is very little "EMS research". Usually the ACLS inclusion/removal of medications and interventions are done at Hospitals ad nauseam before they are instituted.

I would hazard a guess that none of the protocols we operate under were the result of actual EMS research. Some studies are done periodically and included in much broader studies. But for the most part, research is not a part of EMS and that is unfortunate.

[systemet]

Glad to hear I missed my foot. So was ACLS started on "it seemed good on paper" kind of deal and as time progressed/EMS became a recognized health field that required its own research and Data collecting they began removing alot of therapies?

I think that's a reasonable assessment of the situation.

EMS is probably still a little ways away from being truly recognised / accepted as a healthcare field, but it seems like there's more research each year. Whether the research really belongs to EMS as in it's "its own research" is hard to say. The stuff I've seen / participated in (a few years ago now), has mostly been driven by cardiology or emergency medicine, rather than by paramedics. But that's part of a bigger problem of who owns / is responsible for EMS.

I think a lot of us would like to have paramedics running large RCTs of prehospital sepsis management or resuscitation, etc. But the reality is, we don't have that expertise. The medicine is always going to be dictated by the physicians (and rightly so). But it should be done in partnership with paramedics, in a mentoring environment, even if it's an unequal partnership.

Put bluntly, if we're participating in the research, we should be getting something out of it. I think the most reasonable exchange is for the physicians conducting the research to involve as many paramedics / EMTs as possible and help push forward paramedicine as a profession.

There is very little "EMS research". Usually the ACLS inclusion/removal of medications and interventions are done at Hospitals ad nauseam before they are instituted.

I agree that there's relatively little EMS research. Change takes time, and it takes a long time to filter down to EMS.

I think some of the changes now are occurring as a result of research in the field, e.g. therapeutic hypothermia, de-emphasis of antiarrhythmics. Practice just changes quicker in the ER because physicians actively read the literature and adapt their own practice. In EMS, we tend to be forced to wait for medical advisory committees to do their job and update guidelines / protocols. Some committees carry out their job with more enthusiasm and vigour than others.

I would hazard a guess that none of the protocols we operate under were the result of actual EMS research. Some studies are done periodically and included in much broader studies. But for the most part, research is not a part of EMS and that is unfortunate.

This is an attempt to do that in Canada:

http://emergency.medicine.dal.ca/ehsprotocols/protocols/toc.cfm

I realise that the sample protocols seem very "old-fashioned" and basic, but if you click on the titles on the left side of the page you get a pretty good list of references for therapies that they haven't included.

Edited February 17, 2012 by systemet

[zmedic]

I think EMS research is valuable, but it's worth remembering that the that big thing in research is having enough of whatever event you are studying to be able to detect a difference between the study group and the control group. Take cardiac arrest as an example. If you want to know if a certain drug has an effect of cardiac arrest survival it is much easier to study in a hospital than in the field. For one thing it is easier to train one or two people who sit in the hospital all day and go to every cardiac arrest than it is to train 50 paramedics in a study protocol knowing that most of them will not have a cardiac arrest in a given shift. It is also easier to record data in a hospital because there are so many people there (ie it is hard to have a medic record information for a study while also providing patient care). Finally, in a hospital there are less variables. Again take cardiac arrest. When someone arrests in a witnessed setting there is often immediate CPR, and rapid ALS. In the field you have more variables (dispatch time, arrival time, ALS v BLS v first responder first on scene, transport time to ER etc). Furthermore, since so many prehospital patients aren't going to survive their cardiac arrest no matter what because of no bystander CPR, no early defib etc, it is harder to see the difference in outcomes between say two drugs.

I guess as far as ACLS goes I feel like "if it doesn't work in the hospital, where the patient has the best chance of getting lots of help from highly trained people, there is no way it is going to work in the field." I think show that something works in the hospital, then test it to see if it makes sense to have in the field. If it doesn't work in the hospital, don't even bother studying it in the ambulance.

I'd also mention that one reason it is so hard to change things in EMS is that once something becomes standard of care, it is very very hard to test, because it could be considered unethical to withhold standard treatment from a patient. I'd love to randomize people who have been in low speed MVCs to backboard or no backboard, but I don't see that happening any time soon.

[JPINFV]

Atropine is stillused here, however there is talk that they will remove it, however we wont lose it as it is the only prehospital drug we carry for the dreaded funnel web spider bite.................

So, what do you use for organophophate poisoning if not atropine?

[Kiwiology]

So, what do you use for organophophate poisoning if not atropine?

I do not know of any ambulance service outside North America that carries anything for organophophate poisoning; either for the patient or the crew.

Personally I think the massive over-subscription of various services' within the US to atropine auto-injector for "biochemical terrorism" might be conducive to ingestion of the Kool Aid

[chbare]

I do not know of any ambulance service outside North America that carries anything for organophophate poisoning; either for the patient or the crew.

Personally I think the massive over-subscription of various services' within the US to atropine auto-injector for "biochemical terrorism" might be conducive to ingestion of the Kool Aid

A function of environment perhaps? One of the first services I worked at was in a rural, farming community. Organophosphate insecticide exposure was not uncommon. I remember a particularly bad case that I was not involved with, but it made quite an impression on many of us in any event. The patient apparantly had a very complicated inpatient course. Eventually, it was realised that he had large enough concentrations of insecticide under his nails to cause ongoing problems.

[JPINFV]

Personally I think the massive over-subscription of various services' within the US to atropine auto-injector for "biochemical terrorism" might be conducive to ingestion of the Kool Aid

This I do agree with. Heck, even the EMT ambulances around here have duodote autoinjectors for the crew. However, the atropine used for OP wasn't autoinjectors.