No difference in epi survival.

a former idiot paramedic (who has since had his cert yanked by the DOH) once told me he could give epi to a rock and it would get a pulse, but once the epi wore off so would the pulse. it's probably the only thing I ever learned from him.
Linuss said:
but you can't have survival without ROSC.
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Linuss is saying it best. if you don't have a ROSC, you won't have survival. plain and simple, if the heart isn't beating on it's own, no matter what else you do, what drugs you push, the person is gonna die.

you take epi out of equation, and how many more people are not going to have a ROSC? those people's (who epi would have given a ROSC to) chance for survival becomes exactly 0.

yes, the goal is to get them to "walk out of the hospital" but without a ROSC, they won't be walking anywhere
 
DrParasite said:
you take epi out of equation, and how many more people are not going to have a ROSC? those people's (who epi would have given a ROSC to) chance for survival becomes exactly 0.
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Yes. The evidence supports that epinephrine increases the number of people with ROSC. And if you don't have ROSC, you're dead.

But if you have ROSC after receiving a bucket of epinephrine, and die in the ICU, or receive severe neurologic disability, it probably doesn't matter that you had ROSC in the first place.

The general message seems to be, that epi gets more hearts beating, but at the end of the day, if you delay / don't use epi, there's not much difference in the total number of people who walk out of the hospital with a decent neurologic outcome.

Or put another way, despite a greater proportion of people who receive epinephrine getting ROSC, a smaller proportion of them survive the hospital with a decent neurologic outcome.
 
How about "three kinds of dead"?

Clincially dead, organically dead, and the third one something like "Chemically animated"? In other words, ROSC is not as simple as it was once considered. This sort of tricotomy would help encompass the concept that, as satisfying as those on-scene or enroute QRS's are, and even though they are the harbingers of successful resuscitations at the current state of the art, that "stem" of the resuscitation "tree" may be a shorter one than we think.

We can't stop looking for the next thing. If we had stopped with "palpable pulse equals life" we would bnot have developed the apical puilse, and is "apical pulse equals life" were our goal, we would not have gone on to EKG, defirillation, and AED.

We need to better define "death" so we can address it properly, or recognize that there are some situations where ther is no "plan A, plan B" (at least in current state of the art) to address it.

How we label and express about something decides how we can think about something, research it, get grants, tell family members.
 
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There is a study review in this months issue of JEMS where they found surprising results with vasodilation instead of vasoconstriction in cardiac arrest.

Instead of using a vasopressor like epinephrine, they used a vasodilator. It was an interesting read so maybe something to watch out for down the road with further study.
 
18G said:
There is a study review in this months issue of JEMS where they found surprising results with vasodilation instead of vasoconstriction in cardiac arrest.

Instead of using a vasopressor like epinephrine, they used a vasodilator. It was an interesting read so maybe something to watch out for down the road with further study.
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It'll be a little while before it gets to humans, and if it does, hopefully someone studies it adequately. As for now, if I ever work a pig with induced cardiac arrest, I know what could work for the little squealer. Don't forget the basis of epi use was animal studies... so, uh, the nitoprusside study has no more promise than any of the early epi studies in animals.
 
medicsb said:
It'll be a little while before it gets to humans, and if it does, hopefully someone studies it adequately. As for now, if I ever work a pig with induced cardiac arrest, I know what could work for the little squealer. Don't forget the basis of epi use was animal studies... so, uh, the nitoprusside study has no more promise than any of the early epi studies in animals.
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I don't agree that it holds no more promise. It's early research to hopefully fuel even more. I think that it is great the standard of epi and principle of vasopressors has been challenged. Honestly, I find the results kinda exciting.

Maybe it will make it to humans, maybe not. But at least people are actively looking for better ways and are challenging the status quo. And it should get us all thinking too.
 
Here's the relevant citations for the SNP study. I found it interesting to read about. There's a couple of problems, as medicsb alluded to:

(1) It's an electrically-induced arrest, which doesn't really mimc what we see in the field.

(2) Along with SNP other interventions were used, such as an impedence threshold device, and "abdominal binding". So these may obscure the effect of SNP, or we may be seeing the effect of these interventions.

(3) The animals were anesthetised with isoflurane during the procedure. Isoflurane also has hemodynamic effects, and can affect cardiac irritability.

I don't think we can dismiss animal studies just because epinephrine was introduced on the basis of animal data. They're a necessary first step. We can't just randomise 40 patients to receive a potentially dangerous / beneficial intervention without doing animal trials first. It's just not ethical. But, as pointed out earlier, sometimes the findings even in large animals don't translate.


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Yannopoulos D, Matsuura T, Schultz J, Rudser K, Halperin HR, Lurie KG. Sodium nitroprusside enhanced cardiopulmonary resuscitation improves survival with good neurological function in a porcine model of prolonged cardiac arrest.Crit Care Med. 2011 Jun;39(6):1269-74. PMID:21358401

Fumagalli F, Ristagno G.The patient is in cardiac arrest! Let's be snappy: prepare a bolus of sodium nitroprusside, while I compress the chest. It's not a joke! Crit Care Med. 2011 Jun;39(6):1548-9. No abstract available.
PMID 21610615

Schultz JC, Segal N, Caldwell E, Kolbeck J, McKnite S, Lebedoff N, Zviman M, Aufderheide TP, Yannopoulos D. Sodium nitroprusside-enhanced cardiopulmonary resuscitation improves resuscitation rates after prolonged untreated cardiac arrest in two porcine models. Crit Care Med. 2011 Jun 30. [Epub ahead of print]PMID: 21725236


Schultz J, Segal N, Kolbeck J, McKnite S, Caldwell E, Yannopoulos D.
Sodium nitroprusside enhanced cardiopulmonary resuscitation (SNPeCPR) improves vital organ perfusion pressures and carotid blood flow in a porcine model of cardiac arrest.Resuscitation. 2011 Aug 22. [Epub ahead of print]PMID: 21864483
 
What about tourniqueting legs and non iv arm to provide peripheral constriction via blockage?
 
This studies are still flawed to begin with.

Of course there won't be much of a difference no matter what you do. We are talking about raising the dead here. Many of those people were deader than a doornail to begin with and epi or not, they were not going to ROSC let alone survive to live a normal life. This is the same reason I think the atropine study is flawed.

The other post is right. You can't have survival without ROSC.
 
Of course there won't be much of a difference no matter what you do. We are talking about raising the dead here. Many of those people were deader than a doornail to begin with and epi or not, they were not going to ROSC let alone survive to live a normal life. This is the same reason I think the atropine study is flawed.
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It's not "flawed". It simply doesn't show what certain persons would like it to show. To say a study is flawed would require proof that the data used was statistically invalid or that the study population was stacked in such a way to purposefully skew the results. When you're studying cardiac arrest (and the research project I was on prior to my current one involved one of the largest and longest running in-hospital arrest databases in the world), everyone is clinically dead so expecting anything but a marginal level of benefit from anything is not an indication of a flawed study.
 
NO study is perfect

...unless it meets my prejudices. Especially if I paid for it.
 
Thought I would add to this here, as I've spent my professional career designing and executing studies.

The alternative hypothesis to this could be:

Epinephrine works extremely well at ROSC, even in cases where significant brain damage and/or organ failure has occurred.

A corollary to this hypothesis would be that absent a clinically meaningful and successful intervention at mitigating brain damage, Epi does not produce a statistically significant increase in survival to discharge.

I think what may be lacking in these studies is a detailed examination of the pathology behind the cardiac arrest. If the person went into arrest because of "X", which in itself causes long-term organ/brain damage, then survival to discharge would then become a multivariate analysis. If epi is good at ROSC, then a patient simply cannot be discharged without having achieved ROSC first.

Statistically significant does not always mean clinically meaningful. More evidence is definitely required for this, the kind that the FDA would grant approval for a specific indication. Then at least we'd know that a well-powered and meticulously designed study is behind the interpretation.

Clinically meaningful is dependent on the primary/secondary outcomes, as well as the assessment tools used to gather data. See the clinical trials for use of atypical antipsychotics in dementia patients. NONE of those trials showed efficacy, yet clinicians swear by them for short-term, low-dose usage for chronically agitated patients. That is because sometimes clinically meaningful can't be captured in a standardized 45 question patient assessment.
 
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Localmotion34 said:
If epi is good at ROSC, then a patient simply cannot be discharged without having achieved ROSC first.
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While that's true, we can't necessarily make the leap to, "Any intervention that improves ROSC will improve survival to discharge", or, "the best strategy to improve survival to discharge is to first improve ROSC".

I agree that there's definitely subgroups within the OHCA population that have different risks for survival. The problem is that it's difficult to identify these groups a posteriori, let alone a priori, where we could actually attempt to target them with specific therapies.

The use of epinephrine is based largely on tradition, and partly on animal data. There's a lack of real evidence to support the statement, "epinephrine improves survival to discharge", but we're starting to build a body of evidence that "epinephrine does not improve survival to discharge". I think a lot of people are starting to question its routine use in cardiac arrest.
 
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