EMCrit Wee – Vasopressin, Steroids, and Epinephrine for Cardiac Arrest

vse

New Study in JAMA:

JAMA. 2013 Jul 17;310(3):270-9. doi: 10.1001/jama.2013.7832.

Vasopressin, steroids, and epinephrine and neurologically favorable survival after in-hospital cardiac arrest: a randomized clinical trial

Mentzelopoulos SD, Malachias S, Chamos C, Konstantopoulos D, Ntaidou T, Papastylianou A, Kolliantzaki I, Theodoridi M, Ischaki H, Makris D, Zakynthinos E, Zintzaras E, Sourlas S, Aloizos S, Zakynthinos SG.

Source  First Department of Intensive Care Medicine, University of Athens Medical School, Athens, Greece. sdmentzelopoulos@yahoo.com

Abstract

IMPORTANCE:  Among patients with cardiac arrest, preliminary data have shown improved return of spontaneous circulation and survival to hospital discharge with the vasopressin-steroids-epinephrine (VSE) combination.

OBJECTIVE:  To determine whether combined vasopressin-epinephrine during cardiopulmonary resuscitation (CPR) and corticosteroid supplementation during and after CPR improve survival to hospital discharge with a Cerebral Performance Category (CPC) score of 1 or 2 in vasopressor-requiring, in-hospital cardiac arrest.

DESIGN, SETTING, AND PARTICIPANTS:  Randomized, double-blind, placebo-controlled, parallel-group trial performed from September 1, 2008, to October 1, 2010, in 3 Greek tertiary care centers (2400 beds) with 268 consecutive patients with cardiac arrest requiring epinephrine according to resuscitation guidelines (from 364 patients assessed for eligibility).

INTERVENTIONS:  Patients received either vasopressin (20 IU/CPR cycle) plus epinephrine (1 mg/CPR cycle; cycle duration approximately 3 minutes) (VSE group, n?=?130) or saline placebo plus epinephrine (1 mg/CPR cycle; cycle duration approximately 3 minutes) (control group, n?=?138) for the first 5 CPR cycles after randomization, followed by additional epinephrine if needed. During the first CPR cycle after randomization, patients in the VSE group received methylprednisolone (40 mg) and patients in the control group received saline placebo. Shock after resuscitation was treated with stress-dose hydrocortisone (300 mg daily for 7 days maximum and gradual taper) (VSE group, n?=?76) or saline placebo (control group, n?=?73).

MAIN OUTCOMES AND MEASURES:  Return of spontaneous circulation (ROSC) for 20 minutes or longer and survival to hospital discharge with a CPC score of 1 or 2. RESULTS:  Follow-up was completed in all resuscitated patients. Patients in the VSE group vs patients in the control group had higher probability for ROSC of 20 minutes or longer (109/130 [83.9%] vs 91/138 [65.9%]; odds ratio [OR], 2.98; 95% CI, 1.39-6.40; P?=?.005) and survival to hospital discharge with CPC score of 1 or 2 (18/130 [13.9%] vs 7/138 [5.1%]; OR, 3.28; 95% CI, 1.17-9.20; P?=?.02). Patients in the VSE group with postresuscitation shock vs corresponding patients in the control group had higher probability for survival to hospital discharge with CPC scores of 1 or 2 (16/76 [21.1%] vs 6/73 [8.2%]; OR, 3.74; 95% CI, 1.20-11.62; P?=?.02), improved hemodynamics and central venous oxygen saturation, and less organ dysfunction. Adverse event rates were similar in the 2 groups.

CONCLUSION AND RELEVANCE:  Among patients with cardiac arrest requiring vasopressors, combined vasopressin-epinephrine and methylprednisolone during CPR and stress-dose hydrocortisone in postresuscitation shock, compared with epinephrine/saline placebo, resulted in improved survival to hospital discharge with favorable neurological status.

Play

You finished the 'cast,
Now get CME credit

Not a subcriber yet? Why the heck not?
By subscribing, you can...

  • Get CME hours
  • Support the show
  • Write it off on your taxes or get reimbursed by your department

Sign Up Today!

.

Subscribe Now

If you enjoyed this post, you will almost certainly enjoy our others. Subscribe to our email list to keep informed on all of the ED Critical Care goodness.

This Post was by , published 9 months ago. We never spam; we hate spammers! Spammers probably work for the Joint Commission.

Comments

  1. Sean Marshall says:

    Interesting study for sure. I am unclear why they elected to only give steroids post-ROSC if the pt was in shock.

    • Justin Yee says:

      I believe they did give other vasopressors prior to the 4 hour mark as defined by what they called “post resuscitation shock” (sustained, new post arrest circulatory failure or post arrest need for 50% or greater increase in any pre arrest vasopressor/inotropic support…)

      You are correct though. It seems difficult to deduce this piece of information.

  2. Seth Trueger says:

    This is certainly a compelling study, but not sure what we can do with the results. While we all know that epi is “standard care” all over the world for cardiac arrest, epi has only been shown to increase ROSC, not RONF. I would love to see this study repeated with VSE vs no epi (or even better, a good 3-arm RCT with VSE vs epi vs placebo). This study just seems like it shows that 3 meds that don’t work are better than 1 med that doesn’t work.

    • Trueg-
      VSE vs. placebo would be rather useless if you think it through logically. VSE 3 arm would be reasonable, but doubtful it would ever be done. Why don’t you get the properly powered epi vs. placebo done.

      Unless you have stopped using epi during your arrests, then you know exactly what to do with the results. Have you stopped giving epi?

  3. What role is solumedrol playing during the arrest? The onset time is at least an hour in most cases…I’m confused by this…

    The other thought provoking thing here, the dose of steroids following ROSC, I have to wonder if it’s neuroprotective by reducing swelling, and or ICP. It seems like very high dose of Vasopressin…120IU? I know the AHA reccomends 40IU once, and I’m all about challenging the dogma..is vasopressin better than epi?

  4. Adam Hagar says:

    For clarification

    The purpose for the Solu-Medrol is to reduce swelling? By what mechanism? Sorry if this is a basic question, just a pre-med.

    • Justin Yee says:

      Adam,

      The mechanism is probably more so via a “stress response” i.e. using corticosteroids for adrenal insufficiency in the setting of refractory hypotension.

  5. I like the study, and the implications…from my perspective (as a paramedic), Solu-Medrol would be an easy drug to add to a resuscitation, given that we carry it already for RAD/anaphylaxis. And I like the idea of pre-empting reperfusion injury. That said, I’d be interested to see the effects of single-dose versus tapered doses…it’s sometimes (read: often) very difficult to get multiple EMS systems and hospitals on the same page for post-resuscitation care in my neck of the woods. I’m not sure what the implications of single-dose intra-arrest Solu-Medrol without tapered-dose in ICU would be….any thoughts?

    • Since they only started the continuous steroids in patients with post-arrest shock, a bunch of them only got the single dose of solumedrol so we can imagine there may be benefit (though as you said, it would be great to see a study actually proving that).

  6. My default prejudice is that vasopressin doesn’t offer any long-term survival advantages and that steroids are kind of a catch-all treatment for any sort of (sometimes critical) illness, whose use often exceeds any proven indications. From the start, I’m a bit biased in that my plausibility level is low…

    Unlike, say, Rivers’ work where I think the simple act of bundling treatment is actually an important intervention, I really wish they hadn’t combined the treatments here because both therapies seem somewhat unlikely from the start. In larger studies, vasopressin has been shown to offer no real survival advantages in humans over epi, and the literature on steroids is wrought with hand-wringing and flip-flopping in critical illness. I think it’s an interesting theory to treat these patients with steroids since the post-arrest syndrome does indeed resemble severe sepsis (though that presumes that steroids in that case are proven…), but I wish they had done just that and not thrown in the vasopressin wrench so that it would be easier to work out which treatment was having what effect.

    In both studies they managed to improve both ROSC and long-term survival to discharge to similar extents. It’s easy to attribute the increased ROSC to vasopressin and increased discharge survival to the steroids on top of that, since that makes some theoretical sense with the limited science we already have. The problem is that a bundled package could also mask bias inherent in how the study was carried out and how patients were randomized and treated on-scene that might never be picked up in statistical analysis or a well described methods section. It’s no revelation that a few paragraphs in a paper can’t adequately describe or control just what happens in the midst of a busy resuscitation like these patients were receiving.

    Let’s imagine that they performed this study using only the steroids and still got the same results. It would seem a bit odd that they had such a high initial ROSC, and we would be justified in being rather skeptical. Or, perhaps they used only vasopressin but still doubled their neurologically-intact survival; that would seem to clash with prior research.

    So, just because they combined the two drugs and each seemed to offer an independent and additive benefit, it also introduces a bit of faith to the science. What I mean is that it’s a sort of black box experiment in figuring what effect, if any, each individual medication was having. You take a cocktail of medications with theoretical (but not proven effects), mix them up in the patients, and out come beneficial results in terms of both ROSC and discharge survival. While the experimental design may be otherwise flawless, it still introduces a modicum of faith and uncertainty to the actual treatment effect that isn’t going to be reflected in statistical analysis. Based on these two papers alone, you’ll never know quite what’s happening in the black box of the treatment arm, only that the patients come out better than placebo.

    Maybe they really had an additive or synergistic effect together.

    Or maybe there was a form of bias affecting the survival of the treatment group that we cannot account for. Without a way to pick apart the individual treatment effects of the two main interventions studied, there’s no way to compare them to historical or experimental controls and decide what extent of the results were due to actual treatment effects and how much was the result of factors not accounted for.

    End nit-picking. I’ve looked through the authors’ other work and some of the supplemental material available online and I’m willing to believe they are working in good-faith to give us the best data possible, but that doesn’t quell my nagging doubts concerning this study and it’s predecessor. But at least there’s no apparent Pharma involvement, so kudos to them on that.

    I think it’s a good study on-paper and a great theory worth examining, and positive results are certainly worth pursuing, but I also can’t help but examine it with a critical eye. There’s a whole lot of pseudo-science that gets pushed with the argument that experimental data shows statistically significant positive results, but the authors fail to address concerns like prior probability and good experimental design. It’s only prudent that we apply the same cold logic that we use to tear apart homeopathy papers to the real science of medicine, especially when it’s “groundbreaking.” Lord knows we get fooled enough, and still more than we realize.

    • Vince,

      Your points are all true and well made, but I think I see studies like this slightly differently.

      We both agree that a superior study would have been simply epi vs. epi + steroids (or a three arm with a placebo arm as Trueger would like). But obviously the authors believe (their hypothesis) that vasopressin is bringing something to the table. So that is how they did their two studies.

      Since they did, all we can say is VSE is superior to epi alone IF we believe in the internal validity of the trial. I’ve seen no arguments to the internal validity in your comments.

      I do not quite understand these lines:
      “There’s a whole lot of pseudo-science that gets pushed with the argument that experimental data shows statistically significant positive results, but the authors fail to address concerns like prior probability and good experimental design.”

      Pseudo-science does not get pushed with statistically significant positive results unless the study is biased, misinterpreted, or the Statistically Sig. effects have no actual patient-oriented clinical significance. RCTs will get things wrong due to Type I error, but this is now the 2nd positive RCT.

      We have had a spate of recent treatments in which the data are completely made up; that is always a possible problem.

      It is really not the responsibility of the researchers to address prior probability. The Bayesian responsibility is on the part of the interpreter not the researcher, though of course they take a crack at it in the discussion section. But great good would come of never reading a discussions section of a study.

      I am not defending VSE–it very well may turn out to be another flash in the pan, I am solely defending proper EBM analysis of studies.

      • Thanks for the thoughtful response!

        I agree that my point in the section you expressed confusion about was poorly defined. Thankfully you helped lead me where I wanted to go by later stating, “The Bayesian responsibility is on the part of the interpreter not the researcher…” which is the only real discussion point where I think we diverge (probably since the foundation of my understanding of EBM was forged from your book…).

        While it’s true that a portion of the Bayesian analysis will always fall on the interpreter, I happen to believe that we are at the point where a significant burden should also lay on the researcher. While the basic use of likelihood ratios is finally gaining some traction in the medical research, there’s still a large portion of the Bayesian approach that extends beyond those simple values. In an RCT like this, I think that means that the design of the experiment should reflect the prior probability of the null hypothesis and that the statistical analysis should be solidly based in Bayesian analysis, not thrown on as an afterthought (if at all).

        So in regards to the experimental design, since we’re mostly interested in the steroids vs. placebo question, I think it’s a fundamental flaw that vasopressin was included here because the likelihood of a benefit was low. Based on prior research, all it really offered was a chance to muck up our ability to interpret the data, so even if the researchers believed that it really offered potential benefit as a bundle, that should have been left to further study or individual practice outside of this research and not included in this already rather novel trial.

        Some may think it’s a minor quibble since positive outcomes in an RCT are positive outcomes regardless of the mechanism, but it goes a little bit deeper than that. The problem I see is that you can have an RCT like this that looks flawless as an RCT in and of itself, but it’s still poorly designed because of that one fatal flaw affecting the prior probability of its results. The treatments appear well randomized, the participants well blinded, and there’s a legitimate placebo group (though Trueger would disagree), but by designing a study where the intervention has two levels of implausibility (the null hypothesis is that steroids don’t work AND that vasopressin doesn’t work), it fundamentally decreases the likelihood of the results supporting the null hypothesis and decreases the overall strength of the trial.

        This is where the design of the study starts to merge with its statistical analysis if we buy in to the benefits of a true Bayesian approach. My ability to discuss this topic is restricted by the limited extent of my own understanding (and the attention of any readers making it this far), but it suffices to say that Bayesian analysis should form the basis of the statistical analysis most trials being performed today. Instead, even when likelihood ratios are included in the results, it’s only as an add-on to frequentist values and the fundamentals of Bayesian inference are chiefly ignored. It’s well understood that the frequentist approach hamstrings our ability to perform usable research, but still p-values and confidence intervals persist for a multitude of reasons (including the fact the p-value is an inflated number and poorly understood).

        With all that said, I do not take any of these gripes out on the authors themselves. We both agree that they seem to have performed this study to the best of their abilities and executed it well, and the results sure are interesting. My issue is that we operate in a field where a study can appear well-designed on paper and still have the power to lead us astray, yet the flaws leading to these erroneous conclusions and the possible solutions are rarely discussed or given the pedestal they deserve. My true position on this paper is far more positive than the above paragraphs would have you believe.

        As an individual practitioner using the best data available to you, I think your conclusions and the consideration of incorporating these interventions into your practice as you discussed are perfectly valid. My reason for sounding so nihilistic in my own approach to this paper is two-fold: First, as a medic, I don’t even have to consider adding this to my own practice yet, and two, I greatly worry about the repercussions when this goes up to the AHA and ILCOR for inclusion in their next guidelines. Already I saw a piece on Medscape (absolutely glowing) where the lead author describes the results as corresponding to a “level B recommendation.” At this point, and based on their prior decisions, I can’t imagine the committees seeing it any differently.

  7. Matthew says:

    I’m with Adam and Ryan, what’s the pathophysiology behind using steroids in cardiac arrest? Plus, it takes about 45 minutes to take affect…

    • I think, as Ben alluded to above, it’s the massive SIRS response after the global ischemia-reperfusion. The authors reference their own prior study in 2009 (the initial spyros et al in annals of internal medicine, jan 2009 12;169(1): 15-24). In that study, the intro + discussion goes over why they chose intra-arrest + post-arrest steroids, and they do a good job of citing prior evidence/support.

      To loosely paraphrase, the intra-arrest dose was thought to augment post-arrest perfusion pressure, and the post-arrest steroid was essentially used to treat the post-arrest syndrome similar to a “sepsis-like syndrome”. Because of that, they used the post-arrest steroids in a similar manner as they would in sepsis (I believe they even used it as a drip, which is what was “2D-recommended” by the surviving sepsis campaign).

      This makes some physiologic sense, as cardiac arrest is kind of a continuum (the peri-arrest period requiring medical augmentation of perfusion pressure vs the arrest period, which requires manual augmentation of perfusion pressure), so whatever can help augment perfusion pressure during the transition between the two may help achieve ROSC and keep it.

      It makes sense, too, especially with their selected patient population. If the cardiac arrest is prolonged (looks like most took over 20 minutes to achieve ROSC), it seems like there would be more difficulty maintaining perfusion pressure in the immediate peri/post-arrest period, and it may elicit a more robust SIRS response. Instead of just giving empiric, prolonged doses of steroids to all post-arrest patients (which we have to be careful NOT to do based on this study…may be easy for us to get carried away), it makes sense to use it in the select patient population they chose.

      On the surface, this is a great study. May be usable, especially when you consider all the stuff we do in the intra/peri-arrest period with less evidence. Would take another couple of years to get the numbers in this patient population again, but would like to see it independently repeated. In the mean time, definitely something I will consider doing in the right patients.

  8. I think the big problem here is that they were in hospital arrests. We (in the ED, at least in our set up) don’t look after in hospital arrests. From my time as an intern and ICU doc, responding to all the cardiac arrests in the hospital, they were a very different population from the out of hospital patients.

    I suspect (though as I write this I realise i should really do a pub med search first) that there’s a lot less VT/VF and the big killers are PEs, electrolyte disorders and post op sepsis. Vasopressin/steroid might be the drug of choice for those.

    The numbers of the outcome we’re looking for (intact neuro survival) are low too; it was only 18 v 7 patients favouring the vasopressin/steroid. Statistically significant as they may be, it’s reasonable to hope for bigger numbers than that before I start giving the vasopressin/steroid.

  9. rfdsdoc says:

    thanks for the comments. very useful!
    Andy, I am surprised by your request for bigger numbers!
    18 v 7 is over double intact neuro survival!
    How much bigger numbers do you want?
    In an arrest patient population!!??
    I find the skepticism remarkable in some of the comments and yes Trueger and I debated this online.
    This is the second +ve RCT for this Rx bundle. There are a heck of a lot of Rx we do that have much less supportive evidence : Prehospital cervical spine immobilisation comes to mind, cricoid pressure ( yes I will admit that one even!), magnesium in severe asthma,
    I am puzzled what people’s skepticism is based on..adverse side effects of Rx? ( well arrested patients dont have many complications..death or coma or vegetable or neuro intact survival)
    This Rx bundle actually seems to lead to more neuro intact survivors..isnt that what we want?!
    Cost of Rx concerns?? well these drugs are certainly cheaper than what Xigris costed..or ECMO!
    Its baffling to me!

  10. rfdsdoc says:

    hang on..my only theory why there is some skepticism to this paper..is that some ..(maybe many) of us have stopped using epinephrine in cardiac arrest care..and this paper suggests that was a wrong decision…and this causes sufficient cognitive dissonance to adopt the position. ..that this paper is wrong..rather than the decision to stop using epi in arrest ..was wrong instead

    right?

    • I agree somewhat. This actually was a follow-up on a 2009 single-center study by the same authors – also well done. Ideally, it would be replicated by different authors to be totally above reproach (and they need to separate steroids and vaso, as discussed above), but I think we might be able to start applying this. We would do that mostly out of knowing epi by itself doesn’t really work, and trying other various ways to augment perfusion pressure (particularly during the transition from intra-arrest to post-arrest) may be helpful.

      It seems like there are a couple different aspects of physiology at work, and I’m only somewhat glad they lumped them together. The first is augmentation of perfusion pressure in the intra –> peri –> post arrest period, and it may have been the vasopressin +/- an early effect of steroids as there is a transition from the peri-to-post arrest period. The second is an attenuation of the massive, post-arrest SIRS response.

      Both of these make quite a bit of sense, and I feel like we can use this as a “bundle” and it will improve neuro-intact survival as long as we match the patients used in the study with our patients (i.e. refractory arrest, refractory post-arrest shock…it should NOT be used empirically for all post-arrests, which would be easy to do). It would be interesting to know which aspect of the VSE arm was beneficial, and if we can use steroids for refractory shock and not intra-arrest, etc.

    • Most of my own skepticism boils down to the fact that we’ve not only been burned a few times by steroids for several disease states, but also oversold on “lifesaving” cardiac arrest interventions in the past. Combining the two sounds like a great way to set up an evidence-based minefield and I fear we’ve been down this path before…

      The authors did the right thing by chasing their initial data, but results that more than double favorable outcomes sound way too good to be true unless we get these interventions verified by an independent set of investigators. Individual practitioners are probably supported if they want to try this out in their own practice, but I really worry about what’s going to happen when this ends up in the guidelines and becomes “standard of care.” Though we’re going to have to work with the data we’ve been given for the next few years, I’m making the weightless prediction that future study will severely diminish, if not overturn this initial research.

  11. rfdsdoc says:

    thanks Trent, agree.
    One thing. Epi does work in arrest..it just doesnt work enough by itself!
    Consistently improves ROSC in past studies of arrest care…just not RONF!

  12. I’m so glad you have posted on this paper Scott as I read this one and have been hanging out to see what debate could come of it. My default position is that a) anything showing a new set of drugs in cardiac arrest is useful will probably be misleading and b) any new intervention that looks good in medicine usually starts to look pretty awful shortly afterwards when it has been studied a bit more. That said, I couldn’t really fault this study. There were two primary outcome measures which really means you are getting a second lottery ticket for free but since they were both positive I suppose that really strengthens things a lot (if one were positive and one negative the study would be open to the argument that you are bound to get lucky sooner or later if you have enough outcome measures). Otherwise it looks like a significant treatment effect and effect size and a very implementable intervention.

    For a resuscitation paper it is a big series and a bit effect size. It would be great to see it replicated in the put of hospital arrest population. I do wonder how much the presence of several days of illness in hospital makes a difference to steroid requirements and responsiveness and whether such a benefit would be seen in the single coronary occlusion VF arrest in the community.

  13. Hi,

    Just a thought, but I think RFDSDOC’s post highlights a good point: the arrest population offers a unique study group in that a majority of patients who arrest die, so there are no major harms that we can do with these medications (except for ROSC without RONF, which is no small issue) that would warrant being overly cautious about their use. In fact, these treatments have all been used, albeit not as a bundle, and so it seems to me we could produce a lot of data just by using this treatment algorithm in a larger population. Granted, I think separating each intervention for the sake of being more targeted in our treatments is valid, as previous posts suggested with a 3-arm study, but overall this seems to me a situation of a lot of potential benefit and little risk of further harm– a luxury we don’t often get in studying novel treatment approaches.

  14. rfdsdoc says:

    thanks for the additional useful comments here!

    in fact no one commenting has given a single good reason NOT to follow VSE Rx in hospital arrest situations.

    And for all those who stopped giving epi in ACLS, then some reconsideration on that stance is warranted!

    The evidence based medicine door swings BOTH ways!

    • I would say that people who are already using epi should consider vse, those who believe in not using it may choose to ignore this study.

  15. Ah, so this is where the discussion brews.

    I didn’t like this article. I do have issues with internal validity, re: baseline differences between groups, different follow-up interventions, the multiple interventions, and confounding associations with good outcome. It also troubles me this is the same group x2, rather than independent verification.

    There is the issue of “well, ain’t they dead?” but I’d rather be more confident in the cognitive outcomes before I start VSE during arrest – unless my goal is simply keeping the husk alive for organ harvest – before I start a multi-day ICU pathway of resource utilization.

    • I guess the ? I ask you Ryan is do you still use epi. If the answer is no, then your points are entirely consistent with your practice. If you are using it, how do we justify that drug?

  16. abdullah alsugair says:

    Great discussion as always.
    Thanks scott.l totally agree with you , If you believe in epi why not go ahead for VSE & give it a shot.
    A large study whether 2 or 3 arm RCT would be of intersest to validate these results.
    As RFDSDOC said EBM doors swing both ways.
    Thsnks.

  17. Robbie Mc Mahon says:

    Hi Scott and all involved in the discussion re this paper.
    I have a slightly different issue with the results and presentation of them. While the numbers certainly look favourable for the VSE group and any benefit is welcomed in this area of practice,
    my issue is with the other treatments given and the baseline survival rates.

    Firstly, no patient in either the control group or the intervention group appears to have received defibrillation (Table 2) despite the fact that almost 17% of cardiac arrest rhythms in each group are reported as VF/VT and that over 90% of arrests in each group were reported as witnessed.
    The fact that the average duration of CPR was 5 cycles (mean cycle duration 3.2 minutes) for the control group and 4 cycles (mean cycle duration 3.3 minutes) for the intervention group implies that at least some of those patients should have received a minimum of 1 DC shock during their resuscitation.
    This is also of interest in regards to the cause of cardiac arrest between the 2 groups as the reported incidence of life threatening/fatal arrhythmia in the control group was 8% in the control group versus 6.2% in the intervention group (Table 1).
    The apparent lack of defibrillation may provide some reason for the overall decreased survival rates for patients with cardiac arrest within the study population versus other published international results.
    This then presents the question as to whether the results found represent an overall improvement in functional survival rates despite the lack of the use of defibrillation, or whether the results represent an overall decrease in the functional survival due to the lack of early defibrillation within the study population versus comparable international populations.

    Secondly, there appears to be a difference in the rates of Myocardial Ischaemia/Infarction as a cause of cardiac arrest (Table 1) between the 2 groups. The control group having a rate of 17.4% versus the intervention group rate of 23.1%. This may have provided an increased potential for curative intervention within the intervention group which may have contributed towards the overall improved outcome (RONF) seen within this group.

    Any thought or comments welcomed!

  18. There’s a small trial from the 1980s where dexamethasone was given prehospital as a single dose. Seems underpowered though. Only about 45 patients in each arm. Plus they did some other weird stuff too, MAST trousers, etc.
    Annals emerg med vol13 issue 11 November 1984

Trackbacks

  1. […] Dr. Weingart’s VSE Emcrit Wee is of course also worth a listen here […]

  2. […] Steroids and Epinephrine in Cardiac Arrest. Scott Weingart previously weighed in on this study on EMCrit. […]

Speak Your Mind (Along with your name, job, and affiliation)