A week ago on the EMS EdUCast the topic was resuscitation. The big disagreement was about the IV vs No IV epinephrine study.[1]
One of the criticisms of the study is that Blair Bigham states that therapeutic hypothermia would lead to improved outcomes. However, the Oslo hospitals started routinely using therapeutic hypothermia only four months after the start of the study. So, almost all of the eligible patients did receive therapeutic hypothermia.[2] The therapeutic hypothermia study does show a doubling of survival to discharge with good neurological function at one year after discharge, so this does not appear to be any justification for doubting the effectiveness of treatment in Oslo.
Another concern is that PCI (Percutaneous Coronary Angiography or cardiac catheterization) might affect outcomes, but cardiac catheterization was also part of standard treatment in Oslo at the time.
Bill Toon mentions that some of the ambulances are staffed by physicians, but what difference is there between what a physician will do on scene and what a medic will do on scene? Physician staffed ambulances were present at 37% of no IV patients and 38% of IV patients, so this should not have affected either group more than the other.
A concern raised by Rob Theriault was the change in the CPR (CardioPulmonary Resuscitation) and ACLS (Advanced Cardiac Life Support) guidelines during the study period.
Until January 2006, ACLS was performed according to the International Guidelines 2000,14 with the modification that patients with ventricular fibrillation received 3 minutes of CPR before the first shock and between unsuccessful series of shocks.15 [1]
While they were not using the 2005 guidelines prior to January 2006 in Oslo, they were using a form of CPR that could be described as closer to the 2005 guidelines than the 2000 guidelines. According to the study –
Both groups had adequate and similar CPR quality with few chest compression pauses (median hands-off ratio, 0.15 for the intravenous group and 0.14 for the no intravenous group) and the compression and ventilation rates were within the guideline recommendations (Table 1).[1]
It appears that the compression interruptions are much less than what we would expect from a similar study done in the US, except where CCR (Continuous Compression Resuscitation or CardioCerebral Resuscitation) is being used correctly.
If you believe, as Blair appears to, that the improved outcomes in the US after the 2005 guidelines are at least partially due to epinephrine, likewise the improvements in the places using CCR, then you anticipate that when the first large enough randomized placebo-controlled study of drugs during cardiac arrest is published, it will show significantly better outcomes for those receiving epinephrine.
I doubt it. I expect something similar to the many studies of traditional treatments that could only be shown to improve surrogate end-points. Surrogate end-points are like alcohol. In moderation, the effects can be pleasant, while intemperate use distorts reality.
Some examples of being misled by surrogate end-points are the routine use of antiarrhythmic medication in post-MI (Myocardial Infarction) patients with PVCs (Premature Ventricular Contractions). The drugs did a great job of getting rid of the nasty looking PVCs, but making the rhythm look better did not improve outcomes. In spite of the wonderfully improved heart rhythms, the fatality rate more than tripled.[3]
We used to give furosemide (Lasix) to almost all patients presenting with symptoms of CHF (Congestive Heart Failure). Single-mindedly, we would try to remove as much water from CHF patients, because fluid in the lungs is a sign of fluid overload. Research, going back to the 1980s, shows that fluid in the lungs and fluid overload are not the same thing. Giving furosemide causes the body to dump water almost as dramatically as if we gave the patient an enema. Medical directors have responded to research showing harm from furosemide, and many have restricted the use of furosemide.
MAST/PASG (Medical Anti-Shock Trousers/Pneumatic Anti-Shock Garment) was the answer to blood loss. The same argument, that you have to have a pulse to leave the hospital alive, reared its head. Rather than focus on pulses in the ED, medical directors chose the meaningful outcome of more patients leaving the hospital able to care for themselves.
At one point, Buck Feris points out that post-resuscitation care is largely a matter of dealing with the side effects of epinephrine. Blair presents a paper that suggests that there are no post-resuscitation guidelines (not his conclusion). No post-resuscitation guidelines? There is an entire section of the ACLS guidelines on post-resuscitation care.[4] Just because there is no particular flow sheet to be memorized, does not mean that there are no guidelines. When I taught ACLS, post-resuscitation care was one of the essential parts I covered.
CPR/CCR, defibrillation, potentially reversible causes, and post resuscitation care are the things that make a difference in outcome. Why do we spend so much time on trying to resuscitate people, if we are not going to prepare them to actually deal with what happens after the return of a pulse?
Post-resuscitation care is not just about treating vital signs. Perhaps part of our problem is that we do not see this as part of resuscitation. If we understood this, maybe we would see that giving epinephrine is just about vital signs. Giving epinephrine is not about resuscitation. When we produce a pulse with epinephrine, we need to switch from resuscitation to trying to counter epinephrine toxicity.
Perhaps, if epinephrine were in any way considered good for the heart, I would be less cynical. There are not many drugs more toxic to the heart than epinephrine.
Narrative Fallacy –
How did this happen? – Research
C A S T and Narrative Fallacy comment from Shaggy
Some Research Podcasting Comments
Shaggy Comments on Some Research Podcasting Comments.
Spine Immobilization in Penetrating Trauma: More Harm Than Good?
EMS EdUCast – Journal Club 2: Episode 43
Education Problems, Autism, and Vaccines
Updated 9/14/2012 at 03:00 for formatting.
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Footnotes:
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[1] Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial.
Olasveengen TM, Sunde K, Brunborg C, Thowsen J, Steen PA, Wik L.
JAMA. 2009 Nov 25;302(20):2222-9.
PMID: 19934423 [PubMed – in process]
I wrote about this in Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial. If you want to read the full text of the study, it is available in PDF at the EMSEdUCast page for this episode.
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[2] Implementation of a standardised treatment protocol for post resuscitation care after out-of-hospital cardiac arrest.
Sunde K, Pytte M, Jacobsen D, Mangschau A, Jensen LP, Smedsrud C, Draegni T, Steen PA.
Resuscitation. 2007 Apr;73(1):29-39. Epub 2007 Jan 25.
PMID: 17258378 [PubMed – indexed for MEDLINE]
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[3] Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial.
Echt DS, Liebson PR, Mitchell LB, Peters RW, Obias-Manno D, Barker AH, Arensberg D, Baker A, Friedman L, Greene HL, et al.
N Engl J Med. 1991 Mar 21;324(12):781-8.
PMID: 1900101 [PubMed – indexed for MEDLINE]
CONCLUSIONS. There was an excess of deaths due to arrhythmia and deaths due to shock after acute recurrent myocardial infarction in patients treated with encainide or flecainide. Nonlethal events, however, were equally distributed between the active-drug and placebo groups. The mechanisms underlying the excess mortality during treatment with encainide or flecainide remain unknown.
I have written about this in C A S T and Narrative Fallacy and elsewhere.
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[4] 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Circulation. 2005;112:IV-84 – IV-88.
Part 7.5: Postresuscitation Support
Free Full Text Free PDF
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You made some excellent points there. I did a search on the topic and barely found any specific details on other sites, but then happy to be here, seriously, thanks.
– Andre
Andre,
Thank you.