Without evidence of benefit, an intervention should not be presumed to be beneficial or safe.

- Rogue Medic

How Effective Is Epinephrine for Improving Survival Among Patients in Cardiac Arrest?

   

There have been two studies comparing epinephrine with placebo to treat out of hospital cardiac arrest. The Jacobs study was stopped early, because of interference by those who do not want to know if their medicine actually works.[1] The purpose of research is to determine, as objectively as possible, if a treatment is better than placebo nothing.  

Click on the image to make it larger.  

Even the small sample size shows a impressive p values of <0.001 for both ROSC (Return Of Spontaneous Circulation) and being admitted to the hospital. Unfortunately, that does not lead to outcomes that are better than placebo.

The Perkins study (PARAMEDIC2) did not find a significant difference between adrenaline (epinephrine in non-Commonwealth countries) and placebo.[2] The Jacobs study also did not find a difference, but the numbers were small, due to the interference by the less than knowledgeable. Following the Jacobs study, some intervention proponents have suggested that the problem is not a lack of evidence of benefit, but need to look at the evidence from the right perspective. The inadequate evidence is not “inadequate”, but really just misunderstood. All we need to do is use a method of analysis that compensates for the tiny sample size. A Bayesian approach will produce the positive outcome that is not justified by so few patients.[3]

What happens when the numbers are combined, so that the sample size is large enough to eliminate the need for statistical chicanery to come up with something positive?

The outcomes do not improve.  

Neither standard dose adrenaline, high-dose adrenaline,vasopressin nor a combination of adrenaline and vasopressin improved survival with a favourable neurological outcome.[4]
 

If the Bayesian approach were appropriate, then the much larger sample size would have provided more than enough patients to confirm the optimism of the epinephrine advocates. The result is still not statistically significant. Maybe a much, much larger study will show a statistically significant, but tiny, improvement in outcomes with epinephrine, but don’t hold your breath for that. It took half a century to produce the first study, then seven more years for the second. With the cost of research and the problems coordinating such a large study, it is more likely that the guidelines will continue to recommend spending a lot of time and money giving a drug that diverts attention from the interventions that do improve outcomes.

There is still no evidence that adrenaline provides better outcomes than placebo in human cardiac arrest patients.

  –  

Footnotes:

  –  

[1] Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial Jacobs IG, Finn JC, Jelinek GA, Oxer HF, Thompson PL. Resuscitation. 2011 Sep;82(9):1138-43. doi: 10.1016/j.resuscitation.2011.06.029. Epub 2011 Jul 2. PMID: 21745533

Free Full Text PDF Download from semanticscholar.org  

This study was designed as a multicentre trial involving five ambulance services in Australia and New Zealand and was accordingly powered to detect clinically important treatment effects. Despite having obtained approvals for the study from Institutional Ethics Committees, Crown Law and Guardianship Boards, the concerns of being involved in a trial in which the unproven “standard of care” was being withheld prevented four of the five ambulance services from participating.

In addition adverse press reports questioning the ethics of conducting this trial, which subsequently led to the involvement of politicians, further heightened these concerns. Despite the clearly demonstrated existence of clinical equipoise for adrenaline in cardiac arrest it remained impossible to change the decision not to participate.

  –  

[2] A Randomized Trial of Epinephrine in Out-of-Hospital Cardiac Arrest. Perkins GD, Ji C, Deakin CD, Quinn T, Nolan JP, Scomparin C, Regan S, Long J, Slowther A, Pocock H, Black JJM, Moore F, Fothergill RT, Rees N, O’Shea L, Docherty M, Gunson I, Han K, Charlton K, Finn J, Petrou S, Stallard N, Gates S, Lall R; PARAMEDIC2 Collaborators. N Engl J Med. 2018 Aug 23;379(8):711-721. doi: 10.1056/NEJMoa1806842. Epub 2018 Jul 18. PMID: 30021076

Free Full Text from N Engl J Med.

  –  

[3] Regarding “Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial”. Youngquist ST, Niemann JT. Resuscitation. 2012 Apr;83(4):e105; author reply e107. doi: 10.1016/j.resuscitation.2011.09.035. Epub 2012 Jan 18. No abstract available. PMID: 22266068

Free Full Text from Resuscitation.

  –  

[4] Adrenaline and vasopressin for cardiac arrest. Finn J, Jacobs I, Williams TA, Gates S, Perkins GD. Cochrane Database Syst Rev. 2019 Jan 17;1:CD003179. doi: 10.1002/14651858.CD003179.pub2. PMID: 30653257    

.

Closed chest compressions reduce survival in an animal model of haemorrhage-induced traumatic cardiac arrest

   

This is an animal study, rather than a human study, but it has fewer disadvantages than the usual animal studies of medical cardiac arrest. Animals do not develop the comorbidities that humans do, but have artificially created heart attacks, rather than by the development of actual heart disease. In studying trauma, this is less of a problem, since trauma is artificially created. This study is much more representative of penetrating injuries with a low velocity objects, than blunt force trauma, or penetrating injury with a high velocity object.

Are we really killing trauma patients with our chest compressions?

Maybe. This is one small study (39 pigs), but it does raise questions about the ways we can minimize the harm we cause.

 

 
CCC were associated with increased mortality and compromised haemodynamics compared to intravenous fluid resuscitation. Whole blood resuscitation was better than saline.[1]

 
A soft tissue injury was created, with 3 shots to the right thigh using a captive bolt (Cash Special, Accles and Shelvoke, Sutton Coldfield, UK). Two minutes later animals underwent a controlled haemorrhage (30% blood volume) at an exponentially reducing rate as previously described12 until the mean arterial blood pressure (MAP) was 45 mmHg. Blood was collected into CPD (citrate phosphate dextrose) and stored at room temperature until required for later transfusion.[1]
 

Image source

 

This study, conducted in an animal model of haemorrhage-induced traumatic cardiac arrest, has demonstrated that chest compressions confer no benefit over fluid resuscitation alone, and blood should be the fluid therapy of choice.[1]

  That seems to be concluding too much, since this is just one study, but it does reinforce the results of other, similar studies. We should study the outcomes in humans, since there does appear to be equipoise. There never was a physiological justification for chest compressions in traumatic cardiac arrest which appears to be due to hemorrhage. Now there is more evidence that chest compressions produce more harm than benefit in traumatic cardiac arrest which appears to be due to hemorrhage.

 
One study using a baboon traumatic cardiac arrest model found that the improvements in haemodynamics seen with chest compressions for normovolaemic cardiac arrest were not reproduced in hypovolaemic arrest.14 The authors suggested that CCC should not delay correction of the underlying deficit causing TCA, but the study was undertaken in only three animals, perhaps limiting its clinical relevance. A more recent study using a canine model of pulseless electrical activity in TCA found no benefit of chest compressions over fluid therapy alone or fluid combined with chest compressions; in fact the chest compression only group had worse survival, base deficit and ejection fraction.15 The authors concluded that further research was required to determine whether CPR has a role for the patient in haemorrhagic shock.[1]

  Most important is that the outcome is ROSC (Return Of Spontaneous Circulation), not return to normal neurological function. Since these are pigs, even the appearance of normal neurological function may not mean anything in humans. Still, the treatment is not evidence-based, so there does not appear to be a good reason to prefer to continue using compressions for traumatic cardiac arrest which appears to be due to hemorrhage.

Here in America, we are unlikely to do the research, because we are more concerned with appearances than with improving outcomes for patients. Maybe somebody in Britain or Australia will have to demonstrate some responsibility, so we can stop using chest compressions to kill trauma patients.

  Footnotes:

  [1] Closed chest compressions reduce survival in an animal model of haemorrhage-induced traumatic cardiac arrest. Watts S, Smith JE, Gwyther R, Kirkman E. Resuscitation. 2019 May 9;140:37-42. doi: 10.1016/j.resuscitation.2019.04.048. [Epub ahead of print]

PMID: 31077754

Free Full Text from Resuscitation

  .

ILCOR wants the appearance of public comments with less than half the substance

 

The International Liaison Committee on Resuscitation (ILCOR) shows its priorities in the way it handles its problem with public comments.
 

Last week ILCOR posted the two new draft CoSTRs listed below for public comment. It became apparent that the commenting link was broken and those who visited the site could not comment. We apologize for the inconvenience. The commenting link is now fixed and we invite you to comment at ilcor.org/costr.

  • Advanced Airway Management During Adult Cardiac Arrest
  • Vasopressors in Adult Cardiac Arrest
  • As a reminder, the public comment period will close on 4 April 2019.[1]

     

    ILCOR made a mistake that prevented public comments from being submitted for most of the public comment period.

    ILCOR is so interested in your public comments that they have decided to send out an email to let people know that they have the same drop dead date for the comments as before, but this time they might actually be able to get the comments to work. Maybe.

    The lack of evidence of benefit of epinephrine (adrenaline in Commonwealth countries) has lasted over half a century, so what is the rush to get these new guidelines out?

    There is only one outcome that matters – survival without severe brain damage.
     


     

    ILCOR evaluates 23 outcomes.

    ILCOR considers 15 of these outcomes critical, but they are really just 5 outcomes, with some of them repeated over different rhythms. These are (in increasing order of importance to the only one that matters):

    1. For the critical outcome of survival to hospital discharge, 2. For the critical outcome of survival at 3 months, 3. For the critical outcome of favorable neurologic outcome at hospital discharge, 4. For the critical outcome of survival with unfavorable neurologic outcome at 3 months, 5. For the critical outcome of favorable neurologic outcome at 3 months,

    Many of them are repeated for each cardiac arrest rhythm or for each vasopressor, or vasopressor cocktail:

    1. Epinephrine plus vasopressin compared to epinephrine only – Any rhythm 2. Initial vasopressin compared to initial epinephrine – Any rhythm 3. Epinephrine compared to placebo – Non-shockable rhythms 4. Epinephrine compared to placebo – Shockable rhythms 5. Epinephrine compared to placebo – Any initial rhythm

    There is only one outcome that matters – survival without severe brain damage.

    There is only one study that was large enough to answer this:
     

    CONCLUSIONS
    In adults with out-of-hospital cardiac arrest, the use of epinephrine resulted in a significantly higher rate of 30-day survival than the use of placebo, but there was no significant between-group difference in the rate of a favorable neurologic outcome because more survivors had severe neurologic impairment in the epinephrine group.[2]

     

    If the people at ILCOR really think that epinephrine is beneficial in cardiac arrest, they should encourage a much larger study.

    There were 4,000 patients in each group – 4,000 placebo and 4,000 epinephrine.

    Maybe with 8,000 patients in each group, the ever decreasing “trend toward better outcome” will reach significance. Maybe it will be shown to be just another insignificant appearance of a “trend” that is the result of having so few survivors to compare.

    There were only 161 survivors without severe brain damage out of 8,000 cardiac arrest patients – 74 placebo and 87 epinephrine.

    Those resuscitated before receiving epinephrine/placebo were excluded from the study, so this is not a case of EMS that only has a 2% resuscitation rate. The focus on epinephrine is a focus on the patients least likely to be resuscitated and a focus on counterproductive outcomes.

    Almost all of our good outcomes (without severe brain damage) will be without epinephrine, because these resuscitations happen before epinephrine can be give by even the most aggressive epi enthusiast.

    What we are doing is making excuses for memorizing ineffective interventions and requiring their application is a specific way, in order to determine the quality of care. We are promoting fantasy.

    We learned that distracting from the quality of chest compressions is the most deadly thing we can do in resuscitation.

    CPR = only chest compressions – the exception is when the arrest is believed to be due to a respiratory event, such as when the Smurf sign or a respiratory/choking history is present. Chest compressions provide all of the pulmonary resuscitation that a human needs for a non-respiratory event and the respiratory events are not easily missed.

    Why require a whole bunch of skills be applied for such a tiny portion of good outcomes among cardiac arrest patients?

    Why not give up on requiring these skills when the evidence makes it clear that there is no benefit?

    All we are doing is adding cognitive load to make us feel like we are doing something special.

    We could learn something that actually benefits patients, such as how to assess patients when giving high-dose NTG (NiTroGlycerine or GTN GlycerylTriNitrate in Commonwealth countries) for even hypotensive CHF/ADHF (Congestive Heart Failure/Acute Decompensated Heart Failure), where we can make much more of a difference and prevent cardiac arrest, but we don’t.[3],[4],[5]
     


     

    Cognitive load is not just a problem for paramedics and nurses, or med/surg doctors, but also for emergency physicians:

    Cognitive Load and the Emergency Physician
    April 12, 2016
    James O’Shea
    emDocs
    Article

    Why are we distracting everyone from things that do improve the only outcome that matters, in order to promote things that do not improve any outcome that matters?

    Here is what I wrote –
     

    The primary source for the recommendation to keep things the same is a brand new study – PARAMEDIC2.

    This showed no statistically significant improvement in the only outcome that matter – survival without severe brain damage.

    A larger study might show that there is a real improvement – or it may put the epi hypothesis out of its misery.

    I will eventually have a cardiac arrest. If I am resuscitated, whom will ILCOR send to change my diaper, and attend to the other things I can no longer attend to?

    We need evidence of a significant benefit in order to justify distracting everyone from interventions that actually do improve survival without severe brain damage.

    .

     

    The commenting link is now fixed and we invite you to comment at ilcor.org/costr

    Maybe they will pay attention. Dr. Rory Spiegel of EM Nerd has a detailed comment that is also critical of ILCOR’s proposed “strong recommendation” of epinephrine.

    Footnotes:

    [1] Vasopressors in Adult Cardiac Arrest
    Time left for commenting: 11 days 15:49:49
    ILCOR staff
    Created: March 21, 2019 · Updated: March 21, 2019
    Draft for public comment
    Consensus on Science with Treatment Recommendations (CoSTR)
    Vasopressors in Adult Cardiac Arrest page for comments until April 04, 2019 at 06:00 Eastern Time

    [2] A Randomized Trial of Epinephrine in Out-of-Hospital Cardiac Arrest.
    Perkins GD, Ji C, Deakin CD, Quinn T, Nolan JP, Scomparin C, Regan S, Long J, Slowther A, Pocock H, Black JJM, Moore F, Fothergill RT, Rees N, O’Shea L, Docherty M, Gunson I, Han K, Charlton K, Finn J, Petrou S, Stallard N, Gates S, Lall R; PARAMEDIC2 Collaborators.
    N Engl J Med. 2018 Aug 23;379(8):711-721. doi: 10.1056/NEJMoa1806842. Epub 2018 Jul 18.
    PMID: 30021076

    Free Full Text from N Engl J Med.
     

    In a Bayesian analysis that used an assumption of no benefit from adrenaline, the posterior probability that the absolute rate of survival was at least 1 percentage point higher in the epinephrine group than in the placebo group was 37% (Fig. S3 in the Supplementary Appendix). The probability that the absolute survival rate was at least 2 percentage points higher was 0.2%. With respect to the rate of survival with a favorable neurologic outcome at hospital discharge, the probabilities that the rate was at least 1 or 2 percentage points higher with epinephrine were 1.9% and 0%, respectively (Fig. S4 in the Supplementary Appendix).

     

    The probability of a good outcome (no severe brain damage) is not improved with epinephrine.

    If we want to improve outcomes, we need to look elsewhere, because there is nothing to be gained with epi.

    [3] Intravenous nitrates in the prehospital management of acute pulmonary edema.
    Bertini G, Giglioli C, Biggeri A, Margheri M, Simonetti I, Sica ML, Russo L, Gensini G.
    Ann Emerg Med. 1997 Oct;30(4):493-9.
    PMID: 9326864 [PubMed – indexed for MEDLINE]

    [4] Unreasonable Fear of Hypotension and High-Dose NTG – Part I
    Thu, 29 Aug 2013
    Rogue Medic
    Article

    [5] Unreasonable Fear of Hypotension and High-Dose NTG – Part II
    Wed, 04 Sep 2013
    Rogue Medic
    Article

    .

    Cardiac arrest victim Trudy Jones ‘given placebo’ – rather than experimental epinephrine

     

    As part of a study to find out if epinephrine (adrenaline in Commonwealth countries) is safe to use in cardiac arrest, a patient was treated with a placebo, rather than the inadequately tested drug. Some people are upset that the patient did not receive the drug they know nothing about.[1]

    The critics are trying to make sure that we never learn.

    We need to find out how much harm epinephrine causes, rather than make assumptions based on prejudices.

    When used in cardiac arrest, does epinephrine produce a pulse more often?

    Yes.

    When used in cardiac arrest, does epinephrine produce a good outcome more often?

    We don’t know.

    In over half a century of use in cardiac arrest, we have not bothered to find out.
     


     

    We did try to find out one time, but the media and politicians stopped it.[2]

    We would rather harm patients with unreasonable hope, than find out how much harm we are causing to patients.

    We would rather continue to be part of a huge, uncontrolled, unapproved, undeclared, undocumented, unethical experiment, than find out what works.

    Have we given informed consent to that kind of experimentation?

    Ignorance is bliss.

    The good news is that the enrollment of patients has finished, so the media and politicians will not be able to prevent us from learning the little that we will be able to learn from this research.[3]

    Will the results tell us which patients are harmed by epinephrine?

    Probably not – that will require a willingness to admit the limits of what we learn and more research.

    What EMS treatments have been demonstrated to improve outcomes from cardiac arrest?

    1. High quality chest compressions.
    2. Defibrillation, when indicated.

    Nothing else.

    All other treatments, when tested, have failed to be better than nothing (placebo).

    Footnotes:

    [1] Cardiac arrest victim Trudy Jones ‘given placebo’
    BBC News
    23 March 2018
    Article

    [2] Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial
    Jacobs IG, Finn JC, Jelinek GA, Oxer HF, Thompson PL.
    Resuscitation. 2011 Sep;82(9):1138-43. Epub 2011 Jul 2.
    PMID: 21745533 [PubMed – in process]

    Free Full Text PDF Download from semanticscholar.org
     

    This study was designed as a multicentre trial involving five ambulance services in Australia and New Zealand and was accordingly powered to detect clinically important treatment effects. Despite having obtained approvals for the study from Institutional Ethics Committees, Crown Law and Guardianship Boards, the concerns of being involved in a trial in which the unproven “standard of care” was being withheld prevented four of the five ambulance services from participating.

     

    In addition adverse press reports questioning the ethics of conducting this trial, which subsequently led to the involvement of politicians, further heightened these concerns. Despite the clearly demonstrated existence of clinical equipoise for adrenaline in cardiac arrest it remained impossible to change the decision not to participate.

     

    [3] Paramedic2 – The Adrenaline Trial
    Warwick Medical School
    Trial Updates
     

    Trial Update – 19 February 2018:
    PARAMEDIC2 has finished recruitment and we are therefore no longer issuing ‘No Study’ bracelets. The data collected from the trial is in the process of being analysed and we expect to publish the results in 2018. Once the results have been published, a summary will be provided on the trial website.

     

    Edited 12-27-2018 to correct link to pdf of Jacobs study in footnote 2.

    .

    2016 – Amiodarone is Useless, but Ketamine Gets Another Use

    amiodarone-edit-1
     

    I didn’t write a lot in 2016, but 2016 may have been the year we put the final nail in the coffin of amiodarone. Two major studies were published and both were very negative for amiodarone.

    If we give enough amiodarone to have an effect on ventricular tachycardia, it will usually be a negative effect.[1]

    Only 38% of ventricular tachycardia patients improved after amiodarone, but 48% had major adverse cardiac events after amiodarone.

    There are better drugs, including adenosine, sotalol, procainamide, and ketamine for ventricular tachycardia. Sedation and cardioversion is a much better choice. Cardioversion is actually expected after giving amiodarone.

    For cardiac arrest, amiodarone is not any better than placebo or lidocaine. What ever happened to the study of amiodarone that was showing such wonderful results over a decade ago? It still hasn’t been published, so it is reasonable to conclude that the results were negative for amiodarone. It is time to make room in the drug bag for something that works.[2],[3]

    On the other hand, now that we have improved the quality of CPR by focusing on compressions, rather than drugs, more patients are waking up while chest compressions are being performed, but without spontaneous circulation, so ketamine has another promising use. And ketamine is still good for sedation for intubation, for getting a patient to tolerate high flow oxygen, for agitated delirium, for pain management, . . . .[4],[5]

    Masimo’s RAD 57 still doesn’t have any evidence that it works well on real patients.[6]

    When intubating, breathe. Breathing is good. Isn’t inability to breathe the reason for intubation?[7]

    Footnotes:

    [1] The PROCAMIO Trial – IV Procainamide vs IV Amiodarone for the Acute Treatment of Stable Wide Complex Tachycardia
    Wed, 17 Aug 2016
    Rogue Medic
    Article

    [2] Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest
    Mon, 04 Apr 2016
    Rogue Medic
    Article

    [3] Dr. Kudenchuk is Misrepresenting ALPS as ‘Significant’
    Tue, 12 Apr 2016
    Rogue Medic
    Article

    [4] What do you do when a patient wakes up during CPR?
    Tue, 08 Mar 2016
    Rogue Medic
    Article

    [5] Ketamine For Anger Management
    Sun, 06 Mar 2016
    Rogue Medic
    Article

    [6] The RAD-57 – Still Unsafe?
    Wed, 03 Feb 2016
    Rogue Medic
    Article

    [7] Should you hold your breath while intubating?
    Tue, 19 Jan 2016
    Rogue Medic
    Article

    .

    What do you do when a patient wakes up during CPR?

    ResearchBlogging.org
     

    The return of consciousness without the return of a pulse is still rare, but may be more common with our increased focus on high quality chest compressions. There is still no evidence that interrupting chest compressions, for anything other than defibrillation, improves outcomes.

    Is this due to the consistency of the machine? Maybe. Maybe not. We do not have enough evidence to draw that conclusion.

    Is this growing population really growing? Maybe. Maybe not. We do not have enough evidence to draw that conclusion, either.

    It could be that with the ability to use a cell phone camera to record these instances, there is more credibility to the reports. There is a suggestion that this could be common.
     

    Parnia et al. conducted a multi-year, multi-center, prospective study of the frequency of awareness during resuscitation by interviewing cardiac arrest survivors after discharge. They found 55/140 (39%) had perceptions of awareness of being alive and even memories that originated during that time.2 [1]

     

    Should we be giving ketamine to these patients?
     

    Nebraska EMS CPR Sedation Protocol - ALS
    Nebraska CPR Induced Consciousness Sedation Protocol (from the PDF)[1]
     

    We should find out how common it is for people to regain consciousness without regaining a pulse. This is clearly an experimental protocol that is not supported by evidence of improved outcomes that matter – just like all of the rest of cardiac arrest treatment that is not compressions or defibrillation.
     

    RESULTS: The search yielded 1997 unique records, of which 50 abstracts were reviewed. Nine reports, describing 10 patients, were relevant. Six of the patients had CPR performed by mechanical devices, three of these patients were sedated. Four patients arrested in the out-of-hospital setting and six arrested in hospital. There were four survivors. Varying levels of consciousness were described in all reports, including purposeful arm movements, verbal communication, and resuscitation interference. Management strategies directed at consciousness were offered to six patients and included both physical and chemical restraints.[2]

     

    6/1,997 is 0.3% – not anywhere near the 39.3% of 55/140, but it is still a large enough group that we should not ignore them.

    Depression and anxiety following resuscitation are significant problems, so this might even be a way to help decrease those resuscitation side effects.
     

    CONCLUSION:
    One fourth of OHCA-survivors reported symptoms of anxiety and/or depression at 6 months which was similar to STEMI-controls and previous normative data. Subjective cognitive problems were associated with an increased risk for psychological distress. Since psychological distress affects long-term prognosis of cardiac patients in general it should be addressed during follow-up of survivors with OHCA due to a cardiac cause.
    [3]

     

    The similarity to the outcome of STEMI (ST segment Elevation Myocardial Infarction) patients do not inspire confidence in this approach, but that does not mean that it should not be examined.

    It is most important that we not make the mistake that has been made with ventilations, endotracheal tubes, extraglottic airways, antiarrhythmic drugs, pressor drugs, anti-acidosis drugs, antidote drugs, anti-hypoglycemic drugs, et cetera. We should insist that there be valid evidence of some sort of benefit before the ACLS (Advanced Cardiac Life Support) Committee of Failed Treatments adds this to the ACLS algorithms because of an abundance of wishful thinking.
     

    This time will be different.
     

    This use of ketamine is interesting. Ketamine is a sedative that should not depress vital signs, so it may do what we expect. There may be more benefit than harm, but there may be more harm than benefit, or there may be all harm and no benefit. We will not know until we have valid research.

    We have added the other treatments without finding out if they improve outcomes. We continue to remove these treatments as we obtain evidence, because they have one thing in common – they don’t improve outcomes.

    These treatments have increased the ignorance of those who work in EMS (Emergency Medical Services) and EM (Emergency Medicine). We keep convincing ourselves that we know what we are doing, but evidence keeps showing that we are lying to ourselves.

    Maybe ketamine sedation during compressions will be beneficial. It is such a small patient population, that it will be difficult to study. Introducing a treatment without studying it will always be a mistake. Is Nebraska studying this? Probably, but it is not stated in the paper. Has this been approved by an IRB (Institutional Review Board)? I do not know.

    Footnotes:

    [1] CPR induced consciousness: It’s time for sedation protocols for this growing population
    Rice, D., Nudell, N., Habrat, D., Smith, J., & Ernest, E. (2016). Resuscitation DOI: 10.1016/j.resuscitation.2016.02.013
    Free Full Text from Resuscitation.

    [2] Return of consciousness during ongoing cardiopulmonary resuscitation: A systematic review.
    Olaussen A, Shepherd M, Nehme Z, Smith K, Bernard S, Mitra B.
    Resuscitation. 2015 Jan;86:44-8. doi: 10.1016/j.resuscitation.2014.10.017. Epub 2014 Nov 4. Review.
    PMID: 25447435

    [3] Anxiety and depression among out-of-hospital cardiac arrest survivors.
    Lilja G, Nilsson G, Nielsen N, Friberg H, Hassager C, Koopmans M, Kuiper M, Martini A, Mellinghoff J, Pelosi P, Wanscher M, Wise MP, Östman I, Cronberg T.
    Resuscitation. 2015 Dec;97:68-75. doi: 10.1016/j.resuscitation.2015.09.389. Epub 2015 Oct 9.
    PMID: 26433116

    Rice, D., Nudell, N., Habrat, D., Smith, J., & Ernest, E. (2016). CPR induced consciousness: It’s time for sedation protocols for this growing population Resuscitation DOI: 10.1016/j.resuscitation.2016.02.013

    Olaussen A, Shepherd M, Nehme Z, Smith K, Bernard S, & Mitra B (2015). Return of consciousness during ongoing cardiopulmonary resuscitation: A systematic review. Resuscitation, 86, 44-8 PMID: 25447435

    Lilja G, Nilsson G, Nielsen N, Friberg H, Hassager C, Koopmans M, Kuiper M, Martini A, Mellinghoff J, Pelosi P, Wanscher M, Wise MP, Östman I, & Cronberg T (2015). Anxiety and depression among out-of-hospital cardiac arrest survivors. Resuscitation, 97, 68-75 PMID: 26433116

    .

    What is the Best Way to Manage Cardiac Arrest According to the Evidence?

    ResearchBlogging.org
     
    There is an excellent review article by Dr. Bentley Bobrow and Dr. Gordon Ewy on the best management of sudden cardiac arrest from the bystander to the ICU (Intensive Care Unit).

    They point out something that we tend to resist learning. Cardiac arrest that is not due to respiratory causes does not need respiratory treatment. A person who is unresponsive and gasping is exhibiting signs of cardiac arrest, not signs of respiratory problems.
     

    Except in newborns, gasping or agonal breathing is a common sign of cardiac arrest, occurring in slightly more than 50% of patients with primary cardiac arrest.22-25 [1]

     

    Gasping does not mean alive and well. Gasping means dead and having a good chance at resuscitation. Unresponsive and gasping means there is a need for compressions.
     

    If adequate chest compressions are promptly initiated, the patient will continue to gasp.23 [1]

     


     

    Of interest is that only a minority of individuals with noncardiac arrest received CO-CPR.35 In Arizona, the public was generally capable of recognizing respiratory arrest, where chest compressions and assisted ventilations were recommended.[1]

     


     

    It probably has less to do with taking away the ventilation, than with making the compressions continuous and high quality, but ventilations do decrease blood return to the chest and increase the likelihood of vomiting (regardless of what has been eaten), so there are benefits from removing the ventilations.
     


     

    Passive oxygen insufflation means just putting a mask over the patient’s mouth and nose and allowing oxygen to be delivered passively. The rise and fall of the chest, due to compressions, and diffusion will allow for all of the oxygenation the patient will need.

    Standard CPR (Std CPR) means alternating compressions with two ventilations every 30 compressions. Standard CPR is clearly not what we want to do, unless we want to keep patients from being resuscitated.
     

    The problem is that the vast majority of physicians have no idea what the survival rate of patients with OHCA is in their area. This needs to change if major progress is to be made.[1]

     

    Many of us do not know the results of what we do, so it is not surprising that a lot of EMS treatment is mythological.

    Medicine is a field that encourages superstition. Patients provide intermittent reinforcement, which may be the most effect means of creating superstitions. Intermittent reinforcement?[2]
     

    The only way to know the effectiveness of your Emergency Medical System is to know the survival of patients with OHCA and a shockable rhythm. If it is less than 38%,they should be encouraged to institute CCR and reevaluate the results.[1]

     

    Maybe you are already doing better than 38% walking out of the hospital, then you are probably already using continuous compressions and passive oxygen insufflation. If you are not, then you need to improve your patient care.

    Footnotes:

    [1] Cardiocerebral Resuscitation: An Approach to Improving Survival of Patients With Primary Cardiac Arrest.
    Ewy GA, Bobrow BJ.
    J Intensive Care Med. 2014 Jul 30. pii: 0885066614544450. [Epub ahead of print]
    PMID: 25077491 [PubMed – as supplied by publisher]

    [2] Intermittent reinforcements
    Wikipedia
    Article
     

    Pigeons experimented on in a scientific study were more responsive to intermittent reinforcements, than positive reinforcements.[16] In other words, pigeons were more prone to act when they only sometimes could get what they wanted. This effect was such that behavioral responses were maximized when the reward rate was at 50% (in other words, when the uncertainty was maximized), and would gradually decline toward values on either side of 50%.[17] R.B Sparkman, a journalist specialized on what motivates human behavior, claims this is also true for humans, and may in part explain human tendencies such as gambling addiction.[18]

     

    Ewy, G., & Bobrow, B. (2014). Cardiocerebral Resuscitation: An Approach to Improving Survival of Patients With Primary Cardiac Arrest Journal of Intensive Care Medicine DOI: 10.1177/0885066614544450

    .

    Resuscitation characteristics and outcomes in suspected drug overdose-related out-of-hospital cardiac arrest

    ResearchBlogging.org
     

    This study is interesting for several reasons.

    In a system that claims excellence, the most consistent way to identify the study group is by documentation of a protocol violation – but it is not intended as a study of protocol violations.

    This may hint at some benefit from epinephrine (Adrenaline in Commonwealth countries), but that would require some study and we just don’t study epinephrine. We only make excuses for not studying epinephrine.

    The atropine results suggest that the epinephrine data may be just due to small numbers, or that we may want to consider atropine for drug overdose cardiac arrest patients, or . . . .

    The Sodium Bicarbonate (bicarb – NaHCO3) results suggest a flaw in EMS education (probably testing, too). If the patient is acidotic, this is one type of cardiac arrest where hyperventilation may be beneficial. Bicarb is the part of the drug that doesn’t do much, especially if the patient is dead. The sodium is what works, such as when the patient has taken too much of a sodium channel blocker, such as a tricyclic antidepressant or a class I antiarrhythmic. Acidosis is treated by hyperventilation. Use capnography.

    Most important – antidotes probably don’t work as expected during cardiac arrest. Not even naloxone (Narcan).
     

    Despite clear differences in the etiology of suspected OD [OverDose] and non-OD OHCA [Out of Hospital Cardiac Arrest], the International Liaison Committee on Resuscitation guidelines published in 2010 do not specify different treatments for suspected OD-OHCA patients during resuscitation,and state that there is no evidence promoting the intra-arrest administration of the opioid antagonist naloxone.8 [1]

     

    What did they find in the study?

    They may have located the highest concentration of heroin overdose in the country. 93% of OD-OHCA patients were treated with naloxone.
     

    We relied on either naloxone administration or clear description of circumstantial evidence in the PCR [Patient Care Recod] to identify a suspected OD. Clear descriptions are also rare, and most (93%) of the cases were identified by naloxone administration. Naloxone during cardiac arrest is not part of any regional protocol, and all of these administrations are deviations from recommended practice. There may be other cases in which paramedics suspected OD, but did not deviate from protocol to administer naloxone. Therefore, it is impossible to be certain whether the actual number of OD cases is larger or smaller than the reported number. However, the use of naloxone as a proxy indicator of suspected OD has been supported in the literature.11 [1]

     

    The EMS approach to naloxone still appears to be –
     


    Image credits – 123
     

    These results seem to show better response to the prehospital drugs in the OD-OHCA patients, but that ignores the ROSC (Return Of Spontaneous Circulation) rates.
     


    Click on images to make them larger.
     

    Why would OD-OHCA patients do better than non-OD-OHCA patients if they get a pulse back?

    The average non-OD-OHCA patient is 20+ years older. These older patients may not be as capable of recovery nor as capable of tolerating the toxicity of the drugs they were treated with.

    The change after ROSC is dramatic. Is that the important point of this study?

    Are they doing anything special for OD patients in the hospital, or is it just a matter of That which does not kill me by anoxic brain damage, may allow me to recover twice as often as a typical cardiac arrest patient.
     

    Do drugs (antidotes, antiarrhythmics, . . . ) work the same way in dead people as in living people?
     

    Pharmacologic insults are just so massive and normal metabolism and physiology so deranged that no mere mortal can make a meaningful intervention. The seriously poisoned who maintain vital signs in the ED have the best, albeit never guaranteed, chance of rescue from a modicum of antidotes and intensive supportive care.[2]

     

    We should understand that normal metabolism is irrelevant to cardiac arrest.

    We should understand that we do not need to ventilate adult cardiac arrest patients, when the cause is cardiac. An absence of ventilation would not be appropriate in a living adult, but dead metabolism is not normal. If something as basic as oxygen changes, when the patient is dead, how much less do we understand the behavior of other drugs in dead patients?

    Footnotes:

    [1] Resuscitation characteristics and outcomes in suspected drug overdose-related out-of-hospital cardiac arrest.
    Koller AC, Salcido DD, Callaway CW, Menegazzi JJ.
    Resuscitation. 2014 Jun 26. pii: S0300-9572(14)00581-4. doi: 10.1016/j.resuscitation.2014.05.036. [Epub ahead of print]
    PMID: 24973558 [PubMed – as supplied by publisher]

    [2] Dissecting the ACLS Guidelines on Cardiac Arrest from Toxic Ingestions
    Emergency Medicine News:
    October 2011 – Volume 33 – Issue 10 – pp 16-18
    doi: 10.1097/01.EEM.0000406945.05619.ca
    InFocus
    Roberts, James R. MD
    Article

    Roberts, J. (2011). InFocus: Dissecting the ACLS Guidelines on Cardiac Arrest from Toxic Ingestions Emergency Medicine News, 33 (10), 16-18 DOI: 10.1097/01.EEM.0000406945.05619.ca

    Koller, A., Salcido, D., Callaway, C., & Menegazzi, J. (2014). Resuscitation characteristics and outcomes in suspected drug overdose-related out-of-hospital cardiac arrest Resuscitation DOI: 10.1016/j.resuscitation.2014.05.036

    .