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

- Rogue Medic

In Defense of No Improvement by Medic Madness – Part III

ResearchBlogging.org
 

Continuing from Part I and Part II, in response to what I wrote about the failure of the LUCAS,[1] Sean continues with –
 

So do these results reflect on a device that’s over-hyped, or are we missing something in our current CPR guidelines? Keep in mind that this study involved highly trained and prepared responders using the most up-to-date recommendations for CPR delivery. We developed a machine to do exactly what we tell it to. It follows the guidelines exactly as we want, and yet, it can’t produce the results we hoped for. Perhaps the machine isn’t the problem.[2]

 

Maybe the machine was never the answer.
 

In clinical practice, mechanical CPR using the presented algorithm did not result in improved effectiveness compared with manual CPR.[3]

 

This is probably just a reflection of how little we understand of what we are doing.

Everything we do in EMS, and especially in resuscitation, is over-hyped.

If our worry is that we will look like we are not doing enough, then open heart cardiac massage can make it clear that we are doing a lot.[4]   😯
 

Image credit.
 

How many survival studies do we have that randomize patients between a placebo and a vasopressor treatment?

For epinephrine (Adrenaline), vasopressin, norepinephrine (Levophed), or phenylephrine (Neo-Synephrine)?[5]

Here is the evidence of of what happens to survival with epinephrine.[6] I added the two most recent studies.[7],[8] There are no positive epinephrine studies.
 

 

Epinephrine may turn out to be beneficial for some subset of patients, but it is unlikely that epinephrine is beneficial just because the patient remains dead long enough to be given a drug.

A mnemonic for teaching ACLS is – Everybody dead gets epi, because current ACLS (Advanced Cardiac Life Support) guidelines tell us to give epinephrine (or norepinephrine, or vasopressin, or phenylephrine) to all patients who remain dead long enough to be given a drug.

Got a dead patient and can’t think of what to do next? Give epi.

What are we going to do, poison them? Our first dose was so far above the therapeutic range, that it would be considered poisonous if the patient were not already dead.

Vasopressors produce just as much no improvement as a LUCAS.
 

How many survival studies do we have that randomize patients between a placebo and an antiarrhythmic active treatment in cardiac arrest?

Foe amiodarone (Cordarone), lidocaine (Xylocaine), procainamide (Procaine), and magnesium?[9]

In two studies of magnesium, there was no improvement in survival vs. placebo.[10],[11]

In one study of amiodarone, there was improvement in everything except survival to discharge – more patients were resuscitated, but they died in the hospital.[12]

Antiarrhythmics produce just as much no improvement as a LUCAS.
 

There have been other studies of vasopressors and of antiarrhythmics against other unknowns, but does a positive outcome against a different unknown mean more beneficial than the other unknown or just less harmful than the other unknown?

We are aren’t even using Schrödinger’s treatments, because we don’t know if a good outcome means that the patient is surviving because of what we are doing or surviving in spite of what we are doing. We appear to be just happy to be doing something.

Still, we insist on giving these treatments, because we are afraid of doing too little.

We don’t know enough to know what too little is, but it is our fear of doing too little that keeps us from learning what works.

While this is not Sean’s fault, he is aggressively advocating for more of the status quo – the dramatic lack of improvement that we expect from EMS treatments.
 

The LUCAS failed – unless our idea of success is to make no difference in outcomes, because improving resuscitation outcomes is not really our goal.

EMS – we improve nothing more expensively, more dramatically, and more consistently than anyone else!
 

I look at the flawed claims of flaws in the paper in Part IV.

Dr. Brooks Walsh also explains the failure of the LUCAS in this study in “We had a LUCAS save!” – No, you didn’t.

Peter Canning describes the failures of judgment in advocating for the LUCAS in Whup Kits and Chihuahuas.

Footnotes:

[1] The Failure of LUCAS to Improve Outcomes in the LINC Trial
Wed, 05 Mar 2014
Rogue Medic
Article

The LUCAS, Research, and Wishful Thinking
Fri, 07 Mar 2014
Rogue Medic
Article

[2] In Defense of the LUCAS
March 12, 2014
by Sean Eddy
Medic Madness
Article

[3] Mechanical chest compressions and simultaneous defibrillation vs conventional cardiopulmonary resuscitation in out-of-hospital cardiac arrest: the LINC randomized trial.
Rubertsson S, Lindgren E, Smekal D, Östlund O, Silfverstolpe J, Lichtveld RA, Boomars R, Ahlstedt B, Skoog G, Kastberg R, Halliwell D, Box M, Herlitz J, Karlsten R.
JAMA. 2014 Jan 1;311(1):53-61. doi: 10.1001/jama.2013.282538.
PMID: 24240611 [PubMed – indexed for MEDLINE]

Free Full Text in PDF Download format from PEHSC.org.

[4] A Resuscitation Question So Obvious That . . . .
Sun, 19 Jan 2014
Rogue Medic
Article

[5] Vasopressors
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 8: Adult Advanced Cardiovascular Life Support
Part 8.2: Management of Cardiac Arrest
Medications for Arrest Rhythms
Free Full Text from Circulation with link to PDF Download

[6] Vasopressors in cardiac arrest: a systematic review.
Larabee TM, Liu KY, Campbell JA, Little CM.
Resuscitation. 2012 Aug;83(8):932-9. Epub 2012 Mar 15.
PMID: 22425731 [PubMed – in process]
 

CONCLUSION: There are few studies that compare vasopressors to placebo in resuscitation from cardiac arrest. Epinephrine is associated with improvement in short term survival outcomes as compared to placebo, but no long-term survival benefit has been demonstrated. Vasopressin is equivalent for use as an initial vasopressor when compared to epinephrine during resuscitation from cardiac arrest. There is a short-term, but no long-term, survival benefit when using high dose vs. standard dose epinephrine during resuscitation from cardiac arrest. There are no alternative vasopressors that provide a long-term survival benefit when compared to epinephrine. There is limited data on the use of vasopressors in the pediatric population.

[7] Prehospital epinephrine use and survival among patients with out-of-hospital cardiac arrest.
Hagihara A, Hasegawa M, Abe T, Nagata T, Wakata Y, Miyazaki S.
JAMA. 2012 Mar 21;307(11):1161-8. doi: 10.1001/jama.2012.294.
PMID: 22436956 [PubMed – indexed for MEDLINE]

Free Full Text from JAMA.

[8] Impact of early intravenous epinephrine administration on outcomes following out-of-hospital cardiac arrest.
Hayashi Y, Iwami T, Kitamura T, Nishiuchi T, Kajino K, Sakai T, Nishiyama C, Nitta M, Hiraide A, Kai T.
Circ J. 2012;76(7):1639-45. Epub 2012 Apr 5.
PMID: 22481099 [PubMed – indexed for MEDLINE]

Free Full Text from Circulation Japan.

[9] Antiarrhythmics
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 8: Adult Advanced Cardiovascular Life Support
Part 8.2: Management of Cardiac Arrest
Medications for Arrest Rhythms
Free Full Text from Circulation with link to PDF Download

[10] Randomised trial of magnesium in in-hospital cardiac arrest. Duke Internal Medicine Housestaff.
Thel MC, Armstrong AL, McNulty SE, Califf RM, O’Connor CM.
Lancet. 1997 Nov 1;350(9087):1272-6.
PMID: 9357406 [PubMed – indexed for MEDLINE]

[11] Magnesium sulfate in the treatment of refractory ventricular fibrillation in the prehospital setting.
Allegra J, Lavery R, Cody R, Birnbaum G, Brennan J, Hartman A, Horowitz M, Nashed A, Yablonski M.
Resuscitation. 2001 Jun;49(3):245-9.
PMID: 11719117 [PubMed – indexed for MEDLINE]

[12] Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation.
Kudenchuk PJ, Cobb LA, Copass MK, Cummins RO, Doherty AM, Fahrenbruch CE, Hallstrom AP, Murray WA, Olsufka M, Walsh T.
N Engl J Med. 1999 Sep 16;341(12):871-8.
PMID: 10486418 [PubMed – indexed for MEDLINE]

Free Full Text from New England Journal of Medicine.

Rubertsson S, Lindgren E, Smekal D, Östlund O, Silfverstolpe J, Lichtveld RA, Boomars R, Ahlstedt B, Skoog G, Kastberg R, Halliwell D, Box M, Herlitz J, & Karlsten R (2014). Mechanical chest compressions and simultaneous defibrillation vs conventional cardiopulmonary resuscitation in out-of-hospital cardiac arrest: the LINC randomized trial. JAMA : the journal of the American Medical Association, 311 (1), 53-61 PMID: 24240611

Larabee TM, Liu KY, Campbell JA, & Little CM (2012). Vasopressors in cardiac arrest: a systematic review. Resuscitation, 83 (8), 932-9 PMID: 22425731

Hagihara A, Hasegawa M, Abe T, Nagata T, Wakata Y, & Miyazaki S (2012). Prehospital epinephrine use and survival among patients with out-of-hospital cardiac arrest. JAMA : the journal of the American Medical Association, 307 (11), 1161-8 PMID: 22436956

Hayashi Y, Iwami T, Kitamura T, Nishiuchi T, Kajino K, Sakai T, Nishiyama C, Nitta M, Hiraide A, & Kai T (2012). Impact of early intravenous epinephrine administration on outcomes following out-of-hospital cardiac arrest. Circulation journal : official journal of the Japanese Circulation Society, 76 (7), 1639-45 PMID: 22481099

Thel MC, Armstrong AL, McNulty SE, Califf RM, & O’Connor CM (1997). Randomised trial of magnesium in in-hospital cardiac arrest. Duke Internal Medicine Housestaff. Lancet, 350 (9087), 1272-6 PMID: 9357406

Allegra J, Lavery R, Cody R, Birnbaum G, Brennan J, Hartman A, Horowitz M, Nashed A, & Yablonski M (2001). Magnesium sulfate in the treatment of refractory ventricular fibrillation in the prehospital setting. Resuscitation, 49 (3), 245-9 PMID: 11719117

Kudenchuk PJ, Cobb LA, Copass MK, Cummins RO, Doherty AM, Fahrenbruch CE, Hallstrom AP, Murray WA, Olsufka M, & Walsh T (1999). Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation. The New England journal of medicine, 341 (12), 871-8 PMID: 10486418

.

Comments

  1. In the past 14 months I’ve “worked” nine cardiac arrests in the field. Of those, five had ROSC, two walked out of the hospital neurologically intact and one arrested in front of me, survived to the cath lab but I never found out what his outcome was.

    In every case the Lucas was used

    Those are good numbers.

    Did the Lucas do this? Well, it certainly is a tool I’m glad to have but is merely one asset that augments my training and experience. Having said that, it has been my opinion that the Lucas may be the biggest reason I’m having more ROSC since we put them on the ambulance several years ago.

    That’s not just my thought but the opinion of the other 140 medics I work with. In addition, I spoke with a couple of our Emergency Physicians at the Level One Trauma Center I work for and they are solidly convinced of the Lucas’ efficacy – despite the LINC trial.

    My first ambulance call was in 1971 with my first medic job in 1980. Prior to the Lucas, I never saw a patient in cardiac arrest open their eyes and look around during manual CPR. We have seen this with the Lucas. Within the last few months, one of our crews had to sedate a patient in cardiac arrest due to his violent objection to the machine while in asystole.

    Perfusion is obviously better with mechanical CPR. Peripheral pulses are prominent in many cases. Oximetry, with good wave form is the norm.

    Is the Lucas more important than early activation of EMS, electricity, or training and experience? No, its not. But in our area it has become a very important adjunct and one we intend to keep.

    • Duke Powell,

      In the past 14 months I’ve “worked” nine cardiac arrests in the field. Of those, five had ROSC, two walked out of the hospital neurologically intact and one arrested in front of me, survived to the cath lab but I never found out what his outcome was.

      In every case the Lucas was used

      Those are good numbers.

      Those are anecdotes.

      To be relevant, they should be part of a controlled trial that randomizes patients to treatment/no treatment/placebo/different treatment.

      If I flip an unbiased coin nine times and it comes up heads nine times out of nine, does it mean that I have some way of influencing the result?

      If I take a group of nine patients and five of them have a good outcome, do I have any valid information on which to base any conclusions?

      No.

      I only have a bunch of anecdotes.

      Did the Lucas do this? Well, it certainly is a tool I’m glad to have but is merely one asset that augments my training and experience. Having said that, it has been my opinion that the Lucas may be the biggest reason I’m having more ROSC since we put them on the ambulance several years ago.

      Anecdotes can make anything seem impressive, even if it is irrelevant.

      That’s not just my thought but the opinion of the other 140 medics I work with. In addition, I spoke with a couple of our Emergency Physicians at the Level One Trauma Center I work for and they are solidly convinced of the Lucas’ efficacy – despite the LINC trial.

      This is one of the reasons that expert opinion is the lowest level of evidence.

      Many experts are not able to understand the difference between anecdote and evidence.

      This is something that we need to change, so that we can improve the outcomes that matter to our patients.

      My first ambulance call was in 1971 with my first medic job in 1980. Prior to the Lucas, I never saw a patient in cardiac arrest open their eyes and look around during manual CPR. We have seen this with the Lucas. Within the last few months, one of our crews had to sedate a patient in cardiac arrest due to his violent objection to the machine while in asystole.

      With such impressive improvement in surrogate endpoints, the LUCAS still fails to show improvement in outcomes that matter.

      This appears to demonstrate that even though these surrogate endpoints are impressive, they do not matter.

      We can raise the blood pressure of the patient who is bleeding out by dumping liters of saline into him. He may open his eyes and communicate with us, but we are probably just killing him more quickly by forcing blood out of his body and replacing it with saline.

      That is an impressive result, but a worse outcome – probably because of the treatment that made things look better.

      We used to think that ROSC was important, but you can see from the research on epinephrine and amiodarone that ROSC is not important.

      ROSC persuades us that we are doing something beneficial, when we are just changing the place where death is pronounced and possibly decreasing the survival of cardiac arrest patients.

      Perfusion is obviously better with mechanical CPR. Peripheral pulses are prominent in many cases. Oximetry, with good wave form is the norm.

      So why aren’t the outcomes better in the fair tests (research)?

      Is the Lucas more important than early activation of EMS, electricity, or training and experience? No, its not. But in our area it has become a very important adjunct and one we intend to keep.

      I will stick to treatments that make a difference that matters.

      Patients leaving the hospital alive and thinking is what matters.

      There is no evidence that the LUCAS makes a difference that matters.

      .

  2. An alternative view on the use of epi…

    http://www.medicsbk.com/2014/02/03/the-silver-lining-of-epi/

Trackbacks

  1. […] is not the only argument Sean makes. I will address the rest in Part II, Part III, and Part […]

  2. […] started last week when I shared my post as a comment to something he put up in regards to working a CPR with a LUCAS device and the relation of using epinephrine in cardiac […]

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