Furosemide is good for filling the patient’s bladder, but the patient probably did not call for help filling his/her bladder.

- Rogue Medic

Opponents of EBM Now Have More Evidence to Justify Their Rejection of Evidence


 

Those scientists clearly can’t get it right. They are constantly changing the guidelines to correct their mistakes. Why don’t they just do it right the first time.

Finally, somebody is recognizing that a treatment should only be eliminated when there is clear evidence that it harms patients – and only when we have run out of excuses to ignore the irrefutable evidence.
 

The 2015 American Heart Organization (AHO) Cardiovascular Care Guidelines will introduce three new levels of evidence in addition to the current existing levels of evidence
In addition to the current levels of evidence classes the AHO’s 2015 guidelines will include Class IVa (Anecdotal Evidence), Class V (Provider Opinion) and Class XI (Treatments Not Proven to Not Work)
[1]

 

When I was in paramedic school we were told the rules. Intubation is the most important treatment, because the airway is the most important part of patient care, because Airway begins with A, Breathing begins with B, and Circulation begins with C. A comes before B and B comes before C.

Do you think that is a coincidence? No. There’s a reason for that. We are supposed to treat the airway first – no matter what. A paramedic can only have one thought in his head at a time, so it has to be the one best thought. Airway always comes first. Did you ever try to live without an airway? Well, did you? It just doesn’t happen. The Gold Standard of Airway is intubation, so we have to intubate people or they will be dropping like flies. You don’t hear about people surviving in places where medics don’t intubate. Dead! All of ‘em. Dead! It’s a fact.

This is serious business people. Every second counts, but there are a lot of seconds, so we don’t count seconds. We count minutes. So every minute counts, but only with an Airway. Without an Airway, you are dead, but you are only dead after we race your cadaver to the hospital and a doctor pronounces you dead and mutters something under his breath about us being straight out of the Dark Ages. We do respect the classics. We have to honor our roots. We can’t be eliminating traditional treatments just because they seem to harm patients.
 

AHO includes the following in the new guidelines, section IVa (Anecdotal Evidence): “Many people have seem something work or they know of someone who has seen something work, or perhaps have heard of someone who knows someone that has seem something work. If a treatment has been said to work in the past then it stands to reason that it will work again. The AHA now accepts anecdotal evidence as equivalent to and just as valid as a Class I intervention provided that the evidence is no more than 4 degrees of separation from the person.”[1]

 

They shouldn’t have left out treatments based on animal research. We have to include everything. It doesn’t matter that people do not do as well with these treatments as animals do. Don’t you love dogs and cats, or are you some kind of monster? If a treatment can bring a dog back to life then that is good enough for grandpa. If cancer can be cured in animals, but we don’t give the treatments to people we are killing people. It is a Big Pharma conspiracy to find cures and then hide them from everyone, because that is why these scientists do all of this research – so they can have the cures for themselves and watch us die. If it works in animals, there is no reason to not use it in people.

All of this research is just too expensive.

We need to just use what we know works.
 

Go read the full article.

Footnotes:

[1] Heart Organization Endorses New Level of Evidence Guildlines
Call The Cops
Posted by: RJ Beam
8/20/2014
Article

.

The Controversy of Admitting ‘We Do Not Know What Works’

ResearchBlogging.org

 

There are several news articles today criticizing a study because the patients might be deprived of a drug that has not been adequately studied in humans. This criticism is coming from journalists – the people who publicized the fraudulent vaccines research by Andrew Wakefield, who was trying to sell his competing vaccine and was being paid to produce negative research by lawyers suing the vaccine companies.[1]

The real controversy is that this untested drug became the standard of care with no evidence that it improves outcomes that matter.

Is it controversial to give a placebo, rather than a drug not yet adequately tested in humans?

No.

We are not informing patients that there is no evidence that the standard treatment is effective. We are not obtaining consent to give the unproven drug – epinephrine (Adrenaline in Commonwealth countries). How are the ethics different when we substitute a placebo for a mystery medicine?

What is less ethical than continuing the tradition of giving an inadequately studied drug to people who cannot consent to treatment?

Are we depriving patients of effective medicine or are we depriving them of witchcraft?

If you think that epinephrine is effective medicine at improving survival to discharge, provide the evidence and stop this study. The reason the study is being done is that evidence of benefit does not exist.
 

Click on image to make it larger.[2] The studies are in the footnotes.[3],[4],[5],[6],[7],[8],[9],[10]
 

Is Adrenaline beneficial in cardiac arrest?

Probably, but only for some patients and we do not know which patients benefit.

Is Adrenaline harmful in cardiac arrest?

Probably, but only for some patients and we do not know which patients are harmed.

What is the right dose of Adrenaline in cardiac arrest?

Pick a number – any number. We do not know the right dose.
 

 

Even the patients who only received the minimum dose – 1 mg – had worse outcomes.[11]

Wrong timing? Wrong dose? Wrong drug?

We do not know.
 

We have used this untested treatment for half a century and not bothered to find out if it works. A recent study shows that epinephrine produces worse outcomes when given by EMS later,[12] but that does not mean that the outcomes are good when epinephrine is given early. The study had no placebo group, so like a study comparing different doses of cyanide, just because one dose is not as bad as another dose, the results do not suggest that cyanide is beneficial.
 


 

This is comparing three different treatments HDE (High-Dose Epinephrine), SDE (Standard-Dose Epinephrine), and NE (NorEpinephrine). The lines for the HDE and NE are so close to each other, that you may not be able to see the gold line.[13] Other studies produce similar results.[3],[14],[15],[16],[17] Only one study showed better ROSC with standard dose epinephrine.[18]
 

Epinephrine does produce more ROSC (Return Of Spontaneous Circulation – at least a temporary pulse) than placebo, but high dose epinephrine produces even more ROSC than standard dose epinephrine, so why do we give the standard dose that only produces middling ROSC?

Is ROSC the goal? No.

For the guidelines (ACLS and ILCOR), ROSC is the basis for giving standard dose epinephrine, but it would make more sense to give high dose epinephrine if the goal is ROSC. More ROSC, but no more survivors leaving the hospital. If all we want is put the patient in a coma long enough to run up a big hospital bill, then the drugs are great.

If we want people to leave the hospital alive, then We Do Not Know What Works.
 

The guidelines are based on wishful thinking and rationalization. They are not based on improved survival. A lot of research is cited (hundreds of papers), but the research does not show improved survival with any drug(s).

Will the guidelines be revised to remove epinephrine? Maybe.
 

The exciting development is that these data create equipoise about the current standard of resuscitation care. The best available observational evidence indicates that epinephrine may be harmful to patients during cardiac arrest, and there are plausible biological reasons to support this observation. However, observational studies cannot establish causal relationships in the way that randomized trials can.[19]

 

Some cocktails have produced better results than epinephrine in tiny studies. It is too probably too early to tell if these are just statistical aberrations. I will write about them later.

Continued in Does a Placebo vs. Adrenaline Study Deprive Patients of Necessary Care According to the Resuscitation Guidelines?

Footnotes:

[1] “Piltdown medicine” and Andrew Wakefield’s MMR vaccine fraud
Science-Based Medicine
Posted by David Gorski
January 6, 2011
Article
 

In a mere decade and a half, several decades of progress in controlling this scourge had been unravelled like a thread hanging off a cheap dress, all thanks to Andrew Wakefield and scandal mongers in the British press.

[2] 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.

[3] High dose and standard dose adrenaline do not alter survival, compared with placebo, in cardiac arrest.
Woodhouse SP, Cox S, Boyd P, Case C, Weber M.
Resuscitation. 1995 Dec;30(3):243-9.
PMID: 8867714 [PubMed - indexed for MEDLINE]

[4] Adrenaline in out-of-hospital ventricular fibrillation. Does it make any difference?
Herlitz J, Ekström L, Wennerblom B, Axelsson A, Bång A, Holmberg S.
Resuscitation. 1995 Jun;29(3):195-201.
PMID: 7667549 [PubMed - indexed for MEDLINE]

[5] Survival outcomes with the introduction of intravenous epinephrine in the management of out-of-hospital cardiac arrest.
Ong ME, Tan EH, Ng FS, Panchalingham A, Lim SH, Manning PG, Ong VY, Lim SH, Yap S, Tham LP, Ng KS, Venkataraman A; Cardiac Arrest and Resuscitation Epidemiology Study Group.
Ann Emerg Med. 2007 Dec;50(6):635-42. Epub 2007 May 23.
PMID: 17509730 [PubMed - indexed for MEDLINE]

Free Full Text Download in PDF format from prdupl02.ynet.co.il

[6] 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 - indexed for MEDLINE]

Free Full Text from JAMA

[7] Outcome when adrenaline (epinephrine) was actually given vs. not given – post hoc analysis of a randomized clinical trial.
Olasveengen TM, Wik L, Sunde K, Steen PA.
Resuscitation. 2011 Nov 22. [Epub ahead of print]
PMID: 22115931 [PubMed - as supplied by publisher]

[8] 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 of In Press Uncorrected Proof from xa.yming.com
 

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.

 

[9] 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.

[10] 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.

[11] Wide variability in drug use in out-of-hospital cardiac arrest: A report from the resuscitation outcomes consortium.
Glover BM, Brown SP, Morrison L, Davis D, Kudenchuk PJ, Van Ottingham L, Vaillancourt C, Cheskes S, Atkins DL, Dorian P; Resuscitation Outcomes Consortium Investigators.
Resuscitation. 2012 Nov;83(11):1324-30. doi: 10.1016/j.resuscitation.2012.07.008. Epub 2012 Jul 31.
PMID: 22858552 [PubMed - indexed for MEDLINE]

Free Full Text from PubMed Central.

[12] Time to administration of epinephrine and outcome after in-hospital cardiac arrest with non-shockable rhythms: retrospective analysis of large in-hospital data registry.
Donnino MW, Salciccioli JD, Howell MD, Cocchi MN, Giberson B, Berg K, Gautam S, Callaway C; American Heart Association’s Get With The Guidelines-Resuscitation Investigators.
BMJ. 2014 May 20;348:g3028. doi: 10.1136/bmj.g3028.
PMID: 24846323 [PubMed - in process]

Free Full Text from BMJ.

[13] A randomized clinical trial of high-dose epinephrine and norepinephrine vs standard-dose epinephrine in prehospital cardiac arrest.
Callaham M, Madsen CD, Barton CW, Saunders CE, Pointer J.
JAMA. 1992 Nov 18;268(19):2667-72.
PMID: 1433686 [PubMed - indexed for MEDLINE]

[14] A comparison of standard-dose and high-dose epinephrine in cardiac arrest outside the hospital. The Multicenter High-Dose Epinephrine Study Group.
Brown CG, Martin DR, Pepe PE, Stueven H, Cummins RO, Gonzalez E, Jastremski M.
N Engl J Med. 1992 Oct 8;327(15):1051-5.
PMID: 1522841 [PubMed - indexed for MEDLINE]

Free Full Text from NEJM.

[15] Standard doses versus repeated high doses of epinephrine in cardiac arrest outside the hospital.
Choux C, Gueugniaud PY, Barbieux A, Pham E, Lae C, Dubien PY, Petit P.
Resuscitation. 1995 Feb;29(1):3-9.
PMID: 7784720 [PubMed - indexed for MEDLINE]

[16] A comparison of repeated high doses and repeated standard doses of epinephrine for cardiac arrest outside the hospital. European Epinephrine Study Group.
Gueugniaud PY, Mols P, Goldstein P, Pham E, Dubien PY, Deweerdt C, Vergnion M, Petit P, Carli P.
N Engl J Med. 1998 Nov 26;339(22):1595-601.
PMID: 9828247 [PubMed - indexed for MEDLINE]

Free Full Text from NEJM.

[17] High dose versus standard dose epinephrine in cardiac arrest – a meta-analysis.
Vandycke C, Martens P.
Resuscitation. 2000 Aug 1;45(3):161-6.
PMID: 10959014 [PubMed - indexed for MEDLINE]

[18] High-dose epinephrine in adult cardiac arrest.
Stiell IG, Hebert PC, Weitzman BN, Wells GA, Raman S, Stark RM, Higginson LA, Ahuja J, Dickinson GE.
N Engl J Med. 1992 Oct 8;327(15):1045-50.
PMID: 1522840 [PubMed - indexed for MEDLINE]

Free Full Text from NEJM.

[19] Questioning the use of epinephrine to treat cardiac arrest.
Callaway CW.
JAMA. 2012 Mar 21;307(11):1198-200. doi: 10.1001/jama.2012.313. No abstract available.
PMID: 22436961 [PubMed - indexed for MEDLINE]

Link to a free 6 1/2 minute recording of an interview with Dr. Callaway about this paper.

On the right side of the page, to the right of the First Page Preview, is a section with the title Multimedia Related by Topic. Below that is Author Interview. Below that is some information about the edition, . . . , and below that is an embedded recording of the interview. Press on the arrow to play. That has the recording of the interview with Dr. Callaway.

The interview with Dr. Callaway is definitely worth listening to.

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

Woodhouse SP, Cox S, Boyd P, Case C, & Weber M (1995). High dose and standard dose adrenaline do not alter survival, compared with placebo, in cardiac arrest. Resuscitation, 30 (3), 243-9 PMID: 8867714

Herlitz J, Ekström L, Wennerblom B, Axelsson A, Bång A, & Holmberg S (1995). Adrenaline in out-of-hospital ventricular fibrillation. Does it make any difference? Resuscitation, 29 (3), 195-201 PMID: 7667549

Ong ME, Tan EH, Ng FS, Panchalingham A, Lim SH, Manning PG, Ong VY, Lim SH, Yap S, Tham LP, Ng KS, Venkataraman A, & Cardiac Arrest and Resuscitation Epidemiology Study Group (2007). Survival outcomes with the introduction of intravenous epinephrine in the management of out-of-hospital cardiac arrest. Annals of emergency medicine, 50 (6), 635-42 PMID: 17509730

Olasveengen, T., Sunde, K., Brunborg, C., Thowsen, J., Steen, P., & Wik, L. (2009). Intravenous Drug Administration During Out-of-Hospital Cardiac Arrest: A Randomized Trial JAMA: The Journal of the American Medical Association, 302 (20), 2222-2229 DOI: 10.1001/jama.2009.1729

Olasveengen TM, Wik L, Sunde K, & Steen PA (2011). Outcome when adrenaline (epinephrine) was actually given vs. not given – post hoc analysis of a randomized clinical trial. Resuscitation PMID: 22115931

Jacobs IG, Finn JC, Jelinek GA, Oxer HF, & Thompson PL (2011). Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial. Resuscitation, 82 (9), 1138-43 PMID: 21745533

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

Glover BM, Brown SP, Morrison L, Davis D, Kudenchuk PJ, Van Ottingham L, Vaillancourt C, Cheskes S, Atkins DL, Dorian P, & the Resuscitation Outcomes Consortium Investigators (2012). Wide variability in drug use in out-of-hospital cardiac arrest: A report from the resuscitation outcomes consortium. Resuscitation PMID: 22858552

Donnino, M., Salciccioli, J., Howell, M., Cocchi, M., Giberson, B., Berg, K., Gautam, S., Callaway, C., & , . (2014). Time to administration of epinephrine and outcome after in-hospital cardiac arrest with non-shockable rhythms: retrospective analysis of large in-hospital data registry BMJ, 348 (may20 2) DOI: 10.1136/bmj.g3028

Callaham M, Madsen CD, Barton CW, Saunders CE, & Pointer J (1992). A randomized clinical trial of high-dose epinephrine and norepinephrine vs standard-dose epinephrine in prehospital cardiac arrest. JAMA : the journal of the American Medical Association, 268 (19), 2667-72 PMID: 1433686

Brown CG, Martin DR, Pepe PE, Stueven H, Cummins RO, Gonzalez E, & Jastremski M (1992). A comparison of standard-dose and high-dose epinephrine in cardiac arrest outside the hospital. The Multicenter High-Dose Epinephrine Study Group. The New England journal of medicine, 327 (15), 1051-5 PMID: 1522841

Choux C, Gueugniaud PY, Barbieux A, Pham E, Lae C, Dubien PY, & Petit P (1995). Standard doses versus repeated high doses of epinephrine in cardiac arrest outside the hospital. Resuscitation, 29 (1), 3-9 PMID: 7784720

Gueugniaud PY, Mols P, Goldstein P, Pham E, Dubien PY, Deweerdt C, Vergnion M, Petit P, & Carli P (1998). A comparison of repeated high doses and repeated standard doses of epinephrine for cardiac arrest outside the hospital. European Epinephrine Study Group. The New England journal of medicine, 339 (22), 1595-601 PMID: 9828247

Vandycke C, & Martens P (2000). High dose versus standard dose epinephrine in cardiac arrest – a meta-analysis. Resuscitation, 45 (3), 161-6 PMID: 10959014

Stiell IG, Hebert PC, Weitzman BN, Wells GA, Raman S, Stark RM, Higginson LA, Ahuja J, & Dickinson GE (1992). High-dose epinephrine in adult cardiac arrest. The New England journal of medicine, 327 (15), 1045-50 PMID: 1522840

Callaway, C. (2012). Questioning the Use of Epinephrine to Treat Cardiac Arrest JAMA: The Journal of the American Medical Association, 307 (11) DOI: 10.1001/jama.2012.313

.

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

.

When is a double dose of defibrillation a good idea?

 
In the comments to Double simultaneous defibrillators for refractory ventricular fibrillation, NCMedic and Ambulance Driver write that they have already begun using variations on double defibrillation.
 

That     is     excellent.

 


 

The changes in when to implement the change, as well as the vector to use, are reasons we need to have people publishing results on what is being done. Please, work with your medical directors and/or others to publish some results.

We have had epinephrine (Adrenaline in Commonwealth countries) in ACLS (Advanced Cardiac Life Support) guidelines, and our protocols, for decades, but we still do not know the best dose or even which patients benefit.

NCMedic writes –
 

Has been in our protocols for sometime now, we are finding it more beneficial sooner than later for obvious reasons, next protocol revision will most likely have it on the 4th shock with the 2nd set of pads placed A/P to cover from a different vector.

 

Epinephrine seems to be harmful when given later, or is epinephrine less beneficial later, or is epinephrine always harmful, just much more harmful later, or something else.[1]

The problem is that we do not know when, or for whom, epinephrine is indicated.

Epinephrine is probably indicated in some patients, but which patients, at what dose, and at what time? If epinephrine should be repeated all of the same questions apply to all further doses. Dr. Scott Weingart points out how little we know about the use of epinephrine, because his approach makes more sense than what ACLS recommends and the evidence is equally lacking.[2]

There are many things in the presentation to discuss, such as Dr. Weingart’s misunderstanding of what nihilism means, but that is for another time.
 

There does not appear to be any harm from double defibrillation. As we use more current more often, we should expect to learn of harms, as we do with almost every intervention. However, as NCMedic states, we may be doing harm by waiting too long to deliver the double dose.

Should it be a double dose?

What about 1 ½ times the maximum?

300 j bi-phasic or 540j mono-phasic or maybe some combination of bi-phasic and mono-phasic, and if a combination, what combination, with drugs or without, which drugs if with drugs, . . . ?

What about 3 times the maximum?

600 joules bi-phasic or 1,080 joules mono-phasic or . . . ?

Should the higher-dose defibrillation be after the fifth shock with a return to VF/pulseless VT (Ventricular Fibrillation/pulseless Ventricular Tachycardia)? After the fourth shock? After the third shock? After the second shock? After the first shock?

Is waiting longer to increase joules making it more likely that epinephrine will be given? Is epinephrine more harmful than a double shock, less harmful than a double shock, or roughly the same?

The amount we do not know is huge.

We should learn what we are doing to our patients and not arrogantly choose to remain ignorant, as we have chosen with epinephrine. That is changing, but some still defend the arrogance of ignorance at the expense of our patients.[3]

Footnotes:

[1] Does Faster Epinephrine Administration Produce Better Outcomes from PEA-Asystole?
Sun, 25 May 2014
Rogue Medic
Article

[2] Podcast 125 – The New Intra-Arrest from SMACCgold
EMCrit
Dr. Scott Weingart
Web page with video and show notes.

[3] 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 of In Press Uncorrected Proof from xa.yming.com
 

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.

 

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Double simultaneous defibrillators for refractory ventricular fibrillation

 
It looks as if the next generation of defibrillators will go to 11. This patient received a double dose of defib.

Is 720 joules too much?

If your answer is Yes, please explain how 720 joules is worse than death.

What about 400 joules? Some older mono-phasic defibrillators go to 400 joules, but we might see 400 joule bi-phasic defibrillators.

Until then, there is the possibility of using two defibrillators to deliver shocks at the same time, or milliseconds apart. By the time that this is a relevant treatment, the patient has been down for several shocks and is still in a shockable rhythm, but a supervisor or second medic unit should have arrived with a second defibrillator.
 


 

It is important to not put the pads from the same defibrillator next to each other.

The paper describes a patient with a BMI (Body Mass Index) of 40, a STEMI, and an onset of VF (Ventricular Fibrillation) in the presence of EMS.

CPR (being performed by the son when EMS arrived at the ED?), 200J x 3, epi x a bunch, amio x 1 by EMS.

High-quality CPR, a bunch more epi, 200 J x 2, lido x 1, bicarb x 1 (bicarb might have been indicated by the patient’s astrological sign), then the shock at 400 joules.
 

The patient then regained a palpable pulse and blood pressure. He had another brief episode of ventricular tachycardia that responded to a second defibrillation with 400 J. The patient had a wide QRS rhythm that quickly narrowed into normal sinus.[1]

 

Maybe the patient was not told about the concerns of some people that too much is too much. If he had been told, he would have remained dead, like a good scenario patient.

Next time he can follow the approved scenario.
 

Five studies have demonstrated safety in patients receiving 720 J of monophasic energy for cardioversion of atrial fibrillation (17,22–25).[1]

 

Five papers demonstrate the safety of 720 joules in living patients with atrial fibrillation, but many in EMS will tell us that it is too dangerous to use on dead people after the failure of standard doses of energy.

Lake Sumter EMS has been providing compression-only CPR, even adding 720 joule defibrillation, and they may have the best resuscitation rates in America. The rest of us should consider catching up. I wonder how things have gone for LEMS, since I wrote about them a couple of years ago.[2]
 

 

While ROSC (Return Of Spontaneous Circulation) is not the right outcome to use to evaluate a treatment, 70% suggests that we should pay attention to what they are doing in Lake Sumter. 46% ROSC in those who could not get ROSC any other way by EMS.

You can’t be too safe is still a lie.

Also read –

When is a double dose of defibrillation a good idea?

Footnotes:

[1] Double simultaneous defibrillators for refractory ventricular fibrillation.
Leacock BW.
J Emerg Med. 2014 Apr;46(4):472-4. doi: 10.1016/j.jemermed.2013.09.022. Epub 2014 Jan 21.
PMID: 24462025 [PubMed - in process]

[2] Optimizing Outcomes in Cardiac Arrest
Mon, 10 Dec 2012
Rogue Medic
Article

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FREE Webinar from Annals of Emergency Medicine, the AHA, Dr. Bentley Bobrow, Dr. Christopher Crowe, Dr. Ashish Kumar Aggarwal, and Mark Venuti (paramedic)

 

Do you have questions about the best way to perform CPR?

If this FREE webinar does not answer them, there will be time to ask questions at the end.

Tuesday, July 8th 2014, 1pm EST (17:00 Universal Time).
 

Register for FREE at this link.
 


 

Dr. Bobrow is one of the people who has been focusing on improving the quality of chest compressions and minimizing interruptions. Two things that we know about CPR are that improving the quality of compressions and minimizing pauses in compressions make a big difference in neurologically intact survival.

These two improvements may be responsible for most of the improvement in survival since the 2005 ACLS guidelines.

That is the difference between the old focus on ALS (Advanced Life Support) because everybody knows the paramedic/nurse/doctor makes all of the difference and the new focus on compressions and keep the paramedics/nurses/doctors from doing things that interfere with compressions.

We are still waiting for some evidence that resuscitation rates would not increase even more if we just kept the paramedics/nurses/doctors away from the patient until after ROSC (Return Of Spontaneous Compressions).

You can read the guidelines, and the protocols, and the research at any time, but there are not many times when you are able to ask the experts responsible for creating all of them.
 

Register for FREE at this link.
 

Tuesday, July 8th 2014, 1pm EST (17:00 Universal Time).
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Emergency Cardiovascular Care Update (ECCU) 2014 Conference – What Will We Get?

 

What should we expect from the Emergency Cardiovascular Care Update (ECCU) 2014 Conference?

The brochure suggests that the next version of the guidelines will be based more on science than the current guidelines, but that is always the suggestion.
 


 

Will the AHA (American Heart Association) actually limit treatments to those that work?

Or will we get more wishful thinking-based guidelines?

There is an examination of the research that will affect the next decade of BLS (Basic Life Support) resuscitation.
 


 

There is also a session where questions are encouraged.
 


 

Will we continue to harm patients with ventilations?

There is still no evidence of benefit from ventilations prior to ROSC (Return Of Spontaneous Circulation). We would still ventilate those who arrested secondary to respiratory causes and children.
 

That format is repeated for ALS (Advanced Life Support).
 


 

And a session where questions are encouraged.
 


 

Will we still be giving eye of newt?

While eye of newt has not been shown to increase the rate of ROSC, it has not been studied, so we do not know if eye of newt does increase the rate of ROSC.

Epinephrine (Adrenaline in Commonwealth countries) is slightly more evidence-based than eye of newt, because it has been shown to increase the rate of ROSC, but who cares?

ROSC is not the goal.

Resuscitation of the heart and brain is the goal.

Epinephrine has failed to demonstrate improved resuscitation.
 

What works?

Teaching CPR effectively works.

Ventilations impair outcomes and impair education.
 


 

What can we do to improve the quality of CPR?
 


 

What can we do to improve the quality of EMS?

EMS resuscitation is not an ALS treatment.

EMS resuscitation is about keeping the medics out of the way of the people providing compressions and defibrillations.
 


 

Resuscitation does not come in a syringe, so prehospital therapeutic hypothermia is not going to be done with chilled IV fluids.

We know that does not work.
 


 

Stutter CPR looks promising, but we are not there, yet.
 


 

What do we do after ROSC?

Higher pressures seem to lead to higher resuscitation rates, but is that just an association of healthier hearts producing higher blood pressures, is it something we can improve with pressors (epinephrine, norepinephrine, phenylephrine – but probably not with dopamine), or is it something that we will make worse with pressors?
 


 

There is even a discussion of mechanical Compression devices.

Should we teach excellent chest compressions to bystanders, while we abandon quality EMS compressions to machines?

If quality is a problem, we should give the machines to bystanders and demand high quality from EMS.

Or is it possible that the machines can act as prehospital ECMO and improve outcomes? We do not know – yet.
 


 

It looks interesting.

I hope the results are a dramatic improvement over the current (2010) guidelines.

The 2005 guidelines made a big difference in compression quality and the resuscitation rates followed.

2015 could cause us to focus on what really works.

If it doesn’t work when we study it, then we were just fooling ourselves about whether it works. If it doesn’t work when we study it, it does not work.
 

Emergency Cardiovascular Care Update (ECCU) 2014 Conference

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