2010 AHA Guidelines | Rogue Medic

If you have a BVM (Bag Valve Mask resuscitator), you should not need naloxone. The problem is inadequate respiration, not inadequate naloxonation.

- Rogue Medic

Drug Shortage Update Affecting a Lot of the Ex-Code Drugs

Wed, 16 May 2012 11:00:57 +0000 By Rogue Medic Leave a Comment

Today’s drug shortage update from the FDA (Food and Drug Administration) includes a lot of drugs that used to be routine drugs for cardiac arrest.

Once upon a time, I was a code drug.

Atropine is the most recent drug to be dumped by the AHA (American Heart Association). In the past week, two manufacturers have stated that they have atropine available. FDA Update.

It was nice to see the AHA admit that there is not a good reason to keep treating every PEA (Pulseless Electrical Activity) or asystole patient with a drug that has never had good evidence that it improves survival. The next revision of the ACLS (Advanced Cardiac Life Support) guidelines will provide more opportunity to get rid of some drugs that are routinely used for cardiac arrest, even though there is no evidence that they improve survival – lidocaine (farther down on this list), amiodarone, and the everybody’s favorite drug to not improve survival – epinephrine (also farther down on the list).

Calcium Chloride has increased availability from one manufacturer, but decreased availability from another. Calcium is still the best drug for hyperkalemia, but it was once used routinely in cardiac arrest, as if there has been a lot of sudden onset hypocalcemia. FDA Update.

Epinephrine 1:10,000 has not yet been dumped by the FDA, but the recent evidence suggests that we are decreasing survival by using epinephrine – and those who do survive the epinephrine are more likely to have significant brain damage. FDA Update

Tomorrow, I will be talking about the evidence for and against epinephrine at the EMS Web Summit.

Lidocaine has new manufacturing delays. Lidocaine is still just barely in the ACLS guidelines –

Amiodarone may be considered when VF/VT is unresponsive to CPR, defibrillation, and vasopressor therapy (Class IIb, LOE A). If amiodarone is unavailable, lidocaine may be considered, but in clinical studies lidocaine has not been demonstrated to improve rates of ROSC and hospital admission compared with amiodarone (Class IIb, LOE B).^[1]

Maybe lidocaine is there to make amiodarone look good, because nothing else makes amiodarone look good.

For victims of witnessed VF arrest, early CPR and rapid defibrillation can significantly increase the chance for survival to hospital discharge.^128,–,133 In comparison, other ACLS therapies such as some medications and advanced airways, although associated with an increased rate of ROSC, have not been shown to increase the rate of survival to hospital discharge.^{31,33,134,–,138} ^[2]

In other words, these drugs are probably only as effective as atropine, and maybe less harmful than atropine, but the AHA has not given up on them, yet. FDA Update.

Magnesium Sulfate is another once-promising code drug, now used for the ever-impressive torsades and for the less impressive hypomagnesemia. FDA Update

Sodium Bicarbonate used to be given almost as much as epinephrine.

Now, Sodium Bicarbonate is only given when it is specifically indicated – the way that real medicine should be used.

Sodium Bicarbonate is second line for hyperkalemia and probably is just the hypertonic saline (5.8% saline) that is working, rather than treatment of acidosis, but acidotic patients may benefit from that, too – if they are well ventilated. Sodium Bicarbonate is CO₂ in a syringe.

FDA Update.

Vasopressin is now available, again. Not useful in cardiac arrest, but we feel we need to inject something, so this permits some variety. FDA Update.

Important non-code EMS drugs on the FDA Current Drug Shortages list are:

Alfentanyl – Possibly substituting for fentanyl, but not having enough to make up for the lack of fentanyl. Probably also due to increased realization that the side effects of opioids are easily managed by competent medical personnel.

Atracurium (Tracrium).

Diazepam (Valium).

Digoxin.

Diltiazem (Cardizem).

Diphenhydramine (Benadryl).

Etomidate (Amidate).

Fentanyl (Sublimaze).

Hydromorphone (Dilaudid).

Ketorolac (Toradol).

Lorazepam (Ativan).

Mannitol.

Metoclopramide (Reglan).

Midazolam (Versed).

Morphine.

Multi-vitamin injection (banana bags?).

Naloxone (Narcan).

Naltrexone.

Ondansetron (Zofran).

Oxytocin (Pitocin).

Pancuronium (Pavulon).

Phentolamine (Regitine).

Procainamide (Pronestyl) – the only ventricular antiarrhythmic that works (of those commonly available in the US – [sotalol also works]).

Prochlorperazine (Compazine).

Promethazine (Phenergan)

Propofol (Diprivan).

Sufentanyl (Sufenta).

Tromethamine (Tham).

Vecuronium (Norcuron).

and something new –

Sodium Chloride 0.9% (5.8mL and 20mL) (Initial Posting Date) – 5/4/2012. FDA Update.

Footnotes:

^[1] Drug Therapy in VF/Pulseless VT
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 8: Advanced Life Support
Part 8.2: Management of Cardiac Arrest
Free Full Text from Circulation

^[2] Overview
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 8: Advanced Life Support
Part 8.2: Management of Cardiac Arrest
Free Full Text from Circulation

Filed Under: 2010 AHA Guidelines, FDA, Heresy, Pharmacology

Keeping ALS Out of Resuscitation

Sun, 13 May 2012 08:00:15 +0000 By Rogue Medic 2 Comments

Why do we work so hard at keeping resuscitation rates low?

Rates of bystander cardiopulmonary resuscitation (CPR) in the United States are dismal. A national study showed that only 31% of patients with cardiac arrest treated out-of-hospital received CPR from a bystander.¹ The low rates of bystander CPR, a procedure developed over 50 years ago, is particularly notable when compared with the great progress that has been made in making a much newer technology—percutaneous coronary angioplasty—highly accessible.^[1]

We could recognize this dismal level of bystander ~~CPR~~ chest compressions.

In America, we seem to be trying to demonstrate how much more intelligent people are in other countries. Here, we have only isolated pockets of high bystander CPR rates.

We spend our time making excuses for the higher resuscitation rates is these places. Seattle is #1, again – and again – and again – and again – . . . .

But they call fine V Fib (Ventricular Fibrillation) asystole! –

Is there any validity to that claim?

Probably not.

Is there any evidence that fine V Fib is in any way more responsive to defibrillation than asystole?

Is there any difference between what the critics of Seattle think of as a shockable rhythm and what is programmed into AEDs (Automated External Defibrillators)?

If these critics are so offended by Seattle’s high resuscitation rates, maybe they should submit their own resuscitation rates with their version of fine V Fib and without. Will removing their fine V Fib result in results that compare to Seattle’s resuscitation rates?

Or is the secret of Seattle not the way they measure V Fib, but the way they encourage bystander ~~CPR~~ chest compressions?

Is a cath lab useful without bystander chest compressions?

Is adding more cath labs an expensive way of avoiding the real problem – low rates of bystander ~~CPR~~ chest compressions?

In addition, angioplasty fits our medical model. A person has a medical problem. A subspecialty physician treats it with a high-technology intervention in a hospital setting. Interventions that can be performed by laypersons in nonhospital settings tend to receive less attention.^[1]

A medical model of cardiac arrest treatment?

The medical model would not be the BLS treatments. Treatments that we know improve outcomes.

The medical model would be the ALS treatments. Treatments that we only hope improve outcomes.

What has dominated our attention in resuscitation?

Drugs, tubes, ventilations, . . .

We still do not have any evidence that these improve survival with good brain function. Is there any other valid way to measure outcomes?

We know that low rates of bystander CPR limit resuscitation rates, but we continue to make excuses for pushing the drugs, for pushing the tubes, and for squeezing the bag.

The captain of that engine is running that cardiac arrest. His job is to make sure there are good chest compressions and to make sure that the medics, when they arrive, don’t get in the way of good chest compressions.

It is an EMT-Basic skill to run a cardiac arrest now. The paramedics just get in the way.^[2]

We can improve resuscitation or we can support paramedic egos.

As a paramedic, I think the choice is easy. We need to improve the rate and quality of bystander chest compressions.

Bystander chest compressions save lives.

Footnotes:

^[1] Increasing bystander CPR rates: the chest compression-only method puts the goal in easier reach.
Katz MH.
Arch Intern Med. 2011 Jan 10;171(1):87-8. No abstract available.
PMID: 21220665 [PubMed]

^[2] Medical Direction Issue
Interventions
Medical Direction Issue.

Dr. Sporer Interview.

Filed Under: 2010 AHA Guidelines, Heresy, V Fib

Comments on Cardioversion – 2010 ACLS – Part II

Mon, 16 Apr 2012 15:35:01 +0000 By Rogue Medic Leave a Comment

In response to Cardioversion – 2010 ACLS – Part II, there are some new comments. Chris from Sweden, had written -

What meds do you use in the hypotensive, but still conscious patient for sedation? Could ketamine and low dose of midazolam be of use here?

Gerardo Gastélum comments –

Not Ketamine for cardioversion. Ketamine rises heart rate and coronary O2 requirements.

Benzos like Midazolam or Diazepam + Opiates such as Fentanyl or Morphine can do the works. AHA also recomends etomidate, thiopental and propofol, but out of these I chose etomidate due to it´s cardiovascular stability.

I disagree.

There may be more of a desire to avoid sedatives that vasodilate and depress cardiac activity. This is one of the reasons that etomidate is recommended. I think that either effect is going to be short-term – if the cardioversion, or series of cardioversions, works.

Some people discourage sedation. One of the things that they do not appear to consider is the possibility of needing to cardiovert more than once.

I can get away with shocking her without sedation, justify it as saving her life, and sedate her afterward to deal with the side effects of such brutal treatment, but the idea of appropriate sedation prior to cardioversion almost scares me into an unstable tachycardia.

Fortunately, nobody here is recommending that we not sedate for cardioversion.

With comments on this topic, I tend to wonder, Has this been covered in an EMCrit podcast? What would Dr. Scott Weingart do? Maybe he can make up some EMCrit screensavers with the slogan WWWD? (What Would Weingart Do?). Dr. Weingart is trying to smooth the transition from treatment in the ED (Emergency Department) to treatment in the ICU (Intensive Care Unit) and possibly take over the world of emergency education.

I think the clever something to give is probably a low dose of etomidate, maybe 5 or 7 mg of etomidate. They’re not going to be fully unconscious, like when we gave the 10 or 15 mg, but it’ll take the edge off.

They’re getting no pain control whatsoever from that, so if you were really a smart guy, give a little etomidate with some ketamine, or even just ketamine alone.^[1]

Listen to the whole podcast – all 9 minutes of it. I just copied a few sentences, but this very short podcast covers a lot of material that is very important to understand before dealing with the unstable tachyarrhythmia patient.

Image credit.

In the second comment, Gerardo Gastélum provides a quote from the 2010 ACLS guidelines that is important for the understanding of the difference between unstable and just symptomatic.^[2]

Thank you for the great description from ACLS.

Footnotes:

^[1] EMCrit Podcast 20 – The Crashing Atrial Fibrillation Patient
by EMCRIT on FEBRUARY 12, 2010
Podcast page

^[2] Management of Symptomatic Bradycardia and Tachycardia
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 8: Adult Advanced Cardiovascular Life Support
Part 8.3: Management of Symptomatic Bradycardia and Tachycardia
Free Full Text from Circulation

Unstable and symptomatic are terms typically used to describe the condition of patients with arrhythmias. Generally, unstable refers to a condition in which vital organ function is acutely impaired or cardiac arrest is ongoing or imminent. When an arrhythmia causes a patient to be unstable, immediate intervention is indicated. Symptomatic implies that an arrhythmia is causing symptoms, such as palpitations, lightheadedness, or dyspnea, but the patient is stable and not in imminent danger. In such cases more time is available to decide on the most appropriate intervention. In both unstable and symptomatic cases the provider must make an assessment as to whether it is the arrhythmia that is causing the patient to be unstable or symptomatic. For example, a patient in septic shock with sinus tachycardia of 140 beats per minute is unstable; however, the arrhythmia is a physiologic compensation rather than the cause of instability. Therefore, electric cardioversion will not improve this patient’s condition. Additionally, if a patient with respiratory failure and severe hypoxemia becomes hypotensive and develops a bradycardia, the bradycardia is not the primary cause of instability. Treating the bradycardia without treating the hypoxemia is unlikely to improve the patient’s condition. It is critically important to determine the cause of the patient’s instability in order to properly direct treatment. In general, sinus tachycardia is a response to other factors and, thus, it rarely (if ever) is the cause of instability in and of itself.

One of my earliest posts was a variation on the distinction between unstable and symptomatic –

Cardioversion – I’m not doing that, you do it!

Filed Under: 2010 AHA Guidelines, Cardioversion, EMCrit, Pharmacology, Sedation

Dr. Ken Grauer on Killing Patients Just to Get a Temporary Pulse With Epinephrine – Part II

Fri, 23 Mar 2012 08:00:35 +0000 By Rogue Medic 3 Comments

Dr. Ken Grauer wrote a couple of extended comments in response to Killing Patients Just to Get a Temporary Pulse With Epinephrine.

Dr. Grauer has provided some commentary on this on his web site – KG-EKG Press.

ISSUE #10: Should We Still Use Epinephrine for Cardiac Arrest?

So, how bad was epinephrine in this study?

Dr. Grauer writes –

I am not a statistician – and I admit to not understanding much of the technical jargon in the methodological portions of this manuscript – BUT – the cited “propensity score” data for Epi administration to my reading seems highly contrived – and I have trouble accepting this concept as being valid in this nonrandomized observational study …

I am not a statistician, either. However, the epinephrine group had a bunch of large advantages in this study.

Click on images to make them larger.

In spite of those large advantages, the only advantage to the no epinephrine group was in response times being 7:18 vs. 7:54, the unadjusted results showed that patients did better without epinephrine.

What did the 2010 ACLS Guidelines recommend about epinephrine before this study was completed?

It is reasonable to consider administering a 1 mg dose of IV/IO epinephrine every 3 to 5 minutes during adult cardiac arrest (Class IIb, LOE A).^[2]

It is only reasonable to consider giving epinephrine.

Not – It is mandatory to consider epinephrine.

Not – It is reasonable to give epinephrine.

Definitely Not – It is mandatory to give epinephrine.

Certainly Not – It is unethical to withhold epinephrine.

Absolutely Not – Giving epinephrine will improve outcomes.

ACLS does not state any of that.

Deemphasis on Devices and Advanced Cardiovascular Life Support Drugs During Cardiac Arrest
At the time of the 2010 International Consensus Conference there were still insufficient data to demonstrate that any drugs or mechanical CPR devices improve long-term outcome after cardiac arrest.⁴⁵ Clearly further studies, adequately powered to detect clinically important outcome differences with these interventions, are needed.^[3]

Clearly further studies, . . . , are needed.

It looks as if the AHA (American Heart Association) is ready to give up on epinephrine in cardiac arrest unless someone provides evidence of actual benefit to real patients.

50 years of traditional use of epinephrine, unimpeded by a lack of evidence.

Thus, properly evaluating this traditional therapy now seems necessary and timely and should consist of a rigorously conducted and adequately powered clinical trial comparing epinephrine with placebo during cardiac arrest. Such a trial has previously seemed unethical, and investigators who have attempted to perform this comparison have received unwarranted criticism in their communities.^17,19 While awaiting results of such a definitive trial, physicians and other practitioners involved in cardiac resuscitation must consider carefully whether continued use of epinephrine is justified.^[4]

You will notice that the list of authors for the 2010 ACLS Guidelines includes the same Dr. Callaway who wrote this editorial. This should be a hint of what we can expect from the next change in the guidelines. Dr. Callaway is not the only doctor involved in writing the guidelines, but the ACLS Committee as a whole has been moving away from medications and has been emphasizing high-quality chest compressions.

Unless there is a miracle and a new study shows some benefit from epinephrine in cardiac arrest, I expect epinephrine to be removed from the next revision of the ACLS Guideline.

The 2015 ACLS Guidelines –

Epinephrine is only recommended for asthma and anaphylaxis.

Why?

Those are the only medical emergencies that have evidence of benefit from epinephrine.

No more voodoo.

Footnotes:

^[1] Prehospital Epinephrine Use and Survival Among Patients With Out-of-Hospital Cardiac Arrest
Akihito Hagihara, Manabu Hasegawa, Takeru Abe, Takashi Nagata, Yoshifumi Wakata, Shogo Miyazaki
JAMA. 2012;307(11):1161-1168.
doi:10.1001/jama.2012.294

Free Full Text in PDF format

^[2] Epinephrine
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Robert W. Neumar, Chair; Charles W. Otto; Mark S. Link; Steven L. Kronick; Michael Shuster; Clifton W. Callaway; Peter J. Kudenchuk; Joseph P. Ornato; Bryan McNally; Scott M. Silvers; Rod S. Passman; Roger D. White; Erik P. Hess; Wanchun Tang; Daniel Davis; Elizabeth Sinz; Laurie J. Morrison
Part 8: Adult Advanced Cardiovascular Life Support
Part 8.2: Management of Cardiac Arrest
Vasopressors
Free Full Text from Circulation with link to PDF Download

^[3] Deemphasis on Devices and Advanced Cardiovascular Life Support Drugs During Cardiac Arrest
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 1: Executive Summary
John M. Field, Co-Chair*; Mary Fran Hazinski, Co-Chair*; Michael R. Sayre; Leon Chameides; Stephen M. Schexnayder; Robin Hemphill; Ricardo A. Samson; John Kattwinkel; Robert A. Berg; Farhan Bhanji; Diana M. Cave; Edward C. Jauch; Peter J. Kudenchuk; Robert W. Neumar; Mary Ann Peberdy; Jeffrey M. Perlman; Elizabeth Sinz; Andrew H. Travers; Marc D. Berg; John E. Billi; Brian Eigel; Robert W. Hickey; Monica E. Kleinman; Mark S. Link; Laurie J. Morrison; Robert E. O’Connor; Michael Shuster; Clifton W. Callaway; Brett Cucchiara; Jeffrey D. Ferguson; Thomas D. Rea; Terry L. Vanden Hoek
New Developments in Resuscitation Science Since 2005
Free Full Text from Circulation with link to PDF Download

^[4] Questioning the Use of Epinephrine to Treat Cardiac Arrest
Clifton W. Callaway
JAMA. 2012;307(11):1198-1200.
doi:10.1001/jama.2012.313

And the accompanying interview in mp3 format on JAMA’s site –

Questioning the Use of Epinephrine to Treat Cardiac Arrest
Clifton W. Callaway
JAMA: March 21, 2012; Vol 307, No. 11,
Author Interview
podcast in mp3 format (06:29, 3.7 MB)

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), 1161-1168 DOI: 10.1001/jama.2012.294

Callaway, C. (2012). Questioning the Use of Epinephrine to Treat Cardiac Arrest JAMA: The Journal of the American Medical Association, 307 (11), 1198-1200 DOI: 10.1001/jama.2012.313
.

Filed Under: 2010 AHA Guidelines, Epinephrine, Heresy, Pharmacology, Research

Dr. Ken Grauer on Killing Patients Just to Get a Temporary Pulse With Epinephrine – Part I

Thu, 22 Mar 2012 13:00:38 +0000 By Rogue Medic 1 Comment

Dr. Grauer,

I love your ACLS 2nd edition and learned more about ACLS from your book than from any other source. You and Daniel Cavallaro did a great job of presenting the material in a way that encourages thinking and assessment. I think that your presentation of the rationale behind the possible treatments ahead of the 1992 ACLS was a great service to those who were able to read your book. I used it long after your third edition came out, because of the way you analyzed the treatments.

Dr. Grauer wrote a lot in two comments, in response to Killing Patients Just to Get a Temporary Pulse With Epinephrine, with only the abstract as a reference for the first comment. I will try to address a point, or two, at a time without distorting his meaning.

Observational studies are just that – observations – NOT proof. Based on observational studies done on large numbers of women we routinely treated with estrogen for many years – until controlled, prospective trials were done and showed the fallacy of that previously uniformly accepted observational dogma …

This is the primary difference in our views of the research.

I am not stating that we should use observational data to add an unexamined treatment.

No, I want much better evidence that any treatment works. It would not be good patient care to treat patients based only on observational data, but what we have to support the use of epinephrine in cardiac arrest epinephrine is not even as good as observational data.

An observational study showing a benefit from the use of epinephrine would be a tremendous contribution to the research supporting epinephrine in cardiac arrest, because there is no outcomes research supporting epinephrine in cardiac arrest. Nothing.

We have several studies showing harm from epinephrine, but no studies showing any benefit. 50 years of absolute failure to produce a single study showing improved outcomes with epinephrine. What is wrong with us?

We are treating patients based only on surrogate endpoints. Improved circulation in the laboratory and improved ROSC (Return Of Spontaneous Circulation).

Surrogate endpoints are only useful for generating hypotheses about possible outcomes studies. Surrogate endpoint studies are much lower quality than observational studies.

When surrogate endpoints are examined, they consistently fail to demonstrate improvement in outcomes.

We are not helping our patients if we do not pay attention to any studies that consistently show harm.

First, do no harm, is supposed to be an important consideration. No harm is impossible,^[1] but we should minimize the potential harm.

After 50 years, where is any evidence of improved survival from epinephrine?

How useless is a drug, that after 50 years of use we cannot show ANY benefit?

The goal is not to produce a temporary pulse. The goal is to produce survivors.

Where are the survivors?

With epinephrine, 2,786 patients had ROSC.

Only 805 patients were alive one month later.

Why do almost all of the patients who get epinephrine die very quickly?

Only 205 patients had good brain function.

Why do almost all of the patients not killed by epinephrine end up with severe brain damage?

93% of the ROSC patients were dead or disabled with epinephrine.

More ROSC, but they don’t survive. All of the research has the same result.

If this is not the typical epinephrine response, then somebody needs to prove it.

We need to stop killing patients with epinephrine.

50 years of trust us, it works, means 50 years of killing patients just to get a quick pulse that often does not even last until the emergency department.

Footnotes:

^[1] A piece of my mind: the harm of “first, do no harm”.
Shelton JD.
JAMA. 2000 Dec 6;284(21):2687-8. No abstract available.
PMID: 11105155 [PubMed - indexed for MEDLINE]

Much of the rest of the world operates on sensible risk/benefit principles and by embracing error. But medicine tries to operate on impossible zero-tolerance principles and by denying error. Paradoxically, the old concept leads to too much harm.

Filed Under: 2010 AHA Guidelines, Epinephrine, Ethics, Heresy, Pharmacology, Research

Killing Patients Just to Get a Temporary Pulse With Epinephrine

Wed, 21 Mar 2012 08:00:47 +0000 By Rogue Medic 43 Comments

Today in JAMA there is a non-randomized observational study of epinephrine vs. no medicine in 417,188 EMS cardiac arrest patients. I will be writing about this study in more detail, but I have already written a lot about the earlier studies that demonstrate the harm of epinephrine in cardiac arrest.

We never had a good reason to make epinephrine the standard of care in cardiac arrest.

Never.

The goal of resuscitation is NOT to get a pulse back.

But . . . but . . . but . . . if we don’t get pulses back, we can’t resuscitate patients.

Yes, but that does not mean that it does not matter how much harm we do in order to get pulses back.

Just because epinephrine increases the rate of return of pulses does not mean that epinephrine increases the rate of survival to discharge.

In the treatment of cardiac arrest, nothing is more important than survival to discharge.

OK, survival to one month is more important. Survival to one year is more important. Survival to ten years is more important.

A pulse for a few days is not important. A pulse for a few hours is not important. A pulse for a few minutes is not important. There is a word to describe these patients who never leave the hospital – dead.

only 1.4% of patients in the epinephrine group had good neurological outcomes, despite a 5.4% survivalrate (Table 1). Thus, only about 25% of survivors had good neurological outcomes.^[1]

Thus, properly evaluating this traditional therapy now seems necessary and timely and should consist of a rigorously conducted and adequately powered clinical trial comparing epinephrine with placebo during cardiac arrest. Such a trial has previously seemed unethical, and investigators who have attempted to perform this comparison have received unwarranted criticism in their communities.^17,19 ^[2]

The only thing unethical has been the resistance from those defending the Standard Of Care, that was nothing more than a refusal to examine tradition.

While awaiting results of such a definitive trial, physicians and other practitioners involved in cardiac resuscitation must consider carefully whether continued use of epinephrine is justified.^[2]

How can we justify a treatment that has never been based on any study of survival? We do not have any good reason to expect that the results of a randomized placebo-controlled study will support continuing use of epinephrine.

Epinephrine should only be used in cardiac arrest as a part of controlled studies.

Expert recommendations must come with an expiration date.

No exceptions.

If the expert recommendation is not followed by appropriate research, then the expert recommendation should not be treated better than the patients.

ROSC (Return Of Spontaneous Circulation) is nice, but ROSC is only a surrogate endpoint. If we are creating a dangerous condition by transporting the patient to the hospital; if the patient never wakes up; if we create false hope for the family; if we generate huge bills that may bankrupt the family; if we takes hospital staff away from the treatment of other patients – where is the benefit?

But . . . but . . . but . . . the family will be able to say goodbye to their loved one while the person has a pulse.

Really?

How many millions of dollars is that worth to make us feel good, regardless of what the family wants?

Why do we assume that this is what the family wants? Do we ask? Of course not – we don’t want to risk learning the truth.

50 years of tradition, unimpeded by progress.

Forget it, Jake. It’s Chinatown.

There is also audio of an interview with Dr. Calloway, who wrote the accompanying editorial.^[3]

Thank you to William Toon, PhD. of the EMS EduCast for bringing this to my attention.

Footnotes:

Free Full Text in PDF format

^[2] Questioning the Use of Epinephrine to Treat Cardiac Arrest
Clifton W. Callaway
JAMA. 2012;307(11):1198-1200.
doi:10.1001/jama.2012.313

^[3] Questioning the Use of Epinephrine to Treat Cardiac Arrest
Clifton W. Callaway
JAMA: March 21, 2012; Vol 307, No. 11,
Author Interview
podcast in mp3 format (06:29, 3.7 MB)

Filed Under: 2010 AHA Guidelines, Epinephrine, Ethics, Heresy, Pharmacology, Research

When Does Post-Resuscitation Care Begin

Wed, 18 Jan 2012 22:22:13 +0000 By Rogue Medic 1 Comment

In the comments to Cardiac Arrest Management is an EMT-Basic Skill, AZCEP wrote -

True enough, but it is an important part of resuscitation all the same. Post-arrest management has been de-emphasized to the point of absence from AHA guidelines until the latest version reintroduced it to us.

When we start post-resuscitation care before the patient is resuscitated, we are not doing any good. Post means after. Post-resuscitation means after resuscitation, not during resuscitation and definitely not before ROSC.

We are just making excuses for interrupting compressions and continuing experimental treatments that most likely decrease survival.

Post-resuscitation treatment should not be de-emphasized. I have always spent time teaching people what to do after ROSC (Return Of Spontaneous Circulation).

First. Assess. Don’t do too much.

Find out what is going on before doing anything.

Suppose the patient’s initial pressure is 60 by palpation.

What do we do?

Second. Reassess.

Things change, so we want to know what the trend is. We do not care what normal is. We are dealing with a patient who is not at all representative of what we do.

60/palp is not a good pressure for a normal patient, but there is nothing normal about this patient. We want to know what direction the blood pressure is going. A minute ago the pressure was 0/0, so things have improved. Rushing to give a catecholamine (something that is just a weaker version of epinephrine, or just epinephrine by drip) is a bad idea. The patient just had his systolic pressure rise by 60 points in one minute without any pressors. Adding a pressor to a dramatically rising blood pressure is a bad idea.

If the pressure stays at 60/palp, then some fluids are not a bad idea. Always listen to lung sounds before giving fluids, but crackles are not an absolute contraindication for a fluid challenge. Crackles may even be an indication for a fluid challenge.

If the next pressure is lower, then a fluids challenge is the first treatment – not a catecholamine!

We just resuscitated the patient. Let’s hold off on the drugs that can kill the patient. At least let him live for a few minutes.

What about cardioversion?

This patient definitely meets criteria for cardioversion.

No. This patient only meets criteria for cardioversion after a full assessment and not after cardiac arrest.

How much epinephrine has the patient received?

Is cardioversion going to metabolize any of that massive dose of epinephrine?

Absolutely not.

Just say NO.

Reassess and then reassess again.

The best management of a cardiac arrest is to prevent it from ever happening to begin with.

Preventing cardiac arrest is much better than responding to cardiac arrest, but should we assume that ALS that failed to prevent cardiac arrest is going to reverse cardiac arrest? These are very different medical presentations, even though they may be in the same patient.

I wrote about this in Dissecting the ACLS Guidelines on Cardiac Arrest from Toxic Ingestions. Calcium chloride is safe and effective at preventing arrest from hyperkalemia. Once the patient is dead (maybe medical command refused orders for calcium chloride, maybe the patient arrested prior to arrival, maybe we didn’t think it was that serious, . . . ), giving calcium chloride may not be anywhere near as successful.

There is an important difference in the way dead people and living people respond to treatments.

Filed Under: 2010 AHA Guidelines, Cardioversion, Heresy, Pharmacology

Vinnie Jones’ hard and fast Hands-only CPR

Wed, 11 Jan 2012 06:30:00 +0000 By Rogue Medic 10 Comments

For a view on what to do for cardiac arrest from across the pond (closed captioning is available at YouTube for those who are accustomed to American accents), there is this nice short video from the British Heart Foundation with Vinnie Jones.

One criticism is that the compressions demonstrated are on an actor, so there is not the ability to demonstrate proper depth of compressions. Especially on the actor portraying the dead guy. He looks bigger than average, so a depth of 3 inches might be more appropriate.

What about breathing?

The 2010 guidelines eliminate ventilations.

Due to a misunderstanding of the scientific method, EMS is still supposed to provide these unproven ventilations.

How will any patient recover without breathing?

The explanation is that metabolism slows down during cardiac arrest, so the oxygen that is already in the body is adequate for the needs of the body. The oxygen that is passively exchanged due to chest compressions keeps the level of oxygen from dropping quickly.

If we were to provide any ventilations, we should probably only use tiny volumes and not bag the patient any faster than 10 times a minute – even after an endotracheal tube is in place.

One huge problem with ventilations is that they increase intrathoracic pressure and keep the blood from getting where we want it.

If the blood does not circulate, then it doesn’t really matter how much oxygen is in the blood, does it?

Ventilations can prevent circulation. PPV (Positive Pressure Ventilation) can be as bad as interruptions in chest compressions. If we have to interrupt chest compressions, just to provide ventilations, we are not doing our patients any favors.

What does it say in the AHA (American Heart Association) CPR guidelines?

How can bystander CPR be effective without rescue breathing? Initially during SCA (sudden Cardiac Arrest) with VF (Ventricular Fibrillation), rescue breaths are not as important as chest compressions because the oxygen level in the blood remains adequate for the first several minutes after cardiac arrest. In addition, many cardiac arrest victims exhibit gasping or agonal gasps, and gas exchange allows for some oxygenation and carbon dioxide (CO2) elimination.^110,111,119 If the airway is open, passive chest recoil during the relaxation phase of chest compressions can also provide some air exchange.^{19,110,111,119–122} ^[1]

So why didn’t the AHA make Hands-Only CPR the treatment used by all people – yet?

Clinical question.
In adult and pediatric patients with cardiac arrest (out-of-hospital and in-hospital) and receiving chest compression only CPR (P), does the addition of any passive ventilation technique (eg positioning the body, opening the airway, passive oxygen administration) (I) as opposed to no addition (C), improve outcome (O) (eg. ROSC [Return Of Spontaneous Circulation], survival)? ^[2]

The problem is that the question is backwards. In evidence-based medicine, the way to state a hypothesis is to ask – Does the addition of the intervention improve outcomes?

Compared to what?

Compared to doing nothing or compared to an inert facsimile of the intervention (placebo).

To turn the question around is to give an unfair advantage to treatments that do not work. This is what the alternative medicine quacks would love, but it is completely dishonest.

If a treatment is not better than doing nothing, then we should do nothing. The treatment is not going to make anything better.

If a treatment is not better than doing nothing, but there are side effects, then we should prohibit the treatment. The treatment will sometimes make things worse, but it cannot be expected to make things better.

Does the addition of ventilations to chest compressions improve survival?

I do not see any evidence that there is any added benefit from adding ventilations.

they permitted paramedics to choose, in a nonrandomized way, whether the patient would receive some interposed ventilations versus passive insufflation of oxygen during the continuous chest compressions. These studies by Kellum do not identify the compliance with providing these additional interventions, but these interventions are associated with almost no complications. ^[2]

almost no complications.

almost?

Is that like almost avoiding a crash?

Is that like almost winning the lottery?

Is that like almost passing a test?

Is that like almost having a safe flight?

Is that like almost resuscitating patients?

As I stated above – If a treatment is not better than doing nothing, but there are side effects (complications), then we should prohibit the treatment. The treatment will sometimes make things worse, but it cannot be expected to make things better.

For example –

Ventilations can cause gastric inflation

Ventilations can cause . . . regurgitation and aspiration^[3]

Image credit.

A carved pumpkin is not going to get any deader by vomiting in its airway.

A cardiac arrest patient who is lying on his back is not going to get any better by vomiting in his airway.

Everything gets worse.

Ventilation increases intrathoracic pressure

Ventilations decreases venous return to the heart

Ventilation diminishes cardiac output^[3]

If the blood does not circulate, then it doesn’t really matter how much oxygen is in the blood, does it?

The logical conclusion is that ventilation interferes with everything good about CPR.

Ventilation diminishes . . . survival

Footnotes:

^[1] Hands-Only CPR
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 5: Adult Basic Life Support
Adult BLS Skills
Free Full Text from Circulation with link to PDF Download

^[2] Passive ventilation techniques
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 5: Adult Basic Life Support
Appendix: Evidence-Based Worksheets
PDF download of worksheet pages

^[3] Pit Crew CPR is Just ADHD CPR
Rogue Medic
12/22/2011
Article

Filed Under: 2010 AHA Guidelines, Heresy, Science