We are there for the good of the patient, not for the good of the protocol, not for the good of the medical director, and not for the good of the company.

- Rogue Medic

PROVE Epinephrine is Harmful

We have several studies that suggest that epinephrine is harmful.

Nobody has to make any claim that these are proof that epinephrine is harmful. No one study is proof and collectively they are not proof, but they are evidence and that evidence says STOP!

After 50 years of use in cardiac arrest, there is no evidence of improved survival with epinephrine.

We should not continue to give epinephrine to everyone who remains dead after defibrillation (or who is not in a shockable rhythm).

It is prudent to stop and re-examine this treatment.

Why don’t we have any evidence of improved survival after half a century of routine use?

Doesn’t anyone want to know if epinephrine works?

If we stop using epinephrine, except in randomized controlled trials, what would our patients possibly be missing?

Since the patients would not miss out on any benefit, only the doctors, nurses, and medics would stop receiving a benefit.

Should we be treating patients for our benefit, or for the patients’ benefit?

There is too much evidence to ignore and say, PROVE it is dangerous.

Why are so many people offended at the possibility that we stop the routine use of epinephrine until evidence of improved survival?

Where is the offense?

Where is the danger to the patient of withholding a drug that only has long-term evidence of harm?

 

Demanding proof of harm is NOT medicine.

 








Where is the danger to the patient of withholding a drug that only has long-term evidence of harm?

 

Demanding proof of harm is NOT medicine.

 

We can believe in whatever we want, as long as we do not harm others.

Medicine is not a harmless belief.

If we are using any treatment on patients, we need to demand evidence that it works.

Our patients deserve treatments that work.

If there is no evidence of benefit, it is NOT medicine.

Other commentary on epinephrine in cardiac arrest –

Epinephrine Death Watch

More Nails In the Coffin For Epinephrine

Prehospital Epinephrine for Cardiac Arrest Reduces Survival and Worsens Neurological Outcomes at 1 Month

Another study questions epinephrine for out-of-hospital cardiac arrest

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

And I have written about the most recent study here –

Killing Patients Just to Get a Temporary Pulse With Epinephrine

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

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

Answer to What is this Treatment and Why Did We Stop Using it

.

Comments

  1. It always did puzzle me that we were cautioned about giving more than 0.3 mg subQ because it might kill somebody, but if they’re in arrest, they get 1 mg q/5 min until they were either dead dead or ROSC.

    • That is 1:1,000 vs 1:10,000. There is a difference.

      • Caleb,

        That is 1:1,000 vs 1:10,000. There is a difference.

        The only difference is the concentration. If we were to give epinephrine IV for anaphylaxis/asthma, we would dilute it, but we would still give a very small dose, because epinephrine can cause a lot of damage.

        Ask anyone who has ever had an EpiPen injection. It is not a pleasant experience.

        According to Dr. Corey Slovis, we should consider using IV epinephrine drips for anaphylaxis/asthma.

        PDF of ‘Using IV Epinephrine Expertly’ presentation from 2012 Gathering of Eagles

        The dose is 1 to 2 micrograms per minute for anaphylaxis/asthma.

        For cardiac arrest, we are giving 1 milligram every 3 to 5 minutes. 200 to 333 micrograms per minutes.

        That difference is not small. The cardiac arrest dose from 100 times larger to 333 times larger than the anaphylaxis dose.

        The difference is that we have survival research showing a benefit from epinephrine in anaphylaxis, while we do not have survival research showing any benefit from epinephrine in cardiac arrest, we only have evidence of worse survival.

        .

      • Yes, there is a difference. The amount of fluid given. And that you generally give the more concentrated form IM/SQ and the more dissolved form IV. I see that old don’t do drugs commercial that ends with the smashed egg from the 80’s. I see some relations between the two. Since we don’t know what the dose should be, why not give 0.3 IM/SQ in cardiac arrest once instead of IV every 3-5 minutes? Would it make a difference in survival to discharge? Discuss.

    • Robert,

      It always did puzzle me that we were cautioned about giving more than 0.3 mg subQ because it might kill somebody, but if they’re in arrest, they get 1 mg q/5 min until they were either dead dead or ROSC.

      There have been studies looking at the dose of epinephrine, but we do not know what the right dose of epinephrine might be. Maybe 0.1 mg one time. Who knows.

      The most disappointing thing is that we know that epinephrine is essentially a heart attack in a syringe. That is why we only give low doses to people who are alive.

      We also know that heart attack is the most common cause for cardiac arrest, but the one thing we do for everyone still pulseless after the first defibrillation? Give them epinephrine.

      We would not give epinephrine to someone with VT (Ventricular Tachycardia) with a pulse, no matter low low the blood pressure, as long as we can feel a pulse. If someone else checks for a pulse on the same patient, but cannot find the pulse, that person is going to give epinephrine.

      The same patient, but two different people treating the same patient.

      One gives epinephrine, because that is what ACLS says to do.

      The other does not give epinephrine, because that is what ACLS says to do.

      There is no difference in the patient. The only difference is the sensitivity of the fingers palpating for a pulse.

      VT with a pulse – never give epinephrine.

      Pulseless VT – give epinephrine.

      It will be more interesting when the sodium nitroprusside studies begin on human cardiac arrest patients.

      EMCrit Podcast 69 – The Future of CPR with Keith Lurie and Demetris Yannopoulos
      by EMCRIT on March 19, 2012
      Page with links to the podcast and other sources of information

      .

      .

      • Ok, now you’ve got me intrigued. I know, shocking. Sodium Nitroprusside? I don’t believe I’ve actually come across that as of yet. Care to enlighten me?

        • Can’t say, clowns will eat me,

          Sodium nitroprusside enhanced cardiopulmonary resuscitation (SNPeCPR) improves vital organ perfusion pressures and carotid blood flow in a porcine model of cardiac arrest.
          Schultz J, Segal N, Kolbeck J, McKnite S, Caldwell E, Yannopoulos D.
          Resuscitation. 2012 Mar;83(3):374-7. Epub 2011 Aug 22.
          PMID: 21864483 [PubMed - in process]

          Sodium nitroprusside enhanced cardiopulmonary resuscitation improves survival with good neurological function in a porcine model of prolonged cardiac arrest.
          Yannopoulos D, Matsuura T, Schultz J, Rudser K, Halperin HR, Lurie KG.
          Crit Care Med. 2011 Jun;39(6):1269-74.
          PMID: 21358401 [PubMed - indexed for MEDLINE]

          Sodium nitroprusside-enhanced cardiopulmonary resuscitation improves resuscitation rates after prolonged untreated cardiac arrest in two porcine models.
          Schultz JC, Segal N, Caldwell E, Kolbeck J, McKnite S, Lebedoff N, Zviman M, Aufderheide TP, Yannopoulos D.
          Crit Care Med. 2011 Dec;39(12):2705-10.
          PMID: 21725236 [PubMed - indexed for MEDLINE]

          Sodium nitroprusside enhanced cardiopulmonary resuscitation prevents post-resuscitation left ventricular dysfunction and improves 24-hour survival and neurological function in a porcine model of prolonged untreated ventricular fibrillation.
          Schultz J, Segal N, Kolbeck J, Caldwell E, Thorsgard M, McKnite S, Aufderheide TP, Lurie KG, Yannopoulos D.
          Resuscitation. 2011 Dec;82 Suppl 2:S35-40.
          PMID: 22208176 [PubMed - in process]

          High dose nitroglycerin treatment in a patient with cardiac arrest: a case report.
          Guglin M, Postler G.
          J Med Case Reports. 2009 Aug 10;3:8782.
          PMID: 19830240 [PubMed]

          Also listen to the following free podcast from EMCrit –

          EMCrit Podcast 69 – The Future of CPR with Keith Lurie and Demetris Yannopoulos
          by EMCRIT on March 19, 2012
          Page with links to the podcast and other sources of information

          .

      • What’s the advantage of Sodium Nitroprusside vs. NTG?

        Also, has anyone done studies of how medications circulate during CPR? From my (admittedly simplistic) viewpoint, with automated CPR compressors (e.g. Autopulse), CT scanners, and some sort of contrast dye, we should be able to at least get animal studies of how much peripheral IV drugs move into the main circulation during CPR.

        • mpatk,

          What’s the advantage of Sodium Nitroprusside vs. NTG?

          I do not know.

          The way to find out is to do the research.

          When we assume that we know what the results of treatments will be, we stop asking the questions that help us to learn.

          the chance is high that the truth lies in the fashionable direction. But, on the off-chance that it is in another direction – a direction obvious from an unfashionable view of field theory – who will find it? Only someone who has sacrificed himself by teaching himself quantum electrodynamics from a peculiar and unusual point of view; one that he may have to invent for himself. I say sacrificed himself because he most likely will get nothing from it, because the truth may lie in another direction, perhaps even the fashionable one. - Richard Feynman. – Nobel Prize speech

          We have assumed that we know that because epinephrine improves some circulation that we believe to be important for resuscitation, and improves ROSC, that epinephrine is a good treatment for cardiac arrest. We even appear to assume that it is the best treatment and an essential treatment.

          We do not know what works, but when we stop becoming curious about what works, we limit our ability to learn.

          When we assume that we understand, we often misunderstand, or overestimate what we think we know.

          Nitrates appear to provide some of their benefit in large doses that result in reduced afterload. Afterload appears to be one of the problems produced by alpha agonists. There are many possibilities, but we have become stuck on pressors. A pressure of zero is not good, but that does not mean that a pressor is the best way to produce a lasting ROSC.

          Also, has anyone done studies of how medications circulate during CPR? From my (admittedly simplistic) viewpoint, with automated CPR compressors (e.g. Autopulse), CT scanners, and some sort of contrast dye, we should be able to at least get animal studies of how much peripheral IV drugs move into the main circulation during CPR.

          The problem with that approach is that we don’t know what the goal is.

          Ischemic preconditioning is showing a lot of promise in the resuscitation of swine to normal function. Will it work out in humans? We do not know, but we may learn a lot about what does work.

          Ischemic preconditioning violates a lot of what we should do to maximize circulation, so maybe the problem with epinephrine is that it is increasing too much, or maybe it is not increasing the right aspects of circulation, or maybe it is both, or maybe it is something else.

          .

          • Rogue,

            Re: nitroprusside vs NTG, I was wondering if you knew of any research (yes, I was trying to avoid wading through pages of google and PubMed searches :-) )

            What I read is that nitroprusside is better than NTG at arterial dilation (thus better at reducing afterload), not as good as NTG at venous dilation (but still significant), and has the potential for serious toxicity if used long-term (I’ve always been nervous about that because, in chemical names, prusside = cyanide).

            Also, has anyone done studies of how medications circulate during CPR? From my (admittedly simplistic) viewpoint, with automated CPR compressors (e.g. Autopulse), CT scanners, and some sort of contrast dye, we should be able to at least get animal studies of how much peripheral IV drugs move into the main circulation during CPR.

            The problem with that approach is that we don’t know what the goal is.

            Ischemic preconditioning is showing a lot of promise in the resuscitation of swine to normal function. Will it work out in humans? We do not know, but we may learn a lot about what does work.

            Actually, I wasn’t thinking that advanced. My thought was to determine how much of the drug (simulated by contrast dye or using a tagged medication) actually circulates during CPR vs. how much of the bolus just sits in the peripheral vein. If little to no medicine actually circulates during CPR, then that would have implications for ALL IV therapy during codes. It would probably be different depending on the cause of the arrest (VF/VT vs cardiogenic shock vs hypovolemic shock vs etc…); but I was wondering if anyone had done that first basic “how much medicine goes anywhere during CPR” study.

            Ischemic conditioning looks very interesting; and appears to hold a lot of promise for planned surgeries. The downside is that the conditioning only lasts for (at most) 72 hours; though one abstract I read showed some interesting results among methadone users.

            • mpatk,

              and has the potential for serious toxicity if used long-term (I’ve always been nervous about that because, in chemical names, prusside = cyanide).

              If cyanide the number of live patients walking out of the hospital with good brain function, is that a problem?

              Also, has anyone done studies of how medications circulate during CPR? From my (admittedly simplistic) viewpoint, with automated CPR compressors (e.g. Autopulse), CT scanners, and some sort of contrast dye, we should be able to at least get animal studies of how much peripheral IV drugs move into the main circulation during CPR.

              Go to the 2010 AHA Guidelines, Part 8.2: Management of Cardiac Arrest, scroll down to Peripheral IV Drug Delivery, and continue through the comedy section – Endotracheal Drug Delivery. That should answer a lot of your questions.

              The problem is not that we don’t know much about what we are doing. The problem is that we have found one way to restore a pulse, then assumed that all solutions must include this treatment.

              We are only treating a symptom, not improving outcomes, but claiming that we are curing the patient.

              Ischemic conditioning looks very interesting; and appears to hold a lot of promise for planned surgeries. The downside is that the conditioning only lasts for (at most) 72 hours; though one abstract I read showed some interesting results among methadone users.

              We still have a lot to learn about what we can do with this treatment. We should not look at it as anything other than one possible part of resuscitation.

              .

  2. EMS is part of a larger experiment we call “Medicine” with a Capital “M”.

    My biggest concern is what will articles and reviews like these do to the sales of Epi?

    For an added perspective, don’t miss this: http://emsoutsideagitator.com/2012/03/epid-to-death/

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