The only reason we get away with giving such large doses of epinephrine to these patients is that they are already dead.

- Rogue Medic

Potentially Reversible Causes of Cardiac Arrest and the Futility of CPR for Trauma Arrest – comment from DocXology

 

DocXology did not like my criticism of the futility of CPR in trauma -
 

I think you are setting up a straw man with your naloxone argument. There is not even biomedical plausibility for the scenario you describe.

 

What did I write?
 

While CPR in the pulseless trauma patient has overall been considered futile, several reversible causes of cardiac arrest in the context of trauma are correctible and their prompt treatment could be life-saving.[1]

This is a non sequitur.

Where is there any evidence that CPR in any pulseless trauma patients is not futile?[2]

 

Then I substituted naloxone for CPR in the argument in order to demonstrate that treatment of a potentially reversible cause has absolutely nothing to do with providing a futile treatment in the mean time.

It does not matter if the futile treatment is CPR in traumatic arrest, naloxone in cardiac arrest, or homeopathy for any medical condition. Providing a useless treatment is still useless.

Doing something useless, just for the purpose of looking like we are doing something, is not useful. This only distracts us from whatever might be useful.

One way of improving the fuel economy of a vehicle is to turn off the air conditioning and other items that make the engine work harder and burn more fuel. If the vehicle is out of fuel, then turning off the air conditioning is not going to matter. It is a futile response, just as CPR is a futile response to traumatic cardiac arrest.

The whole point of what I wrote is to demonstrate that the argument for CPR in trauma lacks biological plausibility.

Is that a straw man argument? My argument is not a straw man. Whether DocXology’s argument is a straw man, or just a misunderstanding, is not clear.
 

Image credit.
 

There is no RCT to say that oxygenation is good for cardiac arrest but there is a good physiological rationale for it. I presume you don’t withhold that?

 

That depends on the bias one uses in interpreting the evidence that is the basis for physiological hypotheses.
 

We started using oxygen for resuscitation because it seemed like a good idea. Now we use it because we always have.[3]

 

WHAT’S KNOWN ON THIS SUBJECT:
The superiority of room air over 100% oxygen for resuscitating asphyxiated term and near-term newborns has been demonstrated. However, results of studies of preterm infants have indicated that room-air resuscitation may not be appropriate for this population.

WHAT THIS STUDY ADDS:
Resuscitation of preterm infants starting with 100% oxygen followed by frequent titration was most effective at achieving a target oxygen saturation while avoiding hyperoxemia. Treatment-failure rates were highest for those resuscitated with room air despite rapid titration of oxygen.
[4]

 

As with most treatments based only on the contemporary understanding of physiology, the good physiological rationale for it is being demonstrated to be an overly optimistic interpretation of what we really know.

Oxygen is a drug that should be titrated to the effect that is best for the patient.

This does not mean that physiology is unimportant, but that treatments based on physiology must be demonstrated to work in real patients before being widely adopted.

What about adult resuscitation?
 

Overall, 56% of patients (n = 3561) met the primary outcome of in-hospital mortality (Table 4). Mortality was highest in the hyperoxia group (732/1156; 63% [95% CI, 60%-66%]) compared with the hypoxia group (2297/3999; 57% [95% CI, 56%-59%]) and the normoxia group (532/1171; 45% [95% CI 43%-48%]). The hyperoxia group had significantly higher in-hospital mortality compared with the normoxia group (proportion difference, 18% [95% CI, 14%-22%]; P < .001). Mortality also was significantly higher in the hyperoxia group compared with the hypoxia group (proportion difference, 6% [95% CI, 3%-9%]; P < .001). On Kaplan-Meier analysis, the survival fractions for the hyperoxia and normoxia groups diverged significantly over time (log-rank P < .001; Figure). In addition, among hospital survivors, patients with hyperoxia had a significantly lower proportion of discharges from the hospital as functionally independent compared with patients with normoxia (29% vs 38%, respectively; proportion difference, 9% [95% CI, 3%-15%]; P = .002; Table 4).[5]

 

Then there is the question of how much physiology really supports the use of supplemental oxygen at high flow rates, rather than just to maintain a normal oxygen saturation.
 

Numerous laboratory investigations have identified a paradox relative to oxygen delivery to the injured brain. Although it is intuitive that insufficient oxygen delivery can exacerbate cerebral anoxia, excessive oxygen delivery can also be harmful by exacerbating oxygen free radical formation and subsequent reperfusion injury.4,–,11 [6]

 

My protocols only require that oxygen saturation be maintained at 94% or above.

Supplemental oxygen is not required if the oxygen saturation is adequate.

You suggest that the physiological rationale is unambiguous on oxygen for resuscitation.

That is not true.
 

I appreciate the issue of withholding ECM (Excternal Cardiac Massage) for traumatic arrest. It was raised at ICEM 2012 by Prof Harris of HEMS and he quoted animal studies with the argument the heart in hypovolaemic PEA is maximally hyper-dynamic and further mechanical augmentation is unlikely to improve output. But again no RCTs or human studies to support this.

 

Routine treatments should not be based on the absence of evidence of harm, otherwise we could justify anything at all that has not been demonstrated to be harmful. That is not medicine.

Medicine has evidence of efficacy.

Where is the evidence of efficacy for CPR in traumatic cardiac arrest?

Where is the physiologic rationale for CPR in traumatic cardiac arrest?

Treatments without evidence of efficacy should be limited to controlled trials.

We need to stop using wishful thinking to justify abuse of patients.

 

There is presentation on resuscitation by Dr. Tim Harris available as a free mp3 download at Free Emergency Medicine Talks, but I did not notice any reference to CPR for traumatic cardiac arrest. There are several skips in the recording, but the skips do not appear to obscure information necessary to understand the points Dr. Harris is making. Did he have another presentation on resuscitation?

Tim Harris (UK): Endpoints of Resuscitation
Published: JULY 25, 2012
2012-06-29 D3T3 1100 Endpoints of Resuscitation

-

Footnotes:

-

[1] Part 12.8: Cardiac Arrest Associated With Trauma
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 12: Cardiac Arrest in Special Situations
Free Full Text from Circulation

-

[2] Potentially Reversible Causes of Cardiac Arrest and the Futility of CPR for Trauma Arrest
Mon, 14 Nov 2011
Rogue Medic
Article

-

[3] Oxygen and resuscitation: beyond the myth.
Lefkowitz W.
Pediatrics. 2002 Mar;109(3):517-9. No abstract available.
PMID: 11875151 [PubMed - indexed for MEDLINE]

-

[4] Room-air versus oxygen administration for resuscitation of preterm infants: the ROAR study.
Rabi Y, Singhal N, Nettel-Aguirre A.
Pediatrics. 2011 Aug;128(2):e374-81. doi: 10.1542/peds.2010-3130. Epub 2011 Jul 11. Erratum in: Pediatrics. 2011 Dec;128(6):1212.
PMID: 21746729 [PubMed - indexed for MEDLINE]

Free Full text from Pediatrics.

-

[5] Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality.
Kilgannon JH, Jones AE, Shapiro NI, Angelos MG, Milcarek B, Hunter K, Parrillo JE, Trzeciak S; Emergency Medicine Shock Research Network (EMShockNet) Investigators.
JAMA. 2010 Jun 2;303(21):2165-71. doi: 10.1001/jama.2010.707.
PMID: 20516417 [PubMed - indexed for MEDLINE]

Free Full Text from JAMA.

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[6] Relationship between supranormal oxygen tension and outcome after resuscitation from cardiac arrest.
Kilgannon JH, Jones AE, Parrillo JE, Dellinger RP, Milcarek B, Hunter K, Shapiro NI, Trzeciak S; Emergency Medicine Shock Research Network (EMShockNet) Investigators.
Circulation. 2011 Jun 14;123(23):2717-22. doi: 10.1161/CIRCULATIONAHA.110.001016. Epub 2011 May 23.
PMID: 21606393 [PubMed - indexed for MEDLINE]

Free Full Text from Circulation.

.

Comments

  1. Did I say give 100% oxygen? I believe Earth’s atmosphere contains 21% oxygen. When I breath it, I oxygenate. Or are you recommending ACLS also abandon EAR or BVM?

    ‘Medicine has evidence of efficacy’.

    Depends on how you define evidence. There are varying types and levels. Do you take a nihilist approach because there are no good quality RCTS for an intervention? Do you ignore lower levels of evidence? If everything we had to do in clinical medicine required Level 1 evidence, then there really wouldn’t be very much else to do. Intellectual rigour would have us twiddle our thumbs in many instances waiting for the evidence to arrive.

    • DocXology,

      Did I say give 100% oxygen? I believe Earth’s atmosphere contains 21% oxygen. When I breath it, I oxygenate. Or are you recommending ACLS also abandon EAR or BVM?

      What is EAR? I am not familiar with that acronym.

      Should we be using the BVM to ventilate during cardiac arrest?

      No.

      The exceptions being for cardiac arrest in children or of respiratory origin.

      -

      ‘Medicine has evidence of efficacy’.

      Depends on how you define evidence. There are varying types and levels. Do you take a nihilist approach because there are no good quality RCTS for an intervention? Do you ignore lower levels of evidence? If everything we had to do in clinical medicine required Level 1 evidence, then there really wouldn’t be very much else to do. Intellectual rigour would have us twiddle our thumbs in many instances waiting for the evidence to arrive.

      Not everything must be a randomized placebo controlled trial.

      however, if a randomized placebo controlled trial is practical, then there is no good reason to make anything a routine treatment based on anything less.

      We have been using epinephrine in cardiac arrest for decades with out any evidence of improved outcomes.

      Some people think ROSC (Return Of Spontaneous Circulation) is some kind of a good outcome.

      We can rationalize the bad outcomes by stating that we have to get a pulse to be able to resuscitate.

      If that were a valid excuse, we would still be using high-dose epinephrine in cardiac arrest.

      High-dose epinephrine is better than standard-dose epinephrine at producing ROSC, so if more ROSC means better outcomes, it makes no sense to remove high-dose epinephrine from ACLS.

      High-dose epinephrine is no longer recommended because it produces worse outcomes than standard-dose epinephrine.

      ROSC does not matter if the result is more people dying in the hospital and more brain damage among those who do manage to survive.

      Is standard-dose epinephrine any better than no epinephrine?

      There is no evidence of improvement in neurologically intact survival to discharge, or beyond discharge, with epinephrine. There is evidence of worse neurologically intact survival to discharge with epinephrine.

      There are hundreds of thousands of patients treated for cardiac arrest every year in the US alone. There is no good reason to treat them without first finding out what works.

      Twiddling our thumbs would have been better than treating patients without evidence.

      We are now having to go back and start from the beginning. Now that we have eliminated treatments and begun to focus on good compressions and rapid defibrillation, the resuscitation rates have risen dramatically.

      If we had just been using defibrillations and compressions, which have good evidence, and otherwise twiddling our thumbs how many more hundreds of thousands of patients would have been resuscitated.

      How many people have we killed with dangerous intervention, when what we should have been doing is compressions, defibrillation, and twiddling our thumbs while we considered potentially reversible causes?

      How many people have we killed by doing something, when we should have been twiddling our thumbs?

      .

  2. Rogue Medic,

    Did I ever argue that ROSC in itself was an argument to support an intervention?

    Did I ever argue that high dose adrenaline was beneficial?

    Did I argue that we have not harmed patient because of an incomplete understanding of pathophysiology or lack of empirical research?

    But as clinicians we are often placed in situations where the body of the medical knowledge is incomplete or individual clinical information is often inadequate. To add further complexity, data can appear contradictory or non-sensical.

    The lesson is true since I was a medical student, “there is no such thing as ‘always’ or ‘never’ in medicine” and it would probably be true whether of adrenaline or cardiac compressions in cardiac arrest.

    Whenever new data comes out that may produces new paradigms, my response is usually to consider how it reconciles with pre-existing knowledge and understanding and see how it modifies (not immediately abandon) my approach. It is certainly not a reason to justify my personal biases nor a moment to delight in its contrariness.

    The true skill of the measured and erudite clinician is to rationally negotiate this ever-expanding complexity yet also accept his mortality and limitations.

    As Osler has been want to say:

    “Medicine is a science of uncertainty and an art of probability.”

    • DocXology,

      Did I ever argue that ROSC in itself was an argument to support an intervention?

      Did I ever argue that high dose adrenaline was beneficial?

      Did I argue that we have not harmed patient because of an incomplete understanding of pathophysiology or lack of empirical research?

      You asked me about what kind of evidence I would accept and followed that with the statement that, Intellectual rigour would have us twiddle our thumbs in many instances waiting for the evidence to arrive.

      You do not provide any statement of what evidence you do consider valid, just suggestions that we should not require evidence for treatments.

      But as clinicians we are often placed in situations where the body of the medical knowledge is incomplete or individual clinical information is often inadequate. To add further complexity, data can appear contradictory or non-sensical.

      Too many studies are poorly designed, cannot add anything to our understanding, and may even confuse our understanding. The way to avoid this problem is to insist on IRBs actually understanding what is necessary to answer the question being asked.

      The lesson is true since I was a medical student, “there is no such thing as ‘always’ or ‘never’ in medicine” and it would probably be true whether of adrenaline or cardiac compressions in cardiac arrest.

      Where have I stated that epinephrine should never be used in cardiac arrest? I have only stated that the routine use of epinephrine is foolish, but we give epinephrine to everyone still being treated as cardiac arrest, unless they are resuscitated before we get to the epinephrine part of the algorithm.

      Heart attack? Give epi.

      Brady/asystole? Give epi.

      Tachy/PEA? Give epi.

      CHF arrest? Give epi.

      Always give epi regardless of the cause.

      This is ridiculous.

      Whenever new data comes out that may produces new paradigms, my response is usually to consider how it reconciles with pre-existing knowledge and understanding and see how it modifies (not immediately abandon) my approach. It is certainly not a reason to justify my personal biases nor a moment to delight in its contrariness.

      Of course, that depends on the quality of evidence that the previous “knowledge” was based on. For epinephrine in cardiac arrest, there is no evidence of benefit in anything that matters. There is only improvement in a surrogate endpoint.

      If you think that being in a coma for a while, running up a large bill for your family, but never waking up is good, then epinephrine makes sense.

      Epinephrine increases the number of patients who go to the hospital in a coma, run up huge bills, and die without ever waking up.

      Epinephrine does not increase the number of people leaving the hospital awake and alert, even though that is the endpoint that matters to real people.

      The true skill of the measured and erudite clinician is to rationally negotiate this ever-expanding complexity yet also accept his mortality and limitations.

      As Osler has been want to say:

      “Medicine is a science of uncertainty and an art of probability.”

      I agree with Osler. That is why I have that quote in my sidebar.

      The art of probability requires evidence on which to make probabilistic decisions.

      Uncertainty and probability are the foundations of science.

      Wishful thinking only works until there is evidence. Then the flaws become a problem.

      CPR for traumatic arrest is based on wishful thinking.

      .

      • You should take your own advice:

        “CPR for traumatic arrest is based on wishful thinking.”

        “Epinephrine does not increase the number of people leaving the hospital awake and alert, even though that is the endpoint that matters to real people.”

        Sounds like an always or never statement.

        • DocXology,

          You should take your own advice:

          “CPR for traumatic arrest is based on wishful thinking.”

          “Epinephrine does not increase the number of people leaving the hospital awake and alert, even though that is the endpoint that matters to real people.”

          Sounds like an always or never statement.

          I do not have any rule about never arguing with a troll.

          You provide good examples of the ways people use misleading statements, and even contradict themselves, just to win an argument.

          “CPR for traumatic arrest is based on wishful thinking.”

          Can you provide evidence that CPR improves outcomes from cardiac arrest?

          Apparently not. You have not provided any evidence.

          We should base our treatment on evidence, not the intellectually vacant wishful thinking that you are defending.

          My statement is not all or nothing. My statement is just a statement of fact. If you have evidence that CPR, stop holding back and share that evidence.

          Why are you criticizing facts?

          “Epinephrine does not increase the number of people leaving the hospital awake and alert, even though that is the endpoint that matters to real people.”

          Can you provide evidence that epinephrine increases the number of people leaving the hospital awake and alert?

          Apparently not. You have not provided any evidence.

          The research on epinephrine in cardiac arrest shows increased ROSC, but a decrease in survival to neurologically intact survival.

          We should base our treatment on evidence, not the intellectually vacant wishful thinking that you are defending.

          My statement is not all or nothing. My statement is just a statement of fact. If you have evidence that epinephrine increases the number of people leaving the hospital awake and alert, stop holding back and share that evidence.

          Why are you criticizing facts?

          Dealing with your logical fallacies is instructive to others who read the comments. This is one of the reasons I write about Creationists, antivaccinationists, alternative medicine pushers, and other denialists and conspiracy theorists.

          Thank you for providing these examples of logical fallacies.

          .

        • DocXology,

          “CPR for traumatic arrest is based on wishful thinking.”

          “Epinephrine does not increase the number of people leaving the hospital awake and alert, even though that is the endpoint that matters to real people.”

          Sounds like an always or never statement.

          They’re not absolute predictions, they’re observations based on studies; and they are factually correct statements based on those studies.

          Saying epinephrine does not increase the number of people surviving to discharge does NOT say that epinephrine is not useful; it merely states that routine use does not result in improved odds in all cardiac arrests. Epinephrine probably improves survival in some people, and hinders/prevents survival in others; the net result being no change or fewer patients surviving to discharge (depending on the study). Determining the effectiveness of epinephrine requires further studies and more detailed analysis of the data (e.g. efficacy vs. cause of arrest), not semantics games.

  3. Rogue, off topic, but I’ve followed your epi argument / cautions in arrest for a while now…

    A lot of it makes “sense”, and one can’t argue against trials / data demonstrating (overall) worse outcomes with epinephrine, ROSC not necessarily being an endpoint in itself, and no evidence for anything better than good BLS / shocking what’s shockable…

    But the real world doesn’t necessarily work the way macro data does, and I’d caution against cause / effect correlation that sometimes just don’t make sense in spite of the “evidence”…

    Anecdotal, but reality : dial back to 3 days ago.

    Secondary hospital, no cath lab or Cardiology capability, no balloon pump assist etc, general Internist = the man.

    Called to OR for code.

    In her 50s, remote ex smoker, hypertension well controlled, no known IHD, routine hysteroscopy. well. Induction with propofol via anaesthetist, LMA in situ, dropped her BP to systolic 60, and coded on the table : brief V tach and into V fib.

    On my arrival : CPR in progress, defib arrived from recovery room, defibrillated, 2 min CPR, pulse present, sinus rhythm, BP 70 systolic, fluid bolus going.

    Stat EKG : massive anteroseptal STEMI – likely silent underlying IHD, and BP drop with induction likely precipitated the STEMI.

    Stat TNKase, 30 mg IV Lovenox, balance SC Lovenox, can’t load ASA or Plavix yet.

    BP tanking again, likely cardiogenic shock, into PEA.

    CPR, epi 1 mg IV, 2 min later perfusing again.

    Repeat EKG reperfusing (STs dropping), reperfusion a fib, BP systolic 70s. Start Levophed infusion. BP tanking again, into PEA again.

    Again epi 1mg IVI, 2 min CPR, reperfusing. BP 60s, cranking up the Levophed. Amiodarone infusion started.

    Repeat EKG STEMI again, STs sky high again, BP tanking again, going into florid pulmonary edema (by now intubated, florid pink froth evident).

    Desperation, need to reperfuse : another 1/2 dose of TNKase off label. PEA again…., CPR again, epi again, reperfusing… BPs still in 70s, adding in Dopamine infusion, cranking it up, right IJ line, art line, etc etc. Repeat EKG no reperfusion.

    This repeated a total of 6 times over 90 minutes in OR.

    No pulses / perfusion, nil BP recordable via art lines, dive in capnography, pukka PEAs. Nil shockable.

    Total Epi 1mg boluses X 5, Vasopressin 40 IU x 1. SAO2 throughout all of this in 70-80s range. Loaded with ASA and Plavix via NG tube. Rock and a hard place, gentle Nitro infusion for the pulmonary edema.

    Eventually admitted into ICU with Dobutamine / Dopamine / Levophed / Amiodarone infusions, vented, acidotic, anuric, BPs in 80 systolic range.

    Dial forward to this morning. Extubated, weaned off all inotropes, peeing admirably. Satting 100 % on room air. 100 % honest dinkum neurologically intact (no therapeutic hypothermia)

    Do I think we would have got her through without those bolus epi doses ?

    No.

    • Thanks Canuck,

      In pure logic, you only need one counter example to defeat the premise. But I don’t want to get into a anecdote war with anyone of which approach is ‘right’. In your case, there was a clear temporal relationship between the adrenaline and ROSC. It was hardly a coincidence.

      The important practical question is what was particular about your case that meant that adrenaline was helping more than it was harming – and how we can usefully extrapolate it to other similar arrest situations. Similarly, are their predictive features in the arrest setting which would more likely benefit from adrenaline. Other interesting questions to explore might include dosing alterations in different scenarious. In your situation, it was clearly pump failure that was problematic and although a pulse was not palpable some degree of contractility was still present. One could argue for perhaps a lower or titrated dose to produce a similar effect (and minimise the deleterious effect of ischaemia or arrhythmia).

      • DocXology,

        In pure logic, you only need one counter example to defeat the premise.

        If the claim was the classic all swans are white, then you would be correct. Only one example of a non-white swan would be needed to show that not all swans are white.

        However, I have not stated that no patients improve with epinephrine. Your suggestion is just another example of you using logical fallacies to try to make a point.

        Using your logical fallacy, that you only need one counter example to defeat the premise, only one example of a patient not resuscitated after epinephrine would be proof that epinephrine does not work.

        This is absurd, but this is what I have come to expect from you.

        You make vague statements disparaging evidence, then you complain that the examples I use are not treatments you disapprove of. Whether you disapprove of the examples is irrelevant, but you appear to be just throwing more logical fallacies out there and hoping that nobody notices what you are doing.

        But I don’t want to get into a anecdote war with anyone of which approach is ‘right’. In your case, there was a clear temporal relationship between the adrenaline and ROSC. It was hardly a coincidence.

        Anecdotes are coincidences until demonstrated to be otherwise.

        Again, I have criticized the routine and indiscriminate use of epinephrine in cardiac arrest, not all use of epinephrine in cardiac arrest.

        I have stated that we need to study epinephrine to find out which patients (if any) benefit from epinephrine, not base our treatment on wishful thinking.

        The important practical question is what was particular about your case that meant that adrenaline was helping more than it was harming – and how we can usefully extrapolate it to other similar arrest situations.

        Was the epinephrine helping?

        Was something else helping?

        Was the epinephrine harming more than it was helping?

        An anecdote does not answer those questions.

        An anecdote can provide hypotheses for actual research, but an anecdote is not proof of anything.

        We already know that some patients have paradoxical responses to treatments.

        Similarly, are their predictive features in the arrest setting which would more likely benefit from adrenaline. Other interesting questions to explore might include dosing alterations in different scenarious. In your situation, it was clearly pump failure that was problematic and although a pulse was not palpable some degree of contractility was still present. One could argue for perhaps a lower or titrated dose to produce a similar effect (and minimise the deleterious effect of ischaemia or arrhythmia).

        That is exactly why we need well done placebo controlled randomized studies of epinephrine in cardiac arrest.

        These are the kinds of questions a well done study can look at.

        Thank you for reinforcing the need for research on epinephrine in cardiac arrest.

        .

      • DocXology,

        In your case, there was a clear temporal relationship between the adrenaline and ROSC. It was hardly a coincidence.

        Correlation is not causation. Given all the different medications that were being thrown into that woman in a short period of time, it is either incredibly ignorant or unconscionably arrogant to claim to know that the epinephrine made the difference. Why claim it was the epi, and not the TNKase, or the NTG, or the amiodarone? Hell, that code ran for 90+ minutes; it might as well have been Divine Intervention for all we know.

        Physiologic rationales are a great STARTING POINT for medicine; but should never be taken as evidence themselves. Studies must be done to support, disprove, or modify the theories we base the treatments on. Remember, all the physiologic rationales are based on theories; and theories must be proved with evidence and data.

        The plural of anecdote is not data.

        We can use anecdotes in the absence of data; but we should be honest in that treating patients based only on our theories and rationales is experimental treatment, not proven treatment. Using the rationales as a reason to refuse to conduct studies is neither science or medicine; it’s unbridled ego.

        • Rogue Medic wrote:

          ‘ Why claim it was the epi, and not the TNKase, or the NTG, or the amiodarone?’

          You really ought to read Canuck’s account….

          “BP tanking > CPR > epi > 2min later reperfusing

          PEA again > epi > CPR > reperfusing

          This is repeated a total of 6x over 90 min.”

          I didn’t hear TNK, NTG and amiodarone repeated 6x each time the patient went into PEA.

          • DocXology,

            Umm, I’m not Rogue Medic.

            Also, does something have to be repeated multiple times in order to be “the one thing that worked”?

            Are you aware that pharmacokinetics differ between different types of drugs? Half lives, etc… are different for amiodarone and NTG than they are for epi? Remember, we’re not talking about ROSC, but SURVIVAL.

            Finally, I can’t believe you’d actually post such a pathetically edited version of Canuck’s code when the original is right above it for comparison. Your version bears no resemblance to what he actually described; at least be honest enough to put in some ellipsis (you know, the “…”) where you hack away large chunks of information.

            • Because amiodarone and NTG kinetics cause levels to peak each time after the patient goes into PEA?

              • Read Canuck’s actual post, not your bastardized revision of it.

                If the epinephrine was what saved the patient, why did she keep going into PEA repeatedly? At best, the epinephrine only did what CPR does: help keep blood flowing until the other meds fixed the problem. At worst, the epinephrine might have caused the code to go longer, and if the other meds had been given with just compressions the patient might have been resuscitated sooner. With that quantity of that many different medications in her system, there’s no way to know.

                ROSC =/= survival. All the epinephrine did was give ROSC.

                • mptak says:

                  ” All the epinephrine did was give ROSC.”

                  But you could apply that argument to most of critical care. Dialysis, ECMO, intoropes and ventilation don’t actually reverse the organ failures.

                  You are supporting physiology until either some other treatment works or the body heals itself. This doesn’t diminish their importance in improving survival.

    • Canuck ER MD,

      As you stated, this is anecdotal. This is not typical.

      Would earlier nitro have improved things before a bunch of catecholamines had been given?

      Maybe. Maybe not.

      We have this bizarre idea that we cannot give nitro to hypotensive patients, but there is evidence that this is just a myth.

      Low dose catecholamines might be safer with nitro, but we tend not to give this combination to patients.

      Reperfusion arrhythmias are a big problem, but the best treatment for them may be benign neglect. Just because we see something, does not mean we need to treat it.

      Without evidence, this is an interesting anecdote that we can endlessly speculate about.

      Did giving every catecholamine in the box to a patient with a massive anteroseptal STEMI improve things?

      Maybe. Maybe not.

      Is there evidence that this is a good way to routinely treat massive anteroseptal STEMI?

      No.

      Congratulations on the great outcome.

      .

      • “Would earlier nitro have improved things before a bunch of catecholamines had been given ?”

        The inherent problem here was not the pulmonary edema per se : it was pulmonary edema as a result of a STEMI, pump failure and cardiogenic shock. Earlier Nitro would have done nada for the recurrent PEA due to the heart muscle problem…

        “We have this bizarre idea that we cannot give nitro to hypotensive patients, but there is evidence that this is just a myth”.

        Fully agreed. Had to override the Internist on this one, he wanted Lasix.

        “Reperfusion arrhythmias are a big problem, but the best treatment for them may be benign neglect.”

        Agreed – the Amiodarone was not necessary.

        “Did giving every catecholamine in the box to a patient with a massive anteroseptal STEMI improve things? Maybe. Maybe not. Is there evidence that this is a good way to routinely treat massive anteroseptal STEMI ? No.”

        Nope : we’re not on the same page.

        We treated the STEMI with TNKase, Lovenox IV and SC, and an ASA / Plavix load once the NG was in.

        The catecholamines were required to deal with the consequences of the STEMI : refractory cardiogenic shock and recurrent PEAs (no emergent PCI / balloon assist device etc available).

        A potential problem is that trials (with their inclusions / exclusions / tertiary settings including advanced technology) seldom capture these anecdotal cases.

        The cases may be anecdotal, but we can’t wish them away : they exist.

        And it worked.

        None of this means that I disagree with your take on Epinephrine.

        But with the caveat (as pointed out by yourself) that judgement needs to be exercised.

        I have no doubt that superb CPR contributed to the neurological outcome.

        But I also have no doubt that there would not have been an outcome to present without the large doses of temporising Epinephrine etc until the pump started working again – you can only do CPR for X amount of time without balloon assist devices being available…

      • Rogue Medic said:

        “As you stated, this is anecdotal. This is not typical. Would earlier nitro have improved things before a bunch of catecholamines had been given? Maybe. Maybe not.”

        So what is your evidence-based management of this critical scenario. Or not enough evidence to actually do anything at all?

        “We have this bizarre idea that we cannot give nitro to hypotensive patients, but there is evidence that this is just a myth.”

        Nothing new here. Inotrope and vasodilator is well accepted treatment for cardiogenic shock. Intensivists have been doing it for years. Anyway who are ‘we’ that have ‘bizarre ideas’. Is this is a syndrome who don’t agree with everything you say?

        “Did giving every catecholamine in the box to a patient with a massive anteroseptal STEMI improve things?”

        Giving a box of catecholamines is not going to do anyone any good. But appropriately titrating the dose to haemodynamic and perfusion parameters can be useful in the right situation.

    • With regards to Canuck ED MD (and with congratulations on the save), mistaking causation and correlation is much more likely in an anecdote than in a controlled study. In other words, with an anecdote like the one above, it is more likely than we just don’t understand all the interactions going on during the code, rather than that epi worked in that code when it appeared harmful in controlled studies. Yes, a small percentage of people will have different (even paradoxical) reactions to medications; but do we want to base treatment on what works for most people, or just hope our patient is one of the “lucky ones” who reacts favorably to epi in cardiac arrest?

      The biggest mistake in ACLS is not placing enough emphasis on reversible causes. We wouldn’t use Calcium Chloride or Potassium Bicarbonate on every cardiac arrest; but there are many anecdotes where both meds clearly were the difference in reviving the patient. Similarly, epi will work for SOME cases, but the studies show that those cases are the minority, not the majority. The only treatment that works for all cardiac arrest is CPR; and that isn’t even so much a treatment as artificially circulating the blood while treatments to reverse the cause are considered.

  4. mptak said:

    “In other words, with an anecdote like the one above, it is more likely than we just don’t understand all the interactions going on during the code”

    And that’s why it is is impossible to say if adrenaline is bad or if adrenaline is good. There are lots of variables at play in any clinical scenario. In my practise I treat individuals not study groups.

    If a trainee asks me if lytics are good or bad for MI, I will answer it depends. Is there ST elevation? How long has the pain been there? Are they in cardiogenic shock? Did they have prolonged CPR? Are they on warfarin? Did they just have a endoscopic banding of an oesophageal varicose?

    • Yes, it is impossible to know if epinephrine is good or bad BASED ON ANECDOTES.

      The point is that studies must be done before we decide on whether epinephrine is good or bad. Some studies HAVE been done, and show that epinephrine has a negative effect on cardiac arrest patients: more ROSC, fewer survivals to discharge.

      Now, what needs to be done is to go back and review the studies, and have some more studies, to determine when epinephrine works, and when it is harmful. Unfortunately, the Powers That Be refuse to allow those studies, and we have the result that epinephrine is used in all cardiac arrests per ACLS protocols.

      Guesswork is unfortunately necessary in medicine; but claiming that it should be the normal method (aka “medicine is an art, not a science” and “but some anecdotes show…”) is anti-science, irresponsible and inhumane.

      Canuck admits this is a rare case; why do you insist on twisting this single anecdote out of shape in order to “win” an argument with Rogue?

      • I wasn’t aware that there exists ‘Powers that Be’ that decide how I manage an arrest. I guess it must be the same powers that ignore the PACA and JAMA journals.

        But what is interesting about reading those articles is that their overall survival rates are quite low for the modern era < 5% (contrast that with the usual figure of 10-12%) and contained a disproportionately high number of patients in the asystolic or non-shockable group.

        What it tells me is that if you any intervention used to resuscitate a dead/dying heart is not likely to benefit. Unfortunately, the PACA analysis for the VF group was underpowered to show a difference (odds ratio 2 but wide confidence limits).

        • With regards to the Powers That Be, I was talking about stuff like this from Resuscitation. 2011 Sep;82(9):1138-43. Epub 2011 Jul 2.:

          While this was a double blind randomised placebo-controlled trial there were a number of limitations. Firstly we were unable to achieve full patient recruitment as planned. 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 331 concerns.
          Despite the clearly demonstrated existence of clinical equipoise for adrenaline in cardiac arrest it remained impossible to change the decision not to participate. As a single centre study with approximately 500 out of hospital cardiac arrests in which resuscitation is commenced per year, it would not have been possible to reach the required sample size. In addition it was not possible to continue as the study drugs reached their expiry date and no additional funding was available. The failure to achieve an adequate sample size left the trial underpowered to detect significant effects on survival to hospital discharge.

          I never claimed the studies were perfect. As I said, more studies are needed (but blocked by politicians, “ethics boards”, etc… as in the study I mention). One thing that is clearly shown by the JAMA study at least is that there is a significant disconnect between ROSC and survival to discharge; enough of one that ROSC should not be considered a valid surrogate endpoint for these studies.

          • There is a also disconnect between ROSC and survival with placebo. This is why we talk about a chain of survival.

            If you look at the PACA study sub-group analysis, this is most pronounced in the non-shockable group. One could imagine asystole and PEA most likely represent a catastrophic event affecting cardiac electrical or mechanical activity.

            However, things look a lot brighter for the shockable group where you almost double survival to discharge but the study was under-powered to demonstrate benefit (wide confidence limits).

  5. mptak said:

    “In other words, with an anecdote like the one above, it is more likely than we just don’t understand all the interactions going on during the code”

    And that’s why it is is impossible to say if adrenaline is bad or if adrenaline is good. There are lots of variables at play in any clinical scenario. In my practise I treat individuals not study groups.

    If a trainee asks me if lytics are good or bad for MI, I will answer it depends. Is there ST elevation? How long has the pain been there? Are they in cardiogenic shock? Did they have prolonged CPR? Are they on warfarin? Did they just have a endoscopic banding of an oesophageal varices?

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