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

- Rogue Medic

Safety and Effectiveness of Field Nitroglycerin in Patients with Suspected ST Elevation Myocardial Infarction

 

Is prehospital use of NTG (NiTroGlycerin; GTN GlycerylTriNitrate in Commonwealth countries) safe for treating prehospital suspected STEMI (ST segment Elevation Myocardial Infarction) patients?

The evidence is limited, but does not suggest that prehospital NTG produces enough harm to discourage use in suspected STEMI. These researchers looked at the emergency department assessments of patients following prehospital NTG for suspected STEMI.  

Despite the theoretical risk, the limited retrospective studies of NTG in the prehospital setting for multiple indications suggest that the medication is safe.(10-13) However, with regard to NTG use for STEMI, the AHA International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care concluded that there was not enough evidence to determine the benefit or harm of out-of-hospital use of NTG.(14) Given the high false positive rates for STEMI identified in the field, an additional concern is that many patients treated with NTG for presumed STEMI will ultimately have an alternate etiology for their pain.(15, 16) Therefore, it is not clear that the benefits outweigh the risks of administering NTG to all patients with suspected STEMI in the field.[1]
 

This paper helps to show the safety of prehospital NTG for suspected STEMI, providing evidence that blood pressure changes were similar in suspected STEMI patients with an SBP (Systolic Blood Pressure) of 100, or higher, regardless of whether they were treated with NTG. The study is a retrospective chart review, so we do not know why some of the patients were not treated with NTG.

One reason mentioned, but not discussed, is that only 22% (96 of 440) suspected STEMI patients not treated with NTG are documented to have had pain, but there is no information on the type of pain or other cardiac symptoms of the patients. Were the paramedics avoiding treating atypical chest pain, such as pressure, heaviness, gastric discomfort, difficulty breathing, et cetera? We do not know. Was only chest pain being documented, rather than shoulder, or arm, or jaw, pain? We do not know. Did the pain resolve prior to EMS arrival? We do not know. Were the paramedics correctly recognizing when the machine interpretation of the ECGs (ElectroCardioGrams) were wrong? We do not know.

The median Initial Pain Score is documented as 8, with an IQR (Inter-Quartile Range) of 5-9 for those treated with NTG. For those not treated with NTG the Initial Pain Score is documented as 0, with an IQR of 0-0. We do not know the Initial Pain Score of those who did have pain, but were not treated with NTG. All of these patients were in an IQR that was not documented in the paper. The good news is that the suspected STEMI patients not treated with NTG act as a control group, although possibly with important differences that are not discussed in the paper.

Click on the image of the LA County protocol to make it larger.[2]

What about the 17% of suspected STEMI patients with SPB <100 mmHg who were treated with NTG?

Was medical command (California has certified MICNs [Mobile Intensive Care Nurses] providing medical command on the radio, with physicians available, as well) contacted for authorization to deviate from the protocol? If so, that is something that should be documented in the charts, which were reviewed for this paper. That information is not included in this paper. Those patients are much more interesting to me.

I do not object to using NTG to treat suspected STEMI with an SBP below 100 mmHg, but the authors seem to think that EMS should not even consider it. Do the outcomes of those patients support the approach of the authors? We do not know.

I suspect that the fears of bottoming out the blood pressure are very exaggerated, but it would be nice to have some evidence either way.

An important secondary end point was the differences between those with inferior/right ventricular STEMI, but treated with NTG.  

By vasodilating all blood vessels, and the venous system in particular, it causes a drop in blood pressure and preload. Thus, there is concern for precipitating hypotension in ACS involving the right ventricle.(1-3) Contraindications to the use of NTG, as outlined by the American Heart Association (AHA) Guidelines on the treatment of ACS, include right ventricular infarction.(4) This raises concern for use in inferior ST-segment elevation myocardial infarction (STEMI) in the prehospital setting, since many inferior STEMI result from proximal right coronary artery (RCA) occlusion and 50% involve the right ventricle.(3) Traditional 12-lead ECG is focused mainly on the left side of the heart and typically EMS protocols do not include acquisition of right-sided ECG leads. Further, in many systems, Basic Life Support (BLS) protocols allow for administration of NTG without differentiating the location of STEMI. There is also risk of other adverse events including bradycardia and cardiac arrest.(5-9)[1]
 

I have aggressively promoted the use of NTG for even hypotensive CHF/ADHF (Congestive Heart Failure/Acute Decompensated Heart Failure). Many physicians are not comfortable with that, even though the available evidence shows that aggressive IV NTG doubled the survival rate for these hypotensive patients. More research is needed on the use of NTG, especially in hypotensive patients.  

Further, we did not find an increased risk of hypotension among patients with proximal or mid RCA occlusions confirmed on coronary angiography. There are several possible reasons for our findings. First, while right ventricular involvement in inferior STEMI is common, hemodynamic instability is actually rare due to the right ventricle’s more favorable oxygen supply-demand ratio compared to the left heart and more extensive collateral flow.(3, 22) In addition, left heart occlusions may also involve the right ventricle and result in a preload dependent condition.(23-25) While limited by sample size, our results suggests that specifically avoiding NTG use in inferior STEMI, which is common in EMS systems, may be misguided. One quarter of the local EMS agencies in the state of California, for example, currently prohibit the use of NTG in inferior STEMI.(26) This analysis would benefit from additional study with a larger sample size and specific information about the infarct territory. Further studies are needed to determine which patients, in particular, are at increased risk for hypotension when treated with NTG.[1]
 

Perhaps NTG is also safe for treating patients with inferior ischemia and even right ventricular ischemia.

Footnotes:

[1] Safety and Effectiveness of Field Nitroglycerin in Patients with Suspected ST Elevation Myocardial Infarction.

Bosson N, Isakson B, Morgan JA, Kaji AH, Uner A, Hurley K, Henry TD, Niemann JT.

Prehosp Emerg Care. 2018 Dec 17:1-9. doi: 10.1080/10903127.2018.1558318. [Epub ahead of print]

PMID: 30556765

[2] Treatment Protocol: Chest Pain */ Acute MI

Reference No. 1244

LA County Paramedic Protocols

Los Angeles County Department of Health Services – Emergency Medical Services

Protocol

.

Association of ventilation with outcomes from out-of-hospital cardiac arrest

 

Does this study compare chest compressions with pauses for ventilation (regular CPR [CardioPulmonary Resuscitation]) against continuous chest compressions with no ventilations (compression-only CPR)?

Absolutely not.

This only compares compressions with pauses for good ventialtions against compressions with pauses for bad ventilations.

Will this be used to justify including ventilations in CPR, in spite of the absence of any valid evidence that ventilations improve outcomes?

Yes. It already has in the editorial about the study, published in the same issue.[1]

The authors of the paper were clear about the actual comparison in the discussion.
 

Why did so few patients in our study receive ventilation during CPR? Ventilation with a BVM device is a difficult skill to perform properly and must be practiced to maintain proficiency.22 The person performing ventilation must extend the neck, or place an oral airway, and/or perform a jaw thrust maneuver in order to maintain an open airway, a tight mask seal on the face must be maintained to prevent air from leaking around the mask, and the rescuer must then simultaneously squeeze the manual ventilator over 1 to 1.5 s. Our study showed no significant difference in the number of pauses between Group 1 and Group 2 patients (11 vs. 12 pauses). However, Group 2 patients received significantly more ventilations than Group 1 patients (8 vs. 3 ventilations). The study suggests that the rescuers in both Groups attempted ventilation about the same number of times per patient, but these attempts frequently did not result in lung inflation in Group 1 patients.[2]

 

In other words, this is a study of 30 compressions with a pause for 2 adequate ventilations to 30 compressions with a pause for 2 inadequate ventilations. This is important to know, but it has nothing to do with compression-only resuscitation.
 


 

Were the ventilations in the bad ventilation group going into the stomach? There are not a lot of possibilities, but not much of the ventilations were not going into the lungs or the ventilations were very shallow.

The authors do not mention if there is any difference in the rate of vomiting, aspiration, or other side effects expected from bad ventilation, between the groups.

The authors appear to be measuring the quality of ventilation, which is has never been shown to improve outcomes over compression-only resuscitation.

There is research showing that ventilations do not improve outcomes:
 

Cardiocerebral resuscitation improves survival of patients with out-of-hospital cardiac arrest.
Kellum MJ, Kennedy KW, Ewy GA.
Am J Med. 2006 Apr;119(4):335-40.
PMID: 16564776 [PubMed – indexed for MEDLINE]

Cardiocerebral resuscitation improves neurologically intact survival of patients with out-of-hospital cardiac arrest.
Kellum MJ, Kennedy KW, Barney R, Keilhauer FA, Bellino M, Zuercher M, Ewy GA.
Ann Emerg Med. 2008 Sep;52(3):244-52. Epub 2008 Mar 28.
PMID: 18374452 [PubMed – indexed for MEDLINE]

Minimally interrupted cardiac resuscitation by emergency medical services for out-of-hospital cardiac arrest.
Bobrow BJ, Clark LL, Ewy GA, Chikani V, Sanders AB, Berg RA, Richman PB, Kern KB.
JAMA. 2008 Mar 12;299(10):1158-65.
PMID: 18334691 [PubMed – indexed for MEDLINE]

Free Full Text at JAMA

Passive oxygen insufflation is superior to bag-valve-mask ventilation for witnessed ventricular fibrillation out-of-hospital cardiac arrest.
Bobrow BJ, Ewy GA, Clark L, Chikani V, Berg RA, Sanders AB, Vadeboncoeur TF, Hilwig RW, Kern KB.
Ann Emerg Med. 2009 Nov;54(5):656-662.e1. Epub 2009 Aug 6.
PMID: 19660833 [PubMed – indexed for MEDLINE]

And more.

 

 

Footnotes:

[1] Ventilation during cardiopulmonary resuscitation-Only mostly dead!
Mosesso VN Jr.
Resuscitation. 2019 Aug;141:200-201. doi: 10.1016/j.resuscitation.2019.06.274. Epub 2019 Jun 22. No abstract available.
PMID: 31238035

 

[2] Association of ventilation with outcomes from out-of-hospital cardiac arrest.
Chang MP, Lu Y, Leroux B, Aramendi Ecenarro E, Owens P, Wang HE, Idris AH.
Resuscitation. 2019 Aug;141:174-181. doi: 10.1016/j.resuscitation.2019.05.006. Epub 2019 May 18.
PMID: 31112744

.

How Effective Is Epinephrine for Improving Survival Among Patients in Cardiac Arrest?

   

There have been two studies comparing epinephrine with placebo to treat out of hospital cardiac arrest. The Jacobs study was stopped early, because of interference by those who do not want to know if their medicine actually works.[1] The purpose of research is to determine, as objectively as possible, if a treatment is better than placebo nothing.  

Click on the image to make it larger.  

Even the small sample size shows a impressive p values of <0.001 for both ROSC (Return Of Spontaneous Circulation) and being admitted to the hospital. Unfortunately, that does not lead to outcomes that are better than placebo.

The Perkins study (PARAMEDIC2) did not find a significant difference between adrenaline (epinephrine in non-Commonwealth countries) and placebo.[2] The Jacobs study also did not find a difference, but the numbers were small, due to the interference by the less than knowledgeable. Following the Jacobs study, some intervention proponents have suggested that the problem is not a lack of evidence of benefit, but need to look at the evidence from the right perspective. The inadequate evidence is not “inadequate”, but really just misunderstood. All we need to do is use a method of analysis that compensates for the tiny sample size. A Bayesian approach will produce the positive outcome that is not justified by so few patients.[3]

What happens when the numbers are combined, so that the sample size is large enough to eliminate the need for statistical chicanery to come up with something positive?

The outcomes do not improve.  

Neither standard dose adrenaline, high-dose adrenaline,vasopressin nor a combination of adrenaline and vasopressin improved survival with a favourable neurological outcome.[4]
 

If the Bayesian approach were appropriate, then the much larger sample size would have provided more than enough patients to confirm the optimism of the epinephrine advocates. The result is still not statistically significant. Maybe a much, much larger study will show a statistically significant, but tiny, improvement in outcomes with epinephrine, but don’t hold your breath for that. It took half a century to produce the first study, then seven more years for the second. With the cost of research and the problems coordinating such a large study, it is more likely that the guidelines will continue to recommend spending a lot of time and money giving a drug that diverts attention from the interventions that do improve outcomes.

There is still no evidence that adrenaline provides better outcomes than placebo in human cardiac arrest patients.

  –  

Footnotes:

  –  

[1] Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial Jacobs IG, Finn JC, Jelinek GA, Oxer HF, Thompson PL. Resuscitation. 2011 Sep;82(9):1138-43. doi: 10.1016/j.resuscitation.2011.06.029. Epub 2011 Jul 2. PMID: 21745533

Free Full Text PDF Download from semanticscholar.org  

This study was designed as a multicentre trial involving five ambulance services in Australia and New Zealand and was accordingly powered to detect clinically important treatment effects. Despite having obtained approvals for the study from Institutional Ethics Committees, Crown Law and Guardianship Boards, the concerns of being involved in a trial in which the unproven “standard of care” was being withheld prevented four of the five ambulance services from participating.

In addition adverse press reports questioning the ethics of conducting this trial, which subsequently led to the involvement of politicians, further heightened these concerns. Despite the clearly demonstrated existence of clinical equipoise for adrenaline in cardiac arrest it remained impossible to change the decision not to participate.

  –  

[2] A Randomized Trial of Epinephrine in Out-of-Hospital Cardiac Arrest. Perkins GD, Ji C, Deakin CD, Quinn T, Nolan JP, Scomparin C, Regan S, Long J, Slowther A, Pocock H, Black JJM, Moore F, Fothergill RT, Rees N, O’Shea L, Docherty M, Gunson I, Han K, Charlton K, Finn J, Petrou S, Stallard N, Gates S, Lall R; PARAMEDIC2 Collaborators. N Engl J Med. 2018 Aug 23;379(8):711-721. doi: 10.1056/NEJMoa1806842. Epub 2018 Jul 18. PMID: 30021076

Free Full Text from N Engl J Med.

  –  

[3] Regarding “Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial”. Youngquist ST, Niemann JT. Resuscitation. 2012 Apr;83(4):e105; author reply e107. doi: 10.1016/j.resuscitation.2011.09.035. Epub 2012 Jan 18. No abstract available. PMID: 22266068

Free Full Text from Resuscitation.

  –  

[4] Adrenaline and vasopressin for cardiac arrest. Finn J, Jacobs I, Williams TA, Gates S, Perkins GD. Cochrane Database Syst Rev. 2019 Jan 17;1:CD003179. doi: 10.1002/14651858.CD003179.pub2. PMID: 30653257    

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Closed chest compressions reduce survival in an animal model of haemorrhage-induced traumatic cardiac arrest

   

This is an animal study, rather than a human study, but it has fewer disadvantages than the usual animal studies of medical cardiac arrest. Animals do not develop the comorbidities that humans do, but have artificially created heart attacks, rather than by the development of actual heart disease. In studying trauma, this is less of a problem, since trauma is artificially created. This study is much more representative of penetrating injuries with a low velocity objects, than blunt force trauma, or penetrating injury with a high velocity object.

Are we really killing trauma patients with our chest compressions?

Maybe. This is one small study (39 pigs), but it does raise questions about the ways we can minimize the harm we cause.

 

 
CCC were associated with increased mortality and compromised haemodynamics compared to intravenous fluid resuscitation. Whole blood resuscitation was better than saline.[1]

 
A soft tissue injury was created, with 3 shots to the right thigh using a captive bolt (Cash Special, Accles and Shelvoke, Sutton Coldfield, UK). Two minutes later animals underwent a controlled haemorrhage (30% blood volume) at an exponentially reducing rate as previously described12 until the mean arterial blood pressure (MAP) was 45 mmHg. Blood was collected into CPD (citrate phosphate dextrose) and stored at room temperature until required for later transfusion.[1]
 

Image source

 

This study, conducted in an animal model of haemorrhage-induced traumatic cardiac arrest, has demonstrated that chest compressions confer no benefit over fluid resuscitation alone, and blood should be the fluid therapy of choice.[1]

  That seems to be concluding too much, since this is just one study, but it does reinforce the results of other, similar studies. We should study the outcomes in humans, since there does appear to be equipoise. There never was a physiological justification for chest compressions in traumatic cardiac arrest which appears to be due to hemorrhage. Now there is more evidence that chest compressions produce more harm than benefit in traumatic cardiac arrest which appears to be due to hemorrhage.

 
One study using a baboon traumatic cardiac arrest model found that the improvements in haemodynamics seen with chest compressions for normovolaemic cardiac arrest were not reproduced in hypovolaemic arrest.14 The authors suggested that CCC should not delay correction of the underlying deficit causing TCA, but the study was undertaken in only three animals, perhaps limiting its clinical relevance. A more recent study using a canine model of pulseless electrical activity in TCA found no benefit of chest compressions over fluid therapy alone or fluid combined with chest compressions; in fact the chest compression only group had worse survival, base deficit and ejection fraction.15 The authors concluded that further research was required to determine whether CPR has a role for the patient in haemorrhagic shock.[1]

  Most important is that the outcome is ROSC (Return Of Spontaneous Circulation), not return to normal neurological function. Since these are pigs, even the appearance of normal neurological function may not mean anything in humans. Still, the treatment is not evidence-based, so there does not appear to be a good reason to prefer to continue using compressions for traumatic cardiac arrest which appears to be due to hemorrhage.

Here in America, we are unlikely to do the research, because we are more concerned with appearances than with improving outcomes for patients. Maybe somebody in Britain or Australia will have to demonstrate some responsibility, so we can stop using chest compressions to kill trauma patients.

  Footnotes:

  [1] Closed chest compressions reduce survival in an animal model of haemorrhage-induced traumatic cardiac arrest. Watts S, Smith JE, Gwyther R, Kirkman E. Resuscitation. 2019 May 9;140:37-42. doi: 10.1016/j.resuscitation.2019.04.048. [Epub ahead of print]

PMID: 31077754

Free Full Text from Resuscitation

  .

The Big Government, Big Religion, Immoral Opposition to Physician Assisted Suicide

 
 

The government should not force people to die painful deaths, in order to please the people who can only think of the ways something can go wrong and/or the Bible thumpers. These patients are not harming anyone else and we should stop condemning them as if they are the ones rejecting morality.

There are ways to protect vulnerable patients from being taken advantage of by family, or by others, without forcing everyone to die painfully. Physician assisted suicide is a way to protect vulnerable patients from being taken advantage of by those who claim to know what is best for everyone and want to force it on everyone, for their own good.

The alternative to physician assisted suicide is to require moral physicians break the law in order to provide the care the patient needs – relief of suffering that cannot otherwise be relieved. Physician assisted suicide should not be opposed by any ethical medical organization.

The older I get, the more I see patients abused by this hypocritical legal prohibition on ethical behavior.

Providing the care that the patient requests, with fully informed consent by the patient, is far more ethical than claiming that other people should control patients’ lives for the patients.

This does not affect me much, as a patient, because I can acquire whatever I need to end my life, whenever I feel it is the best option. I also have the ability to administer whatever medications I might choose to use, but I would probably have to do this sooner than I would like, in order to avoid having to rely on others to do what is right.

I will not ask anyone else to put themselves at legal risk, in order to allow me more time.

I will do whatever I need to do before I lose the ability to do everything on my own. Obviously, this will not apply to many medical conditions that have catastrophic sudden onset. I am not currently experiencing any symptoms and I do not have any diagnosis of any condition that would encourage me to end my life, but I may need to move to a state that does not require patients to be tortured to death, if that changes. If the SCOTUS literalists/originalists imposes a big government sharia decision to prohibit ethical end of life decisions by patients, then I might need to move to another country in order to have a longer life.

.

ILCOR wants the appearance of public comments with less than half the substance

 

The International Liaison Committee on Resuscitation (ILCOR) shows its priorities in the way it handles its problem with public comments.
 

Last week ILCOR posted the two new draft CoSTRs listed below for public comment. It became apparent that the commenting link was broken and those who visited the site could not comment. We apologize for the inconvenience. The commenting link is now fixed and we invite you to comment at ilcor.org/costr.

  • Advanced Airway Management During Adult Cardiac Arrest
  • Vasopressors in Adult Cardiac Arrest
  • As a reminder, the public comment period will close on 4 April 2019.[1]

     

    ILCOR made a mistake that prevented public comments from being submitted for most of the public comment period.

    ILCOR is so interested in your public comments that they have decided to send out an email to let people know that they have the same drop dead date for the comments as before, but this time they might actually be able to get the comments to work. Maybe.

    The lack of evidence of benefit of epinephrine (adrenaline in Commonwealth countries) has lasted over half a century, so what is the rush to get these new guidelines out?

    There is only one outcome that matters – survival without severe brain damage.
     


     

    ILCOR evaluates 23 outcomes.

    ILCOR considers 15 of these outcomes critical, but they are really just 5 outcomes, with some of them repeated over different rhythms. These are (in increasing order of importance to the only one that matters):

    1. For the critical outcome of survival to hospital discharge, 2. For the critical outcome of survival at 3 months, 3. For the critical outcome of favorable neurologic outcome at hospital discharge, 4. For the critical outcome of survival with unfavorable neurologic outcome at 3 months, 5. For the critical outcome of favorable neurologic outcome at 3 months,

    Many of them are repeated for each cardiac arrest rhythm or for each vasopressor, or vasopressor cocktail:

    1. Epinephrine plus vasopressin compared to epinephrine only – Any rhythm 2. Initial vasopressin compared to initial epinephrine – Any rhythm 3. Epinephrine compared to placebo – Non-shockable rhythms 4. Epinephrine compared to placebo – Shockable rhythms 5. Epinephrine compared to placebo – Any initial rhythm

    There is only one outcome that matters – survival without severe brain damage.

    There is only one study that was large enough to answer this:
     

    CONCLUSIONS
    In adults with out-of-hospital cardiac arrest, the use of epinephrine resulted in a significantly higher rate of 30-day survival than the use of placebo, but there was no significant between-group difference in the rate of a favorable neurologic outcome because more survivors had severe neurologic impairment in the epinephrine group.[2]

     

    If the people at ILCOR really think that epinephrine is beneficial in cardiac arrest, they should encourage a much larger study.

    There were 4,000 patients in each group – 4,000 placebo and 4,000 epinephrine.

    Maybe with 8,000 patients in each group, the ever decreasing “trend toward better outcome” will reach significance. Maybe it will be shown to be just another insignificant appearance of a “trend” that is the result of having so few survivors to compare.

    There were only 161 survivors without severe brain damage out of 8,000 cardiac arrest patients – 74 placebo and 87 epinephrine.

    Those resuscitated before receiving epinephrine/placebo were excluded from the study, so this is not a case of EMS that only has a 2% resuscitation rate. The focus on epinephrine is a focus on the patients least likely to be resuscitated and a focus on counterproductive outcomes.

    Almost all of our good outcomes (without severe brain damage) will be without epinephrine, because these resuscitations happen before epinephrine can be give by even the most aggressive epi enthusiast.

    What we are doing is making excuses for memorizing ineffective interventions and requiring their application is a specific way, in order to determine the quality of care. We are promoting fantasy.

    We learned that distracting from the quality of chest compressions is the most deadly thing we can do in resuscitation.

    CPR = only chest compressions – the exception is when the arrest is believed to be due to a respiratory event, such as when the Smurf sign or a respiratory/choking history is present. Chest compressions provide all of the pulmonary resuscitation that a human needs for a non-respiratory event and the respiratory events are not easily missed.

    Why require a whole bunch of skills be applied for such a tiny portion of good outcomes among cardiac arrest patients?

    Why not give up on requiring these skills when the evidence makes it clear that there is no benefit?

    All we are doing is adding cognitive load to make us feel like we are doing something special.

    We could learn something that actually benefits patients, such as how to assess patients when giving high-dose NTG (NiTroGlycerin or GTN GlycerylTriNitrate in Commonwealth countries) for even hypotensive CHF/ADHF (Congestive Heart Failure/Acute Decompensated Heart Failure), where we can make much more of a difference and prevent cardiac arrest, but we don’t.[3],[4],[5]
     


     

    Cognitive load is not just a problem for paramedics and nurses, or med/surg doctors, but also for emergency physicians:

    Cognitive Load and the Emergency Physician
    April 12, 2016
    James O’Shea
    emDocs
    Article

    Why are we distracting everyone from things that do improve the only outcome that matters, in order to promote things that do not improve any outcome that matters?

    Here is what I wrote –
     

    The primary source for the recommendation to keep things the same is a brand new study – PARAMEDIC2.

    This showed no statistically significant improvement in the only outcome that matter – survival without severe brain damage.

    A larger study might show that there is a real improvement – or it may put the epi hypothesis out of its misery.

    I will eventually have a cardiac arrest. If I am resuscitated, whom will ILCOR send to change my diaper, and attend to the other things I can no longer attend to?

    We need evidence of a significant benefit in order to justify distracting everyone from interventions that actually do improve survival without severe brain damage.

    .

     

    The commenting link is now fixed and we invite you to comment at ilcor.org/costr

    Maybe they will pay attention. Dr. Rory Spiegel of EM Nerd has a detailed comment that is also critical of ILCOR’s proposed “strong recommendation” of epinephrine.

    Footnotes:

    [1] Vasopressors in Adult Cardiac Arrest
    Time left for commenting: 11 days 15:49:49
    ILCOR staff
    Created: March 21, 2019 · Updated: March 21, 2019
    Draft for public comment
    Consensus on Science with Treatment Recommendations (CoSTR)
    Vasopressors in Adult Cardiac Arrest page for comments until April 04, 2019 at 06:00 Eastern Time

    [2] A Randomized Trial of Epinephrine in Out-of-Hospital Cardiac Arrest.
    Perkins GD, Ji C, Deakin CD, Quinn T, Nolan JP, Scomparin C, Regan S, Long J, Slowther A, Pocock H, Black JJM, Moore F, Fothergill RT, Rees N, O’Shea L, Docherty M, Gunson I, Han K, Charlton K, Finn J, Petrou S, Stallard N, Gates S, Lall R; PARAMEDIC2 Collaborators.
    N Engl J Med. 2018 Aug 23;379(8):711-721. doi: 10.1056/NEJMoa1806842. Epub 2018 Jul 18.
    PMID: 30021076

    Free Full Text from N Engl J Med.
     

    In a Bayesian analysis that used an assumption of no benefit from adrenaline, the posterior probability that the absolute rate of survival was at least 1 percentage point higher in the epinephrine group than in the placebo group was 37% (Fig. S3 in the Supplementary Appendix). The probability that the absolute survival rate was at least 2 percentage points higher was 0.2%. With respect to the rate of survival with a favorable neurologic outcome at hospital discharge, the probabilities that the rate was at least 1 or 2 percentage points higher with epinephrine were 1.9% and 0%, respectively (Fig. S4 in the Supplementary Appendix).

     

    The probability of a good outcome (no severe brain damage) is not improved with epinephrine.

    If we want to improve outcomes, we need to look elsewhere, because there is nothing to be gained with epi.

    [3] Intravenous nitrates in the prehospital management of acute pulmonary edema.
    Bertini G, Giglioli C, Biggeri A, Margheri M, Simonetti I, Sica ML, Russo L, Gensini G.
    Ann Emerg Med. 1997 Oct;30(4):493-9.
    PMID: 9326864 [PubMed – indexed for MEDLINE]

    [4] Unreasonable Fear of Hypotension and High-Dose NTG – Part I
    Thu, 29 Aug 2013
    Rogue Medic
    Article

    [5] Unreasonable Fear of Hypotension and High-Dose NTG – Part II
    Wed, 04 Sep 2013
    Rogue Medic
    Article

    .

    ACLS Excuses for Causing Harm with Epinephrine

     

    The next ACLS guidelines are available for review and comment, before they are finalized. The Consensus on Science with Treatment Recommendations (CoSTR) from the International Liaison Committee on Resuscitation (ILCOR) are available for two guidelines:

    Vasopressors in Adult Cardiac Arrest

    Advanced Airway Management During Adult Cardiac Arrest

    We have been using these interventions for so long, that there should be great evidence to show that benefits and harms of both interventions, but there is no good evidence to support either intervention.

    For epinephrine (adrenaline in Commonwealth countries), the most commonly used vasopressor and the only one rally being considered, there is no evidence of actual benefit – increased survival without severe brain damage.

    Nothing else matters.

    There is no valid evidence that increasing any surrogate endpoint improves survival without severe brain damage. The evidence cited by ILCOR shows that epinephrine increases the rate of severe brain damage.
     

    Intervention: Vasopressor or a combination of vasopressors provided intravenously or intraosseously during cardiopulmonary resuscitation.[1]

     

    Here are the outcomes that are supposed to indicate that the patient is better.
     

    Outcomes: Short-term survival (return of spontaneous circulation (ROSC) and survival to hospital admission), mid-term survival (survival to hospital discharge, 28 days, 30 days, or 1 month), mid-term favorable neurological outcomes (Cerebral Performance Category score of 1-2 or modified Rankin Scale 0-3 at hospital discharge, 28 days, 30 days, or 1 month) and long-term favorable and poor (modified Rankin Score 4-5) neurological outcomes (after 1 month).[1]

     

    Is ROSC an improvement?

    We aren’t supposed to ask that question. These are faulty assumption that the guidelines are based on.

    1. Doing something more is better than only doing things supported by valid evidence of improved survival without severe brain damage.

    No.

    How much harm is being caused in this rush to get a pulse back?

    We are supposed to ignore our understanding of research, look at a statistically insignificant “trend”, and extrapolate that statistically insignificant “trend” to support the prejudice that our intervention has not been harmful.

    That is not good science.

    That is not good medicine.
     

    Why aren’t there any studies large enough to show improved survival without severe brain damage for anything other than rapid defibrillation (when indicated VF/pulseless VT) and chest compressions?

    The research has only produced excuses and surrogate endpoint. Surrogate endpoints are for hypothesis generation and sales pitches to the least knowledgeable, but not for treatment guidelines.

    ILCOR has told us this before, but that was because the choice was between large doses of epinephrine and small doses of epinephrine, not between epinephrine and no epinephrine.

    The choice is the same.

    Is the more aggressive intervention helping?

    The answer is the same. No. That is not the conclusion of the evidence.
     

    CONCLUSIONS
    In adults with out-of-hospital cardiac arrest, the use of epinephrine resulted in a significantly higher rate of 30-day survival than the use of placebo, but there was no significant between-group difference in the rate of a favorable neurologic outcome because more survivors had severe neurologic impairment in the epinephrine group.[2]

     

    If the goal is a pulse with more severe brain damage, then epinephrine is the way to go.

    If the goal is increased survival without severe brain damage, we have to keep looking.

    We should limit the use of epinephrine to well controlled research until there is evidence of improvement in outcomes that matter.

    If this evidence is never found, our patients will not have been harmed by epinephrine.

    If this evidence is eventually found, it is something that should have been insisted on decades ago. We should not use wishful thinking and surrogate endpoints to justify interventions that harm patients.

    We used to stop compressions to let the medic/nurse/doctor intubate, or start an IV (IntraVenous) line.

    We knew that the tube was more important.

    We knew that the drugs given through the IV line were more important.

    The 2005 guidelines told us to continue compressions during intubation and during IV attempts and to improve the quality of the compressions.

    That focus on high quality compressions is the only time we have improved outcomes that matter.
     

    CONCLUSIONS: Compared with controls, patients with out-of-hospital cardiac arrest treated with a renewed emphasis on improved circulation during CPR had significantly higher neurologically intact hospital discharge rates.[3]

     

    33 1/3% vs 60% increased survival without severe brain damage.
     

    In 2004, we began a statewide program to advocate chest compression-only CPR for bystanders of witnessed primary OHCA. Over the next five years, we found that survival of patients with a shockable rhythm was 17.7% in those treated with standard bystander CPR (mouth-to-mouth ventilations plus chest compression) compared to 33.7% for those who received bystander chest-compression-only CPR.[4]

     

    18% vs 34% increased survival only – not increased survival without severe brain damage.
     

    In the analysis of MICR [Minimally Interrupted Cardiac Resuscitation] protocol compliance involving 2460 patients with cardiac arrest, survival was significantly better among patients who received MICR than those who did not (9.1% [60/661] vs 3.8% [69/1799]; OR, 2.7; 95% CI, 1.9-4.1), as well as patients with witnessed ventricular fibrillation (28.4% [40/141] vs 11.9% [46/387]; OR, 3.4; 95% CI, 2.0-5.8).[5]

     

    9% vs 4% increased survival only – not increased survival without severe brain damage.
     

    Neurologic outcomes were also better in the patients who received CCR (OR=6.64, 95% CI=1.31 to 32.8).[6]

     

    6 2/3 more likely to have increased survival without severe brain damage. The range is 1 1/3 to almost 33 times, because of the small numbers, but unlike epinephrine, this is statistically significant and supported by other research.

    We are still making excuses for using a drug that causes harm and does not appear to provide a benefit that is greater than the harm. If there is more benefit, it is too small to be measured, even in a study with over 9,000 patients. We do not know which patients benefit and which patients are harmed, so we do not know how to minimize the harm that we cause.

    Our patients deserve better.

    Footnotes:

    [1] Vasopressors in Adult Cardiac Arrest
    Time left for commenting: 11 days 15:49:49
    ILCOR staff
    Created: March 21, 2019 · Updated: March 21, 2019
    Draft for public comment
    Consensus on Science with Treatment Recommendations (CoSTR)
    Vasopressors in Adult Cardiac Arrest page for comments until April 04, 2019 at 06:00 Eastern Time

    [2] A Randomized Trial of Epinephrine in Out-of-Hospital Cardiac Arrest.
    Perkins GD, Ji C, Deakin CD, Quinn T, Nolan JP, Scomparin C, Regan S, Long J, Slowther A, Pocock H, Black JJM, Moore F, Fothergill RT, Rees N, O’Shea L, Docherty M, Gunson I, Han K, Charlton K, Finn J, Petrou S, Stallard N, Gates S, Lall R; PARAMEDIC2 Collaborators.
    N Engl J Med. 2018 Aug 23;379(8):711-721. doi: 10.1056/NEJMoa1806842. Epub 2018 Jul 18.
    PMID: 30021076

    Free Full Text from N Engl J Med.

    [3] Implementing the 2005 American Heart Association Guidelines improves outcomes after out-of-hospital cardiac arrest.
    Aufderheide TP, Yannopoulos D, Lick CJ, Myers B, Romig LA, Stothert JC, Barnard J, Vartanian L, Pilgrim AJ, Benditt DG.
    Heart Rhythm. 2010 Oct;7(10):1357-62. doi: 10.1016/j.hrthm.2010.04.022. Epub 2010 Apr 24.
    PMID: 20420938

    Free Full Text from Heart Rhythm.

    [4] The cardiocerebral resuscitation protocol for treatment of out-of-hospital primary cardiac arrest.
    Ewy GA.
    Scand J Trauma Resusc Emerg Med. 2012 Sep 15;20:65. doi: 10.1186/1757-7241-20-65. Review.
    PMID: 22980487

    Free Full Text from PubMed Central.

    [5] Minimally interrupted cardiac resuscitation by emergency medical services for out-of-hospital cardiac arrest.
    Bobrow BJ, Clark LL, Ewy GA, Chikani V, Sanders AB, Berg RA, Richman PB, Kern KB.
    JAMA. 2008 Mar 12;299(10):1158-65. doi: 10.1001/jama.299.10.1158.
    PMID: 18334691

    Free Full Text from JAMA.

    [6] Cardiocerebral resuscitation is associated with improved survival and neurologic outcome from out-of-hospital cardiac arrest in elders.
    Mosier J, Itty A, Sanders A, Mohler J, Wendel C, Poulsen J, Shellenberger J, Clark L, Bobrow B.
    Acad Emerg Med. 2010 Mar;17(3):269-75. doi: 10.1111/j.1553-2712.2010.00689.x.
    PMID: 20370759

    Free Full Text from Acad Emerg Med.

    .

    Protecting Systemic Incompetence – Part I

     

    We demand the lowest standards, because we are willfully ignorant and we do not want to understand. The surprise is that so many of us survive our devotion to incompetence. The loudest voices tend to dominate the discussions and the loudest voices demand that their excuses for incompetence be accepted. The rest of us don’t oppose incompetence enough.

    A nurse was told to give 2 mg Versed (the most common brand of midazolam in the US) for sedation for a scan, intended to give 1 mg Versed, but actually gave an unknown quantity of vecuronium (Norcuron is the most common brand in the US). The patient was observed to be unresponsive and pulseless by the techs in the scan. A code was called. The family learned the details from a newspaper article, not from the hospital.
     

    A Tennessee nurse charged with reckless homicide after a medication error killed a patient pleaded not guilty on Wednesday in a Nashville courtroom packed with other nurses who came in scrubs to show their support.[1]

     

    The nurse intended to give a medication that should be limited to patients who are monitored (ECG and waveform capnography), because different patients will respond in different ways. This is basic drug administration and deviation from that basic competence may even have been common in this Neuro ICU (Neurological Intensive Care Unit). We demand low standards, because we do not want to understand.

    We don’t need to monitor for that, because that almost never happens.

    Except these easily preventable errors do happen. And we lie about it. We help to cover it up, because we demand low standards, regardless of how many patients have to suffer for the benefit of our incompetence.

    This is a common argument used by doctors, nurses, paramedics, . . . . It makes no sense, but we keep demonstrating that we don’t care.

    The people in charge should act responsibly, but they delegate responsibility and we reward them.

    Back to the hospital, Vanderbilt University Medical Center (VUMC) is a university medical center, so the standards should be high. VUMC was founded in 1874 and is ranked as one of the best hospitals in America.

    There is a drug dispensing machine, from which less-than-killed nurses can obtain almost anything and administer almost anything, without understanding enough to recognize the problem. This is an administrative problem. This was designed by someone with no understanding of risk management.

    The over-ride of the selection is not the problem, because emergencies happen and it is sometimes necessary to bypass normal procedures during an emergency. Ambulances are equipped with lights, sirens, and permission to violate certain traffic rules for this reason.

    Some of the many blatant problems are:

    * The failure of the nurse to have any understanding of the medication supposed to be given

    * The failure of the nurse to recognize that the drug being given was not the drug ordered.

    * The failure of the nurse to monitor the patient being given a drug for sedation.

    * Most of all, the failure of the hospital – the nurses, the doctors, the administrators, to try to make sure that at least these minimum standards are in place.

    * How often do nurses in the Neuro ICU give midazolam?

    * Why is a nurse, who is clearly not familiar with midazolam, giving midazolam to any patient?

    * How is a nurse, working unsupervised in a Neuro ICU not familiar with midazolam?

    * What kind of qualifications are required for a nurse to give sedation without supervision?

    * Since this nurse was orienting another nurse, what qualifies this nurse to orient anyone?

    * Given the side effects of midazolam, why was midazolam ordered without monitoring?

    * Given the side effects of midazolam, was it the most appropriate sedative for use in a setting where monitoring is going to be difficult?

    * Was it the more rapid onset of sedation, in order to free up the PET scan more quickly and/or avoid having to reschedule the scan, that led to the choice of midazolam?

    * How well do any of the doctors understand the pharmacology of midazolam if they are giving orders for a nurse to grab a dose, take it down to the scan, give the drug, and return to the unit, abandoning the monitoring of the patient to the techs in the PET scan?

    * This is not a criticism of the techs in PET scan, but are techs authorized to manage sedated patients?

    * Even though they will often scan sedated patients, are the techs required to demonstrate any competence at managing sedated patients?
     

    The nurses being oriented apparently thought that it is customary to give sedation:

    1. without even looking at the name of the medication

    2. without confirming by looking at the name again, it before administration

    3. without double checking with a nurse, or tech, that the label matches the name of the drug to be given
     

    How many of the doctors, responsible for the care of ICU patients, would agree to be sedated, without being monitored, and to have their care handed off to PET scan technicians?

    Why didn’t the doctors and nurses see this as a problem before it made the news?

    If the problems were reported, nothing appears to have been done to address the problems beyond the usual – Nothing to see here. Move along. or That’s above your pay grade.

    That is the primary point I am trying to make.

    The problem is well above the pay grade of the nurse.
     

    Here is the part that experienced nurses have jumped on immediately:

    Why did the nurse think that midazolam needs to be reconstituted?

    Vecuronium (most common brand name is Norcuron) is a non-depolarizing neuromuscular-blocker, which comes as a poweder, that needs to be reconstituted.
     


    Image source
     

    1. Read label instructions?

    This nurse has repeatedly demonstrated a need to be supervised, but those responsible for that supervision have apparently ignored their responsibilities in a way that far exceeds any failures by this nurse.

    Is it possible that this is a one time event and that the nurse has behaved in an exemplary manner at all times while around doctors and other nurses before this day? It is possible, but the number and severity of the failures on the part of the nurse strongly suggest a pattern of not understanding, not caring, or both. I suspect that any lack of caring is due to a lack of understanding, because I have not yet lost all hope in humanity.

    Footnotes:

    [1] Nurse charged in fatal drug-swap error pleads not guilty
    By Travis Loller
    February 20, 2019
    Associated Press
    Article

    .