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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

Mon, 12 Aug 2019 17:46:11 -0400 by
 

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

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Filed Under: ACLS, ACS, Assessment, Cardiology, Chest Pain, Critical Judgment, EBM, Evidence, GTN, Heresy, NTG, Research, RVI

Normal Sinus Rhythm is Not a Good Description

Fri, 03 Feb 2017 12:10:55 -0500 by
What is the rhythm 1a
 

Is Normal Sinus Rhythm a good description of this rhythm?

Is it sinus?

Is it normal?

Dr. Steven Novella writes about normal and some of the meanings of normal.
 

This findings, if confirmed, has several implications. First, it is just good to know how our brains typically work. “Normal” is a combined judgment about what is actually happening and what “should” be happening. This confirms what was observed in health care, especially psychiatry, that there is a moral judgment in deciding what is normal.[1]

 

Too often, we seem to try to apply what we think something should be to our mistaken description of what something is.

As an example, an ECG (ElectroCardioGram) showing a regular, or slightly irregular, sinus rhythm is often described using the misleading term normal sinus rhythm.

Normal suggests that there is nothing wrong with the rhythm, or with the heart, when it is not unusual for a patient to have a heart attack with a normal sinus rhythm being accurately displayed on the ECG.

We are subconsciously telling ourselves, Nothing to see here. Move along.

We are fooling ourselves and discouraging investigation of what may be causing problems by unnecessarily adding the term normal.

In this setting, normal does not add any information, but suggests that we know more than we actually know.

Why lie to ourselves?

Because we trust ourselves and don’t bother to check our assumptions to see if they are valid.
 

What is the rhythm 1
 

It is clearly sinus, but what information do we add by calling it normal?

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Footnotes:

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[1] What Is Normal?
Steven Novella
Feb 02, 2017
Neurologica
Article

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Filed Under: ACS, Cardiology, Critical Judgment, Heresy

Who Needs a 12 Lead ECG?

Tue, 11 Mar 2014 23:55:36 -0400 by
ResearchBlogging.org
 

Do we do too many 12 lead ECGs on patients who do not have chest pain?

This is something that some people worry about.

Save the electrodes!

Those poor little electrodes are being abused!

Are electrodes being abused?
 

Women and the elderly with STEMI are particularly likely to present with atypical chief complaints such as dyspnea and weakness. Such patients experience significant delays in door-to-ECG time and treatment and have increased morbidity and mortality compared with patients who present with chest pain.5,9-12 [1]

 

Tiredness/weakness is the second best predictor of STEMI (ST segment Elevation Myocardial Infarction).

After chest pain (pressure, tightness, heaviness, squeezing, et cetera), the best predictor of STEMI is dyspnea in akll age ranges, but dyspnea indicates 20% of STEMIs in patients over 80 years old.

Are we helping anyone by avoiding 12 lead ECG (ElectroCardioGram) assessment?
 

Presenting chief complaints among 6,464 patients with STEMI. Chest pain decreased in frequency with age, whereas a chief complaint of dyspnea, weakness, syncope, or altered mental status all increased in frequency with age.[1]

 


Click on images to make them larger.
 


 

The advantage of a logarithmic chart is that there is greater distinction among the smaller numbers (such as the other complaints that make up less than 5% in the image above). The disadvantage is that large changes are flattened. I modified the dyspnea line to show how it would look on a linear scale (from 5% to 20%). As you can see, the ability to predict STEMI increases dramatically with age – more dramatically than the logarithmic scale suggests.
 


 

How should we remember all of this?

The authors came up with a nice simple flow chart (below).

This is for the ED, but is there a good reason for EMS to ignore these STEMIs?
 


 

Even in the 18-49 year old patients, dyspnea is about as likely to predict a STEMI as weakness is likely to predict a STEMI in an 80+ year old patient.

Chest pain still indicates about 50% of STEMI patients over 80, but we will miss half of STEMIs in this population if we only do 12 leads on chest pain patients.

Can an 80+ year old patient have a good quality of life after a STEMI?

Absolutely.

Also see When should you get an ECG? at Mill Hill Ave Command.

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Footnotes:

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[1] Development and validation of a prioritization rule for obtaining an immediate 12-lead electrocardiogram in the emergency department to identify ST-elevation myocardial infarction.
Glickman SW, Shofer FS, Wu MC, Scholer MJ, Ndubuizu A, Peterson ED, Granger CB, Cairns CB, Glickman LT.
Am Heart J. 2012 Mar;163(3):372-82. doi: 10.1016/j.ahj.2011.10.021.
PMID: 22424007 [PubMed – indexed for MEDLINE]

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Glickman SW, Shofer FS, Wu MC, Scholer MJ, Ndubuizu A, Peterson ED, Granger CB, Cairns CB, & Glickman LT (2012). Development and validation of a prioritization rule for obtaining an immediate 12-lead electrocardiogram in the emergency department to identify ST-elevation myocardial infarction. American heart journal, 163 (3), 372-82 PMID: 22424007

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Filed Under: ACS, Cardiology, Heresy, Research Blogging

EMS Volunteers, Patient Stress and 200,000 Downloads for EMS Office Hours

Sun, 05 Jan 2014 19:30:02 -0500 by
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Last week on EMS Office Hours, Jim Hoffman, Josh Knapp, and Dave Brenner discussed a variety of topics before I got on the show. We ended up discussing a question Josh had posted on the WANTYNU Facebook page.
 

EMS Volunteers, Patient Stress and 200,000
 

I do not have a link to the original question, but it was along the lines of If you are 99% sure that your patient is having a heart attack, do you tell the patient?

My original comment was along the lines of

1. How did I develop so much certainty about this actually being a heart attack?

2. What is the benefit of telling the patient You are having a heart attack?
 

1.

A. Do we track all of our heart attack patients and compare their final diagnoses with our diagnoses?

Would only STEMIs (ST segment Elevation Myocardial Infarctions) be considered for the You are having a heart attack, with 99% accuracy claim?

Does we have the statistics to back up that claim?

Are we overly confident of our diagnoses and unaware of the difference between our accuracy and reality?

Even if we do track our precision (when we state that it is a heart attack, it truly is a heart attack), do we assume that means that we avoid false negatives(when we do not state that it is a heart attack, there is no heart attack)?

Do we track false negatives?

How do we know if we miss false negatives?

How does awareness of these false negatives affect our confidence in claiming You are having a heart attack?
 

Do our misses count?

Is it a miss, if the machine analysis states ***STEMI***, we disagree, but it turns out to be a STEMI?

Is it a miss, if the machine analysis does not state ***STEMI***, we disagree, and it turns out to not be a STEMI?

Is it a miss, if the machine analysis does not state ***STEMI***, we disagree, but it turns out to be a STEMI? The machine was wrong, but we were right.

All of these affect our diagnosis of STEMI, but how much do we pay attention to any of them?

Is the excuse, Most doctors would have missed that, a valid excuse? We are wrong, but we are as wrong as another group of people would be expected to be.
 

appropriate-cath-lab-activation-1
 

If the goal is to be wrong less than 5% of the time, what evidence do we have that we are wrong less than 1% of the time?
 

In summary, broad awareness should exist regarding evidence-based triggers for appropriate Cath Lab activation. A diverse group of frontline clinicians making these time-pressured decisions need a comprehensive list of precise criteria, because not all “acute MIs” have classic ST-elevation on ECG (eg, STEMI-equivalents and certain OCHA scenarios), not all ST-elevation patterns represent “true STEMI” (ie, STE-mimics), and some “true STEMI” patients are not reasonable candidates for an aggressive treatment strategy involving PPCI. Optimal ECG interpretation proficiency by all clinicians in identifying both classic STEMI and STEMI-equivalents constitutes a major cornerstone of ongoing efforts to maximize STEMI system efficiency.[1]

 

And the most important question may be How much do we know about what we don’t know?

Am I 99% certain, or just convincing myself that I am much more certain than I have any right to claim?

Why should we assume that we do not need to know our limitations?
 

Go listen to the podcast.
 

Also see Tom Bouthillet’s slides from his presentation –

STEMI Mimics and STEMI Equivalents
EMS 12 Lead
Slide presentation.

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Footnotes:

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[1] Appropriate cardiac cath lab activation: optimizing electrocardiogram interpretation and clinical decision-making for acute ST-elevation myocardial infarction.
Rokos IC, French WJ, Mattu A, Nichol G, Farkouh ME, Reiffel J, Stone GW.
Am Heart J. 2010 Dec;160(6):995-1003, 1003.e1-8. doi: 10.1016/j.ahj.2010.08.011. Review.
PMID:21146650[PubMed – indexed for MEDLINE]

Free Full Text from Am Heart J.

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Filed Under: ACS, EMS Office Hours, Heresy, Probability

What is Evidence-Based Medicine?

Tue, 06 Nov 2012 21:45:38 -0500 by
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First, Evidence-Based Medicine is a confusing term. Ironically, many people have different interpretations of what Evidence-Based means.

The whole idea of scientific evidence is to minimize the interference of bias, which is much more difficult than it seems. We all have biases. When our biases affect our treatment of our patients, there is a lot of potential for harm.

If I believe that a treatment is effective, but there is no good evidence that it improves outcomes –

Outcomes?

Outcomes are what matter, not surrogate endpoints.

A surrogate endpoint is something that is measured, because it is easy to measure, not because it is important. In treating patients with antiarrhythmic medication, it is much easier to assess the frequency of PVCs (Premature Ventricular Contractions), than it is to assess survival. This was demonstrated very painfully in CAST (the Cardiac Arrhythmia Suppression Trial).[1],[2]
 

 

After a heart attack, if the patient has frequent PVCs, the patient is more likely to die.

Therefore, getting rid of the PVCs saves lives.

That is not an unreasonable conclusion.

The PVCs may progress to something worse, such as V Tach (Ventricular Tachycardia) or V Fib (Ventricular Fibrillation). Preventing these rhythms is important. We use antiarrhythmic drugs and/or implanted defibrillators for this reason.

But the conclusion assumes too much.

Getting rid of the PVCs does not saves lives.

Fiddling with the conduction system is doing something, but why should we assume that it is doing something good, unless we have good evidence that it improves outcomes?

PVCs are an indicator of an injured heart. Just an indicator. If the pulse oximeter alarm is going off because the patient’s oxygen saturation is low, turning the alarm off, or turning the pulse oximeter off is not going to make things better. If the patient is oxygenating adequately, regardless of the alarm settings, treating the false hypoxia would not be expected to produce a good outcome.

We used to automatically give lidocaine to chest pain patients to prevent V Fib.

We have to do something.

It’s in the algorithm.

What if there is a bad outcome?

We do not give lidocaine for chest pain any more.

Why?

Because almost every treatment is eventually discarded. Some are replaced by safer versions of the same treatment, but maybe even more are found to be harmful.

Lidocaine for chest pain was not based on any evidence of improved outcomes.

Lidocaine for chest pain, outside of a controlled trial, was a bad idea. This was just an uncontrolled, undocumented, experiment on unsuspecting patients without any explanation that the risks and benefits were unknown.
 

In CAST the patients receiving the study drugs encainide (Enkaid) and flecainide (Tambocor) were more than 3 times as likely to die as the patients receiving placebo.

Since these drugs were some of the most widely prescribed drugs at that time, probably tens of thousands of patients died because of these drugs.
 

Today, we use epinephrine in cardiac arrest because it improves outcome in dogs and rats who have cardiac arrest induced in the laboratory. Great news if you are a dog, or a rat, and EMS shows up to treat your cardiac arrest.

We also can show that epinephrine improves ROSC (the Return Of Spontaneous Circulation), but this improvement goes away before discharge from the hospital.

In other words, epinephrine only has good evidence of a surrogate endpoint – ROSC. With only evidence of improvement in producing a surrogate endpoint, epinephrine should never have been approved for use outside of controlled trials.

None of the evidence on epinephrine outcomes is well controlled.

There are two interpretations of the epinephrine evidence.

1. Epinephrine is harmful – in which case we never should have been giving epinephrine in cardiac arrest.

2. Epinephrine is neutral (it produces no improvement in outcomes) – in which case we never should have been giving epinephrine in cardiac arrest.
 

 

I added the two most recent studies to this, since they were not yet published when the review of vasopressors was published.[3] The quality and outcome of the added studies is my interpretation, but I think that others will rank them similarly.

The Hagihara study is more than 100 times larger than the combined numbers of all of the studies that came before it.

The Hagihara study is not positive.

The Hagihara study is not even neutral.

How much negative evidence do we need to make excuses for to keep using epinephrine in cardiac arrest?

If we ignore the evidence, then there is no limitation on what we can do for/to patients.

We can give cyanide for cardiac arrest, because maybe the homeopaths are on to something with their law of similars.

We can give medical marijuana, probably by positive pressure ventilation (being very careful not to inhale any ourselves).

We can give actual voodoo, which does have some scientific evidence, but not outcomes evidence and it is used to put people into a state that looks like cardiac arrest, but is not cardiac arrest.

There are no limits to what we can do to patients, if we do not base treatments on evidence.

We have to stop pretending that we First do no harm. Without evidence, we don’t know and we don’t want to know. Trust us, we don’t stop until we cannot ignore the evidence of harm.

If we are satisfied with surrogate endpoints and think that an expensive coma is better than whatever the outcome would have been without epinephrine, then we are just playing with the results of catecholamine toxicity and hoping we will find something that works as well as not using epinephrine.

What about evidence for using a long spine board and rigid EMS collars for spinal immobilization?

There is evidence of worse outcomes. There is no evidence of improved outcomes.

What about high flow oxygen for everything?

There is evidence of worse outcomes. There is no evidence of improved outcomes.

Too much of what we do can be described that way –

There is evidence of worse outcomes. There is no evidence of improved outcomes.

We need to grow up and start treating our patients with respect. They are not toys.

We are practicing witchcraft, not medicine.

We are pretending mythology is medicine.
 

Why is it ironic that many people have different interpretations of what Evidence-Based Medicine means?

Because reliance on scientific evidence is supposed to be about eliminating the influence of interpretation. If one person can read a paper and come to one conclusion, another person can come to the opposite conclusion, and a third person can come to a conclusion that differs with both of the others, and so on – then there is not enough well controlled research to justify subjecting patients to the risks of the proposed treatment.

Without clear evidence of benefit, we should only be using a treatment in controlled trials – otherwise we may never find out if the treatment is more harmful than beneficial.

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Footnotes:

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[1] Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial.
Echt DS, Liebson PR, Mitchell LB, Peters RW, Obias-Manno D, Barker AH, Arensberg D, Baker A, Friedman L, Greene HL, et al.
N Engl J Med. 1991 Mar 21;324(12):781-8.
PMID: 1900101 [PubMed – indexed for MEDLINE]

Free Full Text Article from New England Journal of Medicine.

CONCLUSIONS. There was an excess of deaths due to arrhythmia and deaths due to shock after acute recurrent myocardial infarction in patients treated with encainide or flecainide. Nonlethal events, however, were equally distributed between the active-drug and placebo groups. The mechanisms underlying the excess mortality during treatment with encainide or flecainide remain unknown.

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[2] C A S T and Narrative Fallacy
Rogue Medic
Mon, 20 Jul 2009
Article

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[3] Vasopressors in cardiac arrest: a systematic review.
Larabee TM, Liu KY, Campbell JA, Little CM.
Resuscitation. 2012 Aug;83(8):932-9. Epub 2012 Mar 15.
PMID: 22425731 [PubMed – in process]

CONCLUSION: There are few studies that compare vasopressors to placebo in resuscitation from cardiac arrest. Epinephrine is associated with improvement in short term survival outcomes as compared to placebo, but no long-term survival benefit has been demonstrated. Vasopressin is equivalent for use as an initial vasopressor when compared to epinephrine during resuscitation from cardiac arrest. There is a short-term, but no long-term, survival benefit when using high dose vs. standard dose epinephrine during resuscitation from cardiac arrest. There are no alternative vasopressors that provide a long-term survival benefit when compared to epinephrine. There is limited data on the use of vasopressors in the pediatric population.

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Filed Under: 2010 AHA Guidelines, ACS, Ethics, Evidence, Heresy, Research

Misrepresenting Current Topics in EMS Research from EMS Expo – IMMEDIATE

Mon, 05 Nov 2012 11:30:24 -0500 by
 

At EMS Expo, I was told that Dr. Paul Pepe also did not mention covering Intramuscular versus intravenous therapy for prehospital status epilepticus[1] without mentioning the doses of midazolam (Versed) and lorazepam (Ativan) used in his presentation on the Eagles conference. So John Studnek, PhD has some company in his omission of important information. I don’t know if Dr. Pepe covered the IMMEDIATE trial, too.[2]

If your protocol doses are to start with 4 mg of IV lorazepam or with 10 mg of IM midazolam, then the doses are not important. These large doses of benzodiazepines appear to decrease the need for intubation.[3]

I suspect that 4 mg lorazepam IV (IntraVenous) or 10 mg midazolam (IntraMuscular) will scare a lot of medical directors. They will worry about the need for intubation with large doses of benzodiazepines and switch to IM midazolam, but at a low dose that is less effective and more likely to result in intubation.
 

The second study – IMMEDIATE.

The GIK (Glucose, Insulin, and Kalium [Latin for potassium]) study was undeservedly hyped when it came out and Dr. Studnek continues that misrepresentation.

Should we ignore that the study was originally supposed to be large enough to produce statistically significant results – 15,450 people?[4]

Dr. Studnek points out that there were 911 people in the study. That is the emergency number in the US, so it can help us remember how many patients there were, but that number is before exclusions. There were fewer than 900 patients included in the study. After eliminating almost all of the 15,000 patients who were supposed to be in the study, even 911 patients is a significant disappointment.

Dr. Studnek points out that this was published in JAMA, which is a prestigious journal, so that means that it is of high quality. The week before JAMA hyped this study, they hyped a paper on helicopters in EMS that is garbage.[5]

Being published in JAMA does not mean a study is of high quality.

Should we ignore that the resulting number of patients is only 6.7% of the original and that the error bars on the results are frequently much larger than the possible benefit of treatment?

So what that there is a statistically significant improvement in one, and only one, of the secondary endpoints of the study? This is to be expected when there are that many targets. It is unlikely that everything will come up negative, especially in a study with a small number of patients.

The statistically significant improvement disappears when reassessed one month later.

Is this the epinephrine effect all over again?

Epinephrine increases the return of pulses, but fewer people treated with epinephrine survive to leave the hospital alive. This is less harmful.

The benefit disappears before discharge from the hospital.

Is that what we call success?

We can provide a statistically significant benefit that disappears when you leave the hospital!

Yawn. Let us know about treatments that make a difference in outcomes that matter.
 


Click on the image to make it larger.
 

Even the authors do not make exaggerated claims.
 

Among patients with suspected ACS, out-of-hospital administration of intravenous GIK, compared with glucose placebo, did not reduce progression to MI.[6]

 

Further studies are needed to assess the out-of-hospital use of GIK as therapy for patients with ACS.[6]

 

Maybe we should listen to the authors encouragement to not read too much into this study. Studies of 20,000 earlier patients did not show benefit.

Further study is needed, not further hype.

This is an interesting treatment idea, but it should only be used as a part of a controlled study.
 

Go read the comments of some astute emergency physicians on this study –

The IMMEDIATE trial: Should EMS give Glucose-Insulin-Potassium? by Dr. Brooks Walsh in Mill Hill Ave Command.

and

Glucose-Insulin-Potassium For MI? By Dr. Ryan Radecki in EM Literature of Note.

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Footnotes:

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[1] Intramuscular versus intravenous therapy for prehospital status epilepticus.
Silbergleit R, Durkalski V, Lowenstein D, Conwit R, Pancioli A, Palesch Y, Barsan W; NETT Investigators.
N Engl J Med. 2012 Feb 16;366(7):591-600.
PMID: 22335736 [PubMed – in process]

Free Full Text from N Engl J Med.

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[2] A View From the Eagle’s Nest: A Recap of the 2012 EMS State of the Sciences Conference
Nov 2 2012 9:30AM
Room: 210
Category: General
Paul E. Pepe
Conference schedule for Friday

Current Topics in EMS Research
Nov 1 2012 4:30PM
Room: 219
Category: Educator
Jonathan R. Studnek, Ph.D
Conference schedule for Thursday

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[3] Misrepresenting Current Topics in EMS Research from EMS Expo – RAMPART
Rogue Medic
Fri, 02 Nov 2012
Article

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[4] Should We Start Using a Glucose-Insulin-Potassium Cocktail
Rogue Medic
Wed, 04 Apr 2012
Article

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[5] Flawed Helicopter EMS vs Ground EMS Research – Part I
Rogue Medic
Wed, 18 Apr 2012
Article

Part II

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[6] Out-of-Hospital Administration of Intravenous Glucose-Insulin-Potassium in Patients With Suspected Acute Coronary Syndromes: The IMMEDIATE Randomized Controlled Trial.
Selker HP, Beshansky JR, Sheehan PR, Massaro JM, Griffith JL, D’Agostino RB, Ruthazer R, Atkins JM, Sayah AJ, Levy MK, Richards ME, Aufderheide TP, Braude DA, Pirrallo RG, Doyle DD, Frascone RJ, Kosiak DJ, Leaming JM, Van Gelder CM, Walter GP, Wayne MA, Woolard RH, Opie LH, Rackley CE, Apstein CS, Udelson JE.
JAMA. 2012 Mar 27. [Epub ahead of print]
PMID: 22452807 [PubMed – as supplied by publisher]

Free Full Text From JAMA

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Filed Under: ACS, EMS Expo, Heresy, Pharmacology, Research

Influence of Sex on the Out-of-hospital Management of Chest Pain – Part II

Tue, 15 May 2012 08:00:22 -0400 by
ResearchBlogging.org

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Part I was written in 2010, so I am a bit late in continuing to ridicule this example of bad research.

How do we determine what is good care for our patients?

By having our treatment follow the category that dispatch dispatch assigned the call? I used to work in a county, where this did appear to be the case. The medics would become very upset with dispatch if they did not receive a lot of information about the patient prior to arriving on scene.

Dispatchers would express surprise when I would tell them that I did not care about the information they could obtain over the telephone from some unknown person.

Why?

Apparently, these medics never learned to assess patients themselves.

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We conducted a population-based retrospective cohort study of 800 randomly selected patients over the age of 30 years for whom EMS were dispatched for a complaint of chest pain during a single year.[1]

These are not patients with a medical complaint of chest pain, but patients dispatched as chest pain – for whatever reason.

These are not patients considered to be cardiac by the emergency physician, but patients dispatched as chest pain.
 


 

The main outcome was adherence to state EMS protocols for treatment of patients over age 30 years with undifferentiated chest pain. Rates of administration of aspirin, nitroglycerin, and oxygen; establishment of intravenous (IV) access; and cardiac monitoring were measured.[1]

Should we give aspirin (as a cardiac treatment) to patients who do not have, and never did have, chest pain?

Should we give nitroglycerin (as a cardiac treatment) to patients who do not have, and never did have, chest pain?

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The role of dispatch is not to determine the treatment for the paramedics or for the physicians. The role of dispatch is to prioritize getting the right people to the patient in the right amount of time.

What information do I want from dispatch?

How many patients they believe are there.

Trauma vs medical.

Reports of any violence or anything suspicious of violence.

Who else is responding.

Any reports of traffic problems in the area, or other unusual events that might affect what we do.

Unusual (or amusing) things picked up during the phone call.

The location of the patient.

Should there be any more of an exchange of information than the following?

Respond to location X for an adult with chest pain. X is also responding.

10-4.

Dispatch has more important things to do than to do assessments for incompetent medics.

According to the authors of the study, if dispatch mentions chest pain, I am supposed to follow my Suspected ACS (Acute Coronary Syndrome) protocol, even though that protocol does not mention anything about receiving medical direction from dispatch. The protocol begins with the words, Initial patient contact. Why doesn’t the protocol begin with Dispatch Diagnosis?

I work in the same state. The protocols have changed since the study, but dispatch is only mentioned three times in my paramedic protocols. All of these times are only related to cardiac arrest.

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Maybe I will write a Part III. Maybe, if I do write it, it will not take over two years.

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Footnotes:

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[1] Influence of sex on the out-of-hospital management of chest pain.
Meisel ZF, Armstrong K, Mechem CC, Shofer FS, Peacock N, Facenda K, Pollack CV.
Acad Emerg Med. 2010 Jan;17(1):80-7.
PMID: 20078440 [PubMed – indexed for MEDLINE]

Free Full Text from Academic Emergency Medicine

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Meisel, Z., Armstrong, K., Crawford Mechem, C., Shofer, F., Peacock, N., Facenda, K., & Pollack, C. (2010). Influence of Sex on the Out-of-hospital Management of Chest Pain Academic Emergency Medicine, 17 (1), 80-87 DOI: 10.1111/j.1553-2712.2009.00618.x

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Filed Under: ACS, Cardiology, Heresy, Irrational Government Oversight, Pharmacology, Research Blogging

Should We Start Using a Glucose-Insulin-Potassium Cocktail

Wed, 04 Apr 2012 14:40:18 -0400 by

ResearchBlogging.org
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For two weeks straight, JAMA released EMS-related papers that received a lot of attention from the media. A clear, irrefutable trend. 😳

OK, this paper is just an early release of a paper that is only available online.

Those unfamiliar with research have been making the usual exaggerated claims that come from wishful thinking and not considering the possible harm from rushing to adopt a treatment based on weak evidence.

Should we rush to make this another standard treatment, that will become a Standard Of Care through inertia and tradition?

 

No.

 

Ignore the media.

There are some other things to consider. This study is examined clearly and thoroughly by a couple of very trustworthy doctors on their blogs.[1] [2]

For some different perspective, look at a graph of the numbers of patients involved and the tiny benefit –


Click on graphs to make them larger.

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OK. We can ignore that the study was originally supposed to be large enough to produce statistically significant results – 15,450 people.

We can ignore that the resulting number of patients is only 6.7% of the original and that the error bars on the results are frequently much larger than the possible benefit of treatment.

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Even looking at just the patients enrolled, the possible benefit loses significance after discharge.

Do we want a repeat of epinephrine?

Half a century of lack of survival benefit based on an unimportant surrogate endpoint. Is appeal to the Standard Of Care anything other than a logical fallacy?

We can provide a statistically significant benefit that disappears when you leave the hospital.

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Even the authors do not make exaggerated claims.
 

Further studies are needed to assess the out-of-hospital use of GIK as therapy for patients with ACS.[3]

Maybe we should listen to the authors encouragement to not read too much into this study. Studies of 20,000 earlier patients did not show benefit. Further study is needed, not further hype.

Go read –

The IMMEDIATE trial: Should EMS give Glucose-Insulin-Potassium? by Dr. Brooks Walsh in Mill Hill Ave Command.

and

Glucose-Insulin-Potassium For MI? By Dr. Ryan Radecki in EM Literature of Note.

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Footnotes:

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[1] The IMMEDIATE trial: Should EMS give Glucose-Insulin-Potassium?
Mill Hill Ave Command
Wednesday, March 28, 2012
Article

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[2] Glucose-Insulin-Potassium For MI?
EM Literature of Note
Friday, March 30, 2012
Dr. Ryan Radecki
Article

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[3] Out-of-Hospital Administration of Intravenous Glucose-Insulin-Potassium in Patients With Suspected Acute Coronary Syndromes: The IMMEDIATE Randomized Controlled Trial.
Selker HP, Beshansky JR, Sheehan PR, Massaro JM, Griffith JL, D’Agostino RB, Ruthazer R, Atkins JM, Sayah AJ, Levy MK, Richards ME, Aufderheide TP, Braude DA, Pirrallo RG, Doyle DD, Frascone RJ, Kosiak DJ, Leaming JM, Van Gelder CM, Walter GP, Wayne MA, Woolard RH, Opie LH, Rackley CE, Apstein CS, Udelson JE.
JAMA. 2012 Mar 27. [Epub ahead of print]
PMID: 22452807 [PubMed – as supplied by publisher]

Free Full Text From JAMA

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Selker HP, Beshansky JR, Sheehan PR, Massaro JM, Griffith JL, D’Agostino RB, Ruthazer R, Atkins JM, Sayah AJ, Levy MK, Richards ME, Aufderheide TP, Braude DA, Pirrallo RG, Doyle DD, Frascone RJ, Kosiak DJ, Leaming JM, Van Gelder CM, Walter GP, Wayne MA, Woolard RH, Opie LH, Rackley CE, Apstein CS, & Udelson JE (2012). Out-of-Hospital Administration of Intravenous Glucose-Insulin-Potassium in Patients With Suspected Acute Coronary Syndromes: The IMMEDIATE Randomized Controlled Trial. JAMA : the journal of the American Medical Association PMID: 22452807

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Filed Under: ACS, Heresy, Pharmacology, Research Blogging
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