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The OMI Manifesto

Pendell Meyers, MD and Stuart Swadron, MD, FRCPC
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Nurses Edition Commentary

Kathy Garvin, RN and Lisa Chavez, RN

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EMRAP_2018_09_September_Written Summary 440 KB - PDF

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Robert N. -

I don't think it is surprising (if one didn't already know) that a STEMI/NSTEMI doesn't always mean occlusion/no occlusion when it comes to the cath lab. When listening to this episode, I was waiting for that shiny piece of useful information to come forth, i.e. "when seeing a patient in the ED with chest pain, these findings on EKG or these symptoms should lead you to activate the cath lab". The episode ended and I was left wanting. Does this information exist and you are just holding out? Are you building the suspense for a follow up podcast next month? If that is not the case, this information is essentially useless when it comes to practical application in the ED as it will not lead to any change in anyone's clinical practice.

Harvey M -

If it is not surprising to you that STEMI criteria frequently misses total coronary occlusions, then you should probably express concern about your patients who suffer bad outcomes from missed total (or near total) occlusions. Since you have known this so long then hopefully you have looked for literature and educational material in the past 10 years or so to help you with your concern. Assuming you have tried to find such material, then you have been very unfortunate to miss all of the content published by EMRAP, Dr. Smith's ECG Blog, Amal Mattu, EMS 12 Lead, as well as the literature publications, etc in the last 10 years, some of which might fulfill your desire for "shiny" information.

For those listeners who did not have your preexisting knowledge, I mentioned specifically in the podcast that the only way to become better at the reperfusion decision is to spend time and effort practicing by correlating EKG findings with patient outcomes. I also mentioned specifically that we have nearly 1,000 individual cases on Dr. Smith's ECG Blog with advanced ECG instruction and patient outcomes to facilitate your learning. Take, for example, my latest post a couple days before your comment ( This post teaches the intricacies of hyperacute T-waves, monitoring for re-occlusion, and shows the difference we can make for a patient if we use such skills to diagnose the occlusion earlier than the STEMI criteria can.

So no, I am not "holding out". I said clearly that information already exists to improve your skills, and I told you where to go if you are truly interested. I am sorry that I must be the first one to tell you that solving the most common and most deadly problems in medicine cannot be accomplished with a quick, "shiny" piece of information.

As I said in the podcast, I do not expect this podcast to change clinical practice anytime soon - OMI is a potential idea for the future of our MI paradigm which will require decades of research and collaboration. What should change your practice in the meantime is the time you will spend learning ECG findings which predict acute coronary occlusion. Take this case for example to see how my practice was changed by what I learned:

This post, also by both of my mentor authors on the OMI Manifesto, may be of some interest for those without time or attention:

Here's the cheat sheet for instant gratification with minimal cognitive effort spent learning!

Also see the end of the OMI Manifesto document for a table showing specific ECG findings for Occlusion MI in various contexts and their publications:

Robert N. -

Apparently I have offended with my above comment. It was not my intention.
A few points:
1) The difficulty I have in calling presumed cardiac ischemia an OMI/NOMI is that it suggests that I know what the future of a potential cath would reveal. If this nomenclature were to be adopted, I would call my cardiologist after seeing a patient/EKG and state that I have a cardiac occlusion sitting in front of me and that they should proceed to the cath lab, when in reality the only way that this disease can be referred to in those terms is post-cath. Stating that I have a patient with chest pain (or other symptom) with features (symptoms/EKG findings) that are generally associated with occlusion is a different story. Maybe I am splitting hairs here.
2) As I understand it, EM:RAP is a podcast that is meant to help people learn and to teach them in a different manner. Of course, listening to a podcast is not expected to supplant all of the potential knowledge one can have. Obviously, time spent reading /studying will be required to gain some level of mastery of any topic. Nearly 20 minutes was spent on this episode to tell people that based on research, our current thinking is wrong 20-25% of the time presumably with the hope that we can do better in the future. Pairing your response to my question above, the podcast went something like this: “Hey listeners, we are wrong 20-25% of the time in both directions when it comes to determining who truly has occlusive disease. I’m not going to spend any time telling you how we can change this. You’re just going to have to read more or visit my EKG blog.”
In my opinion, a better use of time on an episode would look a little more like this: “Hey listeners, we are wrong 20-25% of the time in both directions when it comes to determining who truly has occlusive disease. Here are the symptoms/EKG findings that tend to be more consistent with patients that have occlusion. (Take 2 minutes to list those things). If you want to do some more reading, see these resources.” This is why I was hoping you were going to do a follow up episode addressing these things. Apparently, this is not going to be the case.

I don’t think anyone listening to EM:RAP expects to gain clinical competence from the podcast alone. You obviously spend a great deal of time studying this topic. We would all love to glean some knowledge while driving on the way into a shift to reinforce the work we put into reading/studying. Generally speaking, it’s not the EM people that require convincing. I work at an institution where it is notoriously difficult to get our cardiologists to do anything emergent, including STEMI’s (pardon my language). Trying to convince them to go to cath lab emergently on something that doesn’t look like a tombstone would be even more difficult. Leveraging the knowledge of people smarter than myself in defense of the patient sitting in front of me may help to change the future for that patient. I am pretty sure that I can recognize the subtle and the obvious findings of ischemia on an EKG. But if there is something that I don’t know, some pearl that I have missed/haven’t heard of, and you can provide this with a simple sound byte, why wouldn’t you? In the end of your response, you list resources for these pearls. Happy to read them. But put this stuff into an episode. Its what we all want to hear.

Alexander B. -

Aloe vera

Timothy H., Dr -

OMI vs NOMI is a pathological classification and has management consequences for the patient involved.
It is useful paradigm in that it reframes the patients presentation so that we avoid unconscious bias in our assessment and management of the patient.
However confirmation occurs in the Cath lab for the most part and therefore I question the impact it will have on current practice.
As a practicing ED Physician the biggest issue is information dyssymmetry where you initially just have a history and your bedside examination to guide initial decision making.
Decisions have to be made heuristically and I believe that this already happens with the current concepts; flawed as they are.
At the bedside the ECG has been the most useful tool to decide who to lyse/anticoagulate and progress therapy. A dynamically changing ECG or overt ST segment elevation obviate intervention wither through PCI or thrombolysis as the presumption at that stage is that this is occlusive disease.
Takitsubo Cardiomyopathy can masquerade as an MI and not have occlusive disease but that diagnosis is not obvious at the time of initial assessment and I am sure there are other causes of ECG/biomarker changes that may mimick occlusive disease.
I believe the next evolution of bedside assessment for ACS is echo. This will complement all of the current tools in our arsenal but even that will not differentiate between occlusive versus nonocclusive MI.
Personally I have found bedside echo to be extremely useful as once there has been an ischemic assault there is often myocardial stunning and although the ECG may be normal at the time of assessment there is overt regional wall motion abnormalities present.
As a craft group we need to be open to changes in paradigms of thinking and approaching clinical issues.
I thank you for sharing with us and look forward to hearing more from you in the future.

Harvey M -


Thanks for your thoughtful reply. I would like to comment point by point.

1) "OMI vs NOMI is a pathological classification”
First of all, the STEMI vs. NSTEMI paradigm is already simply a poor surrogate for a pathologic classification (if cardiologists didn’t think STEMIs had an blocked artery to open up, they wouldn’t take them to the lab would they?). Moreover, all vascular occlusion paradigms determining the need for emergent intervention use “pathologic” definitions. The need for vascular intervention on an acutely occluded SMA is defined not by the bedside impression and screening tests, but rather by the fact that the vessel is occluded or nearly occluded on CT angio of the abdomen in an appropriate clinical setting. Same goes for brachial artery occlusion - the clinical exam and beside evaluation is not enough - you must perform emergent confirmatory imaging study to determine whether emergent intervention is warranted or not. If you miss an SMA occlusion, and this is found 2 days later after huge mesenteric infarction, this is an unacceptable false negative. Yet in the MI paradigm, somehow this is not considered a false negative because the bedside screening test was not obvious. This makes no sense.

2) “However confirmation occurs in the Cath lab for the most part and therefore I question the impact it will have on current practice.”
Confirmation for all vascular occlusive emergencies happens via radiographic confirmation and intervention. This is how we perform vascular interventions in stroke, acute limb ischemia, mesenteric ischemia, and essentially all other important arterial ischemia syndromes which have emergent intravascular reperfusion therapies. Simply because it is more difficult to diagnose than other vascular occlusions (which aren’t moving in real time, enabling CT angio), does not mean that the goal of the paradigm is different. It just makes it more difficult. The fact that it takes more effort to perform an angiogram than a CTA does not magically change the fact that an emergent arterial occlusion must be diagnosed.

3) “Decisions have to be made heuristically and I believe that this already happens with the current concepts”
Decisions about emergent management of arterial occlusions resulting in irreversible loss of important tissue are generally not made heuristically in settings where more advanced care is available. Name one other arterial occlusion paradigm where you have the culture of simply NOT diagnosing the occlusion and NOT applying emergent reperfusion based on beside heuristics? Imagine a stroke patient who presents to a hospital capable of emergent CT angios of the brain and emergent large vessel thrombectomy - you do not apply heuristics to decide whether this patient warrants vascular intervention, you emergently evaluate for large vessel occlusions and perform intervention if feasible. An elderly patient presents with abdominal pain out of proportion to exam findings, AFib, and elevated lactic acid - you do not perform “heuristics" to decide whether this man needs vascular surgery, you perform a CT angio of the abdomen.

You don’t have to “believe” or speculate that this already happens, because we have literature telling us what happens with the current concepts. False positive rates currently range from 15-35%, and false negatives are around 25-30%. For the most common, most rapidly deadly (when deadly), and overall most deadly occlusion syndrome on a population level, this is unacceptable.

4) “Takitsubo Cardiomyopathy can masquerade as an MI and not have occlusive disease but that diagnosis is not obvious at the time of initial assessment and I am sure there are other causes of ECG/biomarker changes that may mimick occlusive disease.”
I agree that takotsubo CM can perfectly mimic occlusion MI and STEMI. And I agree that there are MANY other causes of ECG changes that may mimic occlusion MI and STEMI as well, and these things are not always obvious on initial exam. The only thing that can definitively rule out ACS as the cause of these findings is the emergent angiogram.

So this point works in my favor, not yours. The paradigm cannot be defined on nonspecific beside screening tests when an emergent, treatable cause is suspected and can be ruled out emergently. Just like many abdominal pathologies may mimic large vessel occlusion mesenteric ischemia - as the emergency physician we must rule out the most dangerous and most treatable causes, so when we suspect possible mesenteric ischemia we order a CT angio (if available in your practice) to definitively evaluate for acute occlusion rather than simply assume that our initial bedside impression and screening tests were correct.

5) “I believe the next evolution of bedside assessment for ACS is echo.”
I agree that bedside echo is very important helping inform the reperfusion decision. However it is not able to differentiate old from new WMAs. It is not able to differentiate takotsubo CM from occlusion MI. A WMA without ECG findings as you describe cannot be distinguished from a baseline WMA. We have many cases on our blog of how useful cardiac bedside US can be to help with the decision. This is why we even added bedside echo to our prototype diagram of the Occlusion MI paradigm near the end of the OMI Manifesto manuscript (see full text). Overall, echo is just another imperfect surrogate screening tool for what you care about - whether you need to open up an acutely occluded coronary artery. Experts must spend much time to be very good at ECG and echo, however at the end of the day they know that these are imperfect and cannot be used to define a paradigm in isolation.

Timothy H., Dr -

We are essentially saying the same thing.
Bedside tests are not perfect and that acute obstruction needs to be addressed immediately.
This is the standard of care.
NSTEMI/STEMI; NSTEAC/STEAC or OMI/NOMI has not changed that.

Harvey M -

Forgive me, but we are not saying the same thing.

We agree that acute obstruction needs to be addressed immediately, but this is obviously NOT the current standard of care for acute MI. Under the STEMI/NSTEMI paradigm, it is NOT standard of care to emergently treat acute occlusion unless they meet STEMI criteria. I'm pointing out that MI is the only vascular paradigm where the standard of care allows us to miss occlusions and think we did the right thing.

How can you say that identifying acute occlusions is the current standard of care if you agree that STEMI/NSTEMI misses acute occlusions? This is internally inconsistent.

At Dr. Smith's ECG Blog we have collected case after case of patients with "NSTEMI" with total occlusion who suffered death and missed severe MI, who all received the "standard of care." We all know this happens everywhere. And the data proves it with 60,000 NSTEMI patients: 25-30% missed occlusions (these are the ones that are published!) and almost double the mortality (still overall not that high) in the NSTEMI group for the patients who had a missed occlusion.

It is literally the name "STEMI/NSTEMI" that inspires or propagates the belief that total occlusions without STEMI criteria do not need emergent management.

The name STEMI/NSTEMI is a big part of the problem. It must be changed if we want the standard of care to identify acute occlusion. Our theory is that OMI/NOMI might one day change the standard of care, because the current standard of care misses important acute occlusions.

Timothy H., Dr -

Take Home Points

There is a problem with the way we classify and manage acute MI.

I agree. This is why NSTEMI/STEMI became NSTEAC/STEAC (Non ST Elevation Acute Coronary Syndrome) which was an attempt to move away from over reliance on the ECG as the sole discriminator for acute coronary obstruction.
It was replacing a bedside diagnostic test as a primary decision making tool with a syndromic approach which includes not only ECG changes but other signs and symptoms that would predict an increased likelihood of obstruction (National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand: Australian clinical guidelines for the management of acute coronary syndromes 2016).

Patients without STEMI on the ECG may still have acute occlusion of a coronary artery and benefit from revascularization.

Absolutely agree hence the 25-30% miss rate in the article.

There are multiple harms associated with PCI.

Agree also.

The STEMI/NSTEMI paradigm is wrong in identifying acute coronary occlusion about 25-30% of the time.

You’ve provided the evidence for this and I agree.

As I pointed out above; there have been attempts at the highest levels to address this issue including rebranding NSTEMI to NSTEAC and STEMI to STEAC.
That is an ECG based diagnosis (NSTEMI/STEMI) to a syndromic one (NSTEAC/STEAC).

This brings me back to my original point that NOMI/OMI is linked to the underlying cause / pathology as the basis for cognitive assessment and management decisions.

Our regional experts have long recognised the disparate results and tried to address this issue with the previous iterations of the National ACS guidelines.

Ultimately it comes down to the risk assessment of each individual patient and an intercollegiate discussion about patient disposition and management.

As an anecdote I managed a patient who had no risk factors but presented with near syncope and left arm pain which resolved. His initial ECG was normal however bedside echo revealed anterolateral wall motion abnormalities which prompted an emergent discussion with cardiology. Subsequent ECGs demonstrated a rise in the ST segment and at PCI the patient was found to have occlusive LAD disease.

Having a conceptual framework on which to base clinical decision making is important and rebranding to change the way we think or based on an improved understanding of pathology/pathophysiology is always necessary if we are to progress Medicine.

So in summary I agree with the take home points.

And Yes! I forgive you.

Harvey M -

Excellent discussion, thanks Timothy

Sean G., M.D. -

Well I thought it was excellent, and while I knew the issue w STEMI/NSTEMI existed I was not aware how bad the prognostics were. I agree totally that a change in Nomenclature is helpful. We are what we speak to a certain extent and since we are missing a sig number I think changing the nomenclature would help keep us actively aware that we should not blindly just follow the STEMI/NSTEMI paradigm, of course we are still held to the core measure issue, but changing our words is the first step in truly changing our thought process, while one can probably use the current nomenclature and remain aware, I think it makes recall of these issues more challenging when we are pressed. This was my favorite segment this month. thanks much. I worked w a Cards recently who CLEARLY did not get this. The doc is in his 60's.

Harvey M -

Thanks Sean!

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EM:RAP 2018 September Full episode audio for MD edition 213:30 min - 313 MB - M4AEM:RAP 2018 September Canadian Edition Canadian 25:37 min - 35 MB - MP3EM:RAP 2018 September German Edition Deutsche 99:49 min - 137 MB - MP3EM:RAP 2018 September French Edition Français 21:59 min - 30 MB - MP3EM:RAP 2018 September Aussie Edition Australian 39:22 min - 54 MB - MP3EM:RAP 2018 September Spanish Edition Español 78:35 min - 108 MB - MP3EMRAP 2018 08 Sept Individual MP3 277 MB - ZIPEMRAP 2018 09 Sept Board Review Answers 130 KB - PDFEMRAP 2018 09 Sept Board Review Questions 238 KB - PDFEMRAP 2018 September Summary (SPA) 763 KB - PDFEMRAP 2018 09 September Individual Summaries 765 KB - ZIPEMRAP_2018_09_September_Written Summary 440 KB - PDF

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