T.R. Eckler (2): That was the deepest most heavy section we have ever done
on the podcast And if you can just get that from this you're gonna be
the greatest emergency doctor and you will really be carrying water in
your pale for your cardiology folks
Sam : Hi everyone, and welcome to another episode of EMPlify
I'm your host, Sam Ashoo.
Before we dive into this month's episode, I want to say thank you for joining us.
I sincerely hope that you find it to be helpful and informative for your
clinical practice, and I want to remind you that you can go to ebmedicine.net
where you will find our three journals, Emergency Medicine Practice, Pediatric
Emergency Medicine Practice, and Evidence Based Urgent Care, and a multitude of
other resources, like the EKG course, the laceration course, interactive
clinical pathways, just tons of information to support your practice
and help you in your patient care.
And now, let's jump into this month's episode.
Sam (2): Welcome back, ladies and gentlemen to the podcast.
I am one of your hosts, Sam Ashoo, and on the other side of the microphone,
T.R. Eckler (2): Expert at Rural Medicine TN case administration Dr TR Eckler
Sam (2): that is quite the niche.
You are a TN case list.
T.R. Eckler (2): we gotta work on that lytic-ologist is pretty good I'm a lot of
Sam (2): that Oh, I do like, the sound of that.
today we're talking about the emergency medicine practice article.
This is the February 20, 26 issue on acute coronary occlusion.
So things that will occlude your coronary artery, authored by Dr. Horning.
And really a thorough review, I think of this topic.
I thought it was very well written and today we're gonna try and summarize that
all for you quickly in this podcast.
But this is definitely one of those articles you just need to go read.
Lots of figures, lots of EKGs, lots of examples which are very, very helpful.
We'll do our best to convey over the microphone.
But I strongly recommend you just go look at these diagrams and
why are we talking about this?
Well, because this is a pretty significant piece of our population in the emergency
department, and I love the numbers.
So the numbers say somewhere between 25 and 30% of high risk patients
with acute coronary occlusion fail to meet the traditional STEMI criteria.
And that's what we seem to be always talking about, STEMI or non STEMI.
But it turns out somewhere like a third of those patients don't
meet STEMI criteria, and yet they have an acute coronary occlusion.
And conversely, somewhere between 15 and 35% of STEMI activations end up being
false positives without a culprit lesion.
So there's still a significant number of people who fall outside of the
STEMI, non-STEMI categorization, and we're always looking for better
ways to try and redefine them.
And one of them is this scheme of acute coronary syndromes
and acute coronary occlusions.
And what kinds of things are more likely to be occlusions, not just STEMI on EKG.
The American Heart Association and the American College of Cardiology in 2025
published updated guidelines for the management of acute coronary syndromes.
And so we'll talk about some of those today and let you know where we stand
with things that are STEMI equivalents.
And that's a, a very, very important topic that we'll touch on in a little bit.
But first, some interesting nomenclature.
So, ACO acute coronary occlusion is a term that encompasses all things
that will occlude a coronary artery.
So not just STEMI.
And as I mentioned before, there is some newer data that suggests that
the STEMI, non-STEMI categorization system is a little inadequate.
There was a, a large study in 2024 was a meta-analysis of 23,000 patients and found
that the pool sensitivity for STEMI for actually detecting coronary occlusion was
only 43%, which I found shockingly low.
There was another meta-analysis of 40,000 patients with non
STEMIs and about a quarter of them had acute coronary occlusion.
So that suggests that what we are doing, in forcing people into a
categorization system of STEMI versus NSTEMI, is actually inadequate
and there's room for improvement.
So, glad to see the conversation is still ongoing.
The, there is a new nomenclature that's kind of leaching its way into the
literature and in the common practice of occlusion, myocardial infarction
versus non occlusion myocardial infarction, or OMI versus NOMI.
And the, the paradigm there is really more about the underlying physiology
is the coronary artery occluded?
And can we pick up on STEMI or any other EKG pattern that suggests that
this is an occluded coronary artery?
and interestingly enough, the authors suggest that maybe.
As we look at things that are STEMI equivalents, as we look at some adjunct
tools like AI interpreting EKGs or helping us interpret EKGs that maybe we could
get better and improve on our diagnostic capability for acute coronary inclusion,
which I thought is a worthwhile cause.
T.R. Eckler (2): I thought this was a great summary of what I think is kind of
like the big transition in the evidence and the data that we're staring at right
now And I think it's a good thing for you as the emergency provider at the bedside
to basically realize that if you think your patient is sick and if you think
that this patient could be having a heart attack It doesn't just have to rely on
them having elevation of their ST segment on their EKG We're gonna talk about a lot
of other things today that can indicate that and I think this is gonna empower
you to take the the patient in front of you that you're worried about and the
EKGs that you're looking at and take them to your cardiologist and say Hey I know
it's not a STEMI but I see this What do you think And it's gonna give you more
tools to catch more of these patients that really do have an occlusion that isn't
gonna show up by the classic guidelines
Sam (2): Yeah.
Well, well said.
In our typical method, we start talking about a diagnosis, and
the first thing we mentioned is the differential diagnosis for it.
There's a great table, table one on page six, which goes through
all of the diagnoses that should be on your differential for STEMI.
This includes everything from a true MI to pericarditis and myocarditis
and takatsubo cardiomyopathies as well as non coronary things like
pulmonary embolism aortic dissection coronary vasospasm left ventricular
hypertrophy, and on and on and on.
This is a very long list, but it talks about the specific diagnoses
and then what you might see on A EKG that might mimic something going on
like an acute coronary occlusion.
So I thought that was a helpful list.
It's definitely a list of things you need to keep in mind when you are seeing these
patients in the emergency department.
And as I mentioned before somewhere around a quarter of the patients who make it
to the cath lab have normal coronaries or are found not to have a culprit
vessel that has led to the STEMI alert.
So it's important that you keep the differential in mind.
Your patient may end up having another one of these other diagnoses.
For our pre-hospital personnel, the author did a great job of
reinforcing the importance of EMS as a partner in this system.
So if you live in an urban area, hopefully you guys already have a
STEMI alert system that will get a hold of a hospital with PCI capabilities.
Send field EKGs ahead of time.
Maybe do multiple ones if the transport is any kinda lengthy transport.
The goal.
Is an EKG within 10 minutes of first medical contact.
And that includes EMS.
So if you're gonna be on scene for a while, or if it's gonna take you longer
than 10 minutes to get this patient to the hospital, that first EKG is
yours and is very, very important.
And if it's non-diagnostic, a repeat, EKG is equally as important.
Especially if it's starting to show some transient or developing changes.
Those are all very, very important and things you want to be able to transmit
ahead of time or print or transmit and print and provide to the physician when
you arrive at the hospital so that they can look and see that, oh yes, this EKG
is evolving in front of our own eyes.
A second or third field, EKG by EMS was found to identify up to 15% of
additional STEMI cases that were not present on the initial ECG.
So it definitely makes a difference.
And the author corroborated that your typical STEMI protocol
for pre-hospital treatment is exactly what you should be doing.
You're gonna administer that aspirin . You're gonna give the
sublingual nitroglycerin 0.4 milligrams every five minutes for
three doses as needed for the symptoms.
And then you're only going to give oxygen if they're hypoxic
less than or equal to 90%.
So not everybody needs oxygen.
It's only those who are hypoxic that really need the oxygen.
We'll get into this a little later, but there is evidence showing
that it's completely useless.
If they're not hypoxic, it doesn't add anything clinically
relevant for the patient.
So, aspirin, sublingual nitro oxygen.
Get an EKG, get a repeat EKG if there's gonna be any kind of delay.
And most importantly, if you can get them to a PCI capable hospital, if they have
suspected or confirmed STEMI on their ECG.
A very, very important step.
If you're in a rural area your hospital choices are very limited
then 90 minutes is about the cutoff time for first contact, to balloon
time for a PCI capable hospital.
If your first contact as an EMS person to, whenever they can inflate that balloon
in the coronary artery is gonna take longer than two hours, 120 minutes then
they want you to take 'em to a close hospital where they can get thrombolytics.
And hopefully that's all already protocolized for you in
whatever county you are working.
Especially if it's a rural place.
I know for us in our hospital, we have agreements with rural hospitals for
rapid acceptance and rapid transfer.
And so if you're in one of those outlying places and you're brought a patient, you
are expected to give TN K or whatever your thrombolytic is, and then rapidly get them
to our facility because we know they're just not getting here within 120 minutes.
And so, hopefully those hospitals have those agreements and if
you're in the EMS field, already have those protocols established.
They're very, very important, critically important.
So can't overstate the role of EMS in this particular scenario.
T.R. Eckler (2): I think one thing I would add to that is I think there's
such a challenge of rural EMS access and and only having like you know one or two
ambulances for a county in rural places I think there's a role for having these
discussions with your flight teams to see if someone clearly has a STEMI and you
can identify that In the field or identify that on first medical contact then looking
at whether or not you can get them there by flight or whether you can basically
move them to a hospital and bring the helicopter to the hospital and kind of
meet in the middle and then basically they can get lytics and get going I found in
practice that patients get better with lytics but then can sometimes become
unstable and need to still get quickly to a PCI center So I think there's a role
for like you know facilitating as two stage transport as soon as you can to get
these people to where they need to end up
Sam (2): Great points.
. And when they do get to where they need to end up, so hopefully in
our ED and we're trying to obtain a history, it's your typical history.
Not much has changed there.
So acute chest discomfort or dyspnea is usually the presenting symptom, but
they may complain of chest pressure, chest tightness, chest heaviness,
chest burning, whatever it is.
It's all under the blanket of some kind of discomfort.
There's gonna be some kind of radiation.
It might involve the arms or the neck or the jaw.
There might be associated symptoms.
There might.
Only be associated symptoms and no chest pain.
Things like nausea, vomiting, upper abdominal pain shortness of
breath, diaphoresis unexplained fatigue or even syncope.
So it's a wide net.
We cast in a bunch of symptoms that can present under the blanket
of acute coronary syndrome.
But just keep that in mind.
None of that has really changed, but it's important to remember.
T.R. Eckler (2): I think especially having a higher threshold for people that are
minimizers people that are very tough people that are trying to play down their
symptoms cause they need to go take care of family or pets or something else I
don't think I've ever regretted an EKG in my career and there's some tests where
I've been sad that I ordered them cause I wasn't sure the patient really needed
it But an EKG is a harmless test that you know other than driving my my poor EKG
techs crazy sometimes for all the EKGs that I want I would tell you that it's
never something that you're gonna regret getting on a patient And there are times
when they surprise you And I think if you got one and it makes you nervous then
I think you need to consider getting a second for those kind of people because
that's one of those things as you're taking the history and they come in and
they say Hey do you want an EKG on this patient You say yeah And can I get one
again in 15 minutes while you're having that conversation with the patient If
you offload that cognitive task in a busy time and you make it so that somebody
else is gonna make sure and get a follow up on that I've had a lot of luck where
I've caught things that I I don't think I would've caught from that second EKG
Sam (2): and, a prebuilt order set for that could also help.
Like, Hey, why, why do I have to place two orders?
I can just click one button.
The patient's 75 years old here with chest pain, they're
obviously gonna get more than one.
So here, I'm just gonna click the set.
That's gonna get me three.
So, definitely make it easier for yourselves and
definitely get the repeat EKGs.
when it comes to physical exam again, there isn't any single physical exam
finding that's gonna tell you somebody has an acute coronary occlusion.
That's the crux of it.
But you do have to remember that somewhere between seven and 10% of
patients who have mi are gonna be complicated by cardiogenic shock.
So, if they're hypotensive, if they're bradycardic, if they're
hypotensive and tachycardic if they look like they're in shock, just
keep mi in the back of your mind as a possible cause for that presentation.
'cause that definitely complicates matters very quickly.
T.R. Eckler (2): I still think you're looking to consider some of the other
diagnostic things here So like do they have a clot Do they have a recent surgery
Is their leg really swollen Do can you already hear the fluid in their lungs Can
you already notice some jugular venous distension patients like these often
are really easy to put ejs into because they're already backed up So I think
that that's always something that at a glance I'm looking at the patient and
going huh we're already backing up We're already starting to have trouble getting
blood through our heart there's something there I need to figure out whether that's
an occlusion in their their coronary arteries or it's a blood clot or it's new
onset heart failure from something else
Sam (2): Yeah.
And then of course there's the EKG.
So we're gonna spend a little time running through all of the
different methods of identifying acute coronary occlusion on EKG.
And why do we talk about it?
'cause it's one of the most frequently ordered tests that we
have in the emergency department.
There is data.
From a national cardiovascular registry that has over 40,000 patients
diagnosed with STEMI that found that 11% had an initial non-diagnostic
EKG, that's like one in 10 are gonna have a non-diagnostic one.
72% of those had a repeat ECG, where the STEMI was found, and that was
within 90 minutes of the initial one.
So it, there's definitely strong evidence that ECG will change and until we get to
the point where every ED has continuous 12 lead telemetry and you're catching
this live and watching it evolve, your only choice is to do intermittent EKGs
and get them repeated so one begets another, and that's totally okay.
T.R. Eckler (2): Can I make a brief plug to the fine people that are generating
all these electronic medical records I think that this is one of those places
where you could make medicine awesome If when I open an EKG on my computer it
automatically pulls up any old EKGs or any future EKGs Like let's say I pull one up
and there was one already done that was more recent And the last one I honestly
want to grid of four Like show me the four EKGs in this patient that are the
most recent If I pull one up like if it's a one in the future or three in the past
whatever But if you can pull up all four of those EKGs and let me quickly compare
them or just overlay them and let my brain do awesome things by looking at the four
and going oh geez look everyone else look pretty good But now this is up and this is
down huh There we are So I think there's room for not necessarily AI to do this
Just let me do it Show show me the data better and I'll do the the awesomeness
Sam (2): You could click on a lab and trend it with the
most recent past, six months.
Why can't I just click on an EKG and trend it in the same way?
Yeah, there's images involved, but hey, come on, AI can do it.
T.R. Eckler (2): One other piece And now now that I'm getting old I'm starting to
tell like what I was in residency stories but my my program director and just the
people that ran my hospitals in New York every EKG you were handed came with the
patient's most recent prior EKG So you got two EKGs every time you got handed an EKG
which was a heck of a pain in the butt for EKG techs But boy did it do a better job
of making you go wow this is way different And then you you had a clear idea that
you were dealing with something different And that's that doesn't need any smartness
to it other than just your EKG machines have to be enable you to pull up and print
the one that's today and whatever was prior And I would tell you that I think
that's probably a better standard of care than what a lot of places are doing now
Sam (2): Okay, well since we're on this topic, here's what I want epic and Oracle.
Since you're listening in all the technology companies, I want my EKG
Tech to walk into a room, do a 12 lead EKG, and then come to me with an iPad.
I don't want paper.
I want the iPad there.
I wanna be able to scroll to the left to see the previous EKG
from whatever year it was done.
I wanna be able to scroll to the right to see automatic grid lines appear.
I want my St baseline marked.
I want any st elevations in red.
I want the computer AI interpretation to bring my eyes
to any, any of the syndromes.
We're about to discuss any one of these.
And I want all my indices, all my intervals, all of this stuff in
the, in a little column on the left.
And I don't think that's too much to ask.
You know that That's it.
And then I just wanted to say, Hey, sign your name here, or, or it's an iPad.
Read my fingerprint.
I'm just gonna sign it.
Yeah.
Clock it for right now.
I saw it, and if it's a STEMI, I'm gonna push a little button and
that's gonna activate the order set and bring the patient to a room.
That's not too much to ask really.
Now it is.
T.R. Eckler (2): Could not be more jazzed about that idea
Give us what we want Computers
Sam (2): There's a technology company somewhere out there listening.
But back to the topic at hand, let's first talk about STEMI.
So, STEMI definition by EKG criteria has not changed a millimeter of ST segment
elevation in any two consecutive leads.
Starting at the J point, not including V two and V three, right?
So a millimeter in at least two consecutive leads, not
including V two and V three.
If the ST elevation is in V two and V three, it gets a little bit
more complicated because there are age and gender-based criteria.
So, for V two and V three, in the absence of left ventricular hypertrophy or a
bundle branch block, it's greater than two millimeters in men aged 40 years
greater than two and a half millimeters in men under 40 years old and greater
than 1.5 millimeters in women of any age.
Those have been around for a while and those are not changing the
magnitude of st segment elevation.
It starts being measured at the J point.
That's that transition from the, the s the qr s into the the section between the
S and the T. And the ST segment should be measured against some kind of isoelectric.
Baseline.
And that baseline is between the end of the T wave and the
beginning of the next P wave.
And so anything compared to that would be ST elevation or depression.
And then we talk about our STEMI equivalents.
So again, a great table, page eight.
Table number two, STEMI equivalents.
You've got things like left bundle branch blocks or ventricular paced
rhythms with SCARBOSA You've got the Smith modified SCARBOSA criteria.
You've got Hyperacute T waves, posterior STEMI, and the de Winter sign.
So that's five different STEMI equivalents we're gonna touch on real
quick . If there is the presence of a left bundle branch block or some
kind of ventricular paced rhythm.
You can still identify STEMI.
Scarbosa criteria were first published in like 1996, and you have to get a
total score of three or more points.
And those points are awarded based on the presence of three things.
One is concordant ST elevation greater than a millimeter.
In a lead with a positive QRS.
So a positive ST elevation with a positive QRS and the ST elevation
is more than a millimeter.
That's five points.
That's automatic your in.
Concordant ST depression greater than a millimeter in the anterior leads, so V
one through V three, that's three points.
Again, automatically you're in.
The discordance.
So that's the QRS is heading in one direction and the st
segment's heading in another.
This is the most frequent finding we're gonna see in the left bundle branch block.
But if that discordance is bigger than five millimeters, that's worth two points.
Now, alone, that's not enough.
'cause you gotta have three or more.
So you've gotta have it in conjunction with one of the other two.
And that is the traditional scarbosa criteria.
Those were modified that was published by Smith et al. And lovingly titled
the Smith Modified Scarbosa Criteria, which kind of tried to simplify matters.
The first two criteria stayed the same.
The biggest influence was on the third criteria where ST elevation at the J
point relative to the QRS had to be at least 25% 25 of the preceding S wave.
And again, this is way easier to show you on a figure.
Figure six demonstrates that very nicely, and all you're looking at is
the discordance between the ST elevation or depression and the QRS, which is
heading in the opposite direction.
It's the amplitude of the S wave or the R wave, depending on if it's a positive
or negative QRS and the depression or elevation of the ST segment.
And if that discordance is 25% or more, that's highly suggestive of mi. And it
improved upon the original scar bosa criteria by improving on the sensitivity.
T.R. Eckler (2): Okay So I think when we talk about the scar criteria I think
it's something that I've always really struggled with because to really take the
time and look at the EKG and figure it out I found that oftentimes cardiology
was not that impressed with most of the EKGs that I was concerned might meet
scarbosa because you had such a low sensitivity in a lot of those studies But
now with the Smith modified criteria that they give you you're basically taking the
sensitivity up from say 49-52% In some of the the the trials they have now with the
Smith modified criteria you get 80 to 91% sensitive And I think that gives you more
of a leg to stand on when you show these EKGs to cardiology to say Hey I'm looking
at the Smith Modified Scarbosa criteria and this really fits the criteria I really
think this should be considered a STEMI
Sam (2): Yeah, and I cannot overstate how important these figures are.
Please go look at them.
Figure five shows you the traditional scarbosa criteria, and figure
six shows you the modified Smith.
And again, Smith's objective was just to make the, the math simpler.
So we're just looking at a discordance of 25% or more measured in millimeters.
And that's sufficient to, to make the diagnosis.
And that's a, a handy little table to keep in your back pocket.
T.R. Eckler (2): I really like this too Just the the Smith approach to this
cause he went backward from the real pathology into like combing through
their EKGs and things and developed this that way And I think that's why
the numbers got so much better is he started from the the the patients with
disease and built backwards from there
Sam (2): The next STEMI mimic was Hyperacute T Waves.
So again, if you're not new to emergency medicine, you've heard this a bunch of
times already, but this is just saying that hyperacute or markedly tall and wide
T waves be port pretenders of badness.
So this is the the early STEMI sign, and if you sit around and
just watch this long enough, the ST segment's gonna follow soon enough.
But this is a STEMI equivalent.
T.R. Eckler (2): Don't sit around and watch this
Sam (2): Yeah.
T.R. Eckler (2): Take more pictures if the cardiologist isn't convinced but you don't
need to sit around and watch this You can just keep saying hyperacute T waves
until someone takes them to the cath lab
Sam (2): There was a, an interesting point the author made, and that's that it's
not about the height of the T-wave, it's about the area encompassed by the T-wave.
So width and height, the total area under that curve is what you're looking at.
It's not just how tall the T-wave is in, because, you can see peak T waves and
hyperkalemia or something of that sort.
It's gonna look remarkably different.
There's a great figure, figure seven there that shows you the big fat
T wave compared to a QRS complex.
And that's helpful to keep in mind.
Myocardial infarction or posterior STEMI has ST. Depression in
the anterior septal lead.
So V one, V two and V three are gonna show this deep ST depression with the
QRS complex being positive in V two and V three and that should really start
signaling some alarm bells in your brain.
My old attendings in medical school used to love flipping the EKG upside
down and looking at those anterior leads to kind of make it look like
there's st elevation which I still do.
Honestly, it helps me but the presence of those deep st depressions, V one through
V three especially if there's reciprocal ST segment elevation in other leads is, is
diagnostic and that's a STEMI equivalent.
There's usually a big dominant R wave in V two.
You might see some upright T waves in the anterior leads.
All of that adds to it and is incorporated in that, making that diagnosis.
You can do posterior lead placement.
So you can take V seven, V eight and V nine and stick 'em on the
back and get that posterior EKG.
Just know that if you do the posterior leads and you don't see
st elevation, it doesn't matter.
That is not an exclusion for acute coronary occlusion.
You still need to get your cardiologist on the phone and
treat this person like a STEMI.
So,
T.R. Eckler (2): they're always impressed Sam when you have the posterior EKG to
show em and I would tell you that of all the like how To do a diagnostic test
Stuff that lives in my brain nothing lives in my brain like V eight goes right
underneath the bottom of their scapula and then you just put V nine a little
next to their spine and V seven a little bit over laterally to that I've taught
so many EKG teachs that and then I'd love I love writing posterior and slashing 4
5 6 V 4 5 6 and turn it into V seven V eight V nine I feel like I really know
what I'm doing and most of those look pretty normal but I really thought that
this article did a great job of saying Hey if you're still worried about the
patient if the posterior EKG is negative this can still be an occlusion mi Take
those pictures to your cardiologist and say Hey I'm worried about this sweaty
diaphoretic dyspneic patient that looks like they're having a heart attack
Sam (2): Yeah.
And interestingly, you do those posterior leads and your
definition for STEMI is changing.
You only need a half a millimeter of elevation in any of those leads.
But please don't forget that if they don't have those st elevations
posteriorly, that's not an exclusion.
That doesn't tell you that their coronaries are okay.
But if they have the elevation that just really tightens up that diagnosis
for you and get you some bonus brownie points with your cardiologist.
T.R. Eckler (2): I think the the take I had from this article there's so many
diagnostic criteria It it's one of those things where like I think you have to
have a little paradigm shift in your head which is I'm worried about this patient
I think they're having a heart attack I'm gonna go through and test every single
one of these things to make sure there's not an easy way for me to say yes this is.
Cause it's not just about STEMI anymore It's about can I find a picture for
occlusion mi that fits this patient.
And if you're worried about em just keep pushing until you feel like
you've exhausted all routes and all cardiologists that'll listen to you
Sam (2): Yeah.
Yeah, that's a great point.
Really, this should be a checklist that you go through for somebody
who has a positive troponin.
Before you write the words non STEMI you need to make sure there's no
STEMI equivalent, and you should be going through this checklist.
The last one is the de winter sign.
So again, figure 10 is an excellent way to visualize it.
If you have access to the article the diagnostic criteria are one to three
millimeters of ST depression that's up sloping, starting at the J point in leads
V one through V six and associated with a big, tall, upright symmetrical T-wave.
And so it's a very distinct looking pattern and lots of case reports describe
it sometimes as a persistent pattern in patients with acute proximal left anterior
descending coronary artery occlusion.
And so those patients don't tend to do very well at all.
And if you see it on your EKG, you should be talking to a cardiologist very quickly.
So that's five STEMI equivalents, right?
So we haven't started talking about the non STEMI or the, the changes
that are harbinger of ischemia.
We're just talking about occlusion.
If you see any one of those, the ST elevation, the standard ST elevation
the Scarbosa or the Smith Scarbosa criteria, the Hyperacute T waves, the
posterior STEMI or the de Winter sign.
You need to treat all of those like acute occlusion, like an acute STEMI
and set off the alerts and off you go.
Then we move on to the non STEMIs, or these are ECG or EKG findings
that are consistent with some kind of acute or subacute ischemia that
you should still be concerned about, but cath lab activation becomes
more at the cardiologist discretion 'cause there are less clear criteria.
And there's again several of these that we're gonna talk about today.
Let's start with a VR.
So if you don't know what a VR is, it's that lead in the second
column on your EKG at the very top.
And we don't frequently look at it, but just know that if you have ST segment
elevation in that lead combined with depression anywhere else, that that
patient's at high risk for associated morbidity and mortality, usually
represents some kind of diffuse ischemia because of significant
stenosis involving the left main.
So the left main or the proximal LAD, neither one of those is a
place you want to have an occlusion or a narrowing a stenosis.
if you've got significant disease there, usually those patients end
up having to go and get bypass or have multi-vessel involvement.
And so it's important to identify them early.
The medical management for them might be different and your cardiologist looking
at that EKG might suggest a completely different approach to that patient.
And if you're not at a center that can do bypass grafting,
that patient may get sent out.
So just just be aware that ST elevation in a VR is a significant disease harbinger.
And the ST segment elevation can be less than a millimeter.
So it doesn't have to be very significant in order for this to be the case.
It, it is usually associated with ST depression in other leads and
something you need to keep in mind.
T.R. Eckler (2): As we get into these though I think it was important for me to
set my expectations that this is not like if you find this a hundred percent of the
time they have an acute coronary occlusion Like when we're talking about aVR ST
segment elevation Even if you have it with multi lead ST depression only 10% of these
are gonna be in acute coronary occlusion So that's worth it's still worth saying
Hey I'm worried about this patient I don't like the way they look I think this
is what I see This is what I'm thinking But just know that if your cardiologist
says Hey okay I think it's more likely that it's not Let's watch em Let's kind
of see how this develops That's not an unreasonable thing and I think there's
a few of these that are like that It's about having the conversation and alerting
them early and then seeing where it goes
Sam (2): All right.
Let's talk about Wellen syndrome.
So, Wellen Syndrome is a specific EKG pattern that you will see in
a patient when they're pain free.
So the classic board question is that they come in with pain and
they have a normal EKG, and then you give 'em some nitroglycerin
and then you go to repeat it.
And now they're pain free.
And they have this abnormality with a biphasic T wave in V two through V
three, meaning it goes up and down or a deeply inverted T-wave in V two and
V three that when they're pain free, can be a harbinger of disease as well.
And is something you want to bring to the attention of your cardiologist.
. And much like the previous things that we mentioned, you should be concerned
about disease at the proximal left anterior descending, or the proximal LAD.
Again, not a place that you want to have stenosis or disease because
if it occludes, you're looking at some pretty remarkable symptoms
and dysrhythmias and death.
So finding this on EKG is very, very important.
Detecting it early, and especially if there's someone who has
presented with chest pain, now they're already symptomatic.
That person is not somebody you want to send home.
That person is also not somebody you wanna put in like your obs
unit and give a stress test to.
You need to get cardiology involved in that case.
And they need to go get a cath.
All right.
Reciprocal ST segment depression.
So, there are oftentimes where you might see something concerning on your ECG or
your EKG, and it's an ST elevation, and your cardiologist is gonna say, great,
you've got all these ST elevations.
Are there depressions?
Are there some reciprocal changes?
I get that question all the time especially from our interventionalists.
And so table four outlines the reciprocal portions of the EKG anatomically
so that when you have elevations in one section, you should expect
depressions in the reciprocal section.
That's just more proof that what you're seeing in ST elevation is not due to
some kind of electrical conduction disorder, but is due to actual ischemia.
So if they have posterior ST elevation, you're gonna see anterior ST depression.
That's how you're gonna diagnose that.
If they have anterior ST elevation, you're gonna see the ST depression inferiorly.
That's the reciprocal changes.
If they're having an inferior mi, you're gonna see reciprocal changes laterally.
If they're having a lateral mi, you're gonna see the reciprocal
changes in the septal leads.
And if they're having a septal mi you're gonna see posterior ST depression with
posterior leads if you're using that.
So, there's a nice little mnemonic, the PAILS mnemonic which helps remind you
about the posterior, anterior, inferior lateral and septal areas on the EKG and
where those reciprocal changes will occur.
That's a helpful mnemonic to keep in mind, and it's probably a question
you're gonna get from your cardiologist when you call about the STEMI.
T.R. Eckler (2): I think worth looking at these basically like once you've
looked at this table now you go pull up a posterior MI and you see the anterior
depressions You pull up an anterior mi you see the inferior depressions as
you said for the lateral mi Then you're looking for septal or inferior depressions
I think once you see it this is one of those being a more visual human that
that figured this out gradually in his education I think if you show me the
positive and negative changes on the EKG I'm much more likely to recognize
it when I see that pattern in the future
Sam (2): Yep.
And then the last one is inferior mi. So inferior MI is defined
as ST elevation of any degree in two contiguous inferior leads.
So it doesn't matter how much elevation, but if you see ST elevation of any degree
in two contiguous inferior leads with any amount of depression in a VL that's
highly suspicious for inferior mi and a VL in that scenario is the only lead that's
truly reciprocal for the inferior wall.
And that's something that's that's concerning.
You need to bring that up to your cardiologist.
There was a retrospective review, like 150 patients confirmed with inferior
STEMI found that all of them had these st changes and had the ST depression in a VL.
these patients are at higher risk as well for arrhythmias.
They're at higher risk for hypotension.
If you see these changes, you gotta be careful with the
nitroglycerin you're giving them.
So, lots of things you gotta keep in mind when you see these changes.
T.R. Eckler (2): I think the thing that I took away from this too was like now we're
starting to really get down Now we're talking about a quarter of a millimeter
of depression is what they're trying to describe here And I think that you
need to remember when you're doing EKGs if you have a low QRS voltage That was
one of the things they talked about the limiting factor in diagnosing these You
can change the sizes of the waves if you ask your EKG texts nicely So if you think
there's something there but the waves are too small repeat EKG Increase the size
increase the amount that you have the ability to see and it's gonna draw out
more of these things more clearly for you
Sam (2): Yeah, one more plug for whatever tech companies listening
to try and develop that iPad with the EKG readings on it for me.
It'd be nice to be able to change the settings live on the EKG I'm looking at,
instead of having to send the tech back to do another one so we can make this
diagnosis immediately for future tech.
you go.
So that's all of the conditions that are harbinger of ischemia.
So that's not necessarily STEMI equivalents, but these are things
that will tell you something is wrong.
And that's aVR ST elevation.
That's our Wellen syndrome.
That's our reciprocal changes, and that's our inferior mi. Those st
elevations in the inferior leads with ST depression and a VL, all
of those are harbinger of ischemia.
T.R. Eckler (2): Just a brief pause for applause for the
crowd for listening to that
Sam (2): a hundred percent.
. Go look at this issue.
If you have access to it@ebmedicine.net copy these images and stick it in your
favorite image section on your phone.
And just keep this handy.
This is such a powerful issue if.
Laboratory testing is pretty easy.
Everybody's gonna get a troponin, a high sensitivity troponin, they'll
elevate in as little as an hour.
And nothing new in that realm.
So, you're gonna get your labs.
Not a big deal.
When it comes to imaging, again, there's not a whole bunch
of imaging we're relying on.
Everybody gets a screening, chest xray
. Interesting actually, that there's not great evidence to indicate
that there's really much value added within a chest x-ray.
But as they get their chest x-ray, it's not usually taking up a whole
bunch of resources in the department.
And so we still do it, we're looking at the aortic knob, we're looking for
anything else pneumothoraces or anything else that might cause chest pain.
Maybe looking to see that they're not in florid failure, although you've
probably already diagnosed that.
So again, it's not adding a whole bunch, but it's, it gets done all the time.
T.R. Eckler (2): I thought there was a case to be made though when they talk
about transthoracic echo cause these patients STEMI patients NOMI patients
OMI patients these are quick patients you're trying to figure this out quickly
You're looking at that EKG I think if they're unstable especially you should
take the time that you would've used your stethoscope or you would've used
the chest x-ray and put it into an ultrasound because I think you're gonna
get much better data much more quickly.
You're gonna confirm your diagnosis or you're gonna notice other things
developing like a pericardial effusion like fluid in their lungs like pleural
effusions You're gonna just know more about this human as you're trying to
resuscitate them and stabilize them enough to get them to the cath lab And I think
that's the case here is you can get a lot of an echo pretty quickly that's gonna
help you do more to save these patients
Sam (2): Yeah, so the, the echo isn't visualizing coronary anatomy
or diagnosing coronary disease.
The echo is looking for regional wall motion abnormalities.
There is data that suggests that the ventricular movement, the wall motion
of the ventricle, is going to look different before any EKG changes occur.
So this could be your earliest tool for detection.
And there is good data that says that in the hands of emergency medicine
trainees, even that identification of regional wall motion abnormalities
is possible with a sensitivity of 88% and a specificity of 92%.
So we do a pretty decent job with training.
If you've never had that training, go take a course, look at a bunch of echoes.
It's important.
It's a good skill to have.
Also equally important to keep in mind that if they don't have regional wall
motion abnormalities that does not rule out acute coronary occlusion.
So it's one of those things that can help you rule it in,
but it isn't gonna rule it out.
And like you said, if they're unstable or have shock, it's it's definitely your
first go-to for evaluating the ventricle.
T.R. Eckler (2): The caveat to that being and and I liked how the authors
got to this was If the regional wall motion abnormality fits in the area where
you think they have an occlusion that increases the likelihood that they have
an occlusion mi there And that should hopefully push your cardiologist more to
take them for reperfusion And I've seen some of our cardiologists do this where
it's kind of not clear they're taking that echo and looking and seeing what
like that certain region of the heart looks like And if it doesn't look like
it's it's moving normally to them it pushes them to the cath lab And I think
that's something to have in your mind
Sam (2): Yeah, great point.
So that's transthoracic, echocardiography supplemental oxygen.
We touched on this earlier in the EMS section but there
have been several trials.
The air versus oxygen in ST segment Elevation, myocardial
infarction or AVOID trial.
Great.
Name the,
T.R. Eckler (2): With air versus oxygen in an ischemic disease But what a great
team of people making up the names for these trials because then the D two
OX a MI trial I love how they combine detox and oxygen into one word Just
really creative work by these folks
Sam (2): Yeah.
Yeah.
Both of these the first trial had 441 STEMI patients in it.
The second trial had over 6,000 patients with myocardial infarction in it.
And both of them found really no benefit whatsoever to just routinely
applying oxygen to people who have normal oxygen saturation.
So if they're hypoxic, if their saturation's less than
90% then there's a benefit.
Otherwise, there is no benefit to it whatsoever.
T.R. Eckler (2): In some of the patients on oxygen had larger sized infarcts
when they went back and looked at them later and oxygen did not reduce all
cause mortality and did not reduce hospitalization with myocardial infarction
So really like lots of things that didn't help and things that may make it worse
So I'm now more inclined to pull oxygen off my patients if they're coming in
with chest pain and they're over 90%
Sam (2): Yeah.
Very few conditions in medicine benefit from Hyperoxia.
Really, it, it's just, it's not, it's not a great thing for us as human beings.
All right.
Analgesia, you're gonna give them nitroglycerin.
You can give them morphine, you can give them fentanyl.
There is data that your first go-to agent should be some kind of nitrate.
The nitrates themselves really don't have evidence to improve
or reduce myocardial injury.
In patients with STEMI, they can help in vasospasm and they might
clinically relieve some of the pain.
But as far as like reperfusion goes, giving 'em a sublingual nitroglycerin
is not gonna reperfuse them.
And the analgesics there is some mild observational data that says yes, you
can give them medications for pain.
Just remember that their response to pain medication does not become diagnostic.
So if you give them morphine and they get better, it doesn't mean they don't
have an acute coronary occlusion.
It just means their pain got better.
'cause now you're covering it up with morphine and there's nothing wrong
with making the patient comfortable while they're waiting for your
cardiology colleague to make a decision.
That's okay.
T.R. Eckler (2): My takeaway from this was I was gonna make sure if I'm transferring
a patient that if I can control their pain with Nitro I put em on a Nitro drip
and send them that way But I wouldn't be opposed to basically giving my EMS
crews orders to use Nitro and fentanyl and give them kind of short acting things
to address this But I think that was my thought was a nitro drip can be a pain
control adjunct for transporting these patients especially if they responded
to it in the ER while they're moving for an hour or two to another hospital
Sam (2): Yeah.
Or if they're critically hypertensive and you wanna give
it for blood pressure management.
There are other reasons why you might start it.
But just remember it's not diagnostic.
And then there is pharmacotherapy.
So this is an extensive section.
You, your hospital's going to have a protocol.
Your cardiologists are gonna have their preferences.
The greatest benefit ever from anything has been aspirin.
So as far as medication goes, so everybody's getting their aspirin,
either 162 or 325 milligrams as soon as possible, chew this aspirin and you
have given 'em the greatest benefit you can if you're not the cardiologist.
T.R. Eckler (2): I disagree Just for one second I would like to speak on
behalf of my fellow rural providers or lytic-ologists as we like to be called
the NNT for aspirin in STEMI is what Sam
Sam (2): I dunno, what is it?
T.R. Eckler (2): 42
Sam (2): Hey,
T.R. Eckler (2): you know what comes one place behind it
Sam (2): what's that?
T.R. Eckler (2): At 43 TNK
Sam (2): Wow.
Hey, that's pretty good.
T.R. Eckler (2): So I would tell you aspirin is incredible I think every heart
attack should get it But I also think that if they're not close enough to get
PCI you should also be making sure they don't meet any of the exclusion criteria
and they're not gonna explode blood into their brain or from their recent surgery
or arterial catheter site I think that TNK is also going to now and and at
the same time setting expectations for yourself cause you know you wanna be
that ER doctor on TV that saves every life You're not going to win every
one of these acute mis but aspirin and lytics are your best tools in that kit
And when they work they're gonna work and you're gonna make a difference with
them And NNT of 42 and 43 is pretty good
Sam (2): That is very good.
There are other categories.
So you've got P2Y12 inhibitors.
That's your things like clopidogrel and prasugrel and ticagrelor and cangrelor
which is the only one that's iv.
And then you've got your GP2B3A receptor antagonists.
You've got traditional anticoagulation like heparin and then you've
got your fibrinolytic therapies.
So all of these fall under the blanket of pharmacotherapy, starting with
aspirin, which everybody's gonna get when it comes to the P2Y12 inhibitors.
These are anti-platelet agents.
They keep the platelets from aggregating three outta the four are oral.
If the patient's not already taking it your cardiologist or your
hospital protocol may include a loading dose of these for STEMI.
The only time your cardiologist might hesitate is if the EKG suggests something
like a main artery or a large artery occlusion and they're concerned there
might be multi-vessel disease and this person might end up having to go get
shipped off for a bypass graft, then some of these agents are not reversible.
Actually, all of these agents are not reversible.
So once you've given it, you have to wait for it to wash out and that delays
their bypass graft, surgical time.
So ask your cardiologist or give whatever the protocol says.
I do both.
Hey, per protocol I'm supposed to give yada, yada.
Are you good with that?
Yes.
Okay, I'm giving it now.
That kind of thing, it's okay to have that conversation but just know that there's
good evidence that those will help.
The decision for which one to give is purely up to your
hospital and your cardiologist.
Clopidogrel has the best evidence behind it as far as bleeding
goes, and the side effects.
While things like ticagrelor and prasugrel have the best response
as far as anti-platelet aggregation goes, but with higher bleeding risks.
So, I leave that decision up to my cardiology colleagues.
I don't have a preference between all of those.
T.R. Eckler (2): Some of those medications are very expensive though and a lot of
your patients that come in are gonna be quote unquote prescribed these medicines
and it's important to ask them Hey are you really taking it Or did your prescription
run out Or did you not have the money to fill it Because I find that a lot of
patients that come in with occluded stents with mis if you really ask em they're like
yeah I came off my my Brilinta ticagrelor same drug I came off that Month or so
ago cause I couldn't afford it anymore
Sam (2): Yeah.
And
T.R. Eckler (2): So it's
Sam (2): is higher.
So, even if they did take it, you're gonna have to give 'em another dose.
If they're do, if they took 75 milligrams this morning, the loading dose is 600,
you gotta give them the rest of it.
So, so yes, absolutely ask that question.
The glycoprotein or two B three A receptor inhibitors, that's something
we're just not giving in the ed.
That's something they're gonna give in the cath lab.
There are specific times where they might want that extra platelet
aggregation blocking, and that's up to your cardiology colleagues.
This is an adjunct at the time of PCI.
And so there was a brief period of time where we were giving those in the
ed, or at least had them available.
Now it's universally given in the cath lab, When it comes to standard
anticoagulation like heparin versus low molecular weight heparin this again is
very cardiology and hospital specific.
So, unfractionated heparin was established at the standard of care long time ago,
and there is good data that says that low molecular weight heparin can work.
But there are, again, regional and physician specific preferences and
there's no need to get into any of that.
Some of the cardiology colleagues like that, you can turn off IV heparin
and rapid reverse and if there's other issues or complications or
bleeding complications that come up.
So just have that conversation with your cardiology colleague.
Make sure it's in whatever your hospital protocol says.
And then lastly, let's talk about those reperfusion therapies.
So there are fibrinolytics that can be given the American Heart Association
and American College of Cardiology recommendations are that if your
patient with the STEMI can't make it to a PCI center within 120 minutes,
that they should go to somewhere where fibrinolytics can be given, if they
can make it to a PCI Ready Hospital.
The first contact to balloon time in the artery should be 90 minutes.
So that's two different numbers, but don't get them confused.
One is a goal time for PCI centers.
That's 90 minutes.
The other is the overall timeframe for how you decide, okay, should we
get this person all the way to the PCI center that's three hours away,
or should we take 'em to the local hospital where they're gonna get lytics?
And the answer is, 120 minutes is the cutoff.
So if they can't make it to the PCI center in 120 minutes or
two hours, then they need to go somewhere where they can get lytics.
You've given lytics before TR?
T.R. Eckler (2): I would say probably honestly like pretty getting close to like
a hundred times now And I would tell you that I think that I've watched patients
get better in front of me Not every time Sometimes you give it and you're sure
it's a STEMI and the cardiologist's sure it's a STEMI and it doesn't break the clot
down but I've seen patients diaphoretic dyspneic all of a sudden the color returns
to their face and they're like Ah I feel great And then my understanding of sign
language is limited but I I know the sign for helicopter because I love to signal
that to my rural emergency secretary to call the helicopter because now I feel
like you've got a brief window of time where they're open again and you gotta
get em somewhere before they they try to close up on you again So I think that
the other part of this which I think this article assumes aliveness throughout but
I've had patients with N STEMIs that then progressed in rural places while waiting
for their transfer And I had one that walked to the bathroom came back and I
heard him hit the ground in his room while he walked his heparin pipe back And we
came down and he was pulseless apnic he got intubated And I asked for TNK within
the first minute or two cause I figured he had a STEMI And he got the TNK and was
back in four minutes We had to sedate him to to keep him intubated But he did great
He came back like a week later and it said he quit smoking and he was so glad
that that he had come in and and gotten checked out for his chest pain that day
Sam (2): Wow.
That's, that's an incredible story.
T.R. Eckler (2): if they have a STEMI and they got worse you don't have if if you're
at a PCI center this was my big point If there's a STEMI and you're waiting for em
to go to the cath lab and they code you can give them lytics if you can get em
back and they can go to the cath lab great But if you can't get em back you can give
these people lytics and you can make them better there on the spot And especially
if they're young and healthy and you think it's worth the risk like it's another tool
I think you should put in your toolkit
Sam (2): And just for your own personal knowledge, once you've
given the lytics, those people still go on to get coronary angiography.
Typically they'll wait a few hours, so, not within the first two or three
hours, but, but somewhere in the first 24 hours they'll go and get
a cath assuming that they improved.
If they have persistent chest pain, persistent EKG changes, those are
all indications to just treat 'em like they're still having a STEMI and
take 'em to the cath lab immediately.
but the cardiologist definitely, if the person has improved and they're
resolving their EKG changes, they'll let them cool off a little bit.
And then the evidence suggests they'll do better if they cath them sometime in
the first 24 hours instead of emergently.
All right.
Lastly, let's talk about as you just mentioned with that case example,
the patients who have cardiac arrest.
So somewhere around 10% of STEMIs that are transferred by EMS have
an out-of-hospital cardiac arrest.
That's a pretty significant number of STEMIs having arrests.
So one in 10 of those STEMIs that are presenting by EMS
will have a cardiac arrest.
And they're mostly observational data in this population.
Just know that if you get return of spontaneous circulation and the EKG shows
STEMI that you're gonna progress down the STEMI pathway in those patients.
And that there is guidelines from the American College of Cardiology
and the American Heart Association stating just that so you get
spontaneous return of circulation.
The EKG shows STEMI, that patient is still a candidate for a primary PCI.
And that's it.
So that brings us to the end of this article.
There are a lot of things that we covered, so please go take a look, look
at the STEMI equivalents, look at the ischemic changes that you might see
on ECG and try and shift your mental model away from just STEMI or non STEMI
to occlusion versus non occlusion.
And I think you'll find this categorization system much more helpful.
I wanna say thanks to Dr. Horning for being the author for this February, 2026
article on acute coronary occlusion.
It was fantastic.
Just jam packed full of information.
And if you're listening, don't forget to go and claim your CME.
Click the link in the show notes.
Fill out the CME questions.
Hopefully ace them because we did such a fantastic job
walking you through the article.
And don't forget , as always.
clinical pathway in the back of the issue that will walk you through, step
by step, each one of those decisions for this critical patient population.
And that's a wrap.
So until next time, everyone, I'm one of your hosts, Sam Ashoo.
T.R. Eckler (2): TR Eckler wishing you the best of luck and keep your TNK ready
Sam : And that's a wrap for this month's episode.
I hope you found it educational and informative.
Don't forget to go to ebmedicine.net to read the article and claim your CME.
And of course, check out all three of the journals and the multitude of
resources available to you, both for emergency medicine, pediatric emergency
medicine, and evidence based urgent care.
Until next time, everyone be safe.