STEMI vs. demand ischemia

[nikolaite]

Pt in ED was tachypneic, O2 sats in mid-80s, AMS, agitated, under physical restraint by six staff, head of cot declined 45 deg to aid restraint, extreme physical exertion. ECG strip was labeled resting, abnormal. Looks like demand ischemia to me, but colleagues are opining STEMI. Honestly, I see no evidence of acute MI in the strip. What am I missing?

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[Apollyon]

I'm a dummy, but, I see inferior wall STEMI with reciprocal change.

 

[nikolaite]

I'm a dummy, but, I see inferior wall STEMI with reciprocal change.

Pt labs: CPK 147, CK MB 1.3, troponin 0.03, blood glucose 348. Seems like it wouldn’t match acute MI findings.

I am truly a newbie when it comes to ECG, but I’d say there’s evidence of an old anteroseptal MI...and apparently current demand ischemia. Can you hold my hand on this one and correct an idiot? 😆

 

[Apollyon]

Dollars to doughnuts, that troponin is going to rise.

Since you can't undo a completed MI, prudence would dictate the cath lab for this pt. It takes guts to call it demand ischemia, and not intervene (and there's a fine line between "guts" and "stupidity"). You treat the pt, not the labs.

 

[Siggy]

If demand ischemia is bad enough, you will get ST elevations. See EKGs immediately post cardiac arrest with diffuse elevation or AVr (left main) elevation. It's demand ischemia... there's high demand with no supply.

Similarly, I've seen ST elevations go away with transfusions in anemic patients (including one with a HgB of 6).

You know what happened with both of those patients? An immediate discussion with the cardiologist.

Also troponins don't matter for a STEMI vs non-STEMI call because of delay in rise. If the cardiologist wants to cancel the cath lab because of the troponin (either too low and it's not real or too high and it's completed already)... then that's on him or her.

 

[RustedFox]

I'm a dummy, but, I see inferior wall STEMI with reciprocal change.

The ST-segments are depressed in II, III, and aVF - and up or (starting to go up) in V1, V2, V3.
I see anterior STEMI with reciprocal changes inferiorly, which I'm pretty sure is what you meant.

OP: Think about it this way: if :60 or :90 seconds would have elapsed, and the EKG were recorded just a touch later in time... those ST-segments in the anterior leads would be higher, given the clinical presentation. This is where I've said to the lazy cardiologist on the phone:

"Yeah, I know the EKG doesn't meet your strict electrocardiographic criteria at this second in time, but I figured I'd call you now instead of waiting another 2-3 minutes and then record a second EKG when it does."

 

[nikolaite]

The cardiology consult said:

The ekgs show sinus tachycardia. Exertion increases heart rate. There’s no evidence of an acute heart attack or pericarditis. There is T wave inversion in the inferior leads that COULD suggest ischemia.

No cath lab.

😬

 

[Siggy]

The cardiology consult said:

The ekgs show sinus tachycardia. Exertion increases heart rate. There’s no evidence of an acute heart attack or pericarditis. There is T wave inversion in the inferior leads that COULD suggest ischemia.

No cath lab.

😬

Options:
1. At most hospitals clinical/non-interventional cards and interventional cards are separate call lists... if it's different or you know that the admitting doc prefers a specific clinical cards, it should be easy to get a second opinion.

2. Get the patient calmed down and repeat EKG in 5-10 minutes. Either it's gonna be worse or better.

 

[turkeyjerky]

I’m not sure what you guys are talking about. Only STE I see is in avL, which, despite what I’ve read, is oftentimes a nonspecific finding and not always indicative of coronary occlusion.

Also don’t t know about ‘demand ischemia’—the pt isn’t even tachycardic…

Sounds like the patient needs to be tubed and get a repeat EKG after done propofol and a head CT.

 

[NITRAS]

Agitated person being restrained and hypoxia. Not sure how they got the EGK when him being held down so much. . . Not enough artifact to be really fighting. (I’ve having fun with you).

I’m going to guess +meth, +/- COVID, plus unfunded with a phone cardiologist.
In all honesty, if the guy didn’t have chest pain, most of our current crop of fellows would balk at calling it acute MI.

 

[RustedFox]

I’m not sure what you guys are talking about. Only STE I see is in avL, which, despite what I’ve read, is oftentimes a nonspecific finding and not always indicative of coronary occlusion.

Also don’t t know about ‘demand ischemia’—the pt isn’t even tachycardic…

Sounds like the patient needs to be tubed and get a repeat EKG after done propofol and a head CT.

Its hard to see which leads are which, but:

- the ST segment in V2 is for SURE elevated.
- the ST segment in V1 is too close to call.
- II, III, and AVF are depressed in multiple complexes.

Although I 100% agree with (and really, really like) your intubation/CT/repeat EKG strategy.

 

[nikolaite]

Agitated person being restrained and hypoxia. Not sure how they got the EGK when him being held down so much. . . Not enough artifact to be really fighting. (I’ve having fun with you).

I’m going to guess +meth, +/- COVID, plus unfunded with a phone cardiologist.
In all honesty, if the guy didn’t have chest pain, most of our current crop of fellows would balk at calling it acute MI.

He arrived nonverbal with right-sided neuro deficits. ED primary had him dosed with 10 mg Ativan IM approximately 2 hrs prior to applying ECG. Obviously an ativan naive pt; had awful paradoxical reactions. Pt was on continuous ECG for 2+ hrs and this time of resistance was the only time an abnormality showed up.

Pt received head, neck, chest CTA. No atherosclerosis. No repeat labs. Acute CVA, though.

 

[RustedFox]

He arrived nonverbal with right-sided neuro deficits. ED primary had him dosed with 10 mg Ativan IM approximately 2 hrs prior to applying ECG. Obviously an ativan naive pt; had awful paradoxical reactions. Pt was on continuous ECG for 2+ hrs and this time of resistance was the only time an abnormality showed up.

Pt received head, neck, chest CTA. No atherosclerosis. No repeat labs. Acute CVA, though.

So... this data kinda changes a lot of the thought process, amigo.
Doesn't change EKG findings, but changes order of operations.

 

[nikolaite]

So... this data kinda changes a lot of the thought process, amigo.
Doesn't change EKG findings, but changes order of operations.

I'm giving it to you in the order I got it.

Original presentation not mentioned by staff until after pt was 6 hrs in. CTA ordered and resulted roughly 8 hrs after ED entry.

Makes the primary's job a bit difficult, eh?

 

[Apollyon]

which I'm pretty sure is what you meant.

Yeah, you got it. I'm hanging a bit here, at Disney!

 

[RustedFox]

I'm giving it to you in the order I got it.

Original presentation not mentioned by staff until after pt was 6 hrs in. CTA ordered and resulted roughly 8 hrs after ED entry.

Makes the primary's job a bit difficult, eh?

Okay. I get it.
See; most of us here presume that you're seeing the patient in the ER, which now that you elaborate ... makes me think that you're somewhere on the floors.

 

[RustedFox]

Yeah, you got it. I'm hanging a bit here, at Disney!

Drive South a touch and I'll buy you a beer.

 

[Apollyon]

Drive South a touch and I'll buy you a beer.

I'd drink your beer, but, we ain't got a car rented! We are chillin'!! Many thanks, amigo.

 

[dadaddadaBATMAN]

Its hard to see which leads are which, but:

- the ST segment in V2 is for SURE elevated.
- the ST segment in V1 is too close to call.
- II, III, and AVF are depressed in multiple complexes.

Although I 100% agree with (and really, really like) your intubation/CT/repeat EKG strategy.

I agree I see ekg changes there, esp v2 and depressions in 2. 3 has enough artifact I think it might be wandering baseline. V2 definitely not >2mm, is a dude right? Did we say how old?

He arrived nonverbal with right-sided neuro deficits. ED primary had him dosed with 10 mg Ativan IM approximately 2 hrs prior to applying ECG. Obviously an ativan naive pt; had awful paradoxical reactions. Pt was on continuous ECG for 2+ hrs and this time of resistance was the only time an abnormality showed up.

Pt received head, neck, chest CTA. No atherosclerosis. No repeat labs. Acute CVA, though.

can get a lot of fake out ekg changes in hemorrhagic or ischemic stroke that look like mi.

I would call cards for this ekg but the story and ekg aren’t compelling to activate to me.

I actually think you’re more likely to end up at M&M or whatever quality process after you delayed the stroke workup for a stemi workup than the opposite here. I would believe dissection before mi

edit: also demand ischemia or not isn’t really an ekg finding so far as I know, it’s a clinical determination separate from all that. I mostly look for things like tachycardic sepsis or post rosc before I call ekg changes that. Usually when I call demand ischemia I’m ignoring some trivial troponemia

 

[Arcan57]

Not a STEMI based on criteria. If clinically looked like ACS, would repeat. If not looking like ACS, would repeat.

 

[RustedFox]

Not a STEMI based on criteria. If clinically looked like ACS, would repeat. If not looking like ACS, would repeat.

This.

I presumed "cardiac presentation" when I first read the thread title and an EKG was the first thing that I saw.

 

[Mount Asclepius]

Yeah, this thread is a little misleading (although some initial details are there to make you question ACS). Some of my partners come ask me to look at a ‘concerning’ EKG and then tell me a story that is not really suspicious or consistent with ACS, or even atypical CP. I think folks occasionally get caught up in the EKG and miss the forest for the trees.

 

[nikolaite]

Yeah, this thread is a little misleading (although some initial details are there to make you question ACS). Some of my partners come ask me to look at a ‘concerning’ EKG and then tell me a story that is not really suspicious or consistent with ACS, or even atypical CP. I think folks occasionally get caught up in the EKG and miss the forest for the trees.

As the OP, I’d say it is just as misleading, or possibly less so, as this pts admittance to the floor. 😂😂

 

[RustedFox]

As the OP, I’d say it is just as misleading, or possibly less so, as this pts admittance to the floor. 😂😂

So, this patient was admitted with the primary concern of "chest pain, high suspicion for ACS" when the presentation was lateralizing neurologic defecits consistent with ischemic stroke?
I'm not being argumentative. That sounded adversarial, I know.
I'm just trying to get a good grip on what we're looking at here.

 

[southerndoc]

I’m not sure what you guys are talking about. Only STE I see is in avL, which, despite what I’ve read, is oftentimes a nonspecific finding and not always indicative of coronary occlusion.

Also don’t t know about ‘demand ischemia’—the pt isn’t even tachycardic…

Sounds like the patient needs to be tubed and get a repeat EKG after done propofol and a head CT.

I also only see it in aVL, and it's minimal at best. Definitely not 2 leads to qualify as a STEMI.

If this patient came in with a classic story, I would repeat it in 5-10 mins. With the story you describe, my interventionalists would not take that to the cath lab if it were their own parent.

 

[southerndoc]

He arrived nonverbal with right-sided neuro deficits. ED primary had him dosed with 10 mg Ativan IM approximately 2 hrs prior to applying ECG. Obviously an ativan naive pt; had awful paradoxical reactions. Pt was on continuous ECG for 2+ hrs and this time of resistance was the only time an abnormality showed up.

Pt received head, neck, chest CTA. No atherosclerosis. No repeat labs. Acute CVA, though.

One of these days I'll learn to read the entire thread before replying.

 

[Rekt]

Feel like I see at least 20 of these EKGs a shift. Wouldn't even bat an eye at this. You get much more leeway in V2/V3 for STE. Which there isn't any here with a wandering baseline.

Not even concerned for demand ischemia imo.

 

[thegenius]

Sinus tachycardia
STD in II, more in III, aVF
STE in I, aVL
Q waves anterior precordium
this would be inferior wall if anything.

in proper clinical context it would be inferior wall MI
2IVs, 2L IVF, ASA
I would either discuss with cardiologist or repeat in 10 minutes.
I don't think it meets STEMI criteria.

if the guy was agitated and yelling and screaming and all that, I would just repeat.

 

[aafisahar]

sinus tachycardia in most patients having a STEMI is going to be sick as ****, talking electrically unstable, hypotensive, cold as ice. You typically aren't going to get that form an inferior or lateral infarct since there's not enough myocardium at risk unless there's multivessel CAD. This really only happens with a high lateral or anterior MI, indicating LAD territory.

 

[thegenius]

The EKG HR above is in the 90s
That taint that fast

 

[TheComebacKid]

Am I crazy?

This EKG, while abnormal, has nothing on it that would make me want to call a cardiologist emergently. For anything. A dude coming in with localized neuro deficits, sure, i'll do the trops, serial EKGs, but this is really an underwhelming for any kind of emergent intervention. If someone wants to stress or cath this guy in a few days, that's fine. But the acute management of this EKG is to do nothing and maybe get a repeat one if you are concerned.

This is not demand ischemia either.

 

[BoardingDoc]

Am I crazy?

This EKG, while abnormal, has nothing on it that would make me want to call a cardiologist emergently. For anything. A dude coming in with localized neuro deficits, sure, i'll do the trops, serial EKGs, but this is really an underwhelming for any kind of emergent intervention. If someone wants to stress or cath this guy in a few days, that's fine. But the acute management of this EKG is to do nothing and maybe get a repeat one if you are concerned.

This is not demand ischemia either.

Agreed. Inferior depressions. Nothing else of note. Even if this person is having active chest pain, I wouldn't call the cath lab for this EKG, or speak to a cardiologist for that matter. I'm really struggling to understand the concern on this one.

 

[dadaddadaBATMAN]

Am I crazy?

This EKG, while abnormal, has nothing on it that would make me want to call a cardiologist emergently. For anything. A dude coming in with localized neuro deficits, sure, i'll do the trops, serial EKGs, but this is really an underwhelming for any kind of emergent intervention. If someone wants to stress or cath this guy in a few days, that's fine. But the acute management of this EKG is to do nothing and maybe get a repeat one if you are concerned.

This is not demand ischemia either.

Maybe im susceptible to peer pressure (first few comments on this thread) but honestly if you handed me the ekg on shift instead of with the idea that “looked like a missed stemi to my colleagues” I think I would probably say changes in iii were artifact, ii might be actual st depression, and don’t appreciate anything in v1 and minimal in v2.

in a chest pain pt I would call because if the cards guy at my place doesn’t want to keep them I need to know.

in this patient?

if a nervous colleague asked me about it I’d tell them to call cards so they could sleep that night and not think about it. If I was feeling crushed or having decision fatigue I would probably call cards so I could stop thinking about it. When I’m in doubt, I usually call the person who will be judging me later.

My threshold for calling for reassurance increases significantly at 5p and 10p-7a though out of respect for colleagues circadian rhythms. But we all sometimes make stupid consults, same as consultants turf to us for stupid office stuff sometimes.

 

[TheComebacKid]

Maybe im susceptible to peer pressure (first few comments on this thread) but honestly if you handed me the ekg on shift instead of with the idea that “looked like a missed stemi to my colleagues” I think I would probably say changes in iii were artifact, ii might be actual st depression, and don’t appreciate anything in v1 and minimal in v2.

in a chest pain pt I would call because if the cards guy at my place doesn’t want to keep them I need to know.

in this patient?

if a nervous colleague asked me about it I’d tell them to call cards so they could sleep that night and not think about it. If I was feeling crushed or having decision fatigue I would probably call cards so I could stop thinking about it. When I’m in doubt, I usually call the person who will be judging me later.

My threshold for calling for reassurance increases significantly at 5p and 10p-7a though out of respect for colleagues circadian rhythms. But we all sometimes make stupid consults, same as consultants turf to us for stupid office stuff sometimes.

I can respect that. I made a thread a few weeks ago about how as a new attending I feel like a wuss, have a tendency to over consult, over admit etc.

My algorithm for these cases is very simple.
1. STEMI criteria met: call cards/activate cath lab. This EKG, I think we can agree, that maybe has some abnormalities but does not warrant cath lab activation.
2. Evolving MI: dynamic EKG changes, rising trops, persistent chest pain, I call cards. Maybe he will be a "sooner than later" cath.
3. Positive trops, maybe non specific EKG changes, but patient otherwise stable: meh. The inpatient team can call cards in the morning. They will just trend it out and monitor on tele. This patient is not getting an emergent cath regardless, so makes no sense to call emergently IMO.
4. Everything else: don't call cards, ensure good outpatient follow up if discharging, otherwise punt to inpatient team.

I'd say if I'm going to discharge a patient and want someone to take a second look at the EKG, it's not unreasonable, especially so I can get some sleep at night. But if I am squinting really hard at an EKG and convincing myself about a little elevation here, or a little elevation there, chances are I am psyching myself out, and I will continue to get a few more EKGs/trops which will further support my notion that the person is not having a significant MI.

The patient in the original post is getting admitted, so... I probably wouldn't lose any sleep over this one.

 

[nikolaite]

Sinus tachycardia
STD in II, more in III, aVF
STE in I, aVL
Q waves anterior precordium
this would be inferior wall if anything.

in proper clinical context it would be inferior wall MI
2IVs, 2L IVF, ASA
I would either discuss with cardiologist or repeat in 10 minutes.
I don't think it meets STEMI criteria.

if the guy was agitated and yelling and screaming and all that, I would just repeat.

According to the RN, the dude was stone silent. Just got benzo-ed because he kept holding onto his clothes when they tried to strip him in the reception area outside the exam room. Had paradoxical disinhibition requiring an hour of physical restraint, then fell asleep. O2 says dropped to mid-80s. Reportedly “woke up” a couple hours later hooked up to ekg, presumably to urinate, tried to get out of ER cot, physical restraint initiated, after about 5 mins of struggle to rise became inc of urine, then returned to sleep. There’s unfortunately sooo much more. The whole thing is a risk management nightmare right now.

 

[thegenius]

Am I crazy?

This EKG, while abnormal, has nothing on it that would make me want to call a cardiologist emergently. For anything. A dude coming in with localized neuro deficits, sure, i'll do the trops, serial EKGs, but this is really an underwhelming for any kind of emergent intervention. If someone wants to stress or cath this guy in a few days, that's fine. But the acute management of this EKG is to do nothing and maybe get a repeat one if you are concerned.

This is not demand ischemia either.

No you are not crazy. The problem is, or maybe it's a good thing, is that I've read Stephen Smith's ECG blog numerous times and he is always pointing out ECGs that show occlusive MI requiring emergent PCI that do not meet STEMI criteria. The ECG in this post could be an example of one of those.

 

[southerndoc]

According to the RN, the dude was stone silent. Just got benzo-ed because he kept holding onto his clothes when they tried to strip him in the reception area outside the exam room. Had paradoxical disinhibition requiring an hour of physical restraint, then fell asleep. O2 says dropped to mid-80s. Reportedly “woke up” a couple hours later hooked up to ekg, presumably to urinate, tried to get out of ER cot, physical restraint initiated, after about 5 mins of struggle to rise became inc of urine, then returned to sleep. There’s unfortunately sooo much more. The whole thing is a risk management nightmare right now.

Risk management nightmares should never be discussed on a public forum until years have passed. This information is discoverable in case of litigation.

 

[Mount Asclepius]

@nikolaite Do you mind if I ask what your position in the medical field is?

 

[deleted721365]

@nikolaite Do you mind if I ask what your position in the medical field is?

They aren’t a physician.

So, I’m curious if there is some nefarious alternative goal here (hello more useless protocols from clueless non physician admins).

 

[dadaddadaBATMAN]

Risk management nightmares should never be discussed on a public forum until years have passed. This information is discoverable in case of litigation.

was about to post the same. Years in this case being whatever the statute of limitations is for medmal in your state, with close attention to fact that date of injury can be different from discovery of injury in some states and some take the latter.

Edit: or if you’re me, just NEVER

 

[RoyBasch]

I’m not seeing a STEMI, given the presentation I don’t know I would even call cards, sounds more concerning for toxic/metabolic/infectious etiology.
It sounds there are more pressing emergencies here then the ekg (respiratory failure, excited delirium) I would intubate, sedate, abg, repeat ekg and see what it looks like.

 

[nikolaite]

I’m a subcontract reviewer with carte blanche, basically. Most of what I do is in laboratory animal studies and medical device development. I have recently been working on a dual stroke study to see what prevents patients from getting into cath labs according to best laid wishes in hospital stroke protocols. I get first pass on cases before they go on to the research lead and then the team.

Again, I have full consent from my contract and approval from legal for disclosure of anything I post here for discussion.

My practical medical position originated in medical transcription, billing and coding, insurance, etc. As far as academic, premed biology, biomedical engineering, mechanical engineering.

 

[turkeyjerky]

Well that explains the complete lack of insight into medical practice...

Ladies and gentlemen, welcome to the future.

 

[turkeyjerky]

Why would you like that post? This is weird...

 

[nikolaite]

Yes, I’m typically the person that gets called in to prep the MDs for depositions to protect them from malicious litigation. Discussing with you all on things like this helps me get perspective to aid your colleagues.

My colleagues enjoy informal study and discussion on medical topics in addition.

Welcome to the future!

 

[nikolaite]

Why would you like that post? This is weird...

There’s nothing weird about it. Nothing underhanded or nefarious. I simply suspect that most MDs don’t brush up against the research and medicolegal side of things...so it feels weird talking to me.

 

[aafisahar]

No you are not crazy. The problem is, or maybe it's a good thing, is that I've read Stephen Smith's ECG blog numerous times and he is always pointing out ECGs that show occlusive MI requiring emergent PCI that do not meet STEMI criteria. The ECG in this post could be an example of one of those.

I've read his blog and I guarantee he's 100% sensitive but like 30% specific. Moreover, there's selection bias where he's showing his hits but not the ones where the patient had neg trops and clean cors.

There's already a pathway for emergent cath that aren't a STEMI. If they have refractory chest pain, then interventional needs to take them to the cath lab. The problem is that the ED gives 4mg of morphine, which increases mortality/morbidity btw, and the patient is high as **** unable to vocalize anything. At my shop, if someone can't get chest pain with a nitro drip and with rising trops, interventional will take them in the middle of the night.

 

[jw3600]

I only read first 10 posts for now but there is literally a zero percent chance cardiology is taking this at any of the hospitals I work at. Zero.

 

[southerndoc]

Unless there is any objection, I'm going to consider this thread has run its course and lock the thread.

 

[jw3600]

Unless there is any objection, I'm going to consider this thread has run its course and lock the thread.

How about a ban for this poster from the physician section as well?