Do you think this EKG is a STEMI

[thegenius]

90 yo F comes to ED with AMS.

Do you think there is electrocardiographic evidence of STEMI?

Spoiler: Spoiler #1: (Don't look until you've answered question above...)

HR initially 136, RR 22, BP 131/90, SpO2 96% RA. Temp 103. FSG normal
Cursory exam: Pt is very altered but mumbling words. She doesn't know if she is having chest pain. She looks terrible. No other med history available right now.

Spoiler: Spoiler #2: More info...

Cr 2, K+ 6.9, Bicarb 21, Trop 0.035 ng/ml, Lactic 3.3, WBC 15, Hg 14

Spoiler: Spoiler #3: More info...

Cardiologist says not a STEMI, doesn't see elevation in the inferior leads except III

Spoiler: My thoughts....

For what it's worth, I thought it was a STEMI. While I don't necessarily think she would go to cath given her high fever, age, to me it's a STEMI on cath. I annotated the EKG as such:

And when you zoom in on II, aVF....

Those look like inferior elevations to me.

So far...nothing bad has happened to her on the floor. Looks like they are not even cycling her troponins. No cardiology consult noted. So maybe I am wrong...wanted your opinion.

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[bravotwozero]

would do a right sided EKG to check for posterior wall MI. If no st elevation, then likely unstable angina unless trop positive.

 

[Buckeye1992]

Rate related ischemic change? How’d it look when she slowed down?

 

[Buckeye1992]

I would not have activated but would have talked to cards

 

[Rekt]

More myocarditis based on rest of history. Would have definitely called cards though. Covid positive?

 

[deleted547339]

In the right patient, call it all day. In the patient described, fax to cardiologist.

 

[GeneralVeers]

For these equivocal ones, I usually just call the STEMI cardiologist and send them a photo of the EKG for review. They tell me if they want to call it or not. That way I document, and am protected from the retrospectoscope.

 

[dadaddadaBATMAN]

I think I’m less concerned about the elevations that I see than the one that I don’t. Looks like it could definitely be a posterior mi in the right person

I’ve definitely been fooled by weird stuff with hyperkalemia though.

As a side note the absence of p waves and a wider qrs with hyperk are pretty scary, especially if a prior looked like something a human should have

Would love to see a repeat after you gave calcium and bicarbonate/insulin/glucose

 

[Cinclus]

I would have called cardiology immediately and let them decide it isn't a STEMI. That thing is ugly.

 

[harvard_of_the_west]

I love these teaching cases. I'm just an MS1, but have had about 10 hours of EKG instruction and practice over the last few days, so I'll take a stab at this one, ha.

I definitely think lead III shows more than 2 mm of ST elevation, but I can't really tell if it's elevated in any other inferior leads...I'd lean that it isn't elevated elsewhere and I'd say not a STEMI because of technicalities. Glad to see others who are much more qualified have differing opinions.

At first I thought I saw LBBB due to negative overall QRS deflection in V1, and the ever so slight positive terminal QRS deflection in V6, but I guess the QRS isn't wide enough for that at only 80ms. Also, I found it interesting that the T waves aren't more peaked with an elevated K+.

Overall, with the patient's appearance and vitals, this would freak me out.

 

[BAM!]

Lead III is the only "slam dunk" lead with ST elevation. No other contiguous lead, so it doesn't fit the classical definition of STEMI. However definitely a good idea to get Cardiology on board (and on the chart).

I think your vertical line comparing the J point on II and III is a little generous to the STEMI cause. I would move it slightly to the right to hit what I view as a more accurate J point on lead III. This would negate any ST elevation on lead II. Not sure I can tell where the J point on aVL is.

What about hitting them with some bicarb, calcium, d50, insulin etc to correct the K and then recheck EKG?

Really the most important thing is to be right. Do you really think this guy has a clot or ruptured plaque that needs emergent TPA or a stent? Not with that fever, ARF (assuming), hyperK, tachycardia, and altered mental status. STEMIs don't have fever and AMS. This is all demand ischemia.

 

[jw3600]

Give calcium. If it’s still that ugly, I would consult cardiology for emergent revascularization.

 

[WilcoWorld]

Technically speaking it doesn't meet STEMI criteria. But as said above, I am worried about a posterior MI. If it's a 50 yo complaining of new onset anginal-type pain, I'm activating the Cath lab. In the case you describe I'd get posterior leads and let Cards weigh in now so they don't critique me in the chart 3 days later, and then do my standard febrile NH workup.

Cool case, thanks for sharing. And kudos on the way you presented the hidden hints.

 

[SpacemanSpifff]

Based only on the ECG and the chief complaint, the primary reason to activate would be an extra opinion (agree with @GeneralVeers). Diffuse ST changes suggest rate related change in the context of underlying CAD, or a global process (PE, myocarditis). It's not classic for posterior. No elevation in aVR, which is not usually a left main, although often cited as such. I don't think this ECG would benefit from a trip to the cath lab. Prior to look at the additional information: bedside TTE, +/- discuss with cards.

With the extra clinical information fever and metabolic abnormalities really steer me away from a primary occlusion as the cause of her ECG changes. But I could definitely be wrong, and see what you mean by the inferior changes @thegenius - for curiosities sake it's too bad we don't have an angiogram. Did she get a TTE? Prior ECG or cath?

 

[Fox800]

They have multi-lead ST depression, and a lot of reasons to have an elevated troponin:
-Tachycardia
-Fever/sepsis
-Renal insufficiency
-Hyperkalemia

I would not expect a posterior STEMI to have so much lateral precordial and lateral limb lead involvement.

You have at least seven leads with ST-segment depression.

Multi-lead STD is much more likely to be from demand ischemia on top of prior diffuse coronary disease (lots of narrowed arteries but nothing acutely occluded) than from an LAD or proximal LMCA occlusion.

I'd definitely talk to cardiology and get repeat ECGs/troponins but the patient sounds medically sick...fix those and see what happens.

 

[dadaddadaBATMAN]

While I love the increased specificity some of you seem to have, I have absolutely activated the cath lab for stemi in non classic presentation with fever, no chest pain, etc.

Sometimes it’s more than one thing, and sometimes acute Illness precipitates a stemi.

Having said that I would not have activated here without a conversation.

Edit cath not carb lab. I am activating the carb lab in my kitchen right now though

 

[AlmostAnMD]

Agree with not STEMI, metabolic issue should be fixed first

also someone said check right sided EKG, IIRC is this correct? For RV infarction that would be ideal but V7-9 would be better, right? We're trying to assess posterior wall for elevations, not the right side with V2R, V3R and V4R, which would be elevated in a purely right ventricular infarction. Purely an academic question, wouldn't change dispo imo

 

[jw3600]

Is anyone else considering Dewinters pattern here? Sub isoelectric origin of ST segment with peaked T waves in precordials.

 

[FirstNobleTruth]

100% - you beat me to it. Particularly V2 is concerning for de Winter's morphology.

 

[Fox800]

Is anyone else considering Dewinters pattern here? Sub isoelectric origin of ST segment with peaked T waves in precordials.

I think the T-waves are typically much larger - larger than the QRS complexes.

 

[ThreadStalker]

Nice case, man! ST elevation in III and reciprocal depressions in I and aVL would have caught my attention, but the questionable elevation of II and aVF throws a bit of a wrench. Plus, the diffuse depressions across V2-V6 are unusual. Given the initial info, I would have suspected a right sided STEMI, held nitro, and called cards right away to have them review the EKG. Could also order a right sided EKG.

Given the extra info you included, my attention is drawn to the K. About 2-3 months ago I had a 27 year old Korean woman present with chest pain and slam-dunk Brugada type 2 on EKG without real significant peaking in T-waves. She was also anorexic and her K came back at 7.2 or so. We treated the hyperK and repeat EKG showed NSR with complete resolution of the Brugada pattern. It makes sense that elevated K would affect ST segments given its role in cell depolarization, so I'm starting to view any ST abnormalities in HyperK as at least suggestive of the influence of potassium on the EKG.

 

[SpacemanSpifff]

Is anyone else considering Dewinters pattern here? Sub isoelectric origin of ST segment with peaked T waves in precordials.

100% - you beat me to it. Particularly V2 is concerning for de Winter's morphology.

It's not classic. As @Fox800 said T waves tend to be large proportionally to the QRS, see below, from LITFL:

 

[turkeyjerky]

What's the lipase?

This a great EKG to demonstrate that not all ST elevation should go to the cath lab. Even if the EKG were diagnostic of coronary occlusion (which it's not), the patient described shouldn't go to the cath lab immediately. The fact that the QRS is a little dysmorphic in the inferior leads makes me think the STE there is more likely repolarization related than ischemia-induced. I do think you're correct in saying that there is inferior STE more than just in lead III--in the right scenario the STE relative to the height of the qrs there would be significant imo.

Would i call cards with this EKG? Yes, but the conversation would go somewhat along the lines of "just had to let you know, k thanks bye" rather than "tough EKG but I think this patient really would benefit from cath".

Given the scenario provided, I'm thinking hyperK > takotsubo > ICH > ACS as the cause of the EKG findings. Hell, I'd be more inclined to believe dissection over ACS.

 

[jw3600]

I think the T-waves are typically much larger - larger than the QRS complexes.

It's not classic. As @Fox800 said T waves tend to be large proportionally to the QRS, see below, from LITFL:

View attachment 324625

I agree not classic. But there is a non negligible chance this patient is having an acute coronary occlusive event. The fact it is not a “STEMI” is irrelevant. I’m aware cardiology is not taking this to the lab unless it’s business hours and they’re bored. Doesn’t mean they shouldn’t (or at the least wouldn’t be reasonable).

edit: as I said before. Really want to see repeat EKG after calcium/medical resuscitation.

 

[SpacemanSpifff]

I agree not classic. But there is a non negligible chance this patient is having an acute coronary occlusive event. The fact it is not a “STEMI” is irrelevant. I’m aware cardiology is not taking this to the lab unless it’s business hours and they’re bored. Doesn’t mean they shouldn’t (or at the least wouldn’t be reasonable).

edit: as I said before. Really want to see repeat EKG after calcium/medical resuscitation.

Fair enough. In the ED we deal in the world of "non-negligible". That said, this is not a clinical picture of someone I think would benefit from LHC.

 

[BAM!]

While I love the increased specificity some of you seem to have, I have absolutely activated the cath lab for stemi in non classic presentation with fever, no chest pain, etc.

Sometimes it’s more than one thing, and sometimes acute Illness precipitates a stemi.

Having said that I would not have activated here without a conversation.

Edit cath not carb lab. I am activating the carb lab in my kitchen right now though

... and that's why cardiologists think we're glorified nurses.

 

[Angry Birds]

Well, I went to a powerhouse residency so this should be easy...

 

[Zebra Hunter]

Because of the atypical presentation, I actually agree with cards about not going immediately to cath in a borderline ECG, but they certainly should be called to make that decision. This is a very interesting ECG. I think someone else mentioned the diffuse ST depressions, which are frequently present with subendocardial ischemia; however, this ECG does not demonstrate subendocardial ischemia given, as you mentioned, evidence of ST elevation in the inferior leads. I typically don't bother with posterior ECGs as posterior MIs are usually pretty obvious without them, however, this is the one type of ECG where they would be useful given that the diagnosis of posterior MI is questionable. I would definitely treat the K aggressively, give plenty of fluids, treat the fever, and then reshoot the ECG. Was the pt COVID+? I think myocarditis is possible, what I suspect more is demand ischemia in the setting of someone with a tight RCA, although certainly could also still be a type I MI. If capable, I'd probably ask cards if they want a stat echo to eval for wall motion abnormalities.

 

[jw3600]

Because of the atypical presentation, I actually agree with cards about not going immediately to cath in a borderline ECG, but they certainly should be called to make that decision. This is a very interesting ECG. I think someone else mentioned the diffuse ST depressions, which are frequently present with subendocardial ischemia; however, this ECG does not demonstrate subendocardial ischemia given, as you mentioned, evidence of ST elevation in the inferior leads. I typically don't bother with posterior ECGs as posterior MIs are usually pretty obvious without them, however, this is the one type of ECG where they would be useful given that the diagnosis of posterior MI is questionable. I would definitely treat the K aggressively, give plenty of fluids, treat the fever, and then reshoot the ECG. Was the pt COVID+? I think myocarditis is possible, what I suspect more is demand ischemia in the setting of someone with a tight RCA, although certainly could also still be a type I MI. If capable, I'd probably ask cards if they want a stat echo to eval for wall motion abnormalities.

Agree very much with this impression and management. Would do my TTE bedside. Early.

 

[RoyBasch]

I'm gonna activate.

It looks like a pretty clearly posterior-inferior STEMI to me.

That being said chief complaint is atypical and pt is quite elderly.

Probably 9 times out of 10 interventional cardiologist will get the family to make the pt DNR and do nothing or say its not a true ACS but demand ischemia related to toxic-metabolic abnormalities.

Likely not going to the lab, but this is definitely a case with a high chance of morbidity and mortality and I'll let the sub-specialist be the one to call off the dogs and downgrade the activation.

edit: answered question before looking at the spoilers. In light of the labs and fever, I would probably have a discussion with cardiology and get them to bless not taking to the cath lab rather than immediately activate.

 

[WheezyBaby]

Good story -> activate

This story, push calcium, initiate basic sepsis mgmt, quick probe on chest primarily for LVEF (I honestly don't think a pocus wall motion assessment is going to be that informative here), get posterior and repeat anterior ekgs, then discuss with cards.

I wouldn't fault someone for activating.

 

[thegenius]

Well thanks for the comments. She was given calcium, IVF, and other hyperkalemia treatment. unfortunately a second EKG was not obtained in the ED for some reason prior to transfer to the floor.

There, there was no cards consult. No repeat trops. Her admitting diagnoses were severe sepsis 2/2 UTI, AKI, metabolic encephalopathy, advanced dementia, chronic Afib, hyperkalemia. Looks like they are having goals of care discussions with family.

There was some variability of analysis which made me feel better...that it isn't an easy EKG. Even my colleague and I disagreed. and sometimes in III I don't see elevation but sometimes I do.

 

[dadaddadaBATMAN]

Well thanks for the comments. She was given calcium, IVF, and other hyperkalemia treatment. unfortunately a second EKG was not obtained in the ED for some reason prior to transfer to the floor.

There, there was no cards consult. No repeat trops. Her admitting diagnoses were severe sepsis 2/2 UTI, AKI, metabolic encephalopathy, advanced dementia, chronic Afib, hyperkalemia. Looks like they are having goals of care discussions with family.

There was some variability of analysis which made me feel better...that it isn't an easy EKG. Even my colleague and I disagreed. and sometimes in III I don't see elevation but sometimes I do.

If I were paid based on the difference in what I ordered and what gets done I’d be a rich man

 

[DrDrummer]

I am always very suspicious of tachycardia in a STEMI or near-STEMI ECG, which in my mind (and I believe literature supports) makes it more likely to be Type II MI than a plaque rupture OMI. Add to that fever, metabolic derangement and you have a lot of reasons to do many more interventions and see what happens to the ECG rather than go to PCI.

 

[WheezyBaby]

I am always very suspicious of tachycardia in a STEMI or near-STEMI ECG, which in my mind (and I believe literature supports) makes it more likely to be Type II MI than a plaque rupture OMI. Add to that fever, metabolic derangement and you have a lot of reasons to do many more interventions and see what happens to the ECG rather than go to PCI.

Can you provide any literature? This is interesting and new to me. I was able to find some stuff on a Dr smith's ekg blog post but was having trouble finding primary literature on a quick search. That blog did say the same, with the exception being cardiogenic shock

 

[AlmostAnMD]

I am always very suspicious of tachycardia in a STEMI or near-STEMI ECG, which in my mind (and I believe literature supports) makes it more likely to be Type II MI than a plaque rupture OMI. Add to that fever, metabolic derangement and you have a lot of reasons to do many more interventions and see what happens to the ECG rather than go to PCI.

Same. I had a squad call in a stroke alert, STEMI alert and sepsis alert a few weeks ago...all on the same guy.

Just a dude septic from a UTI. I'm sure, one day, I'll see a real stemi with sepsis but for the moment I am wildly unlikely to activate STEMI in this setting. Especially after my colleagues have had similar cases and the interventionalist basically refused to cath until the patient had the other medical issues fixed first. Almost always, and I'm sure it'll be the same in the OP EKG, the EKG is from someone under a lot of metabolic stress in the setting of severe three vessel disease.

 

[RoyBasch]

in the OP EKG, the EKG is from someone under a lot of metabolic stress in the setting of severe three vessel disease.

Agreed, this is most likely.

That being said, trop will most likely be elevated as well (for the same reason) so in the setting of anbormal EKG and troponin in a sick patient with high chance of morbidity and mortality, I think immediate cardiology input is warranted, even if you are pretty confident you know what they are going to say.

These poindexters always love to say weeks after the fact, at a Wednesday morning 10:00 AM committee meeting (patient invariably came in at 4:00 AM on Christmas Eve or something like that) "If only the incompetent ER had TOLD US, OF COURSE we would have done x, y, z....!!!"

 

[WheezyBaby]

Agreed, this is most likely.

That being said, trop will most likely be elevated as well (for the same reason) so in the setting of anbormal EKG and troponin in a sick patient with high chance of morbidity and mortality, I think immediate cardiology input is warranted, even if you are pretty confident you know what they are going to say.

These poindexters always love to say weeks after the fact, at a Wednesday morning 10:00 AM committee meeting (patient invariably came in at 4:00 AM on Christmas Eve or something like that) "If only the incompetent ER had TOLD US, OF COURSE we would have done x, y, z....!!!"

I agree. I'd still do the things I recommended in my post prior to discussing with cards, but giving calcium/fluids, pocus TTE, and rechecking anterior/posterior ekg shouldn't take long and it offers cards a lot more information (eg progression of ischemic changes VS some normalization). But regardless I'd discuss with cards

 

[WilcoWorld]

Agreed, this is most likely.

That being said, trop will most likely be elevated as well (for the same reason) so in the setting of anbormal EKG and troponin in a sick patient with high chance of morbidity and mortality, I think immediate cardiology input is warranted, even if you are pretty confident you know what they are going to say.

These poindexters always love to say weeks after the fact, at a Wednesday morning 10:00 AM committee meeting (patient invariably came in at 4:00 AM on Christmas Eve or something like that) "If only the incompetent ER had TOLD US, OF COURSE we would have done x, y, z....!!!"

I agree. I'd still do the things I recommended in my post prior to discussing with cards, but giving calcium/fluids, pocus TTE, and rechecking anterior/posterior ekg shouldn't take long and it offers cards a lot more information (eg progression of ischemic changes VS some normalization). But regardless I'd discuss with cards

Exactly - in this case you page Interventional Cards directly (without activating a STEMI) and page again if they haven't called back after 15 min. Document those times.

In the mean time you provide the care that EM residency taught you. When the cardiologist calls back you tell 'em that the ECG is very concerning, but that the patient is septic and in renal failure, so you wonder if immediate PCI is not the best plan. Cards agrees (the coders see this and you avoid a STEMI metric fallout). Also, you either transfer to a higher level of care or, if you're already at University Receiving, you consult Palliative. Both paths will help avoid an M&M in the 60% of cases where this patient dies prior to discharge regardless of what anyone does.

 

[jw3600]

Exactly - in this case you page Interventional Cards directly (without activating a STEMI) and page again if they haven't called back after 15 min. Document those times.

In the mean time you provide the care that EM residency taught you. When the cardiologist calls back you tell 'em that the ECG is very concerning, but that the patient is septic and in renal failure, so you wonder if immediate PCI is not the best plan. Cards agrees (the coders see this and you avoid a STEMI metric fallout). Also, you either transfer to a higher level of care or, if you're already at University Receiving, you consult Palliative. Both paths will help avoid an M&M in the 60% of cases where this patient dies prior to discharge regardless of what anyone does.

I see you've played Knifey-Spoony before.

 

[GeneralVeers]

I see you've played Knifey-Spoony before.

#ClassicSimpsons

 

[Fox800]

This is pertinent, and came out today: Extreme widespread ST depression, with ST Elevation in aVR. What do you think?