To STEMI or not to STEMI, that is the question...

[TomB]

Isolated posterior wall MI s are definitely a small minority of STEMIs, but they are definitely out there, perhaps on the order of 4% of STEMIs. You probably get the information that you "need" form the standard picture, but getting someone else to get on board might require all the other leads for evidence.

That's true. Without posterior leads showing ST-elevation you may not be able to convince ED personnel that it's a STEMI. On the other hand, ST-depression in the right precordials leads is more likely to represent posterior STEMI than anterior ischemia and in some cases acute isolated posterior STEMI will present with ST-depression in the right precordials but no ST-elevation (or extremely modest ST-elevation) in the posterior leads. When the QRS complexes are small as they often are in leads V7-V9 our threshold for ST-elevation is less but this is often not appreciated.

 

[ekgpress]

Got an interesting call today, and wanted some feedback from you guys.

We received a Priority 2 call to an urgent care center for a 40 y/o male, possible STEMI. (Yes, we asked dispatch to repeat our response priority, too.) U/A, Pt was sitting up in bed, no visible distress, smile on his face. In condensed form, the conversation between me and the RN went something like this:

RN: This is a 40 y/o male who was having chest pain during dialysis this morning. EMS brought him in here. He's not having any chest pain right now, we gave him ASA and Nitro. The doctor noticed some changes when he compared an old EKG to the one we did today. [RN holds up a rhythm strip briefly] He has had three MIs in the past. Now, we're sending him over to ABC hospital to rule out a STEMI.
Me: Was there any elevation?
RN: I don't know. I don't think so.
Me: How are his vitals?
RN: BP in the 170's, Pulse in the 60's.
Me: Do you have his 12 Lead?
RN: Yeah, somewhere.
Me: Can I take a look please?
RN: Here.

The hospital's 12 Lead showed elevation in V3, V4, V5. It was about an hour old. I put him on my monitor (BP 175/102, Pulse 65, BPM 16, SpO2 100), and got this:

Next, I did a 12 lead and got this:

To make a long story short, we arrived at the ED and my 12 Lead was shown to the attending. He shrugged and said, "Not a STEMI" and walked away. I was perplexed; there seems to be clear elevation to me. Had I got this Pt as an emergency call, I would have called in a STEMI to the hospital. Can anyone explain to me why the attending said what he did? I realize that there's a few things going on in the 12 lead, but I don't see why the elevation was not significant. Please tell me what you see, and what you don't see.

Anyone care to take a crack at it? I realize the pics aren't the best, but give it a try anyway.

If I understand correctly- there was an initial hospital ECG (done an hour earlier) - that showed ST elevation in V3,V4,V5 - and then you repeated the ECG and got the following:

First:
- As stated by others, one cannot used ST elevation on a 1- or 3-lead rhythm strip as definitive for ECG interpretation. One can suspect something is going on (and I agree there is clear ST elevation in leads II,III,aVF on the 3-lead rhythm strip) - and this should clearly prompt doing a 12-lead tracing - but one can't "call it" until you see STEMI on a true 12-lead. Note in the rhythm strip that the QRS is predominantly negative (a bit unusual for what one expects in the inferior leads - though totally consistent with the Left Anterior HemiBlock)- and the shape of the ST elevation is concave up in III,aVF as opposed to convex down which is more characteristic of STEMI - so certainly the ST elevation on rhythm strip is of concern - but in no way definitive.

The 12 lead I see is problematic. Note V2 is totally "out of place" (qR, T inverted) - so there is LEAD MISPLACEMENT of lead V2, and this tracing needs to be repeated ... Otherwise - I don't see acute STEMI - but on the other hand I'm not at all sure that something might not be in process ... Would REALLY help to compare this tracing with the one from 1 hour ago .... On this Sept 11 (12:48:17) tracing I see NSR; normal intervals; LAD consistent with LAHB; LVH and strain and/or ischemia; the V2 lead misplacement; q waves in I,aVL that could be normal septal q waves OR could possibly be related to infarct of uncertain age (q in aVL a tad bigger than usual for septal q waves ... ); RAA (peaked P in II); LAA (deep neg P component in V1); persistent S waves (thru to V6); ST coving with some J point depression in esp. I and also aVL (the ST coving a bit uncharacteristic for "strain"); rSr' in V1 with ST elevation (of itself nothing definitive, as this may be seen with rSr' pattern); nondescript, seemingly concave up ST elevation in V3 - with artifact precluding assessment of V4 - and NO true V2 to determine if what I see on this tracing in V3 is anything of concern or not .... Clearly depends on the clinical picture - and comparison with prior tracings - but I'd suspect changes on this tracing are probably old in a patient who clearly has LVH and may or may not have CAD with some ischemia of uncertain age ... Hope that helps - Ken Grauer, MD

 

[ekgpress]

Two points: i) Whether or not there is ST segment deviation is based on the PR segment baseline. In view of this - the ST segment in lead III is clearly elevated (albeit not by a lot) - and the ST segment in lead aVF is probably also up a tad. Point ii) More important than "amount" is ST segment "shape" - so that the ST segment in lead II is coved. Thus, there are some changes in each of the inferior leads (II,III,aVF). That said - I'd guess that these changes are not acute, and are more the "reciprocal" of what we are seeing in leads I,aVL. There is LAHB and LVH, further complicating assessment - but of concern is the ST segment coving particularly in lead I that is usually not seen with pure "strain" from LVH. There is clearly lead misplacement with lead V2 (that looks totally out of place) - and this complicates assessing what looks to be some coved ST elevation in V3 (albeit with artifact) and with the too-much-artifact-to-tell that we see in lead V4. In short - definitely not at all diagnostic on this ECG of STEMI - but possibly something is going on - and follow-up tracings, the clinical course, troponins, and comparison with prior tracings would be needed to know for sure.

 

[Theo]

Awesome thread and great discussion. This weekend, I had my first patient with ST-elevation from causes other than a MI. It was a great experience (for me) that was a perfect reminder of why we have to stay sharp and understand differential diagnosis.

60 y/o male, mild shortness of breath, no pain what so ever, no respiratory distress, a bit lightheaded and said he felt "shaky". Vitals were all stable, BP was a bit on the low side. Patient was being transported from a small ED to a facility that could provide definitive care.

12 Lead revealed ST elevation in V1, V2, II, and III. The strips were cookie cutter ST-elevation, but the guy didn't have any of the corresponding S/S of an MI.

Patient had no prior heart history, no HTN. He had a history of depression and earlier this year had acute renal failure in which he was on dialysis for only one week and then was cleared. He said they never found the cause of his renal failure. ED nurse said patient was again in acute renal failure and was mildly hyperkalemic.

I knew about peaked T waves from hyperkalmeia, but didn't see any peaked T waves on the ECG and the patient's strip never changed throughout transport. Perfect examples of ST-elevation (kicking myself for not making a copy to share). Vitals remained stable, no pain at all.

After the call I did some research and found that in some rare cases, hyperkalemia can produce "pseudoinfarction" patterns on the 12-lead. As the levels of potassium begin to rise, then you will begin to see peaked T waves.

 

[ekgpress]

Awesome thread and great discussion. This weekend, I had my first patient with ST-elevation from causes other than a MI. It was a great experience (for me) that was a perfect reminder of why we have to stay sharp and understand differential diagnosis.

60 y/o male, mild shortness of breath, no pain what so ever, no respiratory distress, a bit lightheaded and said he felt "shaky". Vitals were all stable, BP was a bit on the low side. Patient was being transported from a small ED to a facility that could provide definitive care.

12 Lead revealed ST elevation in V1, V2, II, and III. The strips were cookie cutter ST-elevation, but the guy didn't have any of the corresponding S/S of an MI.

Patient had no prior heart history, no HTN. He had a history of depression and earlier this year had acute renal failure in which he was on dialysis for only one week and then was cleared. He said they never found the cause of his renal failure. ED nurse said patient was again in acute renal failure and was mildly hyperkalemic.

I knew about peaked T waves from hyperkalemia, but didn't see any peaked T waves on the ECG and the patient's strip never changed throughout transport. Perfect examples of ST-elevation (kicking myself for not making a copy to share). Vitals remained stable, no pain at all.

After the call I did some research and found that in some rare cases, hyperkalemia can produce "pseudoinfarction" patterns on the 12-lead. As the levels of potassium begin to rise, then you will begin to see peaked T waves.

----------------
Sorry for my delay in responding - Yes, a picture is worth a 1,000 words - and a beauty of current cell phones is that they enable reasonable quality photos very easy on-the-scene ... There are a number of causes of T wave peaking not due to infarction - including hyperkalemia & repolarization variants. Usually one can surmise what is going on from "gestalt" of the overall tracing - but hard to say more without a copy of the tracing you saw .... Next time!

 

[Brandon O]

Never look at the interpretation first. Try to never look at it all. Nothing is more accurate than a properly trained human brain. This is not a STEMI. V2 & V3 do appear to be swapped. Still no joy on STEMI. No ST elevation. No reciprocal depression. There are inverted T's, but they are chronic in nature from previous multivessel disease with intervention as previously stated.

The fine print on the PDF file stated its accuracy assuming normal parameters. Said pt started out beyond normal parameters.

The Marquette algorithm for STEMI is, as noted, highly specific but not very sensitive. It's true that the specificity depends on various things being in place. However, they're relatively controllable. The big ones are

-- Data quality
-- No tachyarrhythmias (like most humans, it gets confused when the rate is fast)
-- Data quality
-- No notable PR depression (it does use the PR segment to calculate STE, and hence disorders like pericarditis can cause problems)
-- Data quality!

It's not a replacement for a human, but used properly it's a very useful piece of data to add to your overall gestalt when forming a diagnosis. (Mind you this is for calling a STEMI; other interpretations may be more or less accurate.)

Partly due to the above but also because of obvious weirdness (note the R-wave progression), I think the correct response to the given 12-lead is to perform a repeat 12-lead with good quality and work with that instead. Garbage in, garbage out.