Thursday, August 15, 2019

5 Cardiologists said this is not a STEMI. But was it an OMI?

Written by Pendell Meyers

A male in his early 50s presented with waxing and waning chest pain starting at rest. He had multiple cardiovascular risk factors and the EM physician strongly suspected ACS.

Here is his initial ECG:
What do you think?














Sinus rhythm
-STE in V1-V5, possibly a tiny amount in V6, and small amount in I and aVL, and II
-Reciprocal STD (although perhaps isoelectric at J point, immediate STD after the J point) with very ischemic appearance in lead III (down-up T-wave is strongtly suggestive)
-Large T-waves in V2-V4, which may be either a normal variant or hyperacute
-Very tiny Q wave in lead V2, as well as V6, I, and aVL, which is not seen in normal variant
-STEMI criteria are not formally met; although V2 has sufficient STE (greater than 2.0 mm), neither of it's neighbors have enough STE to meet criteria (V1 is close at 0.5 mm of the "required" 1.0 mm)


This is all highly diagnostic of acute anterior MI, with the most likely etiology being OMI of the proximal-mid LAD.

The formulas would be formally contraindicated because of the Q-wave in V2, but if we use them anyway the results are (using QTc 397 ms):


4 Variable formula: 20.32
3 Variable formula: 24.08

Both formulas predict LAD occlusion.





The physician called the on-call cardiologist immediately to discuss this ECG, but the cardiologist reportedly said not to activate the cath lab because he/she was not convinced by the ECG. Over the next few hours, four other general cardiologists "signed off on the initial ECG without recognizing STEMI."


The first troponin I returned elevated at 0.11 ng/mL.

Serial ECGs were obtained, including this one several hours later:
Slightly more STE and longer QT than prior.



Although I do not see much difference between the ECGs, for some reason (perhaps ongoing pain or rising troponins) the case was reevaluated at this time and the decision was made to perform cath.

They found 100% acute mid-LAD Occlusion MI, stented with excellent angiographic result.


Peak troponin I was greater than 75 ng/mL (the assay does not measure higher than this apparently).





Learning Points:

STEMI criteria misses 25-40% of OMI, like this case for example.

Due to our paradigm which lags far behind the current achievable skill level, cases like this will continue to be missed or delayed until we solve the problem by replacing the paradigm.

This is another case demonstrating OMI with all ST segments concave.

Pay attention to even the tiniest Q-waves in the right context and assume they are new until proven otherwise. New Q-waves during MI are NOT wide ("greater than 40 ms") until later.

Any Q-wave in V2 in the presence of an otherwise normal QRS complex is abnormal.

Repeat ECGs are almost always helpful.

Use of the formulas would have improved recognition of this OMI.

Ongoing ischemia (by symptoms, ECG, or troponin) despite maximal medical management is an indication for emergent cath lab activation.


===================================
Comment by KEN GRAUER, MD (8/15/2019):
===================================
Once again, the wrong question was asked in this case. That's because it should not matter IF the initial ECG in this case ( = ECG #1 in Figure-1) represents an acute STEMI or an acute OMI — since initial management should be the SAME:
  • Considering that this patient had multiple cardiac risk factors good story for ongoing new ischemic-sounding chest pain and, the ECG abnormalities seen in ECG #1 — prompt cath to define the anatomy, with goal of acute reperfusion if acute OMI is confirmed is the treatment of choice.
  • Unless a prior ECG on this patient can be found that shows identical findings as we see in ECG #1 — there is NO way to rule out acute OMI. As a result — it’s hard to justify not doing acute cath ...
Figure-1: The 2 ECGs in this case (See text).



MTHOUGHTS on ECG #1: Dr. Meyers has skillfully detailed the abnormal ECG findings. To facilitate visualization — I’ve put both tracings together and labeled the following key points:
  • There is loss of the initial r wave in lead V1 — with development of a small-but-real Q wave in lead Vof ECG #1. Overall QRS morphology in lead V2 is strange, with this qRS complex being “sandwiched in” between an rS complex in lead V1, and an rS complex in lead V3 — so there may be some lead misplacement of lead V2. That said — the small q in V2 is almost certainly a real finding, and clearly abnormal.
  • There is more than 2 mm of ST elevation in lead Vof ECG #1 (Compare the RED horizontal baseline with the RED arrow in this lead). The very wide T wave base, with T wave peak clearly exceeding R wave amplitude in this lead clearly defines the T waves in V2 as being hyperacute.
  • Disproportionate T wave amplitude (compared to R wave height) in leads V3 and V4 define those T waves as also being hyperacute.
  • Note that there is more ST elevation in lead V4 of ECG #1, than there is in lead V3 (Compare the RED horizontal baseline with the RED arrow in these leads). There shouldn’t be more ST elevation in V4 than in V3.
  • Finally (as per Dr. Meyers) — the ST-T wave in lead III is clearly abnormal (curved RED line) — with the scooped ST segment ending in a biphasic (negative-then-positive) T wave.
BOTTOM LINE: Without an identical-looking prior tracing — there is NO way to rule out the possibility (if not probability) of acute ST-T wave findings in at least leads V2-thru-V4 Q in V2 reciprocal change in lead III, in this patient with new chest pain. A millimeter definition of acute STEMI should not be needed to justify the need for prompt cardiac catheterization.
  • NOTE: With proximal LAD OMI — one typically sees: isignificant ST elevation beginning in leads V1,V2; iireciprocal ST depression in each of the 3 inferior leads (II,III,aVF); andiiisignificant ST elevation in lead aVL. Because we only partially see these features in ECG #1 — I would interpret this tracing exactly as Dr. Meyers did = probable “proximal-mid acute LAD occlusion”.

MTHOUGHTS on ECG #2: Several hours later — ECG #2 was obtained. As per Dr. Meyers — for the most part, there has been little change between the 2 tracings. That said:
  • I think there is now more ST elevation in lead Vof ECG #2 than there was in ECG #1 (Compare the BLUE horizontal baseline with the BLUE arrow in this lead).
  • Note that there is once again more ST elevation in lead V4 than in lead V3 of ECG #2. This is not a normal finding.
BOTTOM LINE: Given the clinical history — ECG #2 should not have been needed for making the decision to take this patient to the cath lab ...

Our THANKS to Dr. Meyers for this insightful case!




6 comments:

  1. Hi,
    you say in ECG 1 interpretation...
    "Large T-waves in V2-V4, which may be either a normal variant or hyperacute"
    Can you explain this in more details/Links? because this is so common and impose a diagnostic challenge. How to know the T waves are normal and when they look hyperacute in these leads?

    ReplyDelete
    Replies
    1. Hi MG! Perhaps you sent in your question BEFORE I wrote my comment. I think I expanded on the issues you raise above. Let me know if you still have questions after reading My Comment above — :)

      Delete
  2. whenever T wave towers R it's suspicious for some underlying ischemia, the amplitude of T waves and ST depression with cleat "strain and tatening" in D III caught my eyes.
    thanks for this case Dr smith and thanks to Dr Grauer for his further enrichissement discussion.
    your ENT doctor follower ;)

    ReplyDelete
    Replies
    1. @ Anonymous — THANKS so much for your comment! Just to emphasize — in addition to "size" of T waves (compared to the R in the same lead) — SHAPE of these T waves — plus attention to ALL OTHER leads on the tracing — in context with the History (ie, How worrisome does the chest pain description sound?) — comparison with prior and/or serial tracings — troponin + Echo at the bedside — all of these factors combine to suggest a "likelihood" that the changes seen may be acute. THANKS again for your comment — :)

      Delete
  3. Dr Grauer gets it. Anything but the cath lab on presentation is malpractice. Come on guys. You all know that.

    ReplyDelete
    Replies
    1. @ Unknown — Thanks for your comment. Readers of Dr. Smith's ECG Blog know cath lab on presentation was indicated here. I've always been amazed (throughout my career) — at how differently practice may be in different locations with different providers. Important lessons from Dr. Smith's ECG Blog are to realize this — and to emerge with better understanding of the range of things you "could do" (sometimes more than one option may be reasonable ...) — vs those things that you SHOULD do. Along the way — hopefully we ALL continue to learn — :)

      Delete

DEAR READER: We welcome your Comments! Unfortunately — due to a recent marked increase in SPAM — we have had to restrict commenting to Users with a GOOGLE Account. If you do not yet have a Google account — it should not take long to register. Comments give US feedback on how well Dr. Smith’s ECG Blog is addressing your needs — and they help to clarify concepts of interest to all readers. THANK YOU for your continued support!

Recommended Resources