Tuesday, May 7, 2019

What happens when you don't recognize an OMI?

This was sent by an "avid reader."  The case was from his hospital, which does not have a cath lab.


A 60-something male was sent in from a cardiologists' office after presenting there with chest pain.  The office ECG is unavailable.

The pain had been intermittent for a few days, but worse on the day of admission.

Here was the initial ECG:

To me, and to him, this is an obvious acute LAD occlusion.
There are hyperacute T-waves, especially in V2, plus other more subtle findings.
If you use the 4-variable formula:STE60V3 = 2.5
QTc = 398
RAV4 = 3
QRSV2 = 15
Value = 20.28, confirming LAD occlusion (18.2 is the most accurate cutoff).

The Emergency physician and the cardiologist concluded: "No STEMI.  Admit here.  Do not transfer."

At a minimum, this patient needs ECGs recorded every 15 minutes.  This was not done.  The next ECG was recorded 90 minutes later:
Now it is an obvious anterior STEMI.
The ST Elevation even meets "criteria" now.
Why does the computer not diagnose it?

The first troponin I returned at 1.5 ng/mL.  A repeat returned at 2.5 ng/mL.  Still no 3rd ECG recorded.

At this point, the patient developed cardiogenic shock, and another ECG, at 270 minutes (3 hours after the 2nd ECG), was recorded:
Now there is massive ST elevation.
There are multiple PVCs.
There is clear STE in aVL, with inferior reciprocal ST depression.

The patient was transferred by helicopter to a PCI facility.

Cath: "Entire left system occluded." (including left main).  Ejection fraction 10%.  Too ill for CABG surgery.

I do not have further outcome, but his chances of survival are not good.

Learning point:

Do not wait for STEMI if you find an OMI.

We all have much to learn.  Hopefully this physician will learn from this one, so that future similar patients will not be similarly doomed.

Comment by KEN GRAUER, MD (5/7/2019):
This tragic case is one to learn from. Unfortunately, those in need of the most learning ( = those close-minded colleagues of the “avid reader” who sent in this case) are the least likely to profit from mistakes made. Dr. Smith has already emphasized many KEY points about this case. 
  • I’d add the following thoughts regarding the initial ECG obtained on this 60-something man with new-onset chest pain (Figure-1):
Figure-1: The initial ECG in this case, obtained in the ED on this patient with chest pain. I’ve copied the computerized interpretation of this tracing (See text).
Thought #1:
  • I would wager that the Emergency physician who read the ECG in Figure-1 did not use Systematic Approach. If he/she did — they would surely have noticed that in addition to lead V2 (which as per Dr. Smith — shows an obviously much-taller-and-fatter-at-its-base-than-it-should-be, therefore hyperacute T wave) — there is NO way that lead Vcan be “normal” in a patient with new-onset chest pain. There is at least 2 mm of ST elevation in lead V1 (RED arrow) — and that is virtually never “normal”.
  • There are many systems in use for ECG interpretation. Regardless of whether you use mine, or another one that you prefer — the KEY is to always go through each of the essential parameters to assess in the identical sequence, so that you never forget to assess them all. This entails looking at each of the 12-leads on the ECG.
  • Advantages of Using a Systematic ApproachiWith just a little bit of practice — it will speed up your interpretation! (because you have a step-by-step approach — and will no longer go back-and-forth to reassess things you’ve already looked at)and,  iiA systematic approach will improve your accuracy (because you no longer leave things out …).
Beginning with Descriptive Analysis:
  • Rate & Rhythm — The rhythm is sinus at ~60/minute. There is one late-cycle PVC ( = the 2nd beat in the tracing).
  • Intervals  The PR interval is normal; the QRS complex is not wide; and the QTc is not prolonged.
  • Axis  There is a slightly leftward frontal plane axis (the QRS is all positive in lead I — and probably a little more negative than positive in lead aVF).
  • Chamber Enlargement — None.
  • Q-R-S-T Changes  There is a Q wave in lead aVF. We only see 1 sinus-conducted beat in lead III — and it’s hard to be certain if there is or is not a tiny initial r wave in this lead. There definitely is a small initial r wave in lead II. Otherwise there is a QS complex in lead V1 — but definite precordial lead R waves have formed by V2. R Wave Progression — shows slightly delayed transition (the R becomes taller than the S wave is deep between lead V4-to-V5). ST-T Waves — There are sagging ST segments in each of the inferior leads. The most remarkable finding is the ST elevation in leads V1 and V2 (and probably also a small amount in lead V3— with T waves that look taller-and-fatter-than-they-should-be given relative amplitude of the QRS complex in leads V1-thru-V4.
Putting this Together in your Clinical Impression:
  • The rhythm in Figure-1 is sinus at ~60/minute — there is 1 late-cycle PVC — and, there is evidence of a probable prior inferior MI (ie,a Q in lead aVF [if not also in lead III] — but with inferior lead ST-T waves that do not look acute). Of most concern — there is ST elevation in V1 & V2, and hyperacute T waves in leads V1-thru-V4. Given that this man in his 60s has new-onset chest pain — one has to assume an acute cardiac syndrome (presumed OMI) until you prove otherwise.
  • P.S.  QRS complexes are fragmented (at least in leads V4, V5 and V6— which strongly suggests there is underlying heart disease.
Thought #2:
  • Think Patterns oLeads”. The experienced interpreter saves time and increases accuracy by “taking in” several leads in a given lead area at the same moment in time. For example, the “theme” in the inferior leads is that there has been prior inferior infarction — even though there is definitely no Q wave for the sinus-conducted beat in lead II. And, the reason I think there is slight ST elevation with a hyperacute T wave in lead V3 — is that there is NO doubt about these findings in neighboring leads V1 and V2. This is why the T wave in the next neighboring lead ( = lead V4) is probably also hyperacute (taller-and-fatter-than-it-should-be given the small QRS complex in V4).
Thought #3:
  • What about the Computerized InterpretationIt is hard to believe that the computer is calling chest lead ST-T waves in Figure-1 “probable early repolarization”. This just goes to show How Wrong the computer can be! But we should never be depending on the computerized interpretation to begin with!
  • I happen to like computerized ECG interpretations — because I know how best to use them (CLICK HERE  for My Approach for Using the Computer). I realize many clinicians do not like computerized interpretations. It’s a matter of personal preference and clinical experience with computerized interpretations.
  • The BASICS: Never look at the computerized interpretation until after you have made your own independent assessment! In general — the computer is great for calculating rates, axis, and intervals. In my experience — it is terrible for assessing any rhythm other than sinus! The computer usually does OK for assessing normal tracings — but it may overlook certain findings (such as the ST elevation and hyperacute T waves, as well as the prior inferior MI in Figure-1). BOTTOM Line: The computerized report may help by suggesting certain findings that you may not have thought of — BUT — you must always overread what the computer says. IF you disagree with what the computer says — then cross out those parts in the computer report that you disagree with! In this particular case — I suspect that the computer reading of, “probably early repolarization” may have led one or more of the clinicians astray ...


  1. Do the Qs in inferior leads have any significance ?

    1. I believe the inferior lead Q waves are consistent with prior inferior MI (Please see My Comment above — written after you asked this question — :)

  2. Most likely, the mistake was made because the elevated ST segment is concave up. As this case illustrates, STEMI can have "concave-up ST segment" elevation!!! Does that mean looking for "concave up" or "convex up" is useless? No, I still make a very good use of it.
    K. Wang.

    1. Thanks for your comment K! As I tried to emphasize in My Comment (written after you made your comment) — regardless of what is going on in lead V2, the elevated ST segment in lead V1 is virtually never "normal" in a patient with new chest pain. And as I know you know, in V2 — more than just the ST elevation, it is how disproportionately tall this T wave is that is clearly abnormal ( = hyperacute), regardless of the "smiley" shape to the ST segments. But what is especially disturbing, is that not only the emergency physicians — but also the cardiologist on this case missed these findings ... THANKS again (as always!) for your excellent comments! — :)

  3. Regarding the computer calling "early repolarization", you need a notch at the junction to call early repolarization. This patient does not have it. Also it's important to keep in mind that ~90% of heathy young men have 1-3mmm ST elevation in one or more precordial leads normally. Not "normal variant, just normal!! (pages 222-224 0f Atlas of Electrocardiography by K. Wang) . In that case, the ST segment is concave up. Wouldn't it be nice if all normal ST elevation is concave up while ST elevation in STEMI is convex up? If so, there would be no confusion. Yes, all normal ST elevation is concave up but, unfortunately, not all ST elevation from STEMI is convex up, posing confusion at times as in this case.
    K. Wang.

  4. This was such an unfortunate experience for this patient. I certainly agree with Ken that the ones least likely to benefit from the knowledge presented by this patient outcome were the ones treating the patient. Dogma has no place in medicine.

    I was intrigued by the relatively minimal changes in aVL during all this. I would have expected more (and earlier) STE in aVL with an obviously very proximal LAD lesion and the unlikelihood of a Type 3 LAD. A point I always make when I introduce my students to "Jones's Rule" is that reciprocal changes may sometimes occur in advance of the primary change of ST elevation. ST elevation really doesn't appear in aVL until the 3rd ECG though reciprocal ST depression is present in all 3 ECGs. I also point out that even when the ST elevation makes its appearance, the reciprocal changes may be much more impressive (check out the 3rd ECG).

    Jones's Rule - "Any ST depression on the ECG of a patient with chest pain suggestive of an ACS represents a RECIPROCAL change until proved otherwise."

    1. Thanks, Jerry. While the Jones rule is true, it is specific and not sensitive in anterior MI. 40% of LAD occlusion has no "inferior" ST depression. One cannot rely upon its absence!

    2. Steve...

      By definition, Joness Rule requires the presence of ST depression. But you are absolutely right in that lack of ST depression as a reciprocal change does not rule out any MI that characteristically has no recordable reciprocal leads. Just as a totally normal ECG cannot be used to rule out an MI.

      The Jones's Rule can help when there is a proximal LAD lesion in a Type 1 or 2 LAD in which there will likely be reciprocal changes inferiorly due to STE in aVL caused by 1st diagonal occlusion. Reciprocal changes, as well as STE, in the limb leads are often missed in proximal occlusions of Type 3 LADs due to cancellation of forces.

      But you are certainly correct in that a distal occlusion of a Type 1 or 2 LAD will not result in ST deviations in the limb leads.

  5. I realise this is off topic regarding OMI, but with the negative P wave in V1 and possibly(?) biphasic P in V2, is there a chance that the V1 and V2 electrodes are too high?

    1. It is always possible that there is lead misplacement. In our informal study of tracings posted on the internet — it was amazing how commonly chest lead electrodes were misplaced (and the most common error was placement of V1/V2 too high on the chest). That said — although the P wave in lead V1 is negative — this CAN be a normal finding (ie, right-sided lead V1 normally sees depolarization of the LV as moving away from V1) — and against lead misplacement are: i) lack of an r’ in V1; ii) lack of a clearly negative P in lead V2; and iii) the PQRST in lead V1 really does NOT look much like the PQRST in lead aVR. (Please See My Comment at the bottom of the 11/4/2018 Steve Smith Blog Post — https://hqmeded-ecg.blogspot.com/search?q=lead+misplacement+v1 — :)

  6. Thank you very much for your kind words


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