Saturday, August 1, 2020

Computer and transferring physician say "normal." What do you think?

This was sent by Guillaume Debaty, from the Grenoble Region of France.  He has done a lot of great work on cardiac arrest, including as co-author of our study on esmolol in refractory cardiac arrest, and much more with Keith Lurie.

See his Google Scholar profile here.

A 40-something woman was in a remote alpine location when she complained of crushing chest pain.

The physicians said the ECG was normal, as did the computer.

Guillaume asked for it to be sent.

What do you think?

Guillaume thought that the minimal ST elevation in inferior leads was accompanied by abnormal ST depression and T-wave inversion in aVL.  Note that the voltage of the STD and TWI are VERY small -- but so is the voltage of the QRS.   All ST depression and T-wave inversion is proportional, and must be evaluated in the context of a large or small QRS voltage.

T-wave inversion in aVL and in V2 are both "soft" signs of inferior OMI.

Here the STD in aVL is significant.  He saw it.

They activated the cath lab and found a 100% obtuse marginal occlusion.  It could have been a false positive ECG, but if it had been, no harm done.  It was not.

Of course we do not know for certain that the inferior findings represent ischemia.  It could be that this is the baseline normal ECG and that the marginal occlusion was electrocardiographically silent.  The only way to tell would be to see evolution on subsequent ECGs: if no evolution, then these findings have nothing to do with the occlusion. I will try to get those ECGs!

Learning Points

1. The ECG in OMI may be normal.
2. The ECG in OMI may appear normal at first glance, but actually be highly suspicious or diagnostic
3. Any ST depression in aVL with ANY STE in inferior leads is highly suspicious for OMI.
4. The computer makes this mistake very frequently.  See here over 20 cases of the computer calling the ECG completely normal when in fact it is diagnostic of OMI (some of the many cases here are of other disorders than OMI).

MY Comment by KEN GRAUER, MD (8/1/2020):
For illustrative purposes — the timing of this case is optimal, coming as it does just 1 day after Dr. Smith posted his latest contribution to the challenge of resetting the paradigm away from the problematic “STEMI” vs “non-STEMI” approach — and towards acceptance of the much more practical and effective OMI-NOMI paradigm.
  • Today’s case could have been one of the estimated 25-30% of acute coronary occlusions that are regularly missed by insistence on millimeter-defined STEMI criteria before considering intervention.

For clarity — I’ve labeled and reproduced the initial ECG in today case (Figure-1). It should be emphasized that ECG findings in Figure-1 are subtle — and none of these findings in isolation would compel me to activate the cath lab.
  • As emphasized in My Comment to the July 31, 2020 post — in the setting of new cardiac symptoms — One looks for any of a number of other ECG findings that should raise concern for an acute ongoing event despite lack of millimeter-criteria for STEMI. Several of these are present in this case.

NOTE: The computer did not “make a mistake” in this case. The mistake was made by the clinicians who accepted at face value a computer interpretation of “normal” for an ECG with subtle but definitely-present ECG findings.
  • KEY Point: We should expect that the computerized interpretation will not be sensitive for detecting subtle acute changes. Therefore — Do not look at the computerized interpretation until after you have made your clinical decision. Even then, if you are concerned by the ECG and the clinical history — Do not be swayed by a negative computer report!
  • P.S. — Despite the best of programming — the computer is still not able to “touch” and talk to the patient in front of them. And, in today’s case — the fact that this previously healthy 40-something woman presented with new-onset “crushing” chest pain was of critical importance for optimal clinical decision-making — because this type of history needs to heighten your acuity for seeking out subtle ECG findings that we should not expect the computerized report to pick up.

Figure-1: The initial ECG in today’s case (See text).

MY THOUGHTS on ECG #1: The rhythm is sinus at ~60/minute. All intervals and the axis are normal. There is no chamber enlargement. Regarding Q-R-S-T Changes — I noted the following:
  • There are very small and narrow Q waves in inferolateral leads. These are clinically insignificant.
  • R wave progression is normal — with transition occurring between leads V3-to-V4.
  • There is subtle flattening of the ST segment in a number of leads (horizontal RED lines). Normally, there should be a gradual upsloping of the ST segment in most leads, that then goes on to blend almost imperceptibly into an upright T wave. This is not what we see in leads V2 and V3, and by extension in lead I.
  • It’s a bit more challenging to assess the ST segment in leads V4 and V5 — because ST-T wave morphology is different for the 2 beats that we see. There should be no doubt that the ST segment in leads V4 and V5 for complex -A- is flattened — but not so much for complex -B- (and unfortunately we don’t know which of these 2 complexes show the true ST-T wave morphology in these leads).
  • As noted by Dr. Smith — the T wave in lead aVL is inverted. Although the amplitude of this inverted T wave is tiny — so is the QRS! While true that in isolation — the T wave may normally be inverted in lead aVL when the QRS is predominantly negative (as it is in ECG #1) — the base of this tiny T wave inversion looks disproportionately wide. Conclusion — I did not know for certain if the T wave inversion in lead aVL of ECG #1 was abnormal — but it could be!
  • Also as noted by Dr. Smith — the T wave in lead V2 is inverted. While the T wave may normally be inverted in lead V1 in adults — most of the time, the T wave should not be inverted in lead V2. Adding to my suspicion that this was indeed an abnormal finding is the distinct ST segment straightening in lead V2, that continues on in lead V3.
  • Finally — there are the subtle findings in the inferior leads. I was not as concerned by the slight-but-real upsloping ST elevation in each of these leads. But I wondered (after more than a few looks) if those peaked T waves in leads III and aVF might not be a little bit taller-than-expected given R wave amplitude in these leads ...

BOTTOM Line Regarding ECG #1: If this tracing had appeared in my “daily stack” during the 30 years that I routinely read all out-patient tracings for our 35 medical providers — I would not have thought twice about saying, “Changes do not appear to be acute”. But that is not the clinical scenario that occurred in this case.
  • All of the above findings are subtle! But taken together in the context of a patient presenting with new-onset “crushing” chest pain — I was concerned about a few potentially hyperacute T waves + nonspecific ST segment flattening in multiple leads + potential reciprocal changes in leads aVL and V2 — which taken together, was fortunately enough for Dr. Guillaume Debaty to wisely activate the cath lab.


  1. Hi guys, Very interesting case! This ECG overall strikes me as a pattern of Infero-Lateral OMI. I believe the changes in V2 are likely due to high placement of the lead (the clue lies in the P wave). Acute OM1 Occlusion doesn't really fit with this tracing. Did this patient by any chance have a Left-Dominant Circulation? If so, it's possible that this was Left Circumflex Occlusion that propagated to Occlude OM1 by the time of cath.

    1. Hi Sam! — THANKS so much for your comments, which I totally agree with! I responded to the same point you raise about possible too high placement of leads V1,V2 in my Answer (below) to Arron Pearce. I also would not have predicted OM1 occlusion as the “culprit artery” for the picture I see in ECG #1 … but, as I mentioned in My Comment (above) — I thought we might be seeing very early hyperacute T waves in some inferior leads (and though I chose not to mention this, by extension — possible some “extra peaking” in the T waves of leads V5,V6) — which is why we ALL (for interest purposes) would LOVE to see both serial tracings as well as the complete cath report. THANKS again for your comments! — :)

    2. Agree with both comments, but we do not have that info. All we can say is that the ECG is highly suggestive of inferior MI, from whatever etiology. Not diagnostic however.

    3. Of course we do not know for certain that the inferior findings represent ischemia. It could be that this is the baseline normal ECG and that the marginal occlusion was electrocardiographically silent. The only way to tell would be to see evolution on subsequent ECGs: if no evolution, then these findings have nothing to do with the occlusion. I will try to get those ECGs!

  2. I agree that V2 T wave inversion may or may not be abnormal. I suspect there is high electrode placement as the P waves in V1 and V2 are inverted. I suspect that the T wave inversion may be due to high/close placement of V1 and V2. I think that the T wave inversion in aVL is normal in relation to the negative QRS but the subtle ST depression in the first beat is suspicious in the clinical picture. Inconsistent morphology (beat to beat variation) may cause some to dismiss the subtle ST-T wave findings. An interesting case. Like Dr Grauer I would not be concerned by the ECG if it was not for the patient's symptoms, I wonder if serial ECGs would shown any changes.

    1. @ Aaron — THANKS so much for your comments which I completely agree with! It’s usually me to bring up “questionable lead placement” — but you are completely correct that P wave negativity in leads V1,V2 + marked similarity in QRST morphology of leads aVR, V1 and V2 DOES suggest the possibility of erroneous (ie, too high) placement of leads V1,V2 on the chest (as per My Comment in the Nov. 4, 2018 post = ). That said — the ST segment is flattened not only in lead V2 — but ALSO in lead V3 (if not also V4,V5 if complex -A- reflects true morphology in those leads) — which led me to give greater credence to the T inversion that we see in V2 in this patient with crushing new chest pain. I agree = I’d LOVE to see serial tracings in this patient! But if I correctly understand the history we are given in this case — Guillaume had to make a quick decision — and faced with a VERY worrisome history + a series of very subtle and potentially non-acute (but which also COULD BE acute) ST-T wave changes that are seen in multiple leads — I believe the indication for cath to define the anatomy in this case was made on good grounds. It’s one in which, “Ya gotta be there” — et Guillaume était là! (and he WAS there) — :)


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