Tuesday, March 27, 2018

Do you want to be interrupted to view what the computer calls normal or nonspecific ECGs? 2 cases at once!

Two Cases

Male Patient

I was handed this ECG of a 40-something male patient.  It was recorded at triage.  The chief complaint was "chest pain."
The computer interpretation was "Nonspecific"
What do you think?

Female Patient

At the exact same time, I was viewing the computer queue of unconfirmed ECGs (read by computer but not yet overread by physician) and saw this one from a 40-something woman, about whom I knew nothing:
The computer interpretation was: "Normal ECG"
What do you think?

Veritas algorithm

Male Patient: When I saw the first one, on a 40-something male, I knew it was a new inferior MI (minimal STE in III with reciprocal STD in aVL, without another explanation), but it looked like it might be subacute or reperfused because the T-wave is inverted in lead III and reciprocally upright in aVL.

Female patient: When I saw the 2nd one, I immediately suspected hyperacute inferior MI.


1. The inferior T-waves are too large
2. There is T-wave inversion in aVL
3. There is T-wave inversion in V2, suggestive of posterior MI

Years later, I sent this to the Queen of Hearts:

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Female patient continued 

I looked in the EHR to find the patient, saw she was in triage, and went to locate her there.  She was sitting quietly in the waiting room.  She stated she had one hour of chest tightness.

I brought her by wheelchair to the ED to a room and recorded this ECG 15 minutes after the first one:
This time the computer called it: "Moderate ST depression."
Of course, it is actually clearly an acute inferior MI, even though (as is so frequent) it does not meet "STEMI criteria."
I activated the cath lab and brought her to our stabilization room.
I called the cardiologists to tell them that we have 2 acute MIs in the ED.

Male patient: I went back to the room of the first patient and he stated that he had been having chest pain on and off for 3 days.  He stated that it had never completely resolved but was constant, with waxing and waning, for the entire 72 hours.  At the moment I was talking with him it seemed to be on the waning end of the spectrum.  This "waning" corresponded with the inverted T-wave in lead III (inverted T-waves are signs of reperfusion -- this is Wellens' of the inferior wall).  The artery was probably open and so his MI was less acute than the woman's.

This is called"Acuteness" of the ECG of MI.

Female patient: I went to tend to the this woman, whose T-waves were upright and hyperacute, and made sure everything was set for the cath lab.

Male patient: Then I returned to the man and he was up out of bed, standing next to the bed and leaning on it, looking ill, holding his chest and stating that he had "terrible gas".

This alarmed me, so I brought him to the stabilization room as well, and recorded this ECG:
Now the inferior T-waves are upright (pseudonormalization) and there is more ST elevation and more reciprocal ST depression in aVL.  Plus ST depression in precordial leads.  
Thus, his artery had re-occluded and this explained why he had suddenly become more ill.

The female patient had just gone to the cath lab, and on that particular day we could not do 2 patients at once, so we gave him aspirin, heparin, ticagrelor and eptifibatide, as well as IV NTG for BP 160/100 (I did not suspect RV MI, though it would be optimal to record a right sided ECG).

His pain started to improve and we suspected that he was reperfusing.  So we recorded another ECG:
The T-wave in III is inverted again, though there is still quite a bit of STE.

The first ECG change after reperfusion is terminal T-wave inversion.
Later, the ST segments resolve. 

A bit later, all pain was resolved, and this ECG was recorded (this is a right sided ECG; that is to say, V1-V6 are V1R-V6R):
Limb leads are nearly identical to the first one.
ST elevation is now resolved.
(The artery is reperfused)
There is no evidence of right ventricular MI, but this means nothing by itself: even if the RV were involved, it would likely not manifest STE after reperfusion.

The cath lab was now open and he went for angiogram.  Here it is:
Obvious mid-RCA severe stenosis, but there is flow (reperfusion, spontaneous, autolysis)

Female patient:

She had a 2nd Obtuse Marginal occlusion (Left dominant, off the circumflex!).  It was actually a dissection, not an atherosclerotic plaque rupture.  Here is her post reperfusion ECG:
Nearly normalized

And the next morning:
Truly normalized T-waves.
Reperfusion early and without T-wave inversion!

Learning Points

1. Again, a "Normal ECG," as read by the computer algorithm in triage, would miss an acute MI.

2. One subtle finding may be normal variant (e.g., large inferior T-waves), but the combination of subtle findings makes the ECG diagnostic (add T-wave inversion in aVL and V2)

3. Acute coronary occlusion frequently presents with subtle ECG findings.  (We will give a systematic explanation of this when we publish our OMI Manifesto -- soon)

4. Inverted T-waves in MI are due to reperfusion or long duration.

5.  When such T-waves suddenly become upright, it is due to re-occlusion (this is often called "pseudonormalization" of the T-wave)

6.  All else being equal, the patient with the upright T-waves in the affected area of infarct is the one who has the persistently occluded artery and needs to have priority in going to the cath lab.

7.  Adjunctive anti-thrombotic, anti-platelet, and anti-ischemic therapy makes early spontaneous reperfusion more likely.


  1. Dr. Smith,

    In the male patient's 2nd ECG, the STE in lead III is > STE in lead II. Did you not suspect RV MI due to the lack of STE in V1? Secondly, does STE in V1 have greater specificity for RV MI over STE III> STE II?


    1. 1. Yes. Although the sensitivity of STE in V1 is not perfect. Also because there was elevated BP.
      2. STE III > II has zero value for RV MI
      3. STE in V1 is very specific for RV MI, pretty sensitive if there is no STD in V2, and very insensitive if there is STD in V2

  2. The fact I can now easily spot those and other important subtle changes is a testament to the value of everything you keep sharing with us. Thank you !

  3. When i say its hyperacute T in the inferior leads?

    1. I do not understand the question

    2. Can You show as Your definition of hyperacute T-Wawe, the deffinition of 6mm T wave if You compare with low amplitude of QRS isn't enough specyfic.
      I think that was the correct question.

    3. Kamila,
      There is no definition. Only recognition.

      See these 10 examples of inferior hyperacute T waves:

      Here are 10 examples of anterior hyperacute T waves:

      Here are 10examples of lateral hyperacute T waves:

    4. Try these links:



  4. Great cases! Would you have given eptifibatide in the male's case if he was able to go straight to the cath lab?

  5. A true “clinic” in acute ECG interpretation by Dr. Smith! Superb step-by-step correlation with how the patient is doing (and with what is likely to be happening anatomically at each point in the process). The only point I’d make would be to emphasize that computer interpretations can NOT be used as part of the “triage” process — as could not be more evident than by these cases. Computerized interpretations can at times suggest a diagnosis that might not have been detected … — but: i) the clinician should always look at the ECG himself/herself FIRST before looking at what the computer said; and ii) knowing that computerized interpretations can (and most definitely do) miss some acute tracings — clinicians should go with THEIR interpretation (and ignore a “normal” read by the computer IF they see anything that is worrisome on the ECG). THANKS to Dr. Smith for this excellent post!

  6. Dr. Smith,

    Is the TWI in avl still significant given the QRS axis? I know you've discussed this topic in the past, still trying to wrap my head around it...

  7. As per Dr Grauer what an excellent presentation on these two patients and positive outcome for the patients. Many thanks as always for your knowledge and experience Dr Smith helping people like myself learn.

  8. Ah such scary cases!!! Thanks for posting, I always learn so much from your blog! :-)

  9. Excellent cases! Thanks for providing it so detailed, really great for learning.

  10. Thanks Dr. Smith for your 2 interesting cases of ACS with interpretation in detail. I have a question about using eptifibatide, sir. When should we use it, or use it routinely for all cases of coronary artery occlusion? And if this drug is not available at that time, what will we do ?. Thank you,sir!

    1. Use it only rarely and in discussion with your interventionalist. Ours wanted it due to the delay to cath. Normally it is only given after the angiogram when you know the pathology and anatomy.

  11. Dr Smith,

    Could you explain mechanism of T wave inversion after reperfusion?

    1. Maks,
      No. No one really knows. "Dispersion of repolarization in ischemia." Not very helpful, right? It doesn't help to know the mechanism, you just have to recognize the pattern.


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