Thursday, February 1, 2018

This ECG was shown to the doctor with no clinical information

Written by Pendell Meyers, with edits from Steve Smith

I was charting at my computer on a busy overnight shift when a triage ECG was placed between my face and computer screen, asking for my signature. Here it is:
What do you think?

--Sinus rhythm.
--There is a tiny amount of STE in the inferior leads, with lead III having possibly a large T-wave compared to its QRS complex.
--Lead aVL clinches the diagnosis with a very small normal QRS complex followed by minimal ST depression and a proportionally massively inverted T-wave.
--Lead I also shows reciprocal STD.
There is obvious STD in V2-V4 which indicates posterior involvement.
This ECG is diagnostic of acute coronary occlusion affecting the inferior and posterior walls.

Let's look at the magnified limb leads:
Now the findings are more clear

And the magnified precordial leads:
Note clear ST depression in V2, subtle in V3

Subtle ST depression in V4

I asked the triage nurse to bring him back into a room in my zone immediately, and to perform serial 15 minute ECGs as well as labs and cardiac monitor. Although these changes are clear to me, I knew this would be somewhat difficult to convince the cardiologists and I may have to get serial ECGs until more obvious findings are present.

I went to assess the patient. I found out the ECG belonged to a male in his 40s with hypertension who presented with chest pain that woke him from sleep. He stated he had similar chest pain last night which subsided, and he was able to go to sleep only to be awoken several hours later by recurrent pain.

Here is his previous ECG on file:
This further confirms that the findings in the presentation ECG are real and acute.

At this point I got a repeat ECG (approximately 20 minutes after arrival):
This shows increased STE in the inferior leads, increased STD in aVL, increased STD in V2-V4. All indicative of progression of acute coronary occlusion.

I activated the cath lab.

He was taken for emergent cath:
Patent RCA.

This is the so-called "spider view," in which you can see the clean bifurcation of the left main coronary artery into the LAD and the LCX. Soon after the LCX splits off, it quickly branches into two vessels. The larger caliber vessel shows complete proximal occlusion with TIMI-0 flow.  
This was diagnosed as a 100% thrombotic occlusion of the (very large) proximal segment of OM1.  PCI was performed and was able to reduce the stenosis to 50%.

The first troponin T returned highly elevated at 1.33 ng/mL. No more troponins were available.

This is a surprisingly high Troponin T.  It suggests that the patitent's infarct has been going on longer than one would have thought, or that the pain the patient had experienced earlier in the night had resulted in significant myocardial infarct (permanent injury).

Here is his ECG after cath:
ST segment and T-wave findings have almost all resolved.
There are new Q-waves, with T-wave inversion, in lead III.
The T-wave in aVL is now upright.

Learning Points:

1. Lead aVL once again holds the key to the interpretation of subtle findings in the inferior leads.

2. If you weren't convinced by limb leads (although you should be), ST depression in precordial leads make this even more certain -- they complete a pattern of coronary distribution.  Any artery that supplies the inferior wall (could be either RCA or Circumflex) also often supplies the posterior wall.

3. Serial ECGs are always helpful.

4. Acute coronary occlusion frequently does not manifest the classic STEMI criteria.


  1. Superb case by Pendell Meyers & Steve Smith! Wonderful description by Pendell, leaving me with little to add. The only point I’d emphasize is how when ECG findings are subtle — the KEY resides in looking a multiple leads. As per Pendell, Lead aVL provides an initial major clue — but it is lead I that then tells me without doubt that the T inversion in aVL is “real” and reciprocal to what we see in lead III. And then the subtle but real flattened and depressed ST segment in lead V2 just cannot be a normal finding. So, as per Pendell — there are no less than 8 leads that show subtle-but-real ST-T wave changes ( = leads I, II, III; aVL, aVF; V2,V3,V4) — and putting these abnormal findings in multiple leads together allows synthesis into a cohesive picture of acute coronary occlusion. THANKS for presenting! P.S. I understand that at times it “may be difficult to convince certain cardiologists” from just the initial tracing — BUT — in a patient with new-onset worrisome chest pain and THIS initial ECG — any capable cardiologist SHOULD be completely convinced of the need for immediate cath. If they aren’t, then they have stuff to learn …

  2. Well I can see the STe in inferior leads if the ST segment is compared to PQ junction and no STe when compared to TP segment. Also PR segment looks like downsloping and ST segment morphology looks concave so can we say with certainty that ST segments are elevated?

    1. yes. measure J -point relative to PQ jct. this eliminates the problem with the atrial repolarization wave. Or measure at 60-80 ms after the J-point, relative to TP segment. either way, elevated. But, really, any measurement is unhelpful. It is subjective interpretation that is far better.

    2. In v3 v4 v5, it's TP segment that shows ST depressions but
      looks normal when compared to PQ junction. But in inferior leads its vice versa. Little confusing but I get the point

  3. excellent...
    i still wonder , when i am handed three ekg's at once from triage, while answering a call from a nurse, answeing a gi consultant, and writing sepsis orders in Cerner, that i don't kill anyone. (or at least hope not to). especially when the findings are less obvious.
    though after the discussion above, now seem blatant.
    thank you three.

    1. Tom,
      The hope is that after seeing many of these, recognition becomes instantaneous. It is that way for me. I see this ECG and within 1 second know what it is.
      It will be for you too.


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