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.

Why?

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.
Why?
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.