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.

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