It was most likely left ventricular hypertrophy with a strain pattern and mild hyperkalemia.
First, let's look at the 12-lead ECG and make the case for LVH. You'll recall from my previous posts on the topic that I've said it's more important to recognize the so-called "strain pattern" than the voltage criteria.
The reason is simple. If the "strain pattern" isn't causing a problem (mimicking an acute anterior STEMI) then you're waisting your time calculating the QRS voltage.
This ECG has the general appearance of "T-wave discordance". In other words, the T-waves are deflected opposite the main deflection of the QRS complex, which is highly suggestive of a secondary ST-T wave abnormality. In this case, the most likey cause is left ventricular hypertrophy.
I say "generally appearance of T-wave discordance" because it's not true in every lead. That's why I mentioned in a previous post that there are "some caveats".
When I'm looking for appropriate T-wave discordance, I mentally remove isoelectric or equiphasic leads, particularly in the transition zone (the point at which a QRS goes from mostly negative to mostly positive in the precordial leads).
Let's circle the leads I would mentally remove from this 12-lead ECG to decide whether or not "T-wave discordance" is present.
With those leads removed, are the T-wave deflected opposite the QRS complexes?
Could that be a coincidence?
The high lateral leads in particular are showing a very typical looking strain pattern.
This can be a problem because it could easily be mistaken for "lateral ischemia" or reciprocal changes secondary to acute STEMI!
Does this ECG meet the voltage criteria for LVH?
Not exactly, but I believe we can make the case using the Romhilt-Estes point scoring system. This ECG would get at least a 4 (probable LVH), and it's right on the borderline for left atrial enlargement and delayed intrinsicoid deflection in leads V5 and V6 which would give it a score of 5 or 6.
But I don't think that's important.
But I don't think that's important.
The next question we want to ask is, is the degree of the secondary ST-T wave abnormality proportional to the amplitude of the QRS complex in the opposite direction?
The answer is yes.
Remember, we're looking at the ST-segments and the T-waves together.
At first glance it looks like there might be more ST-elevation in lead V1 than lead V2. However, I believe this is an optical illusion created by the biphasic P-waves in lead V1, as well as the more defined (less diffuse) J-points in lead V1.
Let's blow this up a little bit.
When we use the TP-segments as a baseline, we can see that it's debatable as to whether or not lead V1 shows more ST-elevation, but it's obvious that lead V2 shows a more pronounced ST-T wave abnormality.
The T-waves seem a little bit narrower than we might have expected with LVH, perhaps with a slightly later take-off. Also, the QTc is well within "normal" at 419 ms.
I don't have the exact lab value, but the feedback I received on this case was that the patient had a potassium level that was "on the high end of mild" (so I'm guessing between a 6 and 7).
Consider the following graphic that compares the T-waves of hyperkalemia to the T-waves of acute anterior STEMI.
There isn't much documentation out there as to what hyperkalemia is supposed to look like in the presence of a secondary ST-T wave abnormality, but you'll notice that with hyperkalemia, the T-waves are narrow and have a late take-off, while with acute anterior STEMI, the T-waves are more "broad-based".
This was a very difficult case. So what can we learn from it?
In my mind, it's very simple (and it needs to be simple for field use -- complicated equations involving calipers are not simple).
T-wave discordance strongly suggests the possibility of a secondary ST-T wave abnormality. That being the case, I would wait for changes on serially obtained ECGs before calling a STEMI Alert.
Remember, in some studies LVH is the most common cause of ST-elevation in chest pain patients, so we need a solid strategy to deal with this STE-mimic!