A 41 year old male is pulled over during morning rush-hour by sheriff’s deputies.
He states that he is on his way to the hospital because he is having chest pain. EMS is called to the scene.
The patient is awake, alert, and oriented to person, place, time, and event.
His skin is pink, warm, and moist.
He appears acutely ill and anxious.
He states that he has a history of high blood pressure and renal insufficiency. He takes several medications, but he can only recall that one of them is a beta blocker.
- Onset: 1 hour ago while sleeping.
- Provoke: Nothing makes the pain better or worse.
- Quality: Patient describes the pain as a poorly localized “fullness” or “pressure”.
- Radiate: The patient cannot tell whether or not the pain radiates.
- Severity: The patient reluctantly gives the pain a 7/10.
- Time: The patient states he has had the pain on several occasions over the past few months but did not seek medical treatment.
Vital signs are assessed.
- RR: 20
- HR: 76
- NIBP: 138/78
- SpO2: 99% on room air
The cardiac monitor is attached.
A 12-lead ECG is obtained.
The treating paramedic was concerned that the T-waves in leads V1-V3 might represent hyperacute anterior STEMI.
However, this was not a STEMI.Â It was left ventricular hypertrophy with a strain pattern and mild hyperkalemia.
First, letâ€™s look at the 12-lead ECG and make the case for LVH.
This ECG has the general patternÂ of “T-wave discordance”. In other words, the T-waves are deflected opposite the majority of theÂ QRS complex, which is suggestive of a secondary ST-T wave abnormality.
In this case the most likely cause is left ventricular hypertrophy with a so-called “strain pattern”.
I say “general pattern” because it’s not true in every lead.Â When I look for 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).
Letâ€™s circle the leads I would mentally remove from this 12-lead ECG to decide whether or not â€œT-wave discordanceâ€ 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 â€œlateral ischemiaâ€ 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 itâ€™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 donâ€™t think thatâ€™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, weâ€™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.
Letâ€™s blow this up a little bit.
When we use the TP-segments as a baseline, we can see that itâ€™s debatable as to whether or not lead V1 shows more ST-elevation, but itâ€™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 â€œnormalâ€ at 419 ms.
I donâ€™t have the exact lab value, but the feedback I received on this case was that the patient had a potassium level thatÂ moderately high.
Consider the following graphic that compares the T-waves of hyperkalemia to the T-waves of acute anterior STEMI.
There isnâ€™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 youâ€™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 â€œbroad-basedâ€.
The take-home point is that 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 Code STEMI.
That’s important because according toÂ some studies LVH is the most common cause of ST-segment elevation amongst chest pain patients, so we need a solid strategy to deal with this frequently-encountered STEMI mimic!
Romhilt D, Bove K, Norris R et al. A Critical Appraisal of the Electrocardiographic Criteria for the Diagnosis of Left Ventricular Hypertrophy. Circulation. 1969;40(2):185-196. doi:10.1161/01.cir.40.2.185.
Van Mieghem C, Sabbe M, Knockaert D. The Clinical Value of the ECG in Noncardiac Conditions. Chest. 2004;125(4):1561-1576. doi:10.1378/chest.125.4.1561.