37 year old male CC: Unconscious – Discussion

Here is the follow-up to: 37 year old male CC: Unconscious.

This is the 12-lead ECG that was presented.

There are a few difficulties involved with this case.

First, we have the syncopal episode with possible seizure-like activity and slurred speech.

Second, we have an abormal ECG.

Third, there is a recent history of chelation therapy which may or may not be playing a role in what's happening.

For any patient who experiences a syncopal episode the ECG should be reviewed for high-risk features like cardiac arrhythmias, a prolonged QT-interval, Brugada's syndrome, a Wolf-Parkinson-White pattern, or hypertrophic cardiomyopathy.

Unfortunately, this is an endurance athlete, and it's notoriously difficult (if not impossible) to distinguish between an "athlete's heart" and hypertrophic cardiomyopathy without the aid of an echocardiogram to examine the exact dimensions and shape of the left ventricle.

To me, this ECG clearly shows left ventricular hypertrophy complete with a "strain pattern" (or secondary ST-T wave abnormality).

Remember, left ventricular hypertrophy is considered a "STEMI mimic" and an acute anterior STEMI mimic in particular.

If you're screening the ECG for STEMI and you don't have ST-elevation in the anterior leads, there's no need to measure for the voltage criteria.

Of course, if you've been reading my blog for a while, there's very little reason to measure the voltage criteria if you can identify a "strain pattern".

Consider the following graphics.

ST-elevation is present and the degree of ST-elevation appears to be proportional to the depth of the S-wave. Note that the S-wave is "cropped" in lead V3 by the bottom of the ECG graph paper.

It's worth mentioning that Stephen Smith, MD from Dr. Smith's ECG Blog has stated:

"[I]t is very difficult to find a case of anterior MI with extreme voltage like this; this is probably because profound ischemia of LAD occlusion (STEMI) alters the QRS voltage and attenuates the severity of the electrocardiographic LVH voltage."

It is so rare in fact that he has asked that anyone who has seen an acute anterior STEMI with deep S-waves suggestive of LVH to please contact him! Keep in mind, he wrote the book The ECG in Acute MI.

So, when ST-elevation in the anterior leads is associated with deep S-waves suggestive of LVH, slow down. Take a closer look. You're probably dealing with a STEM mimic!

Now let's look at the lateral leads.

Here again we see "T-wave discordance". In other words, the T-waves are deflected opposite the main deflection of the QRS complex (which is what we're looking for to identify a "strain pattern" with LVH). In addition, the degree of the ST-T wave abnormality is proportional to the size of the QRS complex, but in the opposite direction.

This can sometimes be difficult to appreciate on the prehospital 12-lead ECG because the QRS complexes run together. So take your time and try to identify the true amplitude in each lead.

Finally, take a look at the transition of the T-wave in the precordial leads. By the "transition" I mean the manner in which the T-wave transitions from positively deflected in lead V1 to negatively deflected in lead V6.

As the QRS complex transitions from negative to positive, the T-wave transitions from positive to negative! This is what is meant by "widened QRS/T angle".

If you look at the QRS and T axis at the top of the ECG the QRS axis is 43 and the T axis is 144 which makes the QRS/T angle 101. That's abnormal and suggests T-wave discordance.

So it's clear we're dealing with left ventricular hypertrophy and a strain pattern. Is it "normal" for an endurance athlete? Quite possibly, but it's not our place to make that determination in the field, particularly with the immediate history of syncope.

The best thing the EMS crew did for this patient was take him to the hospital.

If the syncope wasn't reason enough (and in my opinion it most certainly was) the patient had a recent history of chelation therapy. I don't know if the chelation therapy was oral or IV but it doesn't matter. It can contribute to loss of electrolytes and nutrients.

Finally, the slurred speech and loss of clear eye contact. That's what upset the patient's spouse the most, and sometimes we need to stop and listen to the people who know the patient the best. Occasionally this means listening to a mother about about her baby. In this case it means listening to a wife about her husband.

So what was the outcome?

The patient ended up receiving a CT scan of the head at the receiving hospital. A slow venous bleed was discovered. He was transferred to a tertiary care center for more advanced care.

To the best of my knowledge this was the patient's normal ECG.

Update: Here's what electrophysiologist and cyclist Dr. John M had to say about the patient's ECG:

That ECG is very abnormal. Agree with strain diagnosis. Not only that, but the QRS is notched and fragmented. V1's pattern along with the prominent p-wave voltage suggests the possibility of an ASD. I would agree with you entirely about the non-benignness of this patient's syncope, and I would be very interested in the ECHO report.

See also:

Left ventricular hypertrophy – Part I

Left ventricular hypertrophy – Part II

41 year old male CC: Chest pain

41 year old male CC: Chest pain – Answer