Thanks for all the comments! I’m not allowed to blog while I’m on duty (the policy has nothing to do with me personally) so if it seems like I’m not responding, I’m probably just at work.
The paramedic who submitted this case has requested the follow-up information from his supervisor, but unfortunately she’s out-of-town for the next 2 weeks.
In the meantime, we can lay out the issues.
Obviously, this is a scary looking ECG because there is significant ST-elevation in the precordial leads.
However, this ECG also meets the voltage criteria for LVH.
Could it be a strain pattern (typical secondary repolarization abnormality)?
It’s difficult to tell with the wandering baseline throughout this ECG, but if you line up the point at which the PR-segment hits the QRS complex in leads V1, V2, and V3 you can see that each of these leads shows approximately 4 mm of ST-elevation.
You will recall that with a “strain pattern” the degree of ST-elevation is proportional to the depth of the S-wave in the opposite direction! So the lead with the deepest S-wave should have the most significant ST-T wave abnormality in the opposite direction.
It’s not easy to tell the exact depth of the S-wave because the complexes are running together, but these measurements are probably fairly close.
There’s no way that a typical strain pattern would show the same amount of ST-elevation in one lead with S-waves that are 22.5 mm deep and another with S-waves that are only 6 mm deep.
Here’s the most disturbing finding, in my opinion.
There appears to be reciprocal behavior between the inferior leads and the high lateral leads.
So, if this is a STEMI mimic (for example, benign early repolarization superimposed on top of left ventricular hypertrophy) it’s a darned good one! I wouldn’t blame any paramedic for calling in a STEMI Alert for this patient.
So what should the hospital do when they are in receipt of a patient like this? I asked Stephen Smith MD from Dr. Smith’s ECG Blog and here’s what he said.
“If I were the ED physician, I would aggressively treat the blood pressure with NTG (up to 250 mcg/min or even higher) until the BP came way down. I would do a bedside cardiac ultrasound and look for anterior wall motion. If pain did not go away, and echo did not definitely show good wall motion, I would activate the cath lab.”
It’s always nice to get Dr. Smith’s perspective! I’ve learned a lot from his blog over the past 2 years. If you’re not familiar with his website you should take the time to check it out! His case studies are top notch!
Hopefully we’ll have the outcome in about 2 weeks.