A busy time of year, holidays, travel, end-of-the year obligations for various CME and expense reporting duties. A busy time of year to take Edmodo EKG quizzes. And a busy EKG with a lot going on in it.
Starting as always with the rate, it looks to be about 2 big boxes wide so pretty much spot-on 150. That’s probably the easiest part of this EKG to unravel. The next question is the presence of P waves. I admit you sort of get the sense of a deflection in the V1 rhythm strip, but that’s about it. The V5 rhythm strip looks quite clean and I see no evidence of P waves there. I feel that if there were P waves present we’d see them there. So that leaves us with SVT or 2:1 flutter. I don’t get a strong sense of flutter waves inferiorly where they’re best seen, but I think it would be hard to say that for certain. In either case adenosine will either fix the problem or prove it; we’ll come back to that.
I don’t think that anyone would argue that the QRS is narrow. The T waves are where more of the interest in this EKG is. It’s fairly obvious that there’s ST Depression to the lateral chest leads; that’s also a fairly common finding when someone’s heart is going very fast. There also looks to be some ST depression to the inferior limb leads. There is some questionable ST elevation in V1. I don’t see any in V2, but there is no V0 lead. In theory a person could do some right sided or posterior leads. Let’s come back to that as well. There is also ST elevation in the forgotten lead aVR. We’ll come back to that too.
So at this point we have a patient with a HR of 150 having classic angina and ischemic changes on the EKG. While we do need to involve cardiology, if you’re not fixing a non-sinus HR of 150 in the setting of ischemia you’re probably doing the patient a disservice. I thought this was probably SVT, but wouldn’t have been shocked to see flutter waves uncover with the adenosine. As it turns out, the adenosine converted him to a sinus rhythm, the original EKG was indeed an SVT with rate related ischemic changes. Ten minutes later the chest discomfort resolved. One of you questioned what the approach would be if you couldn’t control the rhythm and whether a person would cardiovert. Given symptoms of angina and ischemic changes on the EKG, I would.
Here’s the post-adenosine EKG:
Clearly now there are P waves, he’s slowed to the 120’s but the rate related changes are still present. Given his symptoms have resolved it would be wise to repeat this EKG in another 20-30 minutes to prove that the EKG is also improving.
Interestingly the patient never had palpitations, just angina when he would flunk his SVT auto-stress test. He’d experienced this previously but since he’d always spontaneously converted he’d never sought medical attention.
While his discomfort resolved, his troponin trended up. Ultimately he ended up in the cath lab where they found a 95% proximal LAD, a 70% mid LAD, an 80% circ, and an 80% ramus narrowing and he ended up going to CABG. Remember the ST elevation in aVR? This has increasingly been recognized to potentially represent L main disease if there is ischemic change elsewhere. While this patient didn’t have left main disease per se, he had enough lesions in enough arteries that he basically had the equivalent.