There’s a lot of gray areas in EM, but there are some places where certain rules can cut through the clutter and allow a person to make decisions with confidence. This EKG is a good example of that.
As always we start with the rate. This EKG is irregular so rate determination is a little difficult. It averages about 4 big boxes probably. There’s 14 complexes, 14×6 is 84 so we’ll go with a rate in the 80’s.
Next the rhythm. Rhythm on this EKG is tricky. I try to not write down Undetermined Rhythm in an interpretation, but this is an EKG where that may be excusable; we’ll return to the reason why later. Are there P waves? There mostly aren’t, but I think there are a couple which I pink-dotted.
They aren’t there consistently however. (As an aside V3 should strike you as very concerning; again we’ll come back to that). Interestingly the QRS complexes with possible P waves are identical to those without (excepting the hybrid complex right where the EKG machine changed from V3 to V6 mid-QRS). Because the complexes are identical it would argue for the same location of origin for the complexes. A combination of sinus beats with some junctional ones is therefore probably less likely. If I had to call the rhythm one thing I would say A fib. Usually the penalty for incorrectly diagnosing A Fib is incorrect initiation of anti-coagulation. On this EKG that doesn’t matter; let’s keep going.
Addressing the QRS’s, it’s clearly not narrow.
Many of you suspected RBBB. There is an RSR’, but the QRS is 3 little boxes wide. That width falls outside of simple RBBB, this patient is likely also working on a fascicular block, pushing into LBBB territory.
Now on to the ST waves. V3 has to leap off the page. The repolarization is in the same direction as a wide complex depolarization. That’s an MI as per one of the Sgarbossa criteria. There’s also clearly a millimeter of STE in V1 and likely in V2 as well (the second beat in V2 doesn’t show it that well; I suspect the patient twitched a little; if you weren’t sure have them print a rhythm strip like you’re giving adenosine, then you’ll have a whole page of complexes in that lead to evaluate). Many of you also noticed the (upcoving) STE in III. The other inferior leads don’t show STE but there is marked reciprocal STD in aVL; I suspect that the patient would develop STE in the remaining inferior leads if they went untreated (and lived long enough!).
The Acute MI is likely also the cause of the odd rhythm. You’re going to heparinize the patient for the ACS on the way to the cath lab; you’re off the hook for not being certain of whether or not it’s A fib! I wish I still had the note for which vessel was involved, but rest assured it was an Acute MI when they took him for cath.