It’s bad. I’ve been reading Malcolm Gladwell’s Blink in which he details how the subconscious plays a major role in many decisions we make. He tries to lay out some theories as to when it’s better to rely on a your subconscious reaction and when it’s better to logic through a process. I haven’t completely digested it yet, but certainly you should have that visceral reaction to this EKG.
Rate looks to be fairly normal (one of the last normal things about this EKG), a little over 4 big boxes wide so likely 70’s. The rhythm is sinus (the last normal thing) given fairly obvious P waves. For those of you who said hyperkalemia as the cause of very wide ST segments note that the normal P waves would make that a lot less likely.
Axis is up in I and down in aVF so Left axis. The QRS is somewhat neither here nor there. In II the ST segment gets out of the way of the QRS and we see a complex that isn’t dagger thin, but is likely 2 little boxes wide so not yet reaching the 3 little box width to declare it wide.
Let’s talk about the ST segments. We see massive elevation in I and aVL, and impressive elevation in V2, V4-V6. (We’ll come back to V3 later). We see deep reciprocal change in III and aVF (and also aVR). So we have a lateral STEMI (which should be a blockage in the circ), but it also involves anterior sections with V2. I would almost question if the V2 and V3 leads are switched but I think the R wave progression argues that they’re correct. Therefore there appears to be some anterior involvement (which would imply blockage in the LAD). Note though the reciprocal change in forgotten aVR. Is there a vessel that feeds both the LAD and the Circ? and one that can cause ischemic changes in aVR? This patient has a STEMI from Left Main Occlusion and went to CABG. This is important to recognize if you end up in a department that gives plavix regularly prior to knowing the anatomy since cardiovascular surgeons are going to be unlikely to operate with plavix on board.