An elderly female with h/o HTN presented with chest pressure. She awoke with bilateral upper sternal chest pressure and tightness, with some SOB, starting at 6 am. Here was her first prehospital ECG at 0623:
Here was another at 0627:
Here was another at 0627:
This is similar, except that the PVC is now seen in V4-V6, and this time the T-wave appears more hyperacute in the PVC than in the normal beat. |
She received nitroglycerin and had near resolution of chest pain. She arrived in the ED at 0639. I looked at the ECG and immediately activated the cath lab. We then recorded another at 0651 while waiting for the cath team:
She went to the cath lab immediately and had co-culprit lesions:
1) 99% thrombotic lesion in the proximal segment of a large obtuse marginal, with TIMI-2 flow
2) 99% mid LAD occlusion with TIMI-2 flow.
Both were stented.
She went to the cath lab immediately and had co-culprit lesions:
1) 99% thrombotic lesion in the proximal segment of a large obtuse marginal, with TIMI-2 flow
2) 99% mid LAD occlusion with TIMI-2 flow.
Both were stented.
how reliable and uniform are ST deviations in PVCs if we use them to determine STEMI? is there some sort of standard methodology, the way we (for the most part) do with normal beats? or in this case, were the PVCs used to augment what you already saw in the normal beats?
ReplyDeleteThere is no standard way. To my knowledge, there are no studies of this. This is my own experience and that of my mentor's, K. Wang. I have found it to be very useful to treat PVCs just as I treat LBBB or paced beats: concordant ST segments or proportionally excessively discordant (ST/S ratio > 0.25) are indicative of STEMI.
DeleteHey Steve,
ReplyDeleteRe: co-culprit lesions- are these really two separate plaques in two separate vessels that concomitantly ruptured? Embolic etiology? Literature on this?
Thanks!
Sam
Sam,
DeleteYes, it is believed that some inflammatory state sets lesions off simultaneously. I have seen literature on it but can't find it right now.
Interesting, huh?
Steve