This is a male in his 50's who was lying face down on the pavement stating that his chest was "killing him." He stated it felt like his previous MI. H/o 2 prior stents. Skin was cool and clammy. He started to vomit. He had this prehospital ECG recorded at time zero:
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| No QTc is available on this. But in this case, you don't need to do any analysis to determine if the ST elevation is normal variant or not. The PVC provides the diagnosis: it is an RBBB configuration (originating in the left ventricle): it has a qS pattern (not rSR' because there is an initial Q-wave typical of old or new MI) and ST elevation. In RBBB, the ST segment should never be in the same direction as the terminal part of the QRS, as it is here. This is ST elevation of myocardial infarction. |
A follow up ECG about 15 minutes later was nearly identical except that there was no PVC:
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| I have estimated the QTc as 418ms. If you do not recognize this as STEMI, you can use the formula (STE60V3 = 2.5, QT = 418, RAV4 = 5.5) and you get 25.85 which is pretty much diagnostic of STEMI. |
The medic called in an anteroseptal STEMI and transmitted the EKG. To the chagrin of the medic, the ED MD thought that it was not a STEMI and did not activate the cath lab.
At t = 4 hours 15 minutes (255 minutes), the troponin returned positive and the patient was becoming hypotensive. He was taken for PCI of a 98% occluded LAD and 100% occluded circumflex.
The patient survived. I don't have further info, but I suspect there was substantial myocardial loss.
Lessons:
1. Listen closely to the medics. They often know more about EKGs than you do (this message is for all emergency physicians and cardiologists).
2. Take advantage of all information. PVC's often give you a lot of information. See also this case and this case.
3. Use the anterior STEMI formula. I have found since my study that it is incredibly accurate. I use it all the time to help confirm or refute my readings.
than you very much for this great case, i have few questions, first how can we explain that only anteroseptal findings are present on ECG though there's 100 % occluded circumflex artery ?
ReplyDeleteMy second question is about the conjunction of two facts ; hypotension and isoelectric ST segment in V1 ; can this be a signof Right venricule involvement ?
thank you again
Lotfi djilali Bensekrane
There is evidence of lateral STEMI with hyperacute T-waves in V5 and V6 and I and aVL. So this is consistent with circumflex occlusion. However, it is common for circ occlusions to show little on the ECG, at least in the literature. My experience is that there is nearly always evidence of it to an expert reader with a discerning eye. As for V1, RV involvement only happens with RCA ACS: with a proximal occlusion in which the RV does not get collateral circulation from the LAD, there can be RV STEMI with ST elevation in V1. These certainly can cause hypotension. In this case, the hypotension was due to poor LV function from LAD STEMI.
DeleteDr. Smith -
ReplyDeleteI was playing around with your calculator and I noticed that there is quite a lot of emphasis on the QTc (due to it's being such a high number). Many patients taking amiodarone have a lengthened QTc which can get up to 500-550 ms, using the calculator it is very difficult for them *not* to have an LAD occlusion.
For example, I used a hypothetical patient with a 1 mm elevation 60 ms after the J-point, QTc of 500 ms, and a R wave amplitude of 10. I got a result of 27.436, although the ECG described could be 100% normal (except for the lengthened QTc.
Do you have some type of correction for people known to have a long QT due to drugs or other reasons?
Thanks.
But the other pre-condition is that the differtial diagnosis be acute STEMI vs. early repolarization. Do any of the EKGs you have look like they could be one or the other? I suspect they look like neither. Send me one that you find confusing. Perhaps I need to tell folks to exclude patients who are on QT lengthening meds, but more likely these ECGs do not fit into the problem: is this early repol or is it anterior STEMI?
DeleteDr. Smith, how in the world are you getting 5.5 mm of R wave amplitude in V4? At best I'm measuring 4 mm. Not that it changes anything, but still ...
ReplyDeleteMaybe we're not measuring the same thing, because I clearly get 5.5 mm on both complexes. Perhaps you're measuring the R-wave on the PVC (although that is substantially less than 4 mm)?
DeleteSteve Smith
GREAT example of how ST-T wave change in the PVCs are more dramatic than the rest of the 12-lead for acute STEMI. I'd add a #4 to your "Lessons" listed at the end of this case = LISTEN TO THE PATIENT. This patient patient showed hemodynamic signs and was complaining of severe chest pain. In that context - it should be very hard to overlook the anterior ST elevation seen on this tracing. As you note - there are also important-to-recognize hyperacute T waves in a bunch of leads ... THANKS for posting. The leads V2,V3 of the PVC in the 1st tracing are wonderfully diagnostic.
ReplyDeleteFirst of all I just want to say great blog, you're a great asset to the healthcare industry. I was curious to see what you thought of this EKG in the presence of 10/10 chest pain:
ReplyDeletehttp://s1277.photobucket.com/user/Justin_Canterberry/media/image_zps8b249676.jpeg.html
PR 164ms
QRS 104ms
QT/QTc 466/520
Vent. Rate 75
100Hz 25.0mm/s 10.0mm/mV
Justin,
DeleteThanks. As for the ECG, long QT and nonspecific t wave inversion. Not necessarily ischemia.
Steve Smith
I am a paramedic I just transfer a patient with Lateral STEMI clearly seen with PVCs
ReplyDeleteAny way, interesting scenario thanks
Send it to me, with outcome: dr.smiths.ecg.blog@gmail.com
Delete