This is a 66 year old male with severe substernal chest pain. He was intermittently bradycardic down to the 30's with a blood pressure in the 80's systolic.
This is the first ECG:
4 minutes later, a Right Sided ECG:
T = 18 minutes:
The patient was taken for immediate angiography and PCI of a 95% thrombotic occlusion of the RCA.
Here is another case in which aVL was critical to the diagnosis of inferior STEMI:
http://hqmeded-ecg.blogspot.com/2010/07/inferolateral-st-elevation-might-be.html
This is the first ECG:
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| There is sinus rhythm with first degree AV Block. The QRS is slightly long (113 ms) but there is no bundle branch block. The T-waves in inferior leads have high voltage proportional to the QRS, very suspicious for inferior MI. aVL has T-wave inversion, which raises suspicion even higher |
4 minutes later, a Right Sided ECG:
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| RIGHT SIDE ECG, t = 4 minutes -- (the limb leads are standard, only the precordial leads are shifted to the right side) -- there is still sinus rhythm with 1st deg AVB. The T-waves in the limb leads have less voltage than in the previous ECG, suggesting evolution (artery opening!), which supports the diagnosis of ACS. The R side leads do not have any significant ST elevation. |
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| t = 18 minutes. There is sinus bradycardia with a very prolonged PR interval and some nodal escape beats. Sinus beats that happen AFTER the nodal beat can be seen in the upstroke of the T-wave in the 2nd, 4th, 5th, 7th, and 9th complexes at the bottom in lead II. MORE IMPORTANTLY, there is now clear ST elevation in inferior leads (artery now closing!), with reciprocal ST depression in aVL and also in V2-V4, diagnostic of simultaneous posterior STEMI. Inferoposterior STEMI. |
The patient was taken for immediate angiography and PCI of a 95% thrombotic occlusion of the RCA.
Here is another case in which aVL was critical to the diagnosis of inferior STEMI:
http://hqmeded-ecg.blogspot.com/2010/07/inferolateral-st-elevation-might-be.html
Great case. Heard about the TWI in L preceding inferior STE at one of Amal Mattu's talks at ACEP 2010.
ReplyDeleteThank you again for the great case Dr. Smith...
ReplyDeletemy question is this: because there appears to be slight ST elevation in leads V2 and V3 in the first 12 Lead, can we infer that amount of ST depression in those leads in the third 12 Lead is really more than the measured 1-2mm? That on a basis relative to the first ECG, the amount of ST depression is really at least 2-3mm? is it helpful to think in these terms?
thanks,
David
for the 3rd ekg, when do you make that leap and call it complete heart block?
ReplyDeleteYes!! Good point. Most ECGs, including this one, have ST elevation in V2 and V3, so any ST depression is even greater than what you see. What is important is indeed relative ST depression, relative to the baseline ST segment.
ReplyDeleteI can't call it complete or even 2nd degree unless there is a non-conducted p-wave somewhere. The only non-conducted p-waves are in the middle of a QRS-T when the ventricle is refractory. Now, it could be that if I had a longer rhythm strip, I might find such non-conducted p-waves, but all the p-waves here that come before the QRS have the same PR interval, 380 ms. To call it a non-conducted p-wave, the PR interval would have to be longer than 380 ms!
ReplyDeleteI too thought it was 3rd degree, the PP is fixed at 685. But the RRs are not regular upon closer inspection. 940, 1150 (PRi 370), 1360 (PRi 360), 860, 1200 (PRi 370), 910, 1150 (PRi 350), and 920.
ReplyDeleteBigeminal PJCs? Or is it alternating a PRi of 360 with one of 520?
I'm not entirely sure! In any case, need to get to the cath lab. And it would be prudent to apply external pacer pads.
ReplyDeleteDr. Smith, or anyone else:
ReplyDeleteWould you mind taking a second to focus on the QRS morphology in lead III, especially how it changes over time? I see the notching in other leads, just curious what would explain that morphology and why it would change.
I recognize this patient has bigger problems, but I'd still like to know what you think is going on there.
Thanks for the posts, as always they are very helpful.
The only explanation I have is varying amounts of ischemia to the conducting system, depending on the state of perfusion, which, as we can see, is dynamic.
ReplyDeleteHi, Dr.Smith, thanks for your work!
ReplyDeleteI recently had a similar case (almost the same with your first ECG), but the other end.
In the evening, I was approached by a patient male 76 y.o. with signs of small ischemic stroke. In the morning before he had a severe chest pain. Took nitroglycerin and pain gone in 15 minutes. On admission was charged ECG (quote below).
Atrial fibrillation, some notched QRS in II, III, aVF, mild ST depression in I, aVL, V6 ( > 0.25 mm) with T-wave inversion. Also like hyperacute T waves in IIII, aVF.
Changes in the anterior leads V1 -V5 I regarded as an old myocardial infarction. Also visible there are a bit enlarged U waves.
In labs: AST 17, ALT 16, CK 122, CK-MB 40, troponin negative. K+ is normal.
In labs of 8 hours without significant dynamics - only CK-MB became 23.
And after 8 hours ECG also stay without changes.
So, changes in the inferior leads were not "acute"?
ST depression in aVL with "hyperacute" inferior T-waves may be not acute?
https://plus.google.com/photos/110517571402825386948/albums/5981449338958192913
Thanks!
Yes, these are suspicious T-waves, especially with the T wave inversion in aVL. If I understand your message correctly (there was no change over 8 hourss), then I already know the answer and it is difficult for me to say whether I would have called them truly positiive for MI or not (I think not, but maybe I'm just too biased now). In any case, they are very suspicious and warrant immediate testing such as looking for an old ECG, recording serial ECGs, and getting an emergency high quality echo to look for wall motion. Interesting!
DeleteSteve Smith