tag:blogger.com,1999:blog-549949223388475481.post7175246721734391935..comments2024-03-28T14:02:08.119-05:00Comments on Dr. Smith's ECG Blog: A man in his 50s with witnessed arrest and ST elevation in aVRUnknownnoreply@blogger.comBlogger11125tag:blogger.com,1999:blog-549949223388475481.post-18128996018626361042019-11-05T21:26:13.390-06:002019-11-05T21:26:13.390-06:00Thank you K for your comment and the reference. Wh...Thank you K for your comment and the reference. While I agree and prefer the end of the PR segment as my reference point — as I mention above, in my experience, this gets complicated in practice for the reasons I stated. I don’t think it is always clear cut where the reference point lies. THANKS again for your comment! — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-28112599067954432602019-11-05T21:17:02.239-06:002019-11-05T21:17:02.239-06:00Glad this was helpful.Glad this was helpful.ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-60574389493650189912019-11-05T02:14:03.210-06:002019-11-05T02:14:03.210-06:00excellent conversations/ dissection of this terrib...excellent conversations/ dissection of this terribly unfortunate case.<br />thanks to all of you.<br />tomtfierohttps://www.blogger.com/profile/15955268501222734373noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-3295710401184379202019-11-04T20:51:18.608-06:002019-11-04T20:51:18.608-06:00The reference point for ST deviation, i.e. elevati...The reference point for ST deviation, i.e. elevation or depression, should be the end of the PR segment because, in some people, there could be a significant Ta wave (atrial repolarization wave) as explained in the Atlas of Electrocardiography by k Wang, pages 197-199.<br />K. Wang.Anonymoushttps://www.blogger.com/profile/04509940285330859355noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-35001802441132811022019-11-04T12:54:29.256-06:002019-11-04T12:54:29.256-06:00This is the link — https://youtu.be/h1MhtLMF-7M?t=...This is the link — https://youtu.be/h1MhtLMF-7M?t=557 — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-14611451069870786782019-11-04T12:53:36.193-06:002019-11-04T12:53:36.193-06:00THANKS for your comment! A prominent (>3mm) R’ ...THANKS for your comment! A prominent (>3mm) R’ in lead aVR seen in ECG #1 is VERY much like that seen with TCA overdose. There is sinus tachycardia — but this patient had a number of reasons to have a fast rate. That said, the QRS is not overly wide (it was upper normal at ~0.10 msec) — and there was no right axis deviation. Finally, there was no apparent history of TCA ingestion. That said — I will add that I looked at this tracing a BUNCH of times, thinking to myself that the terminal R’ in lead V1 was a bit too high and a bit too wide compared to what we usually see with incomplete RBBB. In addition — the terminal r’ in lead V2 of ECG #1 ALSO is wider-than-I-usually-expect with simple incomplete RBBB. I decided NOT to talk about this in My Comment (above) — but my thought was that this patient may well have had a combination of incomplete RBBB + Brugada phenocopy! After all, the patient was in extended bradycardic-asystolic cardiac arrest — and cardiac arrest is a well known predisposing condition to development of Brugada phenocopy. I would have LOVED to see an ECG on this patient a bit BEFORE ECG #1 was done and/or to see a later ECG (since all 3 tracings done on this patient above show a similar V1 pattern …). For more on Brugada and Brugada “Phenocopy” — you could listen to the next few minutes on my ECG video about this subject (This link takes you to 9:17 in the video, which is where the part on Brugada Phenocopy begins) — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-75631013590350814132019-11-03T21:19:55.360-06:002019-11-03T21:19:55.360-06:00The initial ECG looks a bit like a TCA overdose to...The initial ECG looks a bit like a TCA overdose to me - especially the terminal 40 msec in aVR.<br />Anonymoushttps://www.blogger.com/profile/07619567671563097116noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-32682174838435471922019-11-03T21:07:33.272-06:002019-11-03T21:07:33.272-06:00@ Wesoundgoodman — THANK YOU for your comment. As ...@ Wesoundgoodman — THANK YOU for your comment. As I stated toward the end of My Comment in the “PEARL” (above) — CNS catastrophes are notorious for causing the most abnormal (and sometimes bizarre) ECG findings. Pseudo-infarct patterns are common. It sounds like that was exactly what happened in your case. Thanks again for sharing your case.ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-74542435903724880842019-11-03T17:56:26.847-06:002019-11-03T17:56:26.847-06:00I had an eerily similar prehospital case. Mid 40’s...I had an eerily similar prehospital case. Mid 40’s female found down in her home by spouse. He called 911. Police Officer arrived first and found her pulseless and started CPR. He stopped because regained a pulse and pushed him off. When we got there, she was pulseless again and obtained ROSC after 1 cycle (no defibs or drugs given). Post-ROSC 12 lead showed global STD with STE in aVR. She remained GCS 3 and was severely hypotensive. Re-arrested during the short transport in a narrow, brady-PEA. Restarted CPR during transport. ROSC achieved in ED after 2 more cycles. Post-ROSC 12 lead showed high lateral STE. Angio was clean and head CT showed massive subarachnoid hemorrhage. Turns out she was evaluated for a headache and discharged from the same hospital the night before. I’ve always wondered why that second 12 lead showed a high lateral MI.Jose Ramirezhttps://www.blogger.com/profile/10619568773954682781noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-74124656024326004262019-11-03T17:47:56.814-06:002019-11-03T17:47:56.814-06:00@ PB — Thanks for your comment! It’s clear that a ...@ PB — Thanks for your comment! It’s clear that a number of things (including electrolyte abnormalities) might contribute to producing the ECG findings we see in ECG #1. That said, to me — the most remarkable finding (as I highlight by RED and BLUE horizontal lines in my Figure-1 above) — is diffuse ST segment depression (that is significantly more marked than I am used to seeing with hypokalemia), that occurs in association with ST elevation in leads aVR, V1 and aVL. This pattern is most suggestive of diffuse subendocardial ischemia. Not only aVR — but also leads V1, and sometimes aVL may also manifest ST elevation with diffuse subendocardial ischemia (typically with the relative amount of ST elevation in V1 and aVL being clearly less than that seen in aVR). As I discuss in My Comment above — complicating assessment of the amount of ST elevation in this case is the PR segment elevation and depression, the tachycardia, and the incomplete RBBB pattern — so it’s difficult to be certain of what and why we are seeing here from just the initial ECG. As to the QTc — I measure the QT interval in the 2nd ECG at 0.36 second — which when corrected for a heart rate of ~110/minute — comes out to a QTc~ 470msec by my estimation, or a bit long (though not as long as the QTc in ECG #1). In my experience — I’ve not found specific measure (through correction factors) helpful in assessing QTc duration in the presence of tachycardia (which I think throws measurements off) — beyond generalization that the QTc is either “normal”, “borderline”, or “clearly long”. Despite the tachycardia and confusion with the next P wave and determination of the ST baseline — I thought the QTc in ECG #1 was definitely long. And, a long QTc is to be expected given the unfortunate CNS catastrophe (massive subarachnoid bleed) that this patient suffered. THANKS again for your comment! — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-14302710890341011842019-11-03T13:06:43.135-06:002019-11-03T13:06:43.135-06:00Interesting case. When I initially looked at the ...Interesting case. When I initially looked at the first ECG I thought it maybe hypokalemia. It is hard for me to figure out where the QT ends since it terminates somewhere in the P wave, but it appears the QT is long to me. V3 seems clearest QT interval at approx 390 msec, meaning QTC of ~540msec by bazetts. The diffuse ST depression appears to have the "down up" pattern of hypok to me on first blush. However, the STE in aVL doesn't fit with that. <br /><br />Second ECG the termination of the QT is much clearer and does not appear long. PBhttps://www.blogger.com/profile/14649507650320504281noreply@blogger.com