tag:blogger.com,1999:blog-549949223388475481.post6265046748841665331..comments2024-03-28T14:02:08.119-05:00Comments on Dr. Smith's ECG Blog: Test yourself: how many hours between your diagnosis of OMI and positive STEMI criteria?Unknownnoreply@blogger.comBlogger9125tag:blogger.com,1999:blog-549949223388475481.post-86112503504970870402020-05-16T10:49:15.740-05:002020-05-16T10:49:15.740-05:00Hello Bruno. We are glad you are enjoying our ECG ...Hello Bruno. We are glad you are enjoying our ECG Blog! YES — In the very 1st ECG (above) — there IS slight ST elevation in EACH of the 3 inferior leads. The shape of this ST elevation is gently upsloping (ie, “smiley”-configuration) — and what is most important — there is NO reciprocal (ie, “mirror-image” opposite) ST depression in lead aVL. It is often difficult to distinguish between repolarization variants vs acute MI. In the inferior leads — there is a “magic” reciprocal relationship that is almost always present between opposite-lying leads III and aVL when there is acute OMI (occlusion-based acute MI) — and, that is ABSENT here. It’s good to note this slight inferior ST elevation that we see — and it would be important to follow on serial tracings. In this particular case — it turned out that on cath, the RCA was not obstructed; instead it was the LAD that was acutely obstructed (and that initial slight inferior lead ST elevation turned into reciprocal changes from acute LAD OMI. For MORE on that “mirror-image” magical lead III-aVL relatinship — GO TO — http://hqmeded-ecg.blogspot.com/2018/08/a-58-year-old-with-weakness-and-more.html — and — http://hqmeded-ecg.blogspot.com/2018/10/a-normal-ecg-on-busy-night.html — I discuss and illustrate this phenomenon in detail in My Comment at the bottom of the page for these 2 links — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-30963594123576480942020-05-16T10:31:29.374-05:002020-05-16T10:31:29.374-05:00Hi Dr Smith, I have just found your blog on the in...Hi Dr Smith, I have just found your blog on the internet and I feel it will be a good source of knowledge, as well as a paradigm breaker for me. I would to ask a question, hoping it won’t be a silly one. In the first ecg of the case, I saw STE, although small, in inferior leads 2, 3 and aVF. Is my impression right or exaggerated?<br />ThanksBruno Mirandahttps://www.blogger.com/profile/04919094360589901707noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-24757079824649771772018-07-09T15:01:26.388-05:002018-07-09T15:01:26.388-05:00Thanks Tom for your Comment! — :)Thanks Tom for your Comment! — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-62385026420930016052018-07-09T15:00:25.464-05:002018-07-09T15:00:25.464-05:00@ UNKNOWN: I Agree with Pendell regarding his answ...@ UNKNOWN: I Agree with Pendell regarding his answer to your excellent question — which is precisely why “strict stemi criteria” is the wrong way to go in 2018. Of note, comparison of the 1st & 2nd ECGs done in this case (which I put together in Figure-1 in my Comment above) — shows us that the QRS complex in lead aVL is now predominantly negative in the 2nd ECG (it was predominantly positive in the 1st ECG). So, if anything — the T wave will often be inverted in lead aVL when the QRS complex in this lead is predominantly negative — yet, compared to ECG #1 (in which the ST segment in aVL was FLAT) — there is now >1 mm ST elevation with a broad more upright T wave in ECG #2 that occurs in association with reciprocal inferior ST depression … Grazie per la tua domanda. Spero che adesso sia chiaro (Thanks for you question; I hope it's now clear) — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-41533798143903858352018-07-09T08:04:46.487-05:002018-07-09T08:04:46.487-05:001) I agree that there is some small STE in I and a...1) I agree that there is some small STE in I and aVL. Probably 1mm in aVL, but I do not think most people would say that lead 1 meets 1mm (we have to admit that when people look at the same EKG they do not agree on the number of mm STE). So I do not think that this would meet "official STEMI criteria" in most peoples' eyes.<br /><br />thanks for the comment!Pendellhttps://www.blogger.com/profile/01445330667624442976noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-36959928048099126602018-07-09T08:02:22.320-05:002018-07-09T08:02:22.320-05:00Great question. During editing it seems we acciden...Great question. During editing it seems we accidentally deleted the paragraph we wrote about this question preemptively. We replaced it. See above, just after that EKG. <br /><br />Basically, this case is NOT an exception to the rule. We believe this patient was in cardiogenic shock with elevated heart rate making up for very poor stroke volume given the proven large wall motion abnormality even before the re-occlusion. Thanks for the question!Pendellhttps://www.blogger.com/profile/01445330667624442976noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-51379641822402081672018-07-09T01:10:43.458-05:002018-07-09T01:10:43.458-05:00painful.
interesting : when a patient complains of...painful.<br />interesting : when a patient complains of heartburn, his heart is doing exactly that. and worrisome is that , with a mentality by many that is chained to the STEMI strict criteria, by many ER docs and cardiologists, patients are allowed to crash and burn form their "heartburn".<br />i agree with Ken on that first EKG (though i would never dare to disagree with wendell and steve!), that there are suspiciously appearing plump (in NY we might say "zaftig") T waves in aVL, V2 and V3. esp in comparison to their respective R waves. granted , i have the advantage of hindsight. if a tech from triage placed this under my nose while i was talking to a surgeon about another patient with ischemic bowel, i might be less impressed.<br />but i whole-heartedly agree that we must be masters of the electrocardiogram. <br />one ecg begets another , the bible says. and we need to see all the 12 leads done pre-hospital.<br /><br />i think its impossible to get continuous 12 lead monitoring in our ER. we are often so busy thats it's hard to get 3, but our techs are excellent.<br /><br />excellent, but unfortunate case, Wendell and steve. thank you, and to you also ken for your comments.<br />t.tfierohttps://www.blogger.com/profile/15955268501222734373noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-53598112742699916072018-07-08T17:08:20.271-05:002018-07-08T17:08:20.271-05:00Hello Dr. Smith,
I am an Italian fellow pratictio...Hello Dr. Smith,<br /><br />I am an Italian fellow pratictioner in Internal Medicine and an ECG enthusiast who sistematically follows your brilliant blog. I have two questions/observation about this case and it would be great if you gave me your opinion:<br /><br />1. In ECG number 2 (obtained during relapsing chest discomfort), what I see is 1 mm STE in I and aVL, which is a peripheral leads STEMI criteria. Am i counting wrong? Or am I being misled by PR interval depression?<br /><br />2. It is definitey true that high BP can cause left ventricular strain with ECG changes such as anterior ST elevation and peripheral ST depression, but, besides the fact that this usually happens in the setting of an underlying LVH, in this case we see an ANATOMICAL DISTRIBUTION of ECG modificantions that should clue you in! An plus, as you've already stated many times, in case of chest pain ANY change should be interpreted as AMI until otherwise proven!!<br /><br />Thanks a lot for keeping this blog up!Anonymoushttps://www.blogger.com/profile/04763119718496195286noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-29311026494461487972018-07-08T16:48:59.200-05:002018-07-08T16:48:59.200-05:00Regarding the ecg the was done at 22:30 in day 1: ...Regarding the ecg the was done at 22:30 in day 1: Don't you think that its quite extra ordinary that the rate is 125 with that blood preasure? You said a lot of times that sinus thacycardia and OMI almost never present together unless there is cardiogenic shock. So assuming that the lungs are clear that's an exceptionNadav shouahttps://www.blogger.com/profile/17330808847744006766noreply@blogger.com