tag:blogger.com,1999:blog-549949223388475481.post7522833871979456060..comments2024-03-28T14:02:08.119-05:00Comments on Dr. Smith's ECG Blog: Is this ECG diagnostic of coronary occlusion? Also: Inferior de Winter's T-waves on prehospital ECG??Unknownnoreply@blogger.comBlogger9125tag:blogger.com,1999:blog-549949223388475481.post-5987963654725272442018-02-14T18:41:45.234-06:002018-02-14T18:41:45.234-06:00@ Tom Fiero — I learned the "hard way" t...@ Tom Fiero — I learned the "hard way" that when I was Attending, that I ALWAYS needed to see the ECG being reported on. Even when the providers were highly capable — I would catch things often that were missed ... and sometimes I'd catch truly important findings that otherwise would have been overlooked. After a while, the residents KNEW that I was going to ask for the actual ECG (and knowing that actually made THEM pay closer attention because they KNEW I'd be asking them what they saw — so THEY got better at interpreting by paying more attention!). Bottom Line — Keep asking your medics to "dig out that ECG from their pockets" — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-86644434394637459702018-02-13T04:58:04.650-06:002018-02-13T04:58:04.650-06:00interesting.
its not uncommon that the medic i gre...interesting.<br />its not uncommon that the medic i greet at the ambulance bay might say " ekg was just nsr doc".<br />and i'm almost embarrassed to ask then to dig it out of their pockets, or sometimes to go back to the van to retrieve it. i am implying that i , while i highly respect them, am saying "i have to see that ekg", that i might be "better" at interpretation.<br />but this blog, like many others, bring home the overwhelming point that every ekg, and serial ekg's when warranted, are essential.<br />thanks, guys.<br />tomtom fieronoreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-62234462480512451022018-02-02T14:47:19.824-06:002018-02-02T14:47:19.824-06:00You can't let someone like this go home!You can't let someone like this go home!Steve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-63734806933454790012018-02-02T14:44:13.753-06:002018-02-02T14:44:13.753-06:00Good comments. Thanks, Jerry.Good comments. Thanks, Jerry.Steve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-85573733758081588332018-02-01T22:33:48.813-06:002018-02-01T22:33:48.813-06:00I was of the opinion that 1st ED ECG is normal,but...I was of the opinion that 1st ED ECG is normal,but the only thing that was concerning was the subtle ST depression in aVL (? flipped T wave is normal in aVL considering the negative QRS in aVL). Overall difficult to explain this to patients with mild chest discomfort kind of symptoms and who have no prior ecgs to compare with, who then usually sign refusal consent for further observation and leave but I believe patients agree to what you tell them esp when they know you. 🙂. Any suggetions to thist🙂? MGhttps://www.blogger.com/profile/06233522417024317416noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-85518928325180949202018-02-01T05:29:09.503-06:002018-02-01T05:29:09.503-06:00Great teaching case, Steve! In all my ECG courses ...Great teaching case, Steve! In all my ECG courses I emphasize a diligent inspection of aVL. Failure to have a healthy respect for that one lead has resulted in a huge amount of litigation. In fact, for 40 years I've made it a personal rule to never set down an ECG without taking one last look at aVL! <br /><br />I think de Winter T waves are really an expression of REGIONAL subendocardial ischemia (ST depression with upright (usually) hyperacute T waves). This is caused by a partial occlusion of a major vessel or a complete occlusion of a branch vessel. In my own mind I feel that a regional subendocardial ischemia is caused by a partial occlusion that occurs more rapidly than the gradual "strangulation" of one or more major vessels resulting in typical circumferential subendocardial ischemia (ST depression with T wave inversion). Regional subendocardial ischemia can develop into a generalized circumferential ischemia with ST depression and T wave inversion OR the involved vessel may continue to become totally occluded creating a transmural MI that extends to the subepicardium and results in a STEMI. I think that as long as the T waves remain upright there is some localization value. Once the T waves invert, trying to localize the lesion becomes futile. While regional subendocardial ischemia has been said to only affect the LAD, I wholeheartedly agree with you that there is no plausible reason why it couldn't result from occlusion of the other two major coronary arteries (though there are probably very good reasons why it doesn't do so as frequently).Jerry W. Jones, MD FACEP FAAEMhttps://www.medicusofhouston.comnoreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-39747347639002476672018-01-29T06:40:20.729-06:002018-01-29T06:40:20.729-06:00Sinus bradycardia is certainly consistent with inf...Sinus bradycardia is certainly consistent with inferior MI, but has so many different causes (and is usually normal) that by itself it is really useless.Steve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-34667932952667976492018-01-28T19:43:25.029-06:002018-01-28T19:43:25.029-06:00GREAT case! I’ll add some additional subtle but im...GREAT case! I’ll add some additional subtle but important “Learning Points” to the 4 Points emphasized by Dr. Smith. Ready availability of a comparison tracing can at times be a luxury — and this is especially true here. Point #5) The BEST way to compare tracings (in my opinion) — is to first fully interpret one of the two tracings (could either be the baseline ECG or the new presentation ECG) — and then carefully compare LEAD-to-LEAD the QRST complex. Point #6) Carefully assess QRS morphology in the 2 tracings you are looking at to be sure there has been no rotation in the frontal plane and no chest lead positional change. This was KEY in this tracing — because the frontal plane QRS axis is IDENTICAL in the 1st ED ECG and in the baseline ECG from 3 years earlier. R wave progression is nearly the same (transition occurs slightly later between V3-to-V4 in the 1st ED ECG — whereas the R>S by lead V3 in the baseline done 3 years earlier). Awareness of whether there has been ANY positional change is CRITICAL for knowing how to assess whether or not there is likely to have been significant interval change. So, knowing that there has been NO limb lead positional change between these 2 ECGs — TELLS US beyond a doubt that the change to a negative T wave in lead aVL in the 1st ED tracing IS significant in this patient with new chest pain. In that context — leads I (which now shows a smaller positive T wave) — and each of the 3 inferior leads — now clearly show differences compared to the baseline of 3 years earlier. Learning Point #7) When you detect a number of subtle abnormalities (as we now have for EACH of the limb leads except aVR) — this should make you look EVEN CLOSER at the remaining leads on the tracing. And, there IS a subtle-but-real difference in ALL 6 chest leads between the 1st ED tracing and the baseline done 3 years earlier (in addition to subtle lateral chest lead ST elevation as mentioned by Dr. Smith, T waves are now more peaked in the 1st ED tracing). That this observation IS real is confirmed by the ECG done 30 minutes after onset of pain, which clearly shows even more peaked chest lead T waves. Learning Point #8) Learn to love the “Mirror Test”! Anterior chest leads show a mirror image of what you’d expect to see with acute MI. That is, if you flip over an ECG and hold it up to the light — what you see in flipped leads V1,V2,V3 will show a Q wave with ST elevation and T inversion. That’s precisely the picture we see in the 2nd black & white tracing here (done 10 minutes after the first pre-hospital ECG) — in that you have relatively tall R waves in V2,V3 with ST depression and positive T wave (which when flipped over would be a Q with ST elevation and T inversion). Taken in context with the other tracings on this patient, this 2nd B&W ECG done 10 minutes later simply reflects evolution from the B&W ECG done 30 minutes after chest pain onset (which showed prominent T waves in V2,V3 — that by the “mirror-test” look like ischemic T waves). Final Learning Point #9) Consideration of all 4 tracings we have on this patient in context with the history of new chest pain allows us to formulate a sequential evolution of ECG changes that now makes total sense. The BEST way to confirm your hypothesis about what occurred with your patient is when you can “make a cohesive story” that corresponds to the clinical history by explaining sequential evolution for each of the tracings you have available. THANKS for presenting this superb case!ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-24721608829455167082018-01-28T10:33:25.252-06:002018-01-28T10:33:25.252-06:00Thank you again, Dr. Smith. It's very informat...Thank you again, Dr. Smith. It's very informative. But I have a question. The old ecg is normal but the new one is sinus bradycardia. May a sinus bradycardia be a suggestion of inferior STEMI? Do you have any information about this?Redhttps://www.blogger.com/profile/01672610830184805954noreply@blogger.com