tag:blogger.com,1999:blog-549949223388475481.post956085960796339087..comments2024-03-26T22:42:04.176-05:00Comments on Dr. Smith's ECG Blog: 32 yo with right sided chest pain. Zero ST Elevation, but that does not matter. Unknownnoreply@blogger.comBlogger16125tag:blogger.com,1999:blog-549949223388475481.post-10963045309711893962020-02-20T12:29:13.836-06:002020-02-20T12:29:13.836-06:00@ Michelle — Thanks for your comment. Hard to know...@ Michelle — Thanks for your comment. Hard to know about “What IFs?” — but hard for me not to believe that IF this patient with acute mid-LAD occlusion (who consequently developed diffuse chest lead Q waves + troponin > 10,000 ng/L) had been cathed (and reperfused) soon after the initial ECG (instead of the delay until later the next day) — that longterm prognosis would not have been BETTER. Impossible to say “How much better”? — and the only info I see regarding the cath report was that the patient was “without significant LV dysfunction” — which could indicate that there indeed WAS some loss of LV function from before the acute OMI. If it were me — I would like my chances much better being reperfused asap after ECG #1, instead of having to wait until the next day … THANKS again for your comment! — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-3080066650094566172020-02-19T23:00:44.924-06:002020-02-19T23:00:44.924-06:00The submitter writes "their future risk of he...The submitter writes "their future risk of heart failure, arrhythmias and premature death is greatly increased". I would be concerned about the risk for future HF if there were LV dysfunction, a persistent resting wall motion abnormality on echo, or large infarct size and/or microvascular obstruction on cardiac MRI, not solely on the basis of a high troponin and Q waves on EKG.Michelle Carlsonnoreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-3289569894442138102020-02-19T16:38:31.483-06:002020-02-19T16:38:31.483-06:00Steve...
So you are using the TQRSD - as you have...Steve...<br /><br />So you are using the TQRSD - as you have defined it - as a diagnostic aid, whereas Birnbaum and Sclarovsky use it primarily for prognostic purposes (they assume the diagnosis of acute ischemia involving the LAD has already been made). For them it represents 3rd degree ischemia, with 1st degree being hyperacute T waves and 2nd degree being STE 50% or less the R wave height.<br /><br />Thanks for the reference!Jerry W. Jones, MD FACEP FAAEMhttps://www.medicusofhouston.comnoreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-45300608911869525432020-02-19T13:42:11.529-06:002020-02-19T13:42:11.529-06:00I use a different definition of terminal QRS disto...I use a different definition of terminal QRS distortion, as described in this paper: https://www.ncbi.nlm.nih.gov/pubmed/27658331<br /><br />Absence of an S-wave OR a J-wave in EITHER of V2 or V3.<br /><br />I do not use if for prognostic purposes, but for differentiating the ST Elevation of LAD occlusion from normal STE. It should only be applied if there is at least 1 mm STE in at least one of V2-V4 AND that is the differential diagnosis. <br /><br />In this paper we found that zero of 171 cases of benign ST elevation had TQRSD so defined.Steve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-3601866639277395322020-02-19T13:04:39.453-06:002020-02-19T13:04:39.453-06:00Hi Jerry. The concept of TQRSD (Terminal-QRS-Disto...Hi Jerry. The concept of TQRSD (Terminal-QRS-Distortion) is one that Steve has studied and written on for a good number of years now (ie, this 2016 post on this blog = http://hqmeded-ecg.blogspot.com/2016/11/paper-published-terminal-qrs-distortion.html ) — but there are MANY more posts on this Blog in which Steve comments and illustrates the criteria he has used. My understanding of the definition he uses differs from what you are citing in the Birnbaum/Sclarovsky article from 1996 — but Steve is the EXPERT — so I’m sending your comment his way for his thoughts. THANKS as always for your active and valuable participation in this ECG Blog! — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-32107985061488528522020-02-19T12:56:31.648-06:002020-02-19T12:56:31.648-06:00THANKS so much for your comments. So glad Dr. Smit...THANKS so much for your comments. So glad Dr. Smith's ECG Blog has been helpful! — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-65670073982232386572020-02-19T11:04:43.549-06:002020-02-19T11:04:43.549-06:00Paramedic here. This is an EKG that I would have t...Paramedic here. This is an EKG that I would have transmitted, just looking at the anterior leads my immediate thoughts were (similar to the authors) there aren't many reasons for this morphology and these T waves aside from an MI. <br /><br />Reading the cases presented here and reading as many EKGs as possible, makes the abnormalities stand out, (Or like Dr Smith says, makes them stand out like a bad enemy). Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-62276935771543294572020-02-19T08:43:35.822-06:002020-02-19T08:43:35.822-06:00Ken...
Regarding the questions about terminal QRS...Ken...<br /><br />Regarding the questions about terminal QRS distortion, the concept as presented by Birnbaum and Sclarovsky referred to STE > 50% of the R wave height or loss of S wave depth in leads with an rS morphology. I don't see any of that here. This is the original article by Birnbaum et al. if any of the readers are interested: Am J Cardiol 1996;78:396-40<br /><br />Also, I don't think one could diagnose terminal QRS distortion when all you have are hyperacute T waves, which are a repolarization abnormality, and not yet affecting depolarization.Jerry W. Jones, MD FACEP FAAEMhttps://www.medicusofhouston.comnoreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-16912155990580024522020-02-19T07:19:28.600-06:002020-02-19T07:19:28.600-06:00@ Shade — There is "almost" TQRSD — but ...@ Shade — There is "almost" TQRSD — but not quite ... (Please SEE my Answer below to Al, with specifics from Dr. Smith — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-19524429050958548202020-02-19T07:17:33.542-06:002020-02-19T07:17:33.542-06:00@ Al — I asked Dr. Smith about the same thing. Thi...@ Al — I asked Dr. Smith about the same thing. This was his answer: “Technically, by my (Dr. Smith’s) definition in the study, there must be some ST elevation for TQRSD. Also, in ECG #1, there is an S-wave that BARELY goes below the isoelectric line.<br />so strictly speaking, it does not have TQRSD. Of course all dichotomous rules in medicine are fallacious. The less S-wave there is, the more likely to be LADO, and the more S-wave, the less likely, overall.” So, there is “almost” TQRSD in ECG #1 — but not quite — but this of course does not matter, because of all of the other signs of definite acute OMI — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-69519036437298821902020-02-19T07:05:52.300-06:002020-02-19T07:05:52.300-06:00GREAT comments as always Jerry! THANK YOU for your...GREAT comments as always Jerry! THANK YOU for your insights on the above subtleties! — :) ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-71484886031560267032020-02-19T07:02:13.953-06:002020-02-19T07:02:13.953-06:00@ Dr. Taha — THANK YOU so much for your kind words...@ Dr. Taha — THANK YOU so much for your kind words! Our pleasure — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-4517374896668357572020-02-19T05:35:38.595-06:002020-02-19T05:35:38.595-06:00Very informative and an absoluetly enjoyable read ...Very informative and an absoluetly enjoyable read as always .. highlighting the importance of early detection of coronary occlusions transforming ones practice from damage control to function efficient myocardial resuscitation that undoubtedly will preserve and improve quality of life .. absolutely gold! Dr. Taha EMhttps://www.blogger.com/profile/07294429459630679452noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-62632391048364527442020-02-18T17:43:55.084-06:002020-02-18T17:43:55.084-06:00Ken and Steve...
A very interesting and sad case....Ken and Steve...<br /><br />A very interesting and sad case. I also have a few points to make.<br /><br />1. While this chest pain was atypical because it was sharp and on the right, it was also constant for over an hour and radiated to both arms. Neuromuscular pain that is sharp is usually lancinating with sharp, brief and intermittent episodes that are usually affected by a change in position.<br /><br />2. I was immediately struck not only by the very obvious hyperacute T waves but also the flattened and minimally depressed ST segment in aVL. aVL is usually the first lead that I scrutinize closely. This flattening had developed into frank T wave inversion by the second ECG. Enough said.<br /><br />3. There was never any impressive STE, but the hyperacute T waves were very impressive - and there was a dynamic nature to them because there was some subtle change in amplitude from tracing to tracing. Hyperacute T waves are actually a subendocardial phenomenon which is why we don't see them as often. Usually by the time the patient arrives in the ER the ischemia has become transmural and the hyperacute T waves are being replaced with the STE of epicardial ischemia. However, some can persist for quite a while. It's also a great time to catch the ischemia because it is usually just beginning and there is a great opportunity to salvage myocardium.<br /><br />4. The hyperacute T waves in the precordial leads indicate a very proximal occlusion but the lack of STE in aVL indicates an occlusion distal to D1 (which was confirmed at cath). Because of the hyperacute T's in V1 and V2, I'm wondering if D1 was proximal to S1. This would explain why the prominence of the hyperacute T's fizzles out toward V5 and V6.<br /><br />5. The additional disease in the RCA that will require a later stent is very interesting. The ST depression in aVL is reciprocal to something going on in the inferior leads and that could explain it. The bases of the T waves in II, III and aVF are very wide and - though not tall - are likely hyperacute T's as well. The RCA is probably receiving significant collateral circulation from the LAD. When it failed, the myocardium in the RCA distribution became ischemic. When multivessel disease is present and there is collateral circulation being shared, it takes just one vessel to fail and the rest start to fall like dominoes.<br /><br />Quite a learning case.Jerry W. Jones, MD FACEP FAAEMhttps://www.medicusofhouston.comnoreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-38311407896273894172020-02-18T10:42:52.203-06:002020-02-18T10:42:52.203-06:00Terminal QRS distortion in V2-V3 ?
AlTerminal QRS distortion in V2-V3 ?<br /><br />AlAnonymousnoreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-88624091631918377282020-02-18T08:49:10.370-06:002020-02-18T08:49:10.370-06:00I would also like to add Tereminal QRS Distortion ...I would also like to add Tereminal QRS Distortion in V3 on the fisrt ECG, and V2,V3 on the second ECG.Shadehttps://www.blogger.com/profile/17518363587331642477noreply@blogger.com