tag:blogger.com,1999:blog-549949223388475481.post4627723613724915722..comments2024-03-28T14:02:08.119-05:00Comments on Dr. Smith's ECG Blog: 50-something with STEMI and hypotension: What is the infarct artery?Unknownnoreply@blogger.comBlogger15125tag:blogger.com,1999:blog-549949223388475481.post-24170937217656493932020-07-06T14:05:11.964-05:002020-07-06T14:05:11.964-05:00THANK YOU! — :)THANK YOU! — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-47200280874961093452020-07-06T14:03:06.296-05:002020-07-06T14:03:06.296-05:00Nice post.Nice post.Anonymoushttps://www.blogger.com/profile/02093426823544945818noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-71032941923703695932020-06-11T11:24:01.240-05:002020-06-11T11:24:01.240-05:00THANK YOU! — :)THANK YOU! — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-21234545757834019712020-06-07T10:37:14.946-05:002020-06-07T10:37:14.946-05:00@ Stanislav — YES, we should ADD this 3rd possibil...@ Stanislav — YES, we should ADD this 3rd possibility to the differential diagnosis. Clearly, it is far LESS common that the cause of an ECG such as the one in today's case will be simultaneous ACUTE multi-vessel disease — but this COULD happen. That said, NOT at all surprising that your patient had cardiogenic shock associated with 2 large ongoing acute STEMIs of this nature. THANKS for your comment — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-84441691121119440732020-06-07T10:34:13.837-05:002020-06-07T10:34:13.837-05:00@ Anonymous — I LOVE "mental exercises" ...@ Anonymous — I LOVE "mental exercises" of this sort. I just think there are limits to what might be predictable. THANKS for your thoughts! — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-49227889756853316192020-06-07T05:42:47.356-05:002020-06-07T05:42:47.356-05:00I agree with you, but it was only a “mental exerci...I agree with you, but it was only a “mental exercise” about the interpretation of ecg without a historical background, even if ecg must always be interpretated in a clinical setting.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-7906526257032299272020-06-07T01:08:36.774-05:002020-06-07T01:08:36.774-05:00I had seen somewhat like this ECG. The patient had...I had seen somewhat like this ECG. The patient had proximal RCA occlusion and critical (99%) stenosis in proximal LAD. But he had pulmonary edema.Stanislavhttps://www.blogger.com/profile/12080512751622104058noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-9777433165712326622020-06-06T22:46:48.901-05:002020-06-06T22:46:48.901-05:00Sorry — but I’m afraid your questions do go beyond...Sorry — but I’m afraid your questions do go beyond the scope of this blog. They are also difficult to address — since there are a lot of “ifs” (ie, by “unstable” are we talking about hypotension or cardiogenic shock as a direct result of a large stemi?). It’s known that patients with acute RV MI often need volume as a primary treatment. Beyond that I don’t know how much postulating one or another artery as the “culprit” vessel will alter what you do. I’m including this link from EMCRIT — as it features excellent notes and podcast discussion on the subject of various pressors — https://emcrit.org/ibcc/pressors/ — Scroll down under Questions & Discussion to Pitfalls, as the pitfalls in the 8 bullets listed address some of your prehospital (long transit time) concerns. The 2nd bullet seems especially apt = “Failure to aggressively up- and down-titrate vasopressors to determine the physiologic effect of each on any specific patient. Medications may not behave as described in a textbook (even this book!). By continually adjusting infusion rates, it is often possible to get a sense of which agents are most effective. The goal is always to use the minimal total dose of vasopressors necessary to achieve hemodynamic targets, so if a drug doesn't seem to be having any effect then wean it off.” That said — “Ya gotta be there” to figure out what’s going to work for your particular patient in your critical patient who is 1-to-2 hours away from definitive care. THANKS for your interest! Glad you are finding our ECG Blog helpful! — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-23839029298014390282020-06-06T21:53:09.382-05:002020-06-06T21:53:09.382-05:00If the patient had been more unstable and had shor...If the patient had been more unstable and had shortness of breath and pulmonary edema would it be safe to err on the side of wraparound LAD? If so would dobutamine be a good option to increase CO and if it wasnt a wraparound (as in this case) would it significantly affect the patient by increasing the demand as well as vasodilation from the B2 agonism seen with dobutamine? In this case with it being a proximal RCA a better option would be levophed right?<br />I apologize if this goes beyond the discussion of this blog but when i study these posts i try and think of myself as the provider and what I would do on scene. I work prehospital with long transport times (2hrs) to definitive care.<br />Thank you guys for providing such great educational content. Ive become addicted to this blog!Anonymoushttps://www.blogger.com/profile/13665054631776516973noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-1569807902236573542020-06-06T19:34:57.299-05:002020-06-06T19:34:57.299-05:00Thanks so much Jerry (as always!) for your comment...Thanks so much Jerry (as always!) for your comment. I’m well familiar with large posterolateral branches with RCA occlusion causing ST elevation in V5,V6 — though in my experience usually not continuing significantly in other chest leads. Thanks again — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-58232283924199126392020-06-06T19:04:43.107-05:002020-06-06T19:04:43.107-05:00Great case and excellent discussions! I think the ...Great case and excellent discussions! I think the STE in the inferior leads is a bit much for a Type 3 LAD. In those cases, the STE tends to be mild to moderately elevated with more involvement in the lower lateral or apicolateral leads. Typically for a right ventricular MI, the STE decreases as we move leftward, though it can sometimes still be very significantly elevated even in V6. V5 and V6 can have significant STE even without a right ventricular MI if the RCA has a long posterolateral branch. As I recall, there is an ECG somewhere on this website that shows a proximal infarction of a superdominant RCA with STE across the precordium.<br /><br />Jerry W. Jones, MD FACEP FAAEMhttps://www.medicusofhouston.comnoreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-46558064521975609672020-06-06T16:05:44.431-05:002020-06-06T16:05:44.431-05:00@ Anderson — Muito obrigado pelo seu comentário (T...@ Anderson — Muito obrigado pelo seu comentário (Thanks a lot for your comment!). I would slightly amend your comment as follows: When we are dealing with a tracing that shows inferior lead ST elevation but NOT anterior lead ST elevation — then the finding of ST elevation in lead III > II, especially when in association with marked, mirror-image ST depression in lead aVL — suggests acute occlusion of the RCA (and NOT of the LCx = Left Circumflex). But the finding of ST elevation in III > II by itself does NOT reliably predict that RCA occlusion is “proximal” — and it does NOT reliably predict that there is acute RV involvement (it only predicts that the RCA is the culprit). If in addition to ST elev in III > II + marked reciprocal ST dep in aVL you ALSO have ST elevation in lead V1 — THEN you are able to predict probable proximal RCA occlusion, and by implication (since the proximal RCA generally supplies the RV) probable acute RV involvement. You can then easily CONFIRM acute RV invovlement by obtaining right-sided leads (looking for ST elevation in right-sided leads). But that is NOT what we have here. In today’s case — there is marked ST elevation in BOTH the inferior and anterior lead areas — so we can NOT be completely certain from this single ECG alone IF this is due to proximal RCA occlusion or proximal LAD occlusion with wraparound. It would ONLY be IF the proximal RCA is the “culprit” artery — that we could then predict acute RV involvement. I hope the above makes sense. As I state in the Bottom Line to my comment above — I learned from this case, because I was not accustomed to thinking of acute RV involvement as being able to produce SO MUCH ST elevation in leads V3,V4,V5 as it does here. Um caso extraordinário, não é? Extraordinary case, isn’t it? — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-30790210180455969012020-06-06T15:40:22.527-05:002020-06-06T15:40:22.527-05:00Great educational and instructive post, THANKS A L...Great educational and instructive post, THANKS A LOT my teachers! I would like to put some words regarding ECG, if i can. Firt, the rhythm is clearly sinus with 107 bpm, therefore sinus tachycardia. Second, The PR, QRS and QT intervals are normal. As per Dr. Smith and Ken Grauer, there are STE in V1-V6 and inferior leads with reciprocal changes in aVL and I. Also, there are pathologic Q waves in inferior leads and V1-V2.As per Dr. K Wang in your great book, when there are STE in III>II and STD in aVL as well as in I,so we have inferior MI with RV involvement(proximal RCA occlusion).Right ventricular infarction is suggested by ST elevation in V1 too.I LOVE ECG!!! <br />Anderson Santos, medical student from Brazil. O Poder da Eletrocardiografiahttps://www.blogger.com/profile/11143192155299060176noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-44207098405819122672020-06-06T14:56:06.788-05:002020-06-06T14:56:06.788-05:00@ Anonymous — I think that when you get into tryin...@ Anonymous — I think that when you get into trying to predict certain specific kinds of anatomic variants in a patient you are assuming did not have a prior event and does not have multivessel disease — that you are reaching beyond what a single initial ECG in a patient with new chest pain is able to tell you. I thought the main differential in this case was the one stated by Dr. Smith above = 1) proximal LAD occlusion with wraparound vs 2) proximal RCA with RV involvement — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-68563374490853184732020-06-06T11:47:45.495-05:002020-06-06T11:47:45.495-05:00Before echo and angiography what about suspecting ...Before echo and angiography what about suspecting occlusion of a long proximal LAD with small diagonal in an anatomy with a large ramus intermedius/MO?Anonymousnoreply@blogger.com