tag:blogger.com,1999:blog-549949223388475481.post6965339311332845981..comments2024-03-28T14:02:08.119-05:00Comments on Dr. Smith's ECG Blog: 21 year old woman with CP, SOB, then syncope, and with ST depression with T-wave inversion in V1-V3Unknownnoreply@blogger.comBlogger8125tag:blogger.com,1999:blog-549949223388475481.post-62588909279623819702020-09-07T07:06:06.997-05:002020-09-07T07:06:06.997-05:00THANKS so much Jerry. Your comment reminds me of m...THANKS so much Jerry. Your comment reminds me of my anecdote related to this post — being awakened in the middle of the night for what I thought was the umpteenth case of LV failure/acute pulmonary edema — only to find that instead of severe LVH, the ECG showed severe RVH with RV stain ... — which highlighted to me how being able to recognize that uncommon case of severe RVH on ECG could totally change the management approach. THANKS again for your comment! — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-33454277073694787752020-09-06T16:25:24.261-05:002020-09-06T16:25:24.261-05:00Excellent cases. Nothing to add except an anecdote...Excellent cases. Nothing to add except an anecdote. My very first night as a first-year internal medicine resident was ER duty (no EM residencies back then). A young woman around 20 y/o came in complaining of a headache. I noted a BP around 180/110 and asked her about neuro symptoms and did a thorough neuro exam, after which I gave her some medicine for her hypertension expecting that to relieve her headache. A few minutes later a nurse came and got me, telling me that the patient was turning blue and getting short of breath. I rushed back to see her. I put her on O2 with no improvement. I had no idea what was happening. Fortunately for me, there was an older, much more experienced internist in the ER seeing one of his own patients and I enlisted his help. After telling him what had happened, he immediately listened to her chest. I remember wondering why he was listening to her chest when she obviously had a neuro problem. Then he asked her, "Do you have any heart problems?" and she answered, "Yes. I have a patent ductus arteriosus." He had her pull her knees up tightly on her chest and then told me that the O2 would start to help in a few minutes (which it did). I learned so many lessons that night - the importance of a complete history and physical exam, the need to look for a cause of hypertension in a very young person and a thorough, first-hand understanding of Eisenmenger's Syndrome. I had not thought about that night for years until I read this post. Thanks!<br /><br />Jerry W. Jones, MD FACEP FAAEM<br />https://medicusofhouston.comDouble Downhttps://www.blogger.com/profile/09589348333176062815noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-64830698739050249832020-09-02T17:25:11.436-05:002020-09-02T17:25:11.436-05:00Hello MG. I will assume you are talking about ECG ...Hello MG. I will assume you are talking about ECG #1 in my Figure-1 (from Case 1). You ask an EXCELLENT question!<br /><br />FIRST — It is true that there is some overlap between certain cases of RVH that manifest with a predominant R wave in lead V1 and RBBB. And sometimes — both conditions may be present. That said I believe the “theme” in ECG #1 is RVH, RVH, RVH + Pulmonary Hypertension.<br /><br />This clearly isn’t complete RBBB — because the QRS complex is not wide (at most, I measure 0.10 second duration). And this ECG lacks the terminal WIDE S waves that should be seen in leads I and V6 when there is complete RBBB.<br /><br />Everything about this case says, “RVH + Pulmonary H.T.”. The clinical presentation is very typical for primary pulmonary hypertension in a young woman — and the qR in V1 suggests pulmonary hypertension (it lacks the initial small positive deflection that is usually found when there is incomplete or complete RBBB). Supportive findings of RVH include all of the things I mentioned above in My Comment (Tall R in V1; RAA; S waves in I,II,III & persisting through to V6; RV “strain” in inferior and anterior leads).<br /><br />The above said — it IS true that I can’t rule out in addition to RVH, that there may also be incomplete RBBB (because there ARE terminal narrow s waves in I and V6 + an R’ in V1) — but the predominance of RVH features suggest to me that there is no conduction defect.<br /><br />Again — there ARE cases in which distinction from these 2 entities is clearly more difficult.ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-76573217564931407522020-09-02T07:19:12.929-05:002020-09-02T07:19:12.929-05:00Why can't this be RBBB instead of being RVH?Why can't this be RBBB instead of being RVH?MGhttps://www.blogger.com/profile/06233522417024317416noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-62655865633372994702020-09-01T19:17:45.960-05:002020-09-01T19:17:45.960-05:00@ PM — Good question! If posterior MI is acute — t...@ PM — Good question! If posterior MI is acute — there will almost always be associated acute inferior lead changes (because the RCA commonly supplies both the inferior and posterior walls of the LV). However — with RVH — there should be (as I emphasize in my comment above) — additional signs — and THAT is what we see in ECG #1 (RAA, RV strain in inferior and anterior leads, qR in lead V1, persistent lateral precordial S waves, S waves in leads I,II,III). ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-2014721878734278122020-09-01T19:16:48.233-05:002020-09-01T19:16:48.233-05:00@ Giacomo — I think it is hard to know what a prol...@ Giacomo — I think it is hard to know what a prolonged QTc in this patient means given the rapid rate and RV “strain”. I think it’s difficult in this tracing ( = my opinion) to distinguish a biphasic T wave from a U wave (I thought we were primarily seeing biphasic T waves … but hard to be certain). It wasn’t my case — and there is no mention of serum K+ & Mg++ — but electrolyte disturbance could be a contributing factor. So, you ARE correct that the QTc might be prolonged (I would not call it “very” prolonged given the heart rate) — and electrolyte disturbance could be contributing. All that said — the “THEME” of this tracing is severe RVH + pulmonary hypertension — and that’s where I’d focus my attention ( in addition to checking serum lytes). THANKS for your comment!ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-75566445479743241362020-09-01T18:07:51.981-05:002020-09-01T18:07:51.981-05:00What's the best way to differentiate between R...What's the best way to differentiate between RVH and posterior MI?PMhttps://www.blogger.com/profile/02137437568582174388noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-13052001069037173842020-09-01T17:22:13.898-05:002020-09-01T17:22:13.898-05:00Hello Dr. Smith and Dr. Grauer,
apart from the EC...Hello Dr. Smith and Dr. Grauer,<br /><br />apart from the ECG findings typical of RVH, isn't there also a very long QT with U waves in the first ECG? If so, how do you explain that? <br /><br />Thanks!Giacomo Zaccagninihttps://www.blogger.com/profile/16450423102718065881noreply@blogger.com