tag:blogger.com,1999:blog-549949223388475481.post896468378557352346..comments2024-03-28T14:02:08.119-05:00Comments on Dr. Smith's ECG Blog: Syncope Several Times, Complete Heart Block, And a Surprise ECG in the ED!Unknownnoreply@blogger.comBlogger17125tag:blogger.com,1999:blog-549949223388475481.post-54379879579609438482020-07-24T15:41:25.352-05:002020-07-24T15:41:25.352-05:00@ AKS — You are correct that the usual rate of ven...@ AKS — You are correct that the usual rate of ventricular escape rhythms in adults is between 20-40/minute — so IF you had a ventricular rhythm at ~50/minute or faster — but slower than ~110-120/minute — AND — you didn't have P waves — then this would be AIVR ( = Accelerated IdioVentricular Rhythm). But since there are P waves in this 1st ECG rhythm — and especially since it is possible that the early beat toward the end of the tracing may be conducted — it's better to describe this as a manifestation of AV block (in which a slightly accelerated ventricular rhythm arises when P waves are non-conducted) — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-56252114950816564192020-07-24T09:16:55.312-05:002020-07-24T09:16:55.312-05:00Tks Ken. I was looking at the Vent rate. What I ca...Tks Ken. I was looking at the Vent rate. What I calculated is above 50 and as I know Vent escape would go up to 40.AKShttps://www.blogger.com/profile/02154650740617806061noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-43577101587961798502020-07-24T08:59:02.451-05:002020-07-24T08:59:02.451-05:00@ AKS — This wasn’t my case — so I’m commenting on...@ AKS — This wasn’t my case — so I’m commenting on just what I see. The rhythm strip for the 1st ECG in lead II is short, as we only see 8 beats. I believe P waves ARE regular (a P wave occurs just at the beginning of beat #6). The QRS is wide — and although it looks like P waves are not related to neighboring QRS complexes — I believe this rhythm strip is TOO SHORT to know that for certain. This is especially because beat #7 occurs early — and whenever you see early beats like this — you have to wonder if they might be conducted! The problem is that QRS morphology of beat #7 is similar but definitely NOT the same in these 2 leads — so I don’t know if this is arising from the same or a different ventricular focus … But I believe it also IS possible that the reason this beat occurs early — is that the P wave that occurs just at the onset of the 6th beat might be conducting (!!!) — with QRS widening being the result of aberrant conduction. So, this isn’t “AIVR” (which is your question) — because we DO see sinus P waves. At the least this appears to be high-grade 2nd-degree AV block — because a number of P waves that should conduct do not conduct. But in my opinion, a LONGER RHYTHM STRIP is need to really know what this rhythm is — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-79873660137058145652020-07-23T17:39:13.125-05:002020-07-23T17:39:13.125-05:00Given the differential of Transient Stemi, could t...Given the differential of Transient Stemi, could the rhythm in ecg 1 in lead 2 be AIVR ? AKShttps://www.blogger.com/profile/02154650740617806061noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-6872119122288297492016-12-09T06:19:55.482-06:002016-12-09T06:19:55.482-06:00Fantastic case with lots of important lessons to b...Fantastic case with lots of important lessons to be learned! Astute observations by Haim Katalan. There are a host of lead misplacements that are possible (especially when you consider multiple misplacements of more than a single lead) — but as per Haim, lack of change of either PQRST morphology in lead aVR — with identical P wave morphology in leads I,II,III (ie, upright P in lead II that remains greater than P wave amplitude in lead I) — together with the change he notes that DOES occur in the chest leads between these 2 tracings (ST elevation seen in V6 in ECG #6 in which ST segments are up in I,aVL — but no ST elevation in V6 for ECG #7) combine to tell us that there was no lead misplacement here!<br /><br />Interesting comment below by Jerry Jones! THANKS to Dr. Stephen Smith for presenting this fascinating case! ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-5730603779876494942016-12-09T06:17:32.475-06:002016-12-09T06:17:32.475-06:00Jerry,
Yes, I was agreeing with you on your assess...Jerry,<br />Yes, I was agreeing with you on your assessment, but just pointing out that in this case if your theory is correct it would be the RCA and not circ. Normally proximal occlusions occur first, then embolize to more distal ones. Your scenario is much less common, but of course whatever happened is indeed quite uncommon, so it is likely correct!<br />Thanks,<br />SteveSteve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-42112744563167499662016-12-08T15:30:26.110-06:002016-12-08T15:30:26.110-06:00Steve...
Thanks for the cath report. I still feel...Steve...<br /><br />Thanks for the cath report. I still feel that the LCx would have to be involved because of the ST-T changes in ECG #6 UNLESS the RCA is actually a "super-dominant RCA": "The right coronary artery is a large dominant vessel that gives rise to the posterior descending artery and approximately FOUR posterolateral branches. The two most distal are QUITE LARGE." (Caps are mine.)<br /><br />I suppose a problem in a distal RCA with such large posterolateral branches could result at times in an acute inferior subepicardial ischemia and an at other times in an impressive acute posterolateral subepicardial ischemia as seen in ECG #6. However, I've never seen a "super-dominant RCA" cause such elevation in Leads I and aVL (but I've seen it in V1 - V6).Jerry W. Jones, MD FACEP FAAEMhttps://www.blogger.com/profile/10333187745825224414noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-48042921390226330552016-12-08T13:52:29.936-06:002016-12-08T13:52:29.936-06:00Jerry,
Maybe.
Here is the entire cath report. It ...Jerry,<br />Maybe.<br />Here is the entire cath report. It was right dominant, but your theory is possible if you consider all of your comments as applying to the RCA. <br /><br />FINDINGS: A. Hemodynamics. Heart rate is 80 beats per minute. Aortic<br />pressure is 94/60 with a mean of 73. Left ventricular systolic pressure is<br />90. LVEDP is 16.<br />B. Left ventriculography: The left ventricular cavity fills diffusely with<br />contrast. The ventricle is not dilated. There is almost complete<br />obliteration of the apical segment of his LV in a hyperdynamic ventricle<br />that almost appears to have the appearance of hypertrophic myopathy with<br />apical button. There was no mitral regurgitation seen. There is ascending<br />aorta and aortic root are normal in size. No gradient was seen across the<br />aortic valve on pullback.<br />C. Coronary cineangiography.<br />1. The left main coronary artery is a moderate length vessel. It appears<br /> to be diffusely narrowed, but no high grade narrowing, perhaps 20% to<br /> 30% diffuse left main narrowing. It is relatively small caliber in the<br /> left main, felt to be perhaps no more than 2.5 mm diameter.<br />2. The left anterior descending coronary artery is also relatively small<br /> in caliber, 2.5 mm diameter vessel. The vessel has no obvious<br /> narrowing.<br />3. There is a ramus intermedius branch that is a large vessel that is free<br /> of disease.<br />4. The circumflex coronary artery is large, but nondominant giving rise to<br /> two obtuse marginal branches. The circumflex and its branches are free<br /> of any disease angiographically.<br />5. The right coronary artery is a large dominant vessel that gives rise to<br /> the posterior descending artery and approximately four posterolateral<br /> branches. The two most distal are quite large. The posterior<br /> descending artery is also quite large. The proximal right coronary<br /> artery has some modest 10% plaque, but there is no significant<br /> narrowing there. The main body of the right coronary artery is also<br /> widely patent with no significant narrowing. The posterior descending<br /> artery has some mild diffuse midvessel tubular narrowing of 20% to 30%<br /> at most. The posterolateral branches appear to be free of disease.<br /><br />SUMMARY:<br />1. Minor nonobstructive coronary artery disease is seen with 20-30%<br /> diffuse left main narrowing and 10% proximal right coronary artery<br /> narrowing and 20% to 30% mid PDA narrowing.<br />2. Hyperdynamic left ventricle with LVEF greater than 75%. No wall<br /> motion abnormalities are noted. We would consider hypertrophic<br /> myopathy and echocardiography should be done.<br />Steve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-33488765671570511262016-12-08T13:48:18.246-06:002016-12-08T13:48:18.246-06:00Good for you. Yes. See that I already changed it ...Good for you. Yes. See that I already changed it due to comments.Steve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-26881164198763043332016-12-08T13:47:39.458-06:002016-12-08T13:47:39.458-06:00That's correct. Read it again as my initial in...That's correct. Read it again as my initial interpretation may have been incorrect and there is a different opinion written nowSteve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-59952620147815634952016-12-08T13:46:42.926-06:002016-12-08T13:46:42.926-06:00Emboli are organized and well formed and much less...Emboli are organized and well formed and much less likely to reperfuse than fresh in situ thrombusSteve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-63403765687595509502016-12-08T10:26:42.613-06:002016-12-08T10:26:42.613-06:00Steve...
After reviewing all the ECGs I would sus...Steve...<br /><br />After reviewing all the ECGs I would suspect involvement of a single vessel - the LCx. Momentary occlusions - whether due to vasospasm or transient thrombi - first in the distal segment of the LCx could give the pattern of an acute epicardial ischemia of the inferoposterior circulation. Then, after that resolved, a temporary occlusion more proximally could give the (more impressive) pattern of a basal-lateral acute ischemia with extension more posterolaterally. <br /><br />The inferior wall epicardial ischemia pattern is not as impressive as the basal-lateral pattern, probably helped by collateral circulation from either the RCA (which could be weakly co-dominant) or the LAD.Jerry W. Jones, MD FACEPhttps://www.medicusofhouston.comnoreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-11151351708139253792016-12-07T22:31:22.229-06:002016-12-07T22:31:22.229-06:00Very curious! thank you.
Very curious! thank you.<br />Fireflyhttps://www.blogger.com/profile/08178971241578746718noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-40676102417829851162016-12-07T10:20:52.678-06:002016-12-07T10:20:52.678-06:00I will cnalenge this theory by claiming rhat STE s...I will cnalenge this theory by claiming rhat STE shape in the latetal leads is completely different from the STD in the so caled sweached leads. Coronary spasm also no P wave axis change as would expected in leads reversal.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-84855448198250760312016-12-07T09:52:31.639-06:002016-12-07T09:52:31.639-06:00Thanks for posting Dr. Smith.
In EKG #6 does the ...Thanks for posting Dr. Smith.<br /><br />In EKG #6 does the different pattern of STD in V3 and V4 as well as the new STE in V6 mean anything then? The limb leads may have been misplaced but that shouldn't affect the precordial leads right?<br /><br />Thanks.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-7971664942694190692016-12-07T09:28:14.859-06:002016-12-07T09:28:14.859-06:00Do you think it could have been embolic? Any histo...Do you think it could have been embolic? Any history of malignancy or hypercoagulability? Ali Jazayerinoreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-24913240550625484922016-12-07T09:05:41.794-06:002016-12-07T09:05:41.794-06:00Great educational post!Great educational post!Joe C.noreply@blogger.com