tag:blogger.com,1999:blog-549949223388475481.post3852228841388772477..comments2024-03-28T14:02:08.119-05:00Comments on Dr. Smith's ECG Blog: Apparent Pseudo-STEMI patterns are not necessarily Pseudo. Beware.Unknownnoreply@blogger.comBlogger8125tag:blogger.com,1999:blog-549949223388475481.post-45676887229533017562017-04-26T13:55:19.927-05:002017-04-26T13:55:19.927-05:00Kaviraj,
PseudoSTEMI means ST elevation that is no...Kaviraj,<br />PseudoSTEMI means ST elevation that is not due to MI (not due to coronary occlusion), but may appear at first glance or to the non-expert to be an MI.<br />STeveSteve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-4531250524103304472017-04-16T14:54:00.452-05:002017-04-16T14:54:00.452-05:00Explain about pseudo STEMI please.. Explain about pseudo STEMI please.. Anonymoushttps://www.blogger.com/profile/11133722693378823273noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-89819144355369002982016-02-13T06:36:18.503-06:002016-02-13T06:36:18.503-06:00Clopidogrel treatment failure is surprisingly comm...Clopidogrel treatment failure is surprisingly common. No evidence for changing to an alternative P2Y12, though.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-39617218404822879522016-02-10T10:39:33.238-06:002016-02-10T10:39:33.238-06:00Dr. Smith, thank you for your reply
MarioDr. Smith, thank you for your reply<br />MarioAnonymousnoreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-30455517529482989612016-02-09T06:39:29.011-06:002016-02-09T06:39:29.011-06:00Mario,
You pointed out a typo in my case. I did n...Mario,<br />You pointed out a typo in my case. I did not mean to say that about LVH. I have changed it to the following, which is what I meant to say:<br />If the ST segment abnormalities remain, then either angiography or emergency formal echo is indicated. If they resolve, then perhaps the findings are due to the severe hypertension.<br />As for the last question, that is very difficult and very case specific. For this, case, the change is diagnostic. If one did not have that previous ECG, then one would first treat the hypertension and see if that resolves the pain and ECG findings. If not, perhaps activate, or get an emergent formal echo. If there is a WMA, then activate. If there is no wall motion abnormality on a contrast echo read by an expert, then there is not significant ongoing epicardial ischemia.<br />Steve SmithSteve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-21045696076390948412016-02-06T10:39:02.682-06:002016-02-06T10:39:02.682-06:00Another very intersting and very instructive case;...Another very intersting and very instructive case; thanks a lot.<br />Only just a question on your statement 'if the ST segment abnormalities remain, then either angiography or emergency formal echo is indicated. If they resolve, then perhaps the findings are due to LVH'. According to your experience do the repolarization changes due to LVH resolve completely?. <br />Let me make also a general comment. <br />In comparison with other difficult ECGs where there are validated helps (for example LBBB->modified Sgarbossa or differentiation between early repol and MI->formula), 'paradoxically' in very frequent clinical situation such as LVH and chest pain, which all we face every day, there are too many uncertanties in order to proper evalutate these difficult ECGs.<br />I hoped that the Armstrong R/S ratio could be of help until I've read your articles and this blog…<br />Therefore, Dr. Smith, I will very highly appreciate your opinion on that; more precisely I would like to know what is your approach to these cases. In other word, and for the sake of clarity, what do you consider first, besides the clinical context, prior available ECGs (which all we know are the exception than the rule), serial ECGs, echocardiogram: Armstrong's ratio, Tampl/QRSampl ratio (not necessarily in that order) etc.?<br /><br />Mario ParrinelloAnonymousnoreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-929701016285994872016-02-06T07:23:46.595-06:002016-02-06T07:23:46.595-06:00Thanks, Ken. Yes, I will remember to number the f...Thanks, Ken. Yes, I will remember to number the figuresSteve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-74095632086345893622016-02-05T14:33:21.672-06:002016-02-05T14:33:21.672-06:00Overall GREAT post. In the interest of academic di...Overall GREAT post. In the interest of academic discussion — I will present another perspective on how I would interpret the first 5 ECGs that you show.<br /><br />The problem with ECG #3 that is shown here ( = the ECG from 1 week prior) — is that the frontal plane axis is different (ie, lead III is predominantly upright — vs lead III in ECGs #1,2 in which the QRS was predominantly negative in lead III). THIS may account for the lack of LVH voltage seen previously in lead aVL — and in my opinion, makes it very difficult to say whether the change between ECG #3 and ECG #2 is indicative of ischemia (it might be due to the axis shift … which in my experience may account for subtle ST-T wave differences). <br /><br />That said — in a patient with NEW chest pain — there IS (in my opinion) a difference between ECGs #1 and 2 — in that there is subtle-but-real increase in T wave amplitude in leads II and aVF on ECG #2. While true that heart rate in ECG #2 is a bit faster than it was in ECG #1 — the frontal plane axis IS the same — so although subtle and in no way definitive, I would be suspicious of something that may be acute simply based on this subtle difference between ECGs #1 and 2 …<br /><br />ECG #4 (ie, repeated @ 5 hours post-arrival) is of course diagnostic as you emphasize — as frontal plane axis is the same as in ECGs #1,2 and there is now obvious change in ST-T wave morphology in each of the limb leads.<br /><br />Note in ECG #5 (@ 6 hours post-arrival) — that frontal plane axis has again shifted (lead III is predominantly positive again) — and once again, I think it may be this frontal plane axis shift that contributes to the change in QRS amplitude in lead aVL … (It would be so NICE if we could just see baseline tracings in sinus rhythm for these 2 different frontal plane axes … — so that we can say with certainty what the baseline R wave amplitude in lead aVL should look like with each axis …).<br /><br />I like the 3 examples you then give re potential for confusion between LVH and inferior STEMI — although in EACH case, while I couldn’t be certain — I would have suspected the changes seen were from LVH (and/or ischemia) and not from acute STEMI (simply based on morphologic appearance). In contrast — the final 2 ECGs (taken from your excellent June 1, 2012 post) are a WONDERFUL example (as per my comment on that post) of how despite obvious LVH, the ST-T wave appearance clearly indicates acute ongoing STEMI (which of course is confirmed by finding the previous tracing).<br /><br />BOTTOM LINE: You make wonderful points about potential confusion that may arise when assessing for ACS/acute STEMI in the setting of underlying LVH. I just wanted add the importance of integrating frontal plane axis into ECG assessment when comparing serial tracings. I base my comments on many years of religious serial observations within a large family medicine population of patients that this potential effect from shift in frontal plane axis may have on QRST limb lead appearance. THANKS (as always) for your great presentation!<br /><br />------------------<br />P.S. Steve — It would be great if you could NUMBER your figures (would really make it much easier to clarify which ECG is being referred to when comments are made). THANK YOU for considering!ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.com