tag:blogger.com,1999:blog-549949223388475481.post622561754236158620..comments2024-03-28T14:02:08.119-05:00Comments on Dr. Smith's ECG Blog: Are these Wellens' waves?Unknownnoreply@blogger.comBlogger9125tag:blogger.com,1999:blog-549949223388475481.post-35067561029486359362020-03-01T10:51:03.794-06:002020-03-01T10:51:03.794-06:00Just didn't look closely because it was not at...Just didn't look closely because it was not at all important to the subject of the caseSteve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-91697672046964343212020-02-29T16:48:48.501-06:002020-02-29T16:48:48.501-06:00Thanks for your comments Jerry. I believe the main...Thanks for your comments Jerry. I believe the main area of discussion between Dr. Smith and myself on ECG #1 was whether in addition to consideration of chronic and/or acute pulmonary disease (hypoxemia) — there might also have been at some prior point anterior infarction accounting for the no-more than tiny r waves in V1,2,3 — and for at least some component of the chest lead ST-T wave changes. And as you emphasize — this complicated ECG “certainly invites more than one opinion”. THANKS again for your insights — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-54221031719840867672020-02-29T16:37:33.885-06:002020-02-29T16:37:33.885-06:00THANK YOU so much Mario for your detailed commenta...THANK YOU so much Mario for your detailed commentary! Grazie come sempre! (Thanks as always — :)ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-82916596170925140272020-02-29T11:56:50.973-06:002020-02-29T11:56:50.973-06:00An instructive and really challenging case proving...An instructive and really challenging case proving that clinical correlation is always of paramount importance.<br />I must admit that without knowing that the patient's main complain was SOB, I would have first investigate whether this patient's history had shown an old anterior MI given the poor R wave progression combined with ST-T waves abnormalities in chest leads WITHOUT clear (=typical and/or suggestive for acute Pulmonary Embolism) ECG findings in inferior leads (except lead III though greatly biased by QRS morphology changes likely due to dyspnea). Along with lack of suggestive (for PE) changes in inferior leads, here sinus tachycardia is not present: in my experience, the vast majority of acute PE does manifest HR>100 (I'm used to think to acute PE when the HR is, typically and often constantly, around 110/115min in the right clinical context). Thas said, it seems quite clear that the clinical context combined with the initial ECG do not fit with Wellens.<br />Mario ParrinelloAnonymousnoreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-81115545362993685152020-02-29T11:46:38.790-06:002020-02-29T11:46:38.790-06:00Steve and Ken...
I enjoyed your discussions very ...Steve and Ken...<br /><br />I enjoyed your discussions very much. This is a very complicated ECG that certainly invites more than one opinion.<br /><br />I also immediately ruled against ACS and Wellens waves. Wellens waves don’t normally appear simultaneously with T wave inversions in the inferior leads. However, given no history, one might want to consider ARVD/C.<br /><br />What concerns me most is how much "chronic" COPD has affected the ECG as opposed to acute cor pulmonale. COPD often makes the interpretation more difficult. I have seen precordial leads look like this in patients with chronic COPD (and little or no exacerbation) and young patients with acute PE with NO history of COPD. The precordial and inferior leads here favor acute cor pulmonale more than ACS. So, ACS is out (by the way, Steve, where did that positive troponin come from? It just popped up in your assessment but was never mentioned in the original history).<br /><br />Here's why I think this ECG is more consistent with acute cor pulmonale in a patient with either relatively mild chronic emphysema or with the chronic bronchitis/blue bloater form: Never in my career have I ever seen an R wave as tall as the one in Lead I in a patient with advanced COPD. It just doesn't happen! We tend to think only in terms of the frontal plane when discussing the mean QRS axis, but with COPD and acute cor pulmonale it is very important to remember there is a second plane and a third direction. <br /><br />No matter which direction the QRS axis moves in the frontal plane, in advanced COPD, it virtually always points posteriorly in the horizontal plane. The evidence lies (in this ECG) in leads V1 - V3 with their deep S waves. What effect will this have on the frontal plane? First, the QRS complexes will be smaller in general than those in the precordial leads (except maybe for V5-6 which are more leftward than posterior). Second, the QRS in Lead I is going to be very small since the majority of the QRS vector is pointing at 90 degrees from Lead I. So, if the lung disease has been profound enough to create a posteriorly-directed QRS axis, it will also have also resulted in a very small QRS amplitude in Lead I. That isn't happening here - in either ECG!<br /><br />However, diminution of the QRS amplitude in Lead I does NOT happen in ACUTE cor pulmonale. Also, the relatively acute change in pulmonary vascular resistance can cause dilatation of the RV with a resultant rotation of the right ventricle more anteriorly. This contributes to the QRS progression seen in the precordial leads. Such a picture does not HAVE to be due to chronic RV strain/hypertrophy. So, in my opinion, this is an ECG that shows some baseline mild chronic COPD changes. The reason I say mild is because in the previous ECG, the QRS axis is normal and the P wave axis is normal. In any ECG showing changes of advanced chronic cor pulmonale, the P wave in aVL is going to be isoelectric or inverted (more typically inverted). That is not present in either ECG.<br /><br />Even though there is an "S1Q3T3" present on the initial ECG, I'm not convinced that it represents THE S1Q3T3 that is so representative of acute cor pulmonale. In those cases, the S1 is due to conduction delay through the right bundle branch and is typically more slurred, as in RBBB. A simple Q3T3 is not helpful because it is commonly seen on the ECG of patients without any respiratory issues. It is more reflective of an axis rotation (but NOT like that seen in acute cor pulmonale!).<br /><br />I would not minimize the importance of the T wave inversion in Lead III on the presenting ECG. Even under normal circumstances there can be a difference in the QRS axis and T wave axis in Lead III - and this is certainly NOT a normal circumstance. I have seen real S1Q3T3 patterns in which the QRS in Lead III was predominantly (net) negative. I think everything is "typical" for acute cor pulmonale here except for the S1 of the S1Q3T3 which, although present, just doesn't look “typical enough” to me (S wave too narrow).<br />Jerry W. Jones, MD FACEP FAAEMhttps://www.medicusofhouston.comnoreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-21501990682053740582020-02-29T11:36:25.780-06:002020-02-29T11:36:25.780-06:00It's easy to overlook ...It's easy to overlook ...ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-26499250732535052362020-02-28T22:08:02.759-06:002020-02-28T22:08:02.759-06:00Yes, regarding aberrant conduction, there are vary...Yes, regarding aberrant conduction, there are varying degrees of aberration in a given patient or from patient to patient, i.e., mildly aberrant, more aberrant, extremely aberrant, so on, like, mild RBBB, more RBBB..., complete RBBB, etc. We are seeing that in this patient. Steve, how come you didn't see the P wave in front of the QRS that you are calling a PVC?<br />K. Wang.Anonymoushttps://www.blogger.com/profile/04509940285330859355noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-89141083642784534682020-02-28T16:41:30.993-06:002020-02-28T16:41:30.993-06:00THANKS for your insights Dave! I did not get to se...THANKS for your insights Dave! I did not get to see the prior ECG at the time I made My Comment. i) My point regarding the tiny r waves in ECG #1 was simply that in most patients that I’ve seen who manifest poor R wave progression due to longstanding pulmonary disease — there is more r wave than we see in leads V1, V2 and V3. The prior ECG does manifest delayed transtion (the R wave does not become taller than the S wave until between V5-to-V6) — but there IS clearly more initial r wave in leads V2 and V3. So while statistically, chances remain greatest that the reason for poor R wave progression in ECG #1 is pulmonary disease — there HAS been loss of r wave in the anterior leads in ECG #1, such that I would want to learn more history before completely discounting the possibility of prior anterior MI.<br /><br />Otherwise — YES — the 12th beat is indeed a PAC that is conducted with RBBB aberration. The underlying rhythm is sinus with multiple PACs that have some repetition in the pattern they form (ie, similar groups of beats). And as I KNOW you have also observed — as one looks at the simultaneously-recorded 3-lead groups above the long lead II rhythm strip at the bottom — it becomes obvious that MANY of these PACs are conducted with varying degrees of aberrant conduction — the relative amount of which is probably determined by “Ashman-like” parameters (interplay between the PAC coupling interval, and the preceding R-R interval — which I believe is longest preceding the 12th beat, which is probably why it is the most aberrantly conducted).ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-81854124057061480472020-02-28T11:09:09.167-06:002020-02-28T11:09:09.167-06:00This is an interesting case, but the ECG is compli...This is an interesting case, but the ECG is complicated by the fact that the patient had COPD. I suspect that the poor R wave progression is unrelated to acute right heart strain (or previous anterior MI), but due to the COPD: hyperinflated lungs can cause lowering of the diaphragm with consequent inferior displacement of the heart and reduction of anterior R wave amplitude. Additionally, as Ken suggests, I don’t think that the T wave inversion in lead III necessarily has any significance at all because the QRS here is predominantly negative: in the limb leads the QRS and T wave polarities are normally similar. As an aside, the ‘PVC’ in the previous ECG is an aberrantly conducted APC – it is preceded by a premature P wave.Dave Richleyhttps://www.blogger.com/profile/08697826369183641026noreply@blogger.com