tag:blogger.com,1999:blog-549949223388475481.post1175401537149712037..comments2024-03-28T14:02:08.119-05:00Comments on Dr. Smith's ECG Blog: The computer and the cardiologist called this a "Normal EKG"Unknownnoreply@blogger.comBlogger2125tag:blogger.com,1999:blog-549949223388475481.post-4293738539522125772019-06-07T07:54:40.391-05:002019-06-07T07:54:40.391-05:00Indeed. S1 is often after D1.Indeed. S1 is often after D1.Steve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-76363846689816300412019-06-06T21:29:14.047-05:002019-06-06T21:29:14.047-05:00Drs. Smith, Grauer and Mosley...
Thank you for a ...Drs. Smith, Grauer and Mosley...<br /><br />Thank you for a very educational experience here. Unfortunately, it seems like this same theme has played out in several of your posts in the last few months.<br /><br />Leads III and aVF along with V2 and V3 certainly point toward a Type 3 "wrap-around" LAD occlusion. But I think there remains one more bit of information that makes this even more interesting. The ST depression in aVL (and Lead I as well) is critical to this case. I can't help but think that had they just followed (ahem!) "Jones's Rule" ("Any ST DEPRESSION on the ECG of a patient with symptoms compatible with ACS represents a RECIPROCAL change until proved otherwise."), they would have come to a resolution of this problem a lot sooner.<br /><br />But where is the occlusion? If the thrombus were proximal to D1, then the basolateral area would have been ischemic and there would have been STE in aVL as well as Lead III. While we may have had a cancellation of forces resulting in minimal to no STE in any of the limb leads, there certainly would not have been ST depression in aVL. Granted, it would THEORETICALLY be possible IF the STE in Lead III were extremely high and the STE in aVL were much less; but occlusion proximal to D1 in a wraparound LAD is going to produce more STE in aVL than in Lead III. Thus, ST depression in aVL with an occlusion proximal to D1 simply does not occur. So, the occlusion has to be distal to D1 to allow Leads I and aVL to be free to react reciprocally to the STE in III. <br /><br />But V1 - though it does not have any overtly diagnostic STE (it's still within the range of normal) - does have a genuine hyperacute T wave. But how is that possible if the occlusion is distal to D1 and S1 normally precedes D1? Simple! In THIS case, D1 is the first branch off the LAD and S1 likely follows D1. The occlusion, though DISTAL to D1, is PROXIMAL to S1, so occlusion of the septal perforators causes the ST changes in V2 and V3 while D1 is able to continue to provide circulation to the apicolateral area (V4 - V6) - with assistance from the LCx, the RCA and possibly a ramus intermedius. Of course, the continuation of the LAD that wraps around the apex is unable to supply part of the inferior wall with enough circulation, so an acute epicardial ischemia develops (i.e., STE). In the case of this unfortunate patient, infarction most assuredly followed as well.<br /><br />Jerry W. Jones MD FACEP FAAEMJerry W. Jones, MD FACEP FAAEMhttps://www.blogger.com/profile/10333187745825224414noreply@blogger.com