Posted by: medicblog999 | June 8, 2010

ECG Geek 10 – The Discussion

So, here is the ECG again :

click to enlarge

If you need to see the patient presentation, then click here to read part one of this post.

I said that as well as the ECG itself, I wanted to have a bit of a discussion about something that cropped up and made me think a little after the job. But first, the ECG.

Some of you got this as the same interpretation as me. Some of you went into more depth than I know (especially Tom Bouthillet who sent an email to me) and some of you were a little off, but I can only share with you my thoughts about the ECG.

Bearing in mind that the patient was asymptomatic, young and a fit gentleman, I got a bit of a shock when I saw this come out of the Lifepak 12 with an interpretation of “Extensive Myocardial Infarction” on it. I glanced at the patient again, then took a few seconds to really look at the ECG, then come to my interpretation.

I thought this was an STEMI Mimic/imposter and not ‘real’ ST Elevation. The patient has huge QRS complexes especially notable in V1, V2, V3 and V4. The ST Elevation that can clearly be seen in V1, V2 and V3 is what I interpreted as what is commonly referred to as ‘high takeoff’ or Benign Early repolarisation, but he also displayed some characteristics of LVH (left ventricular hypertrophy). All QRS complexes are within normal widths but the depth of the S waves in V1, V2, and V3 make it very difficult to discern between the S waves and the R waves of the lead below. If you take the time and really look, you can figure out where the S wave ends in V1 and V2 and it can be seen that the corresponding height of the ST Elevation increases with the increasing depth of the S wave. This is a finding which is not seen in Acute AMI and helps to make a determination that this is not a STEMI. Take all of these findings along with the fact that there are no reciprocal changes anywhere else on the ECG, and things start to slip into place.

My fellow blogger, Tom Bouthillet has also wrote about the shape/morphology of the ST Segment and what characteristics the ST Segment has for Acute AMI compared to the STEMI Mimics. This tracing shows an upwardly concave ST segment as opposed to an upwardly convex segment.

Take these two diagrams reproduced from Tom’s blog, Prehospital 12 Lead ECG.

and :

Tom goes on to write:

“This finding is not particularly sensitive. It is, however, fairly specific……….The STE-mimics almost always present with upwardly concave ST segments and an absence of reciprocal changes”

But, taking all of this into account, what gave me the biggest sense of security is that it ‘just didn’t look like an MI’ on the 12 Lead ECG.

Maybe this comes with practice and extended self learning, but after a time, you just get a ‘feel’ for ECGs, even if you can’t definitely diagnose everything that you think you can see on the ECG.

This brings me to the main point of this post.

I had a patient in the back of my ambulance who I was sure, after a full assessment, was not having an MI, yet his ECG stated that he was. Everything that I had learned in my own time about STEMI mimics and imposters is not taught in my service and is seen well above the level that is required for an operational paramedic. I was confident to just take this patient to the local Accident and Emergency department rather than transmitting the ECG to the regional PPCI (Primary Percutaneous Coronary Intervention or Angioplasty) centre, however, I was stepping WAY outside of my current guidelines by doing this.

What if I didn’t take him to a PPCI centre and this did turn out to be an MI? I would be hung out to dry!!

If I ended up in a ‘clinical variance committee’ meeting and I was judged by my peers, It would be highly likely that those who were giving their opinions would not know what I do about 12 Lead ECG interpretation, and all they would see was that there was ST Elevation and the LifePak 12`s Interpretation said Extensive Myocardial Infarction.

So, I did what I had to do, and transmitted the ECG to the PPCI Centre. When I spoke to them on the vehicle mobile phone I gave them my assessment and my interpretation of the ECG. The Nurse in charge went off to speak to the consultant then came back to the phone and stated that the consultant agreed with my interpretation and that I had to take the patient to the local A&E Department.

Which begs the question, why do I need to know so much more about 12 Lead ECG than what I teach others in the Paramedic training course our service runs?

I can definitely see the benefit in more education on detecting the more subtle findings of ‘borderline’ MI recognition and I have, on more than a few occasions, referred patients to PPCI who did not initially meet criteria for referral, but whose angiograms had gone on to show a blockage of a coronary artery. I guess you will never get fired for referring someone who wasn’t actually having an MI?

However, deciding that someone isn’t having an MI, even though their ECG makes it look like they are (to the untrained eye), and not referring them or transporting them, is a whole other ball game.

I am confident with my interpretation abilities, and I have yet to be caught out (even though I know it is only a matter of time), but I will still continue to transmit the ECGs to the PPCI centres for someone more senior and on a whole lot more pay than I get, to make the final decision on transport and treatment of ?STEMI Mimics.

Does that mean that I don’t need the level of knowledge that I have?

Maybe…..But I am an ECG Geek and I just always want to know more and more?

What are your thoughts?

Would you ever decide to not transport or refer someone who ‘by the book’ meets criteria even though you know it is a STEMI Mimic?

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Responses

  1. Which begs the question, why do I need to know so much more about 12 Lead ECG than what I teach others in the Paramedic training course our service runs?because there's nothing wrong with learning as much as you can.Would you ever decide to not transport or refer someone who ‘by the book’ meets criteria even though you know it is a STEMI Mimic?i'd do the same thing you did – ask something higher up for permission to not go to cath lab, because just like you said, some call review committee will hang the medic out to dry.

  2. Which begs the question, why do I need to know so much more about 12 Lead ECG than what I teach others in the Paramedic training course our service runs?because there's nothing wrong with learning as much as you can.Would you ever decide to not transport or refer someone who ‘by the book’ meets criteria even though you know it is a STEMI Mimic?i'd do the same thing you did – ask something higher up for permission to not go to cath lab, because just like you said, some call review committee will hang the medic out to dry.

  3. I believe the mantra is treat the patient not the ECG. I do hope the LifePak 15's are better at this kind of thing…I have numerous ECG's with large MI warnings over them despite thefact that the patient was not infarcting!

  4. One of the biggest things that I was looking for was reciprocal change. There is no depression that I could see on the 12-lead… Now I know that is not an absolute, but that sends off the 'warning bell' in my mind more than simply elevation alone. I'd also like to have seen the 15-lead on this patient as well. For the time (or lack of) that placing V4R, V8 & V9 takes, I've gotten into the habit that if the patient gets a 12-lead (practically everybody), then they are going to receive a 15-lead. What's three more electrodes? Possibly a lot. I completely agree with burnedoutmedic; learning as much as you can about cardiology and 12-leads in particular can really open your eyes about an otherwise possibly unremarkable patient. (It helps that your cardiology teacher spent years on the CCU floor learning ECG intricacies.Stovelegs

  5. The one good thing about working in an almost urban area, every facility that we transport to, except 1 (which we rarely go there as it is), is a STEMI receiving facility. So no matter which way we go, they are going to have it ruled in or out by the ED MD

  6. Hmmmm, I do love a good cardiac query. Let me start with going back to the 12 lead for moment. I can understand the difficulty in deciding between BER and LVH for this patient (and I can only assume it's quite possible that the pt presented with both). As the 12 lead shows qualities of both. Let me explain why BER shot into my mind immediately, and why I still stand by BER as the correct answer. First, yes, the large voltage QRS is typically LVH. However, BER is also known for having a fairly good sized QRS. Second, while it is possible to see ST elevation with LVH (thus why it's often taught as a mimic), in my field experience LVH has rarely shown with ST elevation in contiguous leads. On the other hand, BER is notorious for looking like a STEMI with the elevation in contiguous leads.Third, what really sold it as BER as opposed to LVH was the ST segment. The 12 lead appeared to show less of the “strain” that typically shows with LVH (http://www.learntheheart.com/LVH-Repol.jpg) and more of the “j-hook/happyface” of BER (I know it's difficult to see on the ECG from the case in question… but look at v3 and v4. Also check the diagram above showing BER vs STEMI). Also, even though it was possible to be a STEMI, the patient age has me looking elsewhere. Although, I would have liked to have known med and family hx as well as what the pt was doing at the time he fell. I wonder this as the highest risk group for BER is young black males. And usually it presents itself during or just after physical activity. Now onto treatment. I say you prepare for your standard CP protocols. IV, O2, continuous monitor and I'd even go so far as to go ahead and give ASA (c'mon, we do have ECG abnormalities in the presence of possible syncope after all). I would however hold off on NTG or morphine as at this time the patient is not experiencing any pain, discomfort, pressure or SOB. Obviously if CP or pressure begins during transport, then we get NTG as well as immediate repeat 12 lead (I'd do 2 or 3 more anyway) and vitals.Now on the topic of transport. For most people who work or live in a large metropolitan area (at least in the states anyway) this is really a non issue. As there are usually several PCI hospitals close by.However, if you are in a system where the closest hospital and the PCI are far apart, then it's gonna come down to your training, your protocols and your med control (and of course pt consent). In most places I have worked for, we would without doubt go to a PCI, mainly as just a CYA. Even if we called med control, it wouldn't be believed that we could tell a difference and we'd be told to go to a cath available hospital. However I did once have a chance to work for a system that trained and trusted it's medics. Us, our medical director and the local cardiologists where all pretty much on the same page. We were trained and grilled on CP, 12 leads and STEMI. We had an almost 98% accuracy rating for spotting STEMI. And up too and including the time when I was there, all the ones that were incorrectly diagnosed were 12 leads that we believed to STEMI that were actually impostures. What does that mean? It means that of all the 12 lead ECGs that were performed in the system before and during my time there, we did not misdiagnose a STEMI in the field as something else.. Yes, I'm proud of that,so yes I'm bragging a bit. Has that changed since? I'm unsure. I am however sure that they maintain that same high percentage rate. Why? because of training. The reason I mention all that, is because of our training and track record we had the ability to make the decisions on where to transport. We were also one of the first systems (at least in Texas) to be able to activate a cath lab from the patients home or scene of call. And in this case, depending on the scene location, we could have transported to the local (non PCI) hospital. And as long as I was correct in my reasoning, my medical director and education board would have stood behind me, even if it meant putting an uppity ER doc in his place cause he was mad we brought him a chest pain. And of course, if later blood work showed any cardiac complications (such as elevated Triponin) we would transfer that patient over to the PCI. Just a quick side note. I know I probably scared a few people with that crazy word “diagnose”. I know most of us who have been doing this for any decent amount of time were always taught “paramedics do not diagnose”. Well I'm here to tell you that is an antiquated way of thinking, that it is at least being tempered even at the education level. We hide behind the “I'm just following what protocol says” way to much. Guess what, if someone tells you their chest hurts, left side, 8/10 crushing pain, it radiates down their arm and they are nauseated, you're gonna form an opinion. Say you then do a 12 lead and it shows ST elevation in II, III and AvF. Now you say, “ohh, we have an inferior STEMI”, and you follow a treatment pattern based off that. Guess what? You just diagnosed a problem. I like to call it field diagnosis, just to soften the blow. But no matter how you look at it, you are forming a hypothesis based on clues given to you by the patient, then treating bases off that. (Even if our treatments are us just following protocols, our assessment led us to the right one to use). And maybe it's just me, but I'd sure as hell rather say I made a field diagnosis then “ahh, hell I just guessed”. :-)Ok, stepping off soapbox now.

  7. Hmmmm, I do love a good cardiac query. Let me start with going back to the 12 lead for moment. I can understand the difficulty in deciding between BER and LVH for this patient (and I can only assume it's quite possible that the pt presented with both). As the 12 lead shows qualities of both. Let me explain why BER shot into my mind immediately, and why I still stand by BER as the correct answer. First, yes, the large voltage QRS is typically LVH. However, BER is also known for having a fairly good sized QRS. Second, while it is possible to see ST elevation with LVH (thus why it's often taught as a mimic), in my field experience LVH has rarely shown with ST elevation in contiguous leads. On the other hand, BER is notorious for looking like a STEMI with the elevation in contiguous leads.Third, what really sold it as BER as opposed to LVH was the ST segment. The 12 lead appeared to show less of the “strain” that typically shows with LVH (http://www.learntheheart.com/LVH-Repol.jpg) and more of the “j-hook/happyface” of BER (I know it's difficult to see on the ECG from the case in question… but look at v3 and v4. Also check the diagram above showing BER vs STEMI). Also, even though it was possible to be a STEMI, the patient age has me looking elsewhere. Although, I would have liked to have known med and family hx as well as what the pt was doing at the time he fell. I wonder this as the highest risk group for BER is young black males. And usually it presents itself during or just after physical activity. Now onto treatment. I say you prepare for your standard CP protocols. IV, O2, continuous monitor and I'd even go so far as to go ahead and give ASA (c'mon, we do have ECG abnormalities in the presence of possible syncope after all). I would however hold off on NTG or morphine as at this time the patient is not experiencing any pain, discomfort, pressure or SOB. Obviously if CP or pressure begins during transport, then we get NTG as well as immediate repeat 12 lead (I'd do 2 or 3 more anyway) and vitals.Now on the topic of transport. For most people who work or live in a large metropolitan area (at least in the states anyway) this is really a non issue. As there are usually several PCI hospitals close by.However, if you are in a system where the closest hospital and the PCI are far apart, then it's gonna come down to your training, your protocols and your med control (and of course pt consent). In most places I have worked for, we would without doubt go to a PCI, mainly as just a CYA. Even if we called med control, it wouldn't be believed that we could tell a difference and we'd be told to go to a cath available hospital. However I did once have a chance to work for a system that trained and trusted it's medics. Us, our medical director and the local cardiologists where all pretty much on the same page. We were trained and grilled on CP, 12 leads and STEMI. We had an almost 98% accuracy rating for spotting STEMI. And up too and including the time when I was there, all the ones that were incorrectly diagnosed were 12 leads that we believed to STEMI that were actually impostures. What does that mean? It means that of all the 12 lead ECGs that were performed in the system before and during my time there, we did not misdiagnose a STEMI in the field as something else.. Yes, I'm proud of that,so yes I'm bragging a bit. Has that changed since? I'm unsure. I am however sure that they maintain that same high percentage rate. Why? because of training. The reason I mention all that, is because of our training and track record we had the ability to make the decisions on where to transport. We were also one of the first systems (at least in Texas) to be able to activate a cath lab from the patients home or scene of call. And in this case, depending on the scene location, we could have transported to the local (non PCI) hospital. And as long as I was correct in my reasoning, my medical director and education board would have stood behind me, even if it meant putting an uppity ER doc in his place cause he was mad we brought him a chest pain. And of course, if later blood work showed any cardiac complications (such as elevated Triponin) we would transfer that patient over to the PCI. Just a quick side note. I know I probably scared a few people with that crazy word “diagnose”. I know most of us who have been doing this for any decent amount of time were always taught “paramedics do not diagnose”. Well I'm here to tell you that is an antiquated way of thinking, that it is at least being tempered even at the education level. We hide behind the “I'm just following what protocol says” way to much. Guess what, if someone tells you their chest hurts, left side, 8/10 crushing pain, it radiates down their arm and they are nauseated, you're gonna form an opinion. Say you then do a 12 lead and it shows ST elevation in II, III and AvF. Now you say, “ohh, we have an inferior STEMI”, and you follow a treatment pattern based off that. Guess what? You just diagnosed a problem. I like to call it field diagnosis, just to soften the blow. But no matter how you look at it, you are forming a hypothesis based on clues given to you by the patient, then treating bases off that. (Even if our treatments are us just following protocols, our assessment led us to the right one to use). And maybe it's just me, but I'd sure as hell rather say I made a field diagnosis then “ahh, hell I just guessed”. :-)Ok, stepping off soapbox now.

  8. I thought high take off and perhaps a little cynical of me (which is going to get me into trouble one day for sure)!! had this patient been taking any weed? or perhaps NSAID? but I would always advise to take them to hospital for a check.

  9. I thought high take off and perhaps a little cynical of me (which is going to get me into trouble one day for sure)!! had this patient been taking any weed? or perhaps NSAID? but I would always advise to take them to hospital for a check.

  10. You should always learn as much as you can. My service does not have telemetry (we cannot transmit ECG for physician interpretation). When I started out as a medic, I brought one patient that had a similar tracing, but I did not know the difference between early repolarization & STEMI. This was not taught in my class. I did what my protocols said I should & transported to an appropriate ER. The Doc took one look at the ECG and dismissed the ST elevation as not am MI. I felt like a fool. I still struggle with the fine points of ECG (LVH, Axis determination etc.) but I review the educational material as often as time allows. The destination of the patient is my choice and it is my butt if I get it wrong. I have become better, but I am not as comfortable with some aspects (and I am not always sure that I am correct) of interpretation.I will continue to read and learn as much as my brain will hold. I will also teach what I know to anyone who wants to learn. I found that when my peers ask questions I learn more than just by reading.

  11. Hey, the nuances of ECGs can be very difficult to read. Thus why part one of this topic had dozens of different people (both here and on the JEMS fb site) posting different ideas as to what it was, with explanation. Hell, if it was easy their wouldn't be need for cardiologists. With that being said, I've taken at least one ECG every year since getting my medic cert, plus I do a lot of reading/studying on my own. And I still struggle with some points of ECG reading. Me and axis deviation don't get along. I learn it…. then I forget it. It's a vicious circle. All we can do is keep studying and keep practicing.

  12. You should always learn as much as you can. My service does not have telemetry (we cannot transmit ECG for physician interpretation). When I started out as a medic, I brought one patient that had a similar tracing, but I did not know the difference between early repolarization & STEMI. This was not taught in my class. I did what my protocols said I should & transported to an appropriate ER. The Doc took one look at the ECG and dismissed the ST elevation as not am MI. I felt like a fool. I still struggle with the fine points of ECG (LVH, Axis determination etc.) but I review the educational material as often as time allows. The destination of the patient is my choice and it is my butt if I get it wrong. I have become better, but I am not as comfortable with some aspects (and I am not always sure that I am correct) of interpretation.I will continue to read and learn as much as my brain will hold. I will also teach what I know to anyone who wants to learn. I found that when my peers ask questions I learn more than just by reading.

  13. Hey, the nuances of ECGs can be very difficult to read. Thus why part one of this topic had dozens of different people (both here and on the JEMS fb site) posting different ideas as to what it was, with explanation. Hell, if it was easy their wouldn't be need for cardiologists. With that being said, I've taken at least one ECG every year since getting my medic cert, plus I do a lot of reading/studying on my own. And I still struggle with some points of ECG reading. Me and axis deviation don't get along. I learn it…. then I forget it. It's a vicious circle. All we can do is keep studying and keep practicing.

  14. Machine generated interpretations are always suspect. The algorithms are just not as adept as the human eye and mind at understanding what it being seen. One must consider the entire clinical package and not just the ECG. Some commenters seem to have missed that point. A “silent” MI is not the same as a “symptomless” MI, although I know a lot of people who think it is. Silent means that there is no chest pain and that that symptoms might be subtle, but they are there. So called silent MIs are found more often on elderly patients where the presenting symptoms might be things such as unexplained syncope, dyspnea, with or without exertion, and even general malaise that can span several days. Take the entire patient into consideration and don't focus on the ECG. Get used to the fact that you are going to miss one here and there. Really, the hospitals have something like a 6% miss rate for MIs. The difference is, at least in the US, we are STILL taking the patient to the hospital (given that they are willing) and that it is likely that the hospital will pick it up using their higher level of training and much more sophisticated technology. Still my experience is that we're the first line of defense for MI patients. A former medical director always opined that he was amazed at the number of MIs we picked up early on even though the ST segment changes hadn't manifested themselves yet. In his opinion, we were seeing the very earliest changes, ones that didn't fall within the criteria for STEMI. We were not only seeing them, but in most cases we were treating them appropriately even though it wasn't quite within protocol. All of which he supported when other doctors questioned our approach. One story to illustrate that doctors aren't always right. Back in the mid 1990s when we were doing 12 Leads using the LP-10 with single channel adapter, my partner and I had a 42 year old patient with chest pain and dyspnea x 2 days. He also had a prior MI history. Our 12 Lead showed global ECG changes, and he had the signs and symptoms that supported that. Diaphoretic, hypotension, pale, crappy looking. We took him to his ED of choice, which was about five minutes away. We brought the patient in along with the 12 lead strip. The attending physician looked at the strip and pooh poohed our interpretation. “Clearly you boys have mistaken early repolarization for a Global MI.” At the time we got follow up letters from the EDs when we did 12 leads, because we had yet to convince them that our interpretations were correct and they wanted to give us feedback. Two days later we got the letter, which stated that he had had a Global MI with near complete occlusion of the LCA and RCA. He was stented and put on the transplant list due the the amount of damage. Sometimes even Harvard trained doctors get it wrong. 🙂

  15. I'll add something for the more advanced interpreters out there.A rule that has a high specificity in determining benign early repolarization vs. anterior MI is:Per Dr. Smith:If the mean R-wave amplitude in V2 – V4 is > 5mm, BER is highly more likely. This is not conclusive, but take everything into account, including ST-morphology, symptomology, and risk factors.Also, as Tom B. has been advocating, it is better to identify strain pattern than LVH or RVH. After identifying strain pattern enough times, you will never mistake it again. The precordial amplitude rule (ie. S in v1/v2 + R in v5/v6) is not conclusive… there are amplitude rules for the limb leads (Lead I, aVL, & aVF to be exact). This isn't important, however, if you can identify the strain pattern– so says Tom, and I agree.

  16. Mark – Unfortunately I'm getting ready for a vacation so I don't have as much time to devote to this discussion as I would prefer. However, I would like to clarify a couple of points, as left ventricular hypertrophy is a critically important STE-mimic and it's clear our understanding of how to differentiate it from STEMI is far too incomplete.First, on the issue of upward concavity of the ST-segments (smiley face) vs. upward convexity, straight, or non-concave (frown) it's true that upward concavity favors an STE-mimic, but it's not a specific finding for an STE-mimic; nor is upward concavity specific for acute STEMI in the presence of left ventricular hypertrophy.Sorry to confuse the issue, but opinions on this matter have evolved over the past year and a half, in large part due to the work of Stephen Smith from Dr. Smith's ECG Blog. Consider these excerpts from an email exchange I had with him on the EKG Club after I posted “Left ventricular hypertrophy – Part I” (http://ems12lead.blogspot.com/2009/08/left-vent…)http://health.dir.groups.yahoo.com/group/ekg_cl…“You might point out that, frequently, the ST elevation in LVH is NOT upwardly concave but upwardly convex. Furthermore, it is extremely rare to find an example of profound LVH in the precordial leads in the presence of acute anterior STEMI. I have seen this once. I attempted to study it, but could not find examples of LVH with STEMI. Why is this? I found some examples of patients whose previous EKGs showed LVH with anterior ST elevation who later had LAD occlusion. The MI itself changed the voltage drastically so that it no longer looked like LVH…If anyone has an example of profound LVH with very deep S-waves and simultaneous proven LAD occlusion, I would like to see an example!”http://health.dir.groups.yahoo.com/group/ekg_cl…“Because that study (Brady et. al., Electrocardiographic ST-segment elevation: the diagnosis of acute myocardial infarction by morphological analysis of the ST segment. Acad Emerg Med 2001; 8(10): 961-7) did not break down STEMIs into anterior and inferior and lateral, and because Kosuge had shown that many LAD occlusions have upward concavity, I repeated the study for LAD occlusions only. See attached, I think you'll find it interesting. I found that a large percentage of patients with LAD occlusion had upward concavity in all leads V2-V6 (poor specificity of the finding)…In Brady's study, there were not a lot of LVH patients with anterior ST elevation…I have seen many cases of LVH with ST elevation and upward convexity… Attached is an example with upward convexity in V3 and V4. Remember that Brady defined upward concavity as upward concavity in all leads V2-V6…I have seen one case (in my 22 year career of EKG specialization) of profound LVH with repolarization abnormalities that had ST elevation that was due to LAD occlusion, not due to LVH (see case 22-6, lead V4, in my book The ECG in Acute MI). If you have others, send them to me. I'll believe it when I see it. But there is no literature on this. Brady's study does not address this issue. There is no study in my 1800 strong file of EKG studies that does…So, to summarize and clarify, upward convexity with a normal QRS is almost always bad (although I could show you many contrary examples of Early repol with upward convexity). But upward convexity in the presence of profound LVH is usually not bad.”He also provided this example:http://groups.yahoo.com/group/ekg_club/attachme…So I think we have to take ST-elevation in the right precordial leads (V1-V3) with a big grain of salt when the S-waves are deep, and depend on other findings like reciprocal changes (being careful not to mistake a strain pattern in the high laterals as reciprocal changes) and most importantly, changes on serially obtained ECGs.Incidentally, I found a couple of ECGs that are similar to yours in Garcia and Holtz. They also struggled with whether or not it showed BER or LVH (perhaps a Hurst “type 2” strain) but they seemed pretty sure it was a STE-mimic as it was in the “good” column. More on this when I've had time to do a little more research! Thanks for the great case!Tom

  17. Mark – Unfortunately I'm getting ready for a vacation so I don't have as much time to devote to this discussion as I would prefer. However, I would like to clarify a couple of points, as left ventricular hypertrophy is a critically important STE-mimic and it's clear our understanding of how to differentiate it from STEMI is far too incomplete.First, on the issue of upward concavity of the ST-segments (smiley face) vs. upward convexity, straight, or non-concave (frown) it's true that upward concavity favors an STE-mimic, but it's not a specific finding for an STE-mimic; nor is upward concavity specific for acute STEMI in the presence of left ventricular hypertrophy.Sorry to confuse the issue, but opinions on this matter have evolved over the past year and a half, in large part due to the work of Stephen Smith from Dr. Smith's ECG Blog. Consider these excerpts from an email exchange I had with him on the EKG Club after I posted “Left ventricular hypertrophy – Part I” (http://ems12lead.blogspot.com/2009/08/left-vent…)http://health.dir.groups.yahoo.com/group/ekg_cl…“You might point out that, frequently, the ST elevation in LVH is NOT upwardly concave but upwardly convex. Furthermore, it is extremely rare to find an example of profound LVH in the precordial leads in the presence of acute anterior STEMI. I have seen this once. I attempted to study it, but could not find examples of LVH with STEMI. Why is this? I found some examples of patients whose previous EKGs showed LVH with anterior ST elevation who later had LAD occlusion. The MI itself changed the voltage drastically so that it no longer looked like LVH…If anyone has an example of profound LVH with very deep S-waves and simultaneous proven LAD occlusion, I would like to see an example!”http://health.dir.groups.yahoo.com/group/ekg_cl…“Because that study (Brady et. al., Electrocardiographic ST-segment elevation: the diagnosis of acute myocardial infarction by morphological analysis of the ST segment. Acad Emerg Med 2001; 8(10): 961-7) did not break down STEMIs into anterior and inferior and lateral, and because Kosuge had shown that many LAD occlusions have upward concavity, I repeated the study for LAD occlusions only. See attached, I think you'll find it interesting. I found that a large percentage of patients with LAD occlusion had upward concavity in all leads V2-V6 (poor specificity of the finding)…In Brady's study, there were not a lot of LVH patients with anterior ST elevation…I have seen many cases of LVH with ST elevation and upward convexity… Attached is an example with upward convexity in V3 and V4. Remember that Brady defined upward concavity as upward concavity in all leads V2-V6…I have seen one case (in my 22 year career of EKG specialization) of profound LVH with repolarization abnormalities that had ST elevation that was due to LAD occlusion, not due to LVH (see case 22-6, lead V4, in my book The ECG in Acute MI). If you have others, send them to me. I'll believe it when I see it. But there is no literature on this. Brady's study does not address this issue. There is no study in my 1800 strong file of EKG studies that does…So, to summarize and clarify, upward convexity with a normal QRS is almost always bad (although I could show you many contrary examples of Early repol with upward convexity). But upward convexity in the presence of profound LVH is usually not bad.”He also provided this example:http://groups.yahoo.com/group/ekg_club/attachme…So I think we have to take ST-elevation in the right precordial leads (V1-V3) with a big grain of salt when the S-waves are deep, and depend on other findings like reciprocal changes (being careful not to mistake a strain pattern in the high laterals as reciprocal changes) and most importantly, changes on serially obtained ECGs.Incidentally, I found a couple of ECGs that are similar to yours in Garcia and Holtz. They also struggled with whether or not it showed BER or LVH (perhaps a Hurst “type 2” strain) but they seemed pretty sure it was a STE-mimic as it was in the “good” column. More on this when I've had time to do a little more research! Thanks for the great case!Tom

  18. […] week we discuss ECG’s and a recent Case Mark Glencorse had, EMS Research and Delaying […]

  19. Back in the day before all the new ECG monitors with interpretation came out we would use MCL 1 through MCL6 to help dx MI along with the limb leads. We would make the dxs ourselves out in the field and call it in as an MI if it was– to the ER. Then all these new ECGs came out which is great but they took the art of interpretation out of it. Then the ER started demanding that we fax the 12-lead for them to alert the Cath Lab. Of course paramedics were outraged that the ER did not trust us to make that determination in the field. Well as I have gotten older and less egotistical I have come to realize that if I do my job, get a good clear 12-lead and send it to the hospital I have done my job and done what is right for the patient. I still like to make the interpretation for MI myself and tell the ER what I am thinking but ultimately it is up to the ER Doc to alert the Cath Lab not I.

  20. Back in the day before all the new ECG monitors with interpretation came out we would use MCL 1 through MCL6 to help dx MI along with the limb leads. We would make the dxs ourselves out in the field and call it in as an MI if it was– to the ER. Then all these new ECGs came out which is great but they took the art of interpretation out of it. Then the ER started demanding that we fax the 12-lead for them to alert the Cath Lab. Of course paramedics were outraged that the ER did not trust us to make that determination in the field. Well as I have gotten older and less egotistical I have come to realize that if I do my job, get a good clear 12-lead and send it to the hospital I have done my job and done what is right for the patient. I still like to make the interpretation for MI myself and tell the ER what I am thinking but ultimately it is up to the ER Doc to alert the Cath Lab not I.


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