Transcription
So, I want to talk today about an important topic as cardiologists. One of the most important calls we get is uh from the emergency room regarding EKGs and assessing whether it is a STEMI or not. So, I will show a lot of cases regarding that particular topic. Okay. Um, I have enough cases to cover over two hours, but I'll split them in half. So, I will give some today and some at another time. Hopefully, I will give some didactics, but it's mostly cases. I will start with some definitions we all need to know.
The cutoffs that are used in the guidelines in the universal definition of MI for what we call significant ST elevation, they use ST elevation of over two millimeters in men or 1.5 millimeters in women in leads V2 through V3, where it's almost where it is universal and normal to have some degree of ST elevation. So, they use 2 and 1.5 millimeters in those leads, and they use one millimeter in the other leads. The most important thing to realize is that it has to be a shape consistent with ischemic ST elevation; it's not just about the height of the ST; the shape is important as well. And they use for the posterior leads V7, V9, the cutoff is 0.5 millimeters, and I will explain why in a second. They also use isolated or most prominent ST depression in leads V1 through V3 of over half a millimeter as also a STEMI equivalent, as a true posterior STEMI equivalent. So, even if you don't have any ST elevation, you have ST depression in those leads, whether diffused, but even if it's diffused, but most pronounced in these V1 through V3, it's considered a true posterior STEMI. So, all those qualify for emergency perfusion, including with lytics if needed.
This is why V7-V9, we use a lower cutoff because V7 through V9 leads are further away from the heart than the anterior leads. So, if you have a posterior infarct, the ST elevation may not be as high because it gets attenuated through the posterior mediastinal and lung transmission. So, we use a lower cutoff. Similarly, we use a lower cutoff for ST depression in the anterior leads when we're defining posterior impact. ST depression of half a millimeter in V1 through V3 is considered significant, and this is because normally you have a little bit of ST elevation in V1 through V3. So, any ST depression in those leads is significant. The more important thing to me, in my opinion, is this: I mentioned to you cutoffs, but what's more important is that lesser ST elevation, lesser than those cutoff in the right context, may still imply injury and qualify for emergency perfusion, usually PCI. You cannot qualify for lytics if you're below those cutoffs, but you can qualify for emergent PCI below those cutoffs if you have the proper morphology and shape. Conversely, ST elevation over one to two millimeters is frequently not a STEMI; it could be pericarditis, early repolarization, or LVH, left bundle branch block. So, it's very important to focus on the shape.
This is an example of a posterior infarct. Look here how you have isolated ST depression in leads V1 through V3. Look at this. This is another case, also isolated ST depression in V1 through V4 in this case, with the pronounced R wave and an upright T wave. That's a classic morphology: pronounced R, ST depression, upright T, isolated to V1, V3, up to V4, or most pronounced in those leads, typically in those patients you will have some subtle ST elevation somewhere else, like you have it here in AVL, you have it here in an inferior lead III, and this is the V7-V9. In those patients, you have subtle, probably half a millimeter ST elevation in V7 through V9 that shows you again, use lower cutoff for V7 through V9 ST elevation.
Now, how to measure ST deviation? ST deviation is usually measured at the J point and is referenced against the TP segment. This is according to the ACC EKG guidelines. However, some authors, including the Chao textbook, prefer measuring the ST deviation one box, one to two boxes past the J point, at the point when all myocardial fibers are expected to have reached the same level of membrane potential and to form an isoelectric segment. So, there is an exception. How do you reference the ST segment in case of sinus tachycardia? During sinus tachycardia, P wave amplitude increases, and the negative atrial repolarization increases as well. This negative atrial repolarization causes the PR segment to depress, and in fact, sinus tachycardia is a cause of PR depression, and it causes that PR segment to also extend all the way to the initial portion of the ST segment and causes that initial portion of the ST segment to depress. This is what we call junctional ST depression. It is driven by atrial repolarization, not by abnormal ventricular repolarization or by ischemia. It's a fake form of ST segment depression. That's why in this case, it's better to reference the ST segment and the J point to the PR rather than to the TP segment. Referencing the J point to the PR segment, so referencing the ST depression to the PR segment mitigates the effect of atrial repolarization on the ST segment, as they are both affected by atrial repolarization. Referencing it to it neutralizes its effect. Conversely, if you reference the ST segment and the J point to the TP, you'll end up with a fake ST segment depression that is purely driven by atrial repolarization. This is an example here. You have PR depression and junctional upsloping ST segment depression. Don't reference to the TP; reference to that PR point.
I will start now with the more important part of the talk, which is cases. So, this is a patient who's, this is a 60-year-old lady who's having chest pain on the floor, and she has metastatic lung cancer. What is the diagnosis? You know, think about it and think what it could be. I think it's most likely pericarditis because there's diffuse ST elevations in all the leads, inferior and precordial leads, and she probably has some kind of even effusion in her, um, pericardial effusion from the metastatic cancer. Okay. That's uh that answer was actually the answer that the cardiologist was consulted on this patient provided. He considered it pericarditis related to metastatic lung cancer and pericardial effusion, and he thought, well, why is the QRS is very low? You have diffusely low QRS voltage. So, he thought it's pericardial effusion causing the low voltage with pericarditis causing the ST elevation. Unfortunately, that is not the right answer, and a few hours later or a couple of hours later when the troponin came up, came up to 100, then they realized this is not pericarditis. Now, when I looked at it, this to me, and you need to realize it, this is 100 percent not pericarditis; this is 100 percent STEMI. It has several features of STEMI. The most important feature to me is looking at lead V2, V3, but especially all of them, but especially lead V2. You have an ST elevation that is fused with the T in a domed fashion. So, ST and T are forming one dome, it convex dome; the ST is convex and forming one dome with the T, plus the QRS is shrunk so much so that the STT dome is bigger than the QRS. Whenever you have this, a domed STT with a shrunk or shrinking QRS, and STT exceeds or approximates the QRS, this is STEMI; this is not pericarditis. Same thing is happening here: the STT is exceeding the size of QRS; QRS is shrinking with an R wave; it's being pulled up. This is very characteristic of STEMI. This shape here, this shape here as well. Okay. So, this morphology is very important to realize. This is what we call, this has a name; what you see here, this is what we call the tombstone. Okay. And actually, if you look at older EKGs on this lady, look how her QRS was. Now, her QRS is being shrunk. During STEMI, we know that you form Q waves, but before, before you form Q waves, as a first step before Q waves, you get shrinking of the QRS as that area loses its electrical activation. You start having shrinking QRS before you form a full-blown Q wave. Later on, this is a full-blown Q wave; this is a shrinking QRS. So, shrinking QRS, sometimes with a pulled R wave, as you can see here, and with a domed STT that exceeds the size of this or approximates it, is a definite STEMI. So, this is actually STEMI.
Now, another caveat of this is that some people, some people would say this is that a situation is too diffuse. I mean, in STEMI, you should have, or you, you usually have reciprocal ST depression. Well, my answer to this is actually it's not true. Mid-LAD occlusion causing apical infarct causes, causes diffuse ST elevation with no reciprocal changes. Actually, around 30 percent of anterior infarcts have no reciprocal ST depression. So, very important to know. One of the reasons is that the apex looks toward all the leads; the apex looks toward the anterior leads; it looks toward the inferior leads; it looks toward all the leads. So, an injury in the apex will cause diffuse ST elevation. Okay. Uh, and this is an illustration how when you have STEMI, you can start with a concave ST elevation, but eventually evolve into a convex ST elevation, a convex ST elevation that exceeds the size of the QRS that starts to shrink, and this is what we call the tombstone. You can put a cross here, and that becomes like a grave. So, this is the tombstone; it's the elevation. Eventually, you start getting deeper Q waves and more deep Q, and eventually ST elevation resolves, and the T will start inverting at some point as well before the ST fully subsides. Did everybody understand that? All the fellows, did you understand this? Anybody has a question regarding this? All right. So, and here are some criteria I want you to know. By the way, all those slides, cases are from my book, uh, or overwhelming they are from my book. So, this is how STEMI, you have five ST characteristics of STEMI. If you have any of them, it is usually enough to tell you it's STEMI; you don't need the five of them; any of them will tell you it's STEMI. So, one is the ST elevation is straight or convex upward, this thing, although it's not always like this, but it's most commonly like this, or it evolves into this. So, straight or convex upward, blends with T to form a dome like this. Second is wide upright T or or inverted T wave at some point. Third, of course, Q waves at some point. Fourth, and what we have here is this elevation or T wave that approximates or exceeds QRS height, plus or minus shrinking QRS, plus or minus shrinking QRS with a pulled-up R wave, as you see here. Okay. And the fifth is reciprocal ST depression.
Now, I want to highlight several ideas regarding reciprocal ST depression. Okay. As I said, you may not have reciprocal ST depression in apical infarct, and you frequently don't. A second idea related to that is you can have reciprocal ST depression without an infarct, such as in LVH or left bundle branch block. In LVH, you can get ST elevation opposite to QRS. So, you get ST elevation in leads V1 through V3. Here you see it, well, in lead V2 and V1, and you got ST depression where the QRS is upright. So, you see here ST depression. Okay. So, you do get reciprocal ST depression in LVH and left bundle branch block. You get ST elevation in V1 through V3; you get ST depression in V5, V6, and I, AVL. So, be careful when we talk about reciprocal ST depression. Okay. It's the least, it's the mo, is the one with the most pitfalls out of the five. This is a nice illustration also from my book that kind of summarizes the shapes. This is the STEMI shapes again, the dome STT, sometimes with the inversion, uh, distinguish it, distinguish it from pericarditis, which tends to be concave, and distinguish it from early repolarization, which is also concave with a sharp, well-demarcated J-point or notched J-point or slurred J-point.
I want to highlight another thing that could have been um confusing here. This patient has PR depression, right? It's, you know, there is a lot of artifact, but he definitely has PR depression. Look here, this is the P wave; this is the R; you definitely have PR depression compared to the TP segment. How come you have PR depression? I mean, that was another thing that confused the cardiologist. Can you have PR depression in MI? The answer is absolutely yes, and that's why I say so when I put the criteria here, pericarditis has PR depression over one millimeter, but as I said, having pericarditis feature with one STEMI feature makes it STEMI. STEMI always, you always favor diagnosis of STEMI if you have any STEMI feature, regardless of whether you have features of something else. In STEMI, it's not uncommon to have PR depression; it's atrial infarction; atrial infarction gives you PR depression, and that's what you're having here. Also, you can get pericardial irritation with a STEMI that can cause PR depression. So, we have a pronounced PR depression here, but this is not pericarditis. Okay.
This is another case. This is a 34-year-old female, obese, no other risk factors. She had chest pain for three hours, worse with supine position. This is her EKG. So, uh, you know, look at it when we, that I was called about this around 1 AM. All those are personal cases, by the way. So, I was called about this around 1 AM, and you know, there is ST elevation in V2 with concave ST segment. What do you think this is here? [Music] I think a reasonable first consideration is pericarditis; it can fit with pericarditis here. Okay. But there was something concerning to me: lead V2. You see that ST, it's not quite convex; it is concave, but the size of it is worrisome to me; the STT almost approximates the whole QRS. The same thing indeed V3. So, when I saw it, I was a little worried; I wasn't sure it's STEMI, but I was worried. So, what's the next step in this case? Is it another EKG? Exactly. That's the best answer. And am I at such a stage where it's questionable? It will evolve. You do an EKG five, ten minutes later; you may see changes that will help you. You can do an echo as well, but the quicker and better answer I think is repeat the EKG. So, we repeated the EKG 15 minutes later, and this is the EKG. Does this help you? What do you think now? Is it STEMI or pericarditis? It has that sort of almost Q wave, and yes, so STEMI, yes. Lead V3 is very helpful now. Lead V3 now has a clear-cut Q wave and it's a very small QRS overall with an ST elevation that is in this, at this point is straight upward. So, lead V3 suggests STEMI. Also, compare those two, the QRS in V2. QRS in V2 here, it's a shrinking QRS with a rising ST segment that exceeds the QRS in two leads now. This is a STEMI at this point. So, I took her to the, again, no clear reciprocal ST depression in this patient, but that was enough for me. So, I took her, and sorry, I have the still images; this is from my prior job; I only have the still images. This is right caudal, and this is an AP, or a, you know, a shallow area or cranial. So, at first look, uh, you know, one can look and see, well, the LAD looks good; the lady looks good here. Anybody can find something concerning on this? Here is the hint, you know, for if you're more experienced, you will tell that, is this really an LAD? You know, the this artery is going way too much to the border of the heart shadow. As I always teach fellows, the LAD should aim toward the center of the heart shadow in the standard views. So, this artery is aiming and twisting toward the border of the heart shadow. So, it made me question whether, whether this is truly an LAD. Okay. At the same time, I don't see anything feeling late; I don't see any stump anywhere. So, here's what I decided to do. I was still convinced this is not pericarditis, even though she's 34 with positional chest pain; that EKG was striking to me. So, that's why it's so important to understand those EKGs. So, I decided to do IVUS. I saw a hazy area here; I decided to do IVUS. Now, IVUS helped me a lot. After I wire an advanced catheter, here is what happened. I started to see a vessel emerge; we probably massaged the clotted area or a plaque here, and that somehow opened what was fully flush occluded LAD, and now I know what the diagnosis is. Yes, it is a totally occluded LAD, proximal LAD, flush occlusion acutely, and then I wired it, and I fixed it. So, again, that was a STEMI, and you know, it is so important to understand the EKG and not quit. Okay. All right, everybody understood this. And this is the same lady. Eventually, she formed those Q waves. Now she has, later on in her course after PCI, she had the full-blown STEMI EKG. Now you have deep Q waves; it's actually, if you look here, if magnum, it's a notched Q; it's a Q and then an upright, then a deep Q. Okay, it's an arched Q. So, we have EQ with diffuse subtle ST elevation at this point. Now, acute Q waves do not necessarily imply necrotic myocardium; part of it may be stunned. So, I wasn't, we don't worry about those Q waves that we see acutely, whether before or after reperfusion. The problem is persistent Q waves at one to six months when you see them back in clinic; they have a stronger prognostic value. Unfortunately, this lady at the couple of months of follow-up, she still had those deep Q waves, and the echo actually was consistent with that; she still had apical dyskinesis. So, the Q, the persistent Q waves correlate with poor outcome and poor recovery, not the acute Qs; that's important to know. Acute Q wave could be stunned myocardium.
This is another case. He's a 38-year-old man coming with chest pain radiating to the back of the neck. What's the diagnosis here? Is this a STEMI? Yes or no? Can this be pericarditis? All right, I'll answer it. So, here's the thing: this is actually pericarditis, and that's what's more interesting. This EKG is so much more subtle than that one, yet that one is pericarditis; the other one was a STEMI. So, here is why I can tell this is pericarditis: the morphology, it is concave in all leads; you have no Q wave in any lead; uh, you have no dome morphology or STT in any leads; and you have no shrinking QRS in any lead; you don't exceed STT in nowhere; it comes close to the size of the QRS. Okay. So, you don't have any of those five that I showed here; you have none of those. Okay. Furthermore, you have an elevation at the upper limit of what we call pericarditis. Pericarditis elevation never exceeds four or five millimeters; this patient is around five millimeters. So, he's really at the upper limit of ST elevation; that's the only concerning thing about him, but he has no STEMI features, and he has ST elevation up to five millimeters, especially here; it really touches five millimeters with PR depression, especially noticeable indeed AVF. Typically, PR depression, you see it best in lead II and V5, V6, typically. In this patient, we see it best in lead AVF. So, this is pericarditis. Now, do you get ST depression anywhere in pericarditis? You do. Typically, you very often get ST depression in lead AVR and often in lead V1. Here's the thing with pericarditis: pericarditis, you have ST elevation injury throughout the whole myocardium. Okay. Well, what is opposite to the, this is the vector of the polarization; this is the vector of ST elevation; the whole myocardium. Well, there are two leads that are opposite to the whole myocardium where you get ST depression, reciprocal ST depression: AVR and V1. On occasion, you may get ST depression as well in lead III and in lead AVL. Okay. So, you can get ST depression in pericarditis; you often do in AVR and V1; sometimes it needs III and AVL. So, that line III, AVL, V1 and AVR, you can get ST depression on all those, besides the ST depression in AVR because of that, again, the vector of repolarization is going this way; AVL is here, right? So, AVL can be depressed because it can be looking away, depending on the exact, on the exact vector, on the exact axis of that vector; AVL can be negative; ST can be negative, and it can be negative in lead III, which is here; the axis of lead III is like this, right?
I want to mention quickly this; I want to dwell on that. This is early repolarization, the third big type of ST elevation, actually the most common type of ST elevation, and here I'm showing the, the morphology. This is a classic morphology of early repolarization. You have a notched J-point in leads V5, V6 with a concave ST segment. You see that notched J-point; it's very important morphology; it almost forms a wave. There's another type of J-point that we don't see here, which is a slurred J-point, and then the well-demarcated J-point that you see in leads V3 and V2. So, you have a clear-cut J-point of some sort in early repolarization. Now, how do you distinguish early repolarization from pericarditis? They tend to have similar shapes to a degree, but here is the way you distinguish it. One, lead V1 can help because in early repolarization, sorry, in pericarditis, you tend to be depressed, whereas in early repolarization you may be elevated in lead V1. But the more important distinction is this: in early repolarization, you have more T, more big T than ST elevation. So, you have a bigger T, lesser ST elevation. In pericarditis, you have lesser T, more ST elevation. Okay. So, we have more ST elevation relative to the T height; so, STT ratio we call it, over 25 percent in leads II, V5, V6, whereas in early repolarization it's much more T than ST elevation. So, the ratio of ST to T is low. You understand? More T than ST in early repolarization; more ST than T in pericarditis, and that's kind of how you distinguish them the best way. Okay. Another thing, early repolarization, just know, of course, it's very common in young men, whether in V1 through V3 where it's extremely common and it's called normal male pattern, but also in the lateral and inferior leads, it is also fairly common in middle-age and older men, you know. And here's the slides; here is the statistics. So, even in the lateral and inferior leads, you can see early repolarization in five to ten percent of men who are 40 to 65 years of age, and you can see it in 20 to 40 percent of those men in the leads V1 through V3. So, you can see it in middle-age to older men. Even the only caveat, it is uncommon in women, older women especially; it is less common in women in general, two to four times less common, but particularly you take into account the age, older women, it's particularly uncommon. So, if you see older women with a, you know, early repolarization is really low on the list; have a higher threshold to calling it STEMI, as you know. It's also more common in African-Americans and in athletes. Okay. And it can be up to three millimeters; it's usually in the range of one to two millimeters, but it can be up to three millimeters. Uh, so this is a another example of early repolarization; it's an unusual early repolarization; this case I had it here in Iowa not long ago, uh, but that shows you the variety of repolarization. This is here what we, this is the J-point; look at that notch; nice J-point; well demarcated here; notched here; see the J-point here; uh, it is big, but guess what? It may be concerning in lead V2 because the STT may seem to approximate the QRS, but it's only in one lead at the transition between negative and upright QRS. I don't worry when I see those concerning features in one lead that is a transition lead because between going from negative QRS to upright QRS you can have a lead where the QRS is shrinking and where the STT exceeds it. So, it's not worrisome to me that EKG. This is not like uh that EKG. Okay. It's very different because this is more than just one transition lead; this one is just the transition lead. Okay. So, you have variety of shapes; also, early repolarization can be dynamic; it may be, in this patient, you get an EKG next day in a different position; make him stand up; you may get a different EKG. The interesting thing is it never evolved into
A malignant form. It doesn't. It never looks like a STEMI, but it can be variable. It can look dynamic, which can fool somebody who doesn't know earlier polarization well. This is another case. So this is a 32-year-old Black man with sharp chest pain and negative troponin. Anybody knows what's the diagnosis here? You can write in the chat box. Nobody wants to take a pic. What is this? Let's say, uh, is this a STEMI? No, it looks like uh maybe wellens. There's a biphasic T. Wait, okay, good point. It could be. Well, what I don't, I don't think it's a UA. Okay, that's good. Uh, it's not the right answer, but it's a good answer. I'll explain it. Anything else? Anything else that this is possible? All right, it is not Wellens, and I'll tell you why. So Wellens can give you that biphasic, that upsloping ST followed by a sharp inverted T wave in the precordial leads, particularly V2 through V4. Wellens, however, that is not associated with significant ST elevation. You get ST elevation up to one millimeter, not more. This ST elevation is more than you see with Wellens. So this would be either STEMI or something else. I wouldn't call it Wellens. Well, as you should not have significant ST elevation, so that's one reason I wouldn't call it one. Is this STEMI? You need to recognize this pattern. Extremely common, believe it or not, up to 10% of young Black men have this EKG. So that's how you need to know this. It's so, so common. This is what we call the earlier polarization pattern of young Black men. Okay, early representation pattern of young Black men, and it's extremely common. So look at it. So we have earlier polarization here in V2, V3. You see the ST elevation. V4, you have earlier polarization with a nicely notched J-point, or J-wave, even, you want to call it. Okay, but instead of having what I told you, you have an early polarization, big T wave. Instead of having a big T wave, you're having an inverted T, and that's the uh Black, the Black variant earlier polarization pattern where instead of an upright T wave, you can get a deeply inverted T wave. It is so common that the international and European guidelines for athlete screening EKG, athlete screening, they consider it worrisome to have the inversion anywhere beyond lead V2, or lead V2 and beyond in an athlete, in a white athlete, but in an African-American athlete, all the way to V4, it's not concerning. You start getting concerned when you have a deep T wave beyond V4. It's because of the recognition of this pattern. So they don't recommend any workup for such an EKG. And again, all that old paper from the 50s suggests that this is seen in up to 10% of young Black men. Uh, now what else could it have been? So it is not a STEMI. It is that earlier polarization variant, but what else could it have been? I want you to think of other things. You have a young man with this pattern. It's not STEMI. It could be early polarization, but what else could it be? You mentioned Wellens. I said it. I explained why it's not, but there are, there is another differential diagnosis of this ST inversion in V2 to V4. So HCM comes to mind. Exactly, yes, HCM, and another one. The one that is more like, I tell you this, if I tell you this is a white man and he has this EKG, what's another thing that's concerning? So HCM, there is another differential, the particular cardiomyopathy that is actually one of the most common causes of sudden death in athletes. ARVD. Exactly, ARVD. The most sensitive sign of ARVD is actually T inversion beyond the lead V2 in white, beyond the lead V4 in Black. So yes, so when you see this EKG, it is either the earlier polarization variant in a young Black man, or it could be HCM, or it could be ARVD. It could be Wellens if it is not that high, but it's otherwise it's the other two, ARVD, HCM, and the earlier polarization variant. Everybody understand? Understand that very, very common. You need to know it well. Another differential that could, you should think about when you see that, especially a young athlete, pre-participation EKG, is also Brugada. So beside the ones I mentioned, ARVD, HCM, Wellens, the STEMI, early polarization, and Brugada, except the shape doesn't fit. This is how the shape of Brugada is that ST elevation would be downsloping. Okay, would be downsloping, uh, ST elevation, coved ST elevation, not this shape. So that's the other differential. All right, I hope you understood that. I want to show another case. This is a patient, a 40-year-old man who's coming with chest pain. What's the diagnosis here? Is this? This is STEMI, inferior STEMI. So this EKG, at first look, uh, seems like STEMI. You have inferior ST elevation. Look, there is inferior acceleration, inferior Q waves. This Q wave, and it's a posterior, in fact, you get to pronounce R wave in V1 with ST depression. Where there is a catch, what you think is a Q wave is actually a negative delta wave. So you have a positive delta wave. Look at the PR here. Okay, there is the P is riding the QRS. They are almost fused, attached to each other, and here you have a negative delta wave. So you have the P attached to the QRS via a negative delta, which is which looks like a Q, a pseudo Q wave. Same here. This is not a Q, this is a delta, negative delta. You see a positive delta here and simultaneously a negative delta here. Okay, so this is not an inferior infarct. This is a just a pre-excited EKG with pseudo Q. And how, why do you have ST elevation? So in a pre-excitation, as in left bundle and and LVH, you get ST changes opposite to the delta wave. So you have negative delta here, you get ST elevation. You could have got ST depression here, but you didn't. You don't always get it with pre-excitation. It's not as consistent as left bundle branch block, but this is ST elevation secondary to the negative delta wave. This is another case, an interesting case. Did everybody understand the prior stuff? Do you have any questions? All right. This is another case. This is a 27-year-old man. He had V-fib arrest at home while playing a video, uh, video game. He was resuscitated by EMS, and this is his post-EKG. Okay, what does this look like? Is this a STEMI? It's okay, you don't have to be shy. You can, you can say it. It looks like it's STEMI. I would agree here. It looks like a STEMI, but there are some unusual features, uh, I mean the ST segment is elevated, but it is downsloping. It's elevated, but it's downsloping. The J point is elevated, but the ST is downsloping. It's still elevated, but downsloping. It's a hint. Then we repeated the EKG at the time he got to the hospital. This is in the ambulance, when at the time he got to the hospital, this is his EKG. What is, what do you think the diagnosis is here? I'll give you the answer. It's, it's hard for you. It is not uncommon, but it is hard for you. So on the 30-minute EKG, look what you see. You still see some J-point elevation. Look at the J-point. Okay, it is elevated compared to TP and PR, and it is notched, but it's interesting that the, the Q, the ST that comes after it is downsloping. It's almost scooped. You see here the J is elevated, but the ST is scooped down. Okay, maybe I have more. No, I don't. All right. This is a characteristic of what we call malignant earlier polarization. Is elevated J-point and downsloping ST elevation, scooped ST elevation. Okay, and this is what this patient had. Eventually we did rule out CAD. We did, we don't. Initially when I saw those two EKGs, I immediately recognized that this is most likely malignant earlier polarization. Uh, we, I did not cath him. We did eventually do CTA, which was normal. No coronary anomalies. We did cardiac MRI in order to rule out ARVD and sarcoidosis and structural disease causing cardiac arrests. He didn't have any of that. We did procainamide testing to elicit Brugada, that was negative. With the stress EKG to assess QT prolongation, that was negative as well, and to assess for CPVT, that was negative as well. So we ended up with a diagnosis of malignant earlier polarization. I want you to recognize that that pattern, malignant earlier polarization, is a case where the, it has several features. One, you have a J-point. It typically that is notched and fat, and it becomes particularly fat at the time you evolve into cardiac arrest. So this is this EKG with the fat J wave that gets fatter and causes ST, more pronounced ST elevation at the time of cardiac arrest. So just before cardiac arrest and just after it, you will see a much fatter J wave with ST elevation, but even at rest you will see typically a notched fat J-point with a downsloping ST segment. Segment. The J-point tends to be around two millimeters, not in this case, but it tends to be two millimeters or so, and it tends to be more pronounced in the inferior leads. Uh, it's really not relevant in somebody who's asymptomatic, simply because having features that are concerning for malignant early polarization in an asymptomatic patient means absolutely nothing. It is still a very common pattern in patients who are asymptomatic who never develop cardiac arrest. This pattern implies that you have two to three times higher risk of cardiac arrest than the standard earlier polarization. However, two to three times of something that is extremely minute remains very low. So if you have this pattern and you're asymptomatic, you don't do anything for those patients. Their risk of cardiac arrest in absolute value is only 0.07% higher per year than those who don't have this pattern. So just recognize it. Recognize malignant early polarization as a cause of V-fib arrest. Recognize that can mimic STEMI just after cardiac arrest, but also recognize you don't do anything for an asymptomatic patient. Also, I wanted to distinguish, since I'm talking a lot about J wave and J-points, distinguish the J-point from epsilon wave. They tend to be in the neighborhood. J-point is just at the junction between QRS and ST, and it can be, like I said, fat, notched, it could be slurred, or it could be a demarcated point. Epsilon wave, which you see in ARVD, is a little bit past the J-point. Okay, it's usually a twitch like this. It's a twitch a little bit past the J-point. It's really not a fat wave or a notch. It's more of a twitched past the J-point, and typically any ARVD, as I mentioned, the most sensitive feature is not epsilon, is the negative T wave in the precordial leads. This is another case again. I hope you're grabbing the patterns here, the EKG patterns. I hope you're understanding the, the, the shapes and morphologies. This is a 50-year-old man. He's coming with chest pain for two hours, which improves with nitroglycerin but did not resolve. Is this STEMI? I repeated the EKG, uh, maybe 20 minutes later or so, 15, 20 minutes later while we're waiting. We activated the cath lab already, but while we're waiting, I got another EKG. No ST elevation still. So I'll analyze the EKG. You have no ST elevation. You have diffuse, you have ST depression in the inferior and lateral leads, even pronounced ST depression. No ST elevation, but you have a very prominent peak and ample T wave in these V2 through V4 along with an upsloping ST depression of one to three millimeters. It's depressed at the J-point, one, two, three millimeters, and it's upsloping into the T wave. Okay, then you have ST depression of a different morphology in the other leads. This is an absolute ST depression. This is a standard ischemic ST depression morphology. Okay, you also have two-millimeter ST elevation in lead AVR. This is what we call the Winter sign, okay, or the Winter complex. What is the Winter, the Winter complex is an equivalent of ST of an anterior STEMI elevation. You just never develop an ST elevation. You just get upsloping ST depression with a very pronounced T wave. You never get an ST elevation, but it is exactly like a STEMI, and it is treated exactly like a STEMI. It's a perfect STEMI equivalent. You do get reciprocal ST depression with the Winter, as I've shown in the other cases. Okay, this patient was taken to the cath lab, and he had subtotal proximal LAD occlusion with TIMI 2 flow. This was treated with one drug-eluting stent. Okay, this is an EKG, uh, after PCI, and you can see a resolution of that upsloping ST depression and normalization of the reciprocal ST depression. Okay, so what is the, the Winter sign? Hyperacute T waves are very common. If you see somebody with a hyperacute chest pain before he developed an ST elevation, it's very common to see those. If you occlude an LAD and get an EKG, it's, that's the first sign you will see. The only difference is that normally that hyperacuity will evolve quickly into ST elevation within five to ten minutes. The Winter complex is that subgroup of patients who never evolve into ST elevation. They are stuck at that stage of hyperacute T wave with upsloping ST depression. Okay, so 2% of anterior infarction have a pattern of static persistent hyperacute T wave that do not evolve into an ST elevation over the course of an hour despite persistent LAD occlusion. Okay, this pattern is important to recognize as it implies an occluded LAD, as is, and is considered a STEMI equivalent, even though it does not progress to ST elevation. Why does this happen? It's thought that a small subgroup of people have a mutation of the potency potassium 880 phase channels, which are the channels that cause ST elevation in an acute infarct. Those channels abruptly open in an acute infarct, and they cause the voltage gradient that causes ST elevation in phase two of uh repolarization. Those patients are deficient in that channel; therefore, they never form ST elevation. That's one of the theories. There are other theories, but I want you to recognize that. Okay. All right, so, and, and the Winter is very different from Wellens. I will show Wellens at a later time. It's very different from Wellens. Wellens is not a STEMI, and it's not a STEMI equivalent. Actually highlighted a little earlier, you do not get an ST elevation more than one millimeter with Wellens. With the Wellens, you do not get Q waves with Wellens, unlike the Winter. It's very different. Keep that distinction. I will try to, uh, also show a couple of small things here. A patient presents with chest pain that started four hours previously, an inferior ST elevation. We gave him nitroglycerin, aspirin, and heparin. Both his chest pain and his elevation resolve. Okay, so he's doing well now. It is uh 10 p.m. Should you perform emergent cath on this patient? The answer is no. You do not need to take him emergently to the lab. So what happened? What's the diagnosis here? The diagnosis is spontaneous lysis of a thrombus. That's the most likely thrombosis. A less likely thrombosis is that he was having coronary vasospasm that resolved, but this is far less likely in my experience. It is far more likely to be thrombus that spontaneously lies. Now, when it spontaneously lyses and both the chest pain and ST elevation resolve, we call it a transient STEMI, and this happens in about 15% of STEMIs. We call it self-aborted STEMI if the CK remains very low. So it's a transient STEMI, and it a subgroup of transient STEMI is a self-aborted STEMI where your infarct is actually very small, meaning you abort it very quickly. A subgroup of that is the transient STEMI that is less than 20 minutes, and in this case, we don't even call it STEMI. We call it non-STEMI. If the ST elevation persists less than 20 minutes, in retrospect, we change the diagnosis to non-STEMI. Either way, any of those three, whether it's transient STEMI or its subgroups, self-aborted STEMI, and, and non-STEMI with transient elevation, none of those need emergent cath. This was based on that very important European trial called the transient STEMI. The randomized was patient to emergent cath versus waiting till next day, a mean 23 hours, and there was no difference in outcomes between weighting and emergent cath. And importantly, those patients had good prognosis, much better than the prognosis of patients who did not recanalize spontaneously and who are even though they were emergently reperfused. Okay, so they had good prognosis, smaller infarct size, and you could easily wait till next day. I'll show one more here, and then I will stop. Everybody understood that that idea? All right. One more thing I will show. This is a 61-year-old man with no significant past medical history. He developed this EKG at rest, and when the EMS arrived, he was awake, but he fully collapsed and developed PEA arrest while the EMS was at his home, and this was the EKG. What's the diagnosis here? You can put it in the chat box for those who are still here. You see that there is ST elevation. I hope you see ST elevation in leads V1 through V3 with the Q waves in V1, V2. Everybody sees that. Is this anterior STEMI? Can anybody, there saying yes or no? All right. Well, I will tell you this is not. Let's see. Somebody, somebody there saying something. Tyler said no. What's the diagnosis then, Tyler? All right. So it looks like an anterior STEMI. However, keep in mind he went into a PEA arrest. First diagnosis should be anterior STEMI, but the PEA arrest alludes to the second possible diagnosis in this patient, which is what can cause ST elevation in leads V1 through V3 that is not STEMI. You know that mimics STEMI without being STEMI. PE. Excellent. Was a lot. Great, great job. Yes. So PE can cause in a form of an RV infarct. Now, what does RV infarct give you? RV infarct gives you ST elevation. People think of ST elevation in the right precordial leads, V3R, V4R, but in fact, leads V1 and V2 are also right-sided leads. Okay, they overly the right heart. So when you have a right-sided infarct, you get ST elevation leads beyond V2. You do get Q waves in V1, V2, even V3. Okay, and this was the second differential diagnosis in this patient. Two hints allow, allow us to say this is PE, not uh, maybe not an anterior STEMI. Uh, so one, um, the progression, what we know is that PE tends, that an ST elevation that you get somehow tends to be fleeting. You repeat the EKG, that elevation may disappear, and that's what happened exactly in that case. Sorry, I don't have the EKG, but the next EKG showed right bundle branch block with no ST elevation. So that's one. Second, bedside echo in those cases is very important to distinguish, and the echo in this patient showed in between cardiac arrest. He was arresting off and on. In between cardiac arrest, he was having hyper contractile, shrunk small LV and massive RV. So that was the second hint. So much so that based simply on that EKG and the quick echo at the bedside, I gave him a bolus of TNK, based purely on that, and he actually hemodynamically improved. He stopped having cardiac arrest after the TNK bolus within about 15 minutes of the TNK bolus. Okay, so that's kind of the diagnosis here. Um, another hint. I want to ask you a question. In, in massive PE, what's the most common EKG finding? Anybody knows? So you can have ST elevation, V1, V2, V3, but there is something more common. Okay, true. What's the most common specific PE finding? So aside from sinus tachycardia, what's the most common? Because it's not specific. You can see it in any categories, any critical illness, any MI. What's the most common specific PE finding in a massive PE? Anybody? Let's see. Not right bundle branch block, no. And I'm going to tell you it's not S1Q3T3. S1Q3T3, uh, is an indicator of right-sided, it's an indicator that the whole cardiac depolarization is shifted toward the right heart, and that's why you get S1 and Q3. You know, Q is because the left heart is pushed up, but it's not that, neither right bundle nor S1Q3T3. Those are not. Yes. Deep T wave inversion in the anterior leads is the most common specific, specific finding in massive PE. It's seen in 85% of massive PE. And why do you have that? It's the same reason you get ST elevation in V1 through V3. It's the right heart strain, and secondary to the right heart strain, you can get deep T inversion or ST elevation. ST elevation is less common. Deep T inversion or some T inversion is quite common. I've seen a patient once present with chest pain and anterior T inversion. He was cathed. They found 70% LAD. They stented it. Okay, the patient kept having this chest pain. Eventually he got diagnosed with PE. So from the beginning, that patient had PE, but they were fooled, the doctors who took care of it. They saw the inversion anteriorly. They thought anterior ischemia. They found some LAD disease that was incidental. The point I'm trying to make, you have somebody with dyspnea and anterior T inversion, always, always think of PE. It is the most common uh massive and submassive PE finding, found in 85% of those cases, and even in standard, all coming PE, all comers with PE, 20% of them will have anterior T inversion. It's the second most common sign after sinus tachycardia, but the most common specific sign. This is another PE case here, uh, it's, uh, so you can see ST elevation. This is massive ST elevation in V1 through V2, V1, V2 from PE, and diffuse ST depression. PE can give you also diffuse ST depression, particularly when you're having ST elevation in V1, V2. You can have ST elevation in AVR as well. This is such a case of deep T wave inversion in the anterior precordial leads, V1 through V3 in a patient with PE. This patient also has right axis deviation, as you can see, and right ventricular hypertrophy with big R wave in leads V1 and V2. Notice that the S1 component of the S1Q3T3, which is a deep S in lead 1, is actually nothing but a sign of right axis deviation. This is the heart on the frontal plane. When you have PE, the right heart goes from this to this. It enlarges, and this causes the QRS depolarization to shift vertically and toward the right, and this is what creates that deep S wave in lead 1. It's the right axis basically. Also, the left heart is pushed up, and this pushed-up left heart creates the initial Q wave in lead 3 as well as the small R wave in lead 1. So the Q3 is the left heart being pushed up. The S1 is the right heart being pushed down.