 I think everybody's filtering back in, so I'm going to go ahead and get started. Thank you for inviting me to speak today. I'm Susan Sallick. I'm a cardiologist with a specialty in advanced imaging. I did my medical school in London, Ontario, my internal medicine at Henry Ford Hospital in Detroit, and my cardiology and advanced imaging training at UT Southwestern in Dallas, Texas. So I've been in the Tri-Cities area since 2006, and I've been part of MidMichigan since 18 months ago. So that's my quick and easy background, and let's read some EKGs. Basically, I'm going to go through ST and T-wave abnormalities. I'm going to start with the things that you guys not only, you know, you need to recognize, and you all, you know, everybody here knows pretty much what you're looking for. It's just a refresher of what do I need to call for, what do I not need to call for, and how do I not get confused by some of the normal variants or other causes of abnormalities that are not acute ST elevation. So just one of my favorite pictures, and then getting on into our EKGs. So everybody knows just the basics, but let's very quickly review. And can you see, okay, if I just point with this, rather than the red dot, so P-segment, atrial activity, the PR segment, things that, and unless we're looking at rhythm, which we're not looking at at this part of your lecture series today, QRS segment, and then here where we get into what we're interested in is the Q, QRS going into the T-wave, so your ST segment. This initial segment as it comes up is your J point. And then the ST segment, this is where the main decision making occurs. And then the T-wave and U-waves, which very rarely are seen in clinically are probably not that relevant regardless. So the isoelectric line, depending on what book you read and who teaches you, there's different people who are going to tell you to compare your ST segment to different locations elsewhere in the EKG. And I've read it in all different locations. So obviously you want to look to see if the ST is elevated or depressed, but what do you compare it to? Drawing a line that somewhat follows along both the PR segment and TP segment is ideal, but those segments are not always at the same level. So the majority of experts, and when you read the most recent literature, recommend that you compare to the TP segment. The reason why that's important is with PR segments, you can have depression in certain disease states that will falsely make this ST segment look elevated. So really you want to draw an eyeball between the PR and the TP, and you hope that that's isoelectric and fairly consistent so that you have a general baseline to compare your ST segment to. So just an example of a normally EKG, it's always important to know what normal is before you can start looking at abnormal. And you can visually look with your eye at PR segment, TP segment, looks like the same line, and then you don't see any significant deviation of this ST segment. So I won't go into a whole normal EKG or how to read an EKG. We'll get on with the ST segments. And subtle changes, and this is something that I always, I give a lot of lectures to medical students and residents, and this is a really important point, is that subtle changes in the absence of symptoms, and so that's going to be different from what you guys see, you're seeing somebody with symptoms, otherwise you wouldn't be there. So it really becomes a less important issue. But subtle changes, minor depression, subtle changes in the T wave, subtle flattening, maybe a little bit of inversion, especially if you don't even have an old EKG to compare to, those changes are less important. So look here in this lead one, you can see that the ST segment is slightly depressed, the T wave is slightly inverted, or maybe biphasic before it comes back up to the isoelectric TP segment. But these are just minor changes that really shouldn't draw too much of your attention. And the causes, and the reason why it becomes less important is because ST segment changes can occur with so many different disease states, with toxic abnormalities, with metabolic abnormalities, and with a variety of ischemic conditions, infectious conditions, the whole list is here, medications, and with MI, with non-ST segment elevation MI as well as ST segment elevation MI. Again, not going to get into all of this because it's not the purpose of our discussion today. So getting into some more variations in normal that are not truly pathology. So persistent juvenile T waves, so what that means is T wave inversions, which are very common in young children, in leads B1, B2, B3, and sorry, this is not set up as your standard three by four EKG. But you can see how these are just subtly abnormal, but this is considered a normal variant in young persons. But it may also be seen in certain disease states. Obviously, you all know that that could be a scene in ischemia, as well as some electrolyte abnormalities and infiltrative cardiomyopathies. Brugata syndrome, which is a channelopathy, and ARVD, that's a rhythmogenic right ventricular dysplasia, something you're certainly not going to be diagnosing or seeing when you're out in the field. But something that can cause these types of changes. So, but again, these are very subtle changes. You see no ST segment deviation up or down. You're just seeing T wave inversion, which is more in the non specific side or less, less dramatic side of abnormality, if abnormal at all. Athletic T wave changes, and this gets more into the J point abnormality. So even in up to 13% of African American athletes, you can see this variant. It's typically observed in the septal and anterior precordial leads, where you can see this, again, J point elevation right here, but then ST segment elevation. When you compare it to both the TP segment as well as the PR segment, this ST segment is one to one and a half millimeters elevated, but you can also see that it's a domed. The T waves may or may not be abnormal as well. Again, something that you probably are not going to see very often. You're not getting call. Well, I don't know. I guess you maybe do get calls on these young people, but again, a normal variant and sometimes very difficult to distinguish from a true abnormality. So this is a good example of J point elevation. Hopefully you can see these pretty well up here. So this is a good example right here at the very terminal portion of the QRS. You see this sharp upslope and then the ST segment comes back down and you observe that the ST is isoelectric with the following TP as well as the previous PR segment. So that initial spike upward gives that visual impression of ST segment elevation when it's simply elevation in that J point. Early repolarization, it's a very similar kind of morphology on the EKG. And this bottom here is a better example that I got. And kudos to Charles. I got a lot of these slides from him. So a lot of these EKG examples are from his lecture. So thank you for that. But this is a good example of how how spiked appearing this J point is before it comes back down into the ST segment. ST depression. I don't know how much time we need to spend on that. But any abnormality that you see needs to meet certain criteria, a millimeter or greater of deviation, whether you're talking depression or elevation, and two or more contiguous leads. And I have a slide of the contiguous leads just for a refresher. But that depression or elevation needs to be measured 0.08 seconds. So eight milliseconds, 80 milliseconds after the J point, which is two boxes, two of the little boxes. And again, the reference, there's some controversy in that you'll read different things in different locations. But in general, probably the best consensus is TP segment. So when you're looking for ischemic changes, ST segment depression, up sloping ST depression is less ominous than flat ST depression, which is less ominous than down sloping. So down sloping is always the worst. And that may or may not be associated with T wave abnormality, such as inversions. The other thing, just getting back to that for a quick second, it can be very difficult in people who are in atrial fibrillation or atrial flutter with all that disorganized atrial activity, or organized atrial activity that's buried in the ST segment when those flutter waves are occurring. It can be very, very difficult to discern ST segment changes. So and that's a tough thing for anybody looking at an EKG. So obviously slowing them down and maybe getting them out of the rhythm, an entirely different discussion in order to better assess them. But remember that caveat. So these are just examples of what I was mentioning. So a normal ST segment in the leftmost panel right here, as opposed to up sloping ST segment depression, horizontal, which is more ominous. And then the most ominous is this down sloping ST segment depression with T wave inversion. So the ST depression, so you all know that STEMIs, ST elevation, it tells you where the infarct is, is it anterior, lateral, inferior, posterior, high lateral, whatever the case may be. ST segment depression, whether it's an active symptoms or an active non STEMI, or even in the stress testing lab, when we do ischemic evaluations in patients, patients does not localize the area of ischemia. So you'll typically see changes in the inferior leads and then starting out at the lateral leads like B6, 5, and then climbing its way towards the septal leads. And these are just examples where you can see down sloping ST depression here in B6, B5, B4, and then it becomes less as it approaches the septal leads. So this would be an ischemic looking EKG, not an ST elevation MI. Another example more in the format that everybody's used to looking to. Actually, you guys have this format, right? The 3 by 4, it's not 6 followed by 6, right? So you can see that there's significant flat almost down sloping ST depression here in the lateral leads, the anterior leads becoming less by the septal leads, but also here in the inferior leads, high lateral as well. So T wave changes again kind of go with the ST segment depression or ischemic changes. They can be flat, they can be less tall. Remember, normal T waves should be about a third of the height of the QRS complex they're associated with and most patients don't have normal T waves. Most people have some flattening in the population that we deal with. T waves may be biphasic or inverted. Unlikely to see isolated T wave changes, but as you all know, one of the precursors to ST elevation is a peak T wave because of the hyperkalemic changes that occur in the myocardium. So that's something you may see early on, which is why you repeat EKGs. Well in sign is a one of those textbook things that you may or may not have read about suggest proximal LAD disease. So that's symmetric deep T wave inversions. I have an example of that coming up and that's something that you're not going to miss. It's not a subtle abnormality. So you can see here these very deep T wave inversions. These aren't tiny little, this is what I would consider a subtle or a minor minor T wave change that I would not be too worried about. But when I see these dramatic T wave inversions that almost reach the amplitude of the QRS complex, this is much more worrisome. These interestingly you'll see as I show some other examples can be seen in hypertrophic cardiomyopathy as well as apical hypertrophic cardiomyopathy. Again, things that you won't know at the time of just an EKG without a clinical history, without an echocardiogram for example, but are seen in other disease states. So infarction as you all know is typically a transmural as opposed to a only portion of the myocardium involvement. And the usual territory, you notice a lot of this, I say usual or most places you read because you're going to find different things in different locations that you read. There is some variation in the literature as well as an expert opinion. So usually V1, V2 is septal, some places say antro-septal. V3 and V4, antroapicole are just anterior. V5 and V6 are becoming more lateral. 1 and AVL are high lateral and then the inferior leads, everybody agrees on 2, 3 and AVF. I thought this was just a very nice diagram describing the location of the EKG leads as they correspond to the coronary territories. So you can see here V1 and V2, you're right over top of the right ventricle. And so as you approach the left ventricle, here's your LAD and you're getting into 2, 3 and 4. And then as you approach the lateral wall of the left ventricle is the circumflex territory. So that's reflected by V6, 1 and AVL. So getting into the high lateral leads and then looking inferiorly. So as the right coronary reaches its final location, 2, 3 and AVF. And then just laying out those territories on the EKG itself. Inferior is right coronary artery and the majority of patients who are right dominant, left dominant and 10%. So this would be a circumflex distribution. The LAD is covering the majority of your precordial leads unless you have a very large circumflex or if you have a large wraparound or CA, these are unusual findings that you're not expecting. But so most of the precordial leads represent the LAD in its branches. And then the circumflex somewhat out here towards the lateral leads, but also more towards the high lateral leads, 1 and AVL. So everybody knows the tombstone picture. I mean, obviously, if you see tombstones, it's easy. It's just, it's not always this easy. It can be a lot more subtle or it can vary quite a bit. But this very convex appearance of VST segments that look like a sad face or look like a tombstone are a bad finding. So as far as acute infarcts occur, as I mentioned a moment ago, if you catch it early enough in the cascade of events, often people are not, have not presented at this point, will first have hyperacute T waves because of the hyperkalemia in the myocardium. And that's your tall peaked symmetric T waves followed by J point and ST elevation. And you can see here in these in this two and three, as well as it's got to be AVF, you can start seeing this ST segment is becoming elevated and it becomes indistinguishable between J point ST segment and T wave. So if you follow the evolution of ST segment change during an acute ST elevation MI, the first thing is this peak T wave. You can see it's doubled in amplitude from the normal state. And then as the ST segment slowly rises, you lose that contour between the QRS J point and T wave to the point where you get the tombstone or more here tombstone. And then as you start completing the infarct or actually infarcting tissue, you start developing the Q wave and then ultimately you'll invert your T wave. This is an example of an anterior infarct that has been evolving where T wave is inverted, ST is elevated, you've lost that contour between the J point and the ST segment. And you can see that there's very little R wave. Remember the R wave is the voltage from the left ventricle that should grow as you go from V1 through V6. And sure you have R wave out here, but you have no R wave here and infarct a Q wave. So the criteria for measuring a Q wave or making diagnostic criteria for a Q wave is one box wide, which is 0.04 seconds. And it should be about one third of the amplitude of the R wave. So if you have no R wave, it's obviously all Q wave. So it's a no brainer. This one's becoming almost completely a Q. You have this teeny teeny little initial R wave. This is an example of an inferior infarction with reciprocal changes. So you don't want to be distracted by these very dramatic down sloping ST segments with T wave inversions, which are not the primary problem here. These are the changes that occur as a result of the reciprocal changes from this inferior ST elevation MI. So you've lost your your contour and the J point here in lead three. You're already starting to develop Q waves here, seen an F in lead three, not so much of a significant Q wave in lead two, but then your reciprocal anterior changes, even high lateral changes. Infraposterior lateral infarct. So this is circumflex territory or a huge wrap around right coronary artery that supplies a posterior lepentricular branch to the lateral wall of the left ventricle. So these are much more difficult to diagnose. This is a patient who is sicker than you think they are based on what you've seen so far. Like they're hemodynamically unstable, they continue to have symptoms no matter what you do, their blood pressure is down, and your EKG is not showing you as much as you think you should see. So at least in this one, because you have inferior changes, you can see that there's ST elevation, there's already Q waves, you can suspect that there may be some degree of a posterior infarct or even an RV infarct going on in these types of patients. And so what you look for in addition to those inferior changes is a dominant R wave in V1, V2, and then T wave inversions as you go out to the lateral leads. RV infarct, this is your right-sided EKG. So anybody who hasn't, is this a protocol? If anybody has an inferior ST elevation, then you do right-sided leads. And so what you're looking for is exactly that, ST segment elevation of the right ventricle, exact same idea. And so you can see this very dramatic inferior ST segment elevation because these leads stay in the same location. You simply change your precordial leads to go out towards the right rather than to the left. You can appreciate also ST segment elevation here. After someone has already had an MI, the ST segments don't always normalize. So when somebody who has had an infarct before and possibly has developed an aneurysm, their ST segments may never normalize. So you might see a patient who's having chest pain or shortness of breath for something completely different, and they still have ST segment elevation. And there's honestly not much you can really do about that because they have symptoms, they have ST elevation. Even in the presence of Q waves, you're stuck basically in thinking that it's a new event unless you have an old EKG for comparison. Paracarditis, that's where basically the PR segment changes come in. So PR segment depression is a very specific finding in the presence of paracarditis together with your clinical suspicion and the pattern of symptoms. So you have this kind of concave appearing ST segment elevation. This almost looks like J point elevation like we looked at earlier, see here in V5. You can appreciate that sharp upslope of the J point and then the ST comes back down and is isoelectric with this following TP segment. But if you use the PR segment as your reference point, this ST segment is two millimeters elevated. So you can appreciate how that PR segment depression can make you think the ST is up when truly that's the abnormal finding. Paracarditis, two changes do not need to occur in every single lead. It doesn't need to be a global process. You still need your two contiguous leads, but it can be territorial. So don't be dissuaded from the possibility of this diagnosis if you only see changes in two or three contiguous leads. Getting into hypertrophy, both right and left ventricular hypertrophy, the findings associated with this can often get in the way of your interpretation of ST segments, typically by way of strain changes from from LVH or RVH. So often the changes that you see with LVH so and I'll go over some of the diagnostic criteria for LVH and RVH. So the classic criteria that everybody memorizes for LVH is the rule of 35. So you take the tallest S wave in V1 or V2 and add it to the tallest R wave in V5 or V6. And that number, if it's greater than 35, which is seven large boxes indicates the presence of left ventricular hypertrophy. So if you see associated ST segment depression, which typically occurs in the lateral and the inferior leads with that T wave abnormalities, it's most likely strain or at least it may be strain, but you can't say that that's ischemia because of the left ventricular hypertrophy. There are limb lead criteria that I typically will advocate people remembering simply because there's there's other diagnoses that can interfere with with any of your LVH criteria. So in the limb leads, what I ask people to look at are the R waves in one being greater than 14 and the R wave in lead AVL being greater than 11. Those are also too easy to remember criteria. As you all know, there's there's a lot of criteria out there that you could memorize and memorizing them all is not useful for right ventricular hypertrophy. So you're looking at a dominant R wave in lead V1, an R to S ratio of greater than one and the presence of S wave progression. So much like you see the R wave growing as the left ventricular myocardium is being seen by your electrodes. The same thing is true of the right ventricle, which is anterior. So as those electrodes are going out more towards the lateral wall, you'll see that negative wave grow. So that's S wave progression. And if you do have right ventricular hypertrophy, the ST with T wave changes that occur are typically in the septal and anterior leads, not in the lateral or inferior leads. So this is an example of LVH and you can see again, sorry, it's in this different format, but you can appreciate that lateral leads, you have this SD segment depression and T wave inversion, which is again, it's not even that much. It's only about a millimeter or half a millimeter, but the T wave is definitely abnormal. This would be a finding of strain and you can see in one and AVL as well, the high lateral leads that you see the change inferior leads actually look pretty normal. But you can see to that this meets the 14 criteria for the R wave and one in AVL, it meets the 11 criteria, but it actually so we've got about five, 10, 12 here in B2, B1 doesn't have a deep S wave. And over here in B5 or B6, you're at about 11. So you don't have 35 for that 35 criteria, you'd have to recognize it by knowing some of the other criteria. Interventricular conduction delays. So remember, there's left bundle branch block, there's right bundle branch block, but there's also wide QRS that doesn't fit entirely into either left or right bundle. And so that's a catch all phrase for those, those characteristics or those EKGs that don't fit the classic patterns. But what you may also see in these also the examples here are both right and left bundle. So in right bundle and B1, B2 and B3 are where you typically will see your repolarization abnormalities. So you can see T wave inversions, usually in B1 and B2, less often do they extend all the way to B3. And then in left bundle branch block, all bets are off. You have all sorts of abnormalities in your ST segments and your T waves that interfere with your ability to diagnose a STEMI. And you all know that there are criteria that are attempted to be used to diagnose STEMI in the setting of a left bundle branch block, but there's truly no consensus as to what really gives you the right answer. So it's not something that we we do. So just to review what is a classic right and what is a classic left bundle branch block. So you need a wide QRS, which is greater than three small boxes 120 milliseconds. And then you only really need to memorize what two leads would look like in each of those. So for a typical right bundle branch block in lead V1, you should have that RSR or rabbit ears appearance, you don't always have to have a very dramatic RSR pattern. It needs to be all upright though. And the T wave is inverted. For leads one and V six, they look the same in a right bundle branch block, where you have this deep slurred S wave with an upright T wave. So that's all you need to memorize to know a right bundle branch block morphology. Going on to the left bundle branch morphology, again, it's the same leads in lead V1, you would have a negative QRS complex with an upright T wave. So really opposite to what you're seeing in a right bundle. And in leads one and V six for a left bundle branch block, you have an entirely upright QRS complex, it could look RSR prime, it doesn't have to, and it has a negative T wave. So again, it's kind of a little bit opposite to what you're seeing, but that's all you need to memorize. And if you know those specific criteria, doesn't really matter what the other leads look like, that's a classic left or your classic right bundle. If you have some mixed features like V1 looks like a right, and V1 and V6 look like a left, or maybe one doesn't look like either, then you would call that what I just mentioned a moment ago, a non specific interventricular conduction delay. But again, if you can't put it into one of those two baskets, it becomes much more difficult to say anything about your ST segments in your T waves. So hyper acute peaked T waves, to make that diagnosis, you need to have greater than five millimeters in a limb lead or 10 in a precordial lead. Really, it's the visual appearance, like I said earlier, you're not seeing these big tall T waves in the majority of our patients, body habitus and other medical conditions or comorbidities being to blame. But this can be seen in a number of disease states and the symmetry or lack of symmetry of it is what may help you to distinguish. So asymmetrically peaked T wave is typically seen in hyperkalemia or the hyperkalemia associated with acute ischemia, asymmetric T wave peaking is more likely to be seen in other disease states. So your bundle changes or hypertrophic changes, or in somebody who's young and normal and has no pathology, which you're typically not going to be seeing. So these are just a couple of examples before we get into all the EKG readings. So just the, and I don't know how useful this is to just go through it, but use this type of thing. And I can give you all these slides that I have, Charles, in addition to what you gave me, that just have the characteristic appearance of these different disease states and how the QRS is STs and T waves look. So the first panel here, and we're looking at leads V1, V2, V3 and lead two. So a left bundle branch block, like we just talked about, entirely negative QRS with an upright T wave and becoming different out towards the lateral leads as well as as inferior. Pericarditis, you have this kind of pseudo ST segment elevation, but you have significant PR depression. Hyperkalemia, it looks like ST segment elevation. And this is the progression that occurs. You'll first peak the T waves, then you start prolonging the QT, the QRS and the PR segment until you become a sine wave. Antroceptile MI, this domed concave or, excuse me, convex tombstone appearing ST segments. This is not something anybody's going to miss. Right bundle branch block. So predominantly upright, it doesn't always have to have that dramatic RSR prime appearance with a negative T wave. And then Brugata, don't worry about. All right. So this is the audience participation time. And I'll tell you that these are all STEMIs. You just have to tell me that the coronary artery, okay, in 90% of people, right? So good. So you have ST segment elevation, you have a normal TP segment down here. In this particular case, you can use your PR segment, but there's at least three millimeters of ST segment elevation. So what if I told you that this patient came, they called EMS and they said, I had chest pain three hours ago and I want you to come pick me up. And they have this EKG. So what might you think, I'm not asking you to make a decision right now. I mean, the, we'll get to that in a second. But if this is their EKG, what else might you think, what else do you notice in the inferior leads that is going to help explain their lack of symptoms right now? It's good. So this is maybe a completed infarct. And then five minutes later, all their chest pain is back and then it's coming and going. So what do you do? Do you activate or do you not activate? Activate. Oh, one other thing. Tell me about B2 and B3. B1. Reciprocal changes. Good. All right, next. What coronary artery? Circumflex. Good. So where are the changes? What territory are they in in the EKG? Good. Good. So you have ST elevation that's in reference to the TP segment and the high lateral leads. It looks like a little bit here, but yes, even getting into LED territory actually. So this could actually be explained by a huge left anterior descending that has a large diagonal branch that supplies the PLV area that typically the circumflex would, would supply. So activate or not activate? Activate. All right. So yeah, inferior wall, no question about it. Do we have reciprocal changes? Yes. Where are those? B2, B3, B4, 1 and AVL. Look at these huge, huge T-wave inversions with downsloping ST depression. So this is either right coronary artery and 90% of people are a large circumflex branch and 10%. So activate or not activate? Easy. Okay. And this patient's blue and their O2 sad is 80 and they can't breathe either. So I'm giving you a very hemodynamically unstable patient. So let's, let's think past LED. You've got high lateral, lateral, anterior, septal. So this is left main. This is a hemodynamically unstable patient who has global ST changes. So the only thing that's not really being affected is your inferior wall. So they probably have a dominant right, but that's probably what's more likely going on if you have hemodynamic instability with a lot of LED area changes. So obviously activate. Okay. Inferior, lateral. So this might be what coronary artery might this be? Like a super dominant right that gives over a huge posterior left ventricular branch. So it's also affecting lateral wall or it could be a dominant circumflex. That's also affecting other branches of two marginal branches of the circumflex. You have ST elevation and B6 kind of borderline and B5 depression here in the high lateral lead. So those would still be termed reciprocal changes and then inferior ST elevation reciprocal changes and B2, B3, B1. What coronary artery? So starting in B1 you have a millimeter about two to three millimeters and B2, five to six maybe even more here and B3, five and B4 and then leveling out by the lateral leads and not elevated in the high lateral leads. Inferior leads, maybe some non-specific changes, maybe some reciprocal changes. What do you also notice? How much our wave voltage do you have? A little to none right? So this is probably not, I mean if they're having chest pain they go to the lab but there's not a lot of our wave voltage left here anymore. So this is probably not very, very recent. There's only so many territories we can do in these EKGs right? So it's this one. Yeah it's inferior. It's not very impressive in two although it does meet criteria but you have much more impressive ST elevation with T-wave inversion in lead B3 and AVF and then what are these? Reciprocal changes in the anterior leads. So LAD again right? Yep yep yep getting out into the lateral leads as well so probably LAD with a good sized LAD significant ST elevation in B3 and B2. Flattening of the T-wave so I don't know that I would say anything reciprocal but you guys get the idea here of the T-wave being subtly abnormal but not dramatically abnormal. What coronary? LAD. Only three choices. Fork including left main. I think this is the last one. So inferior with reciprocal changes. Okay so let's look at some other things that are not ST elevation MIs and look at some of the contrasting changes or findings on these. So I'm giving you the diagnosis at the top. I suppose I should have put those on there but I have more that don't have labels on them so. So let's look at those criteria so you guys remember what I showed you a moment ago about what are the classic criteria you see with the right bundle branch buck. So what's V1 look like? Rabbit ears right? It's your RSR prime. Check. B6 and 1 should look the same. They should have don't look at everything just look at what the criteria are that you need to memorize. Deep slurred S-wave you shouldn't have an S-wave at all and lead one. Nor should you have an S-wave and a normal patient in B6. So yes you have deep slurred S-waves in 1 and B6. Is my QRS wide? It's really wide. It's probably six small boxes long. So we have classic example of a right bundle branch buck. So let's also remember back to what T-wave abnormalities we typically will see with the right bundle branch buck. Are they in the inferior leads in V1, 2, 3 or V4, 5, 6? A, B or C? So they're typically in the septal in the interior lead. So V1, V2, V3 just like with right ventricular hypertrophy also with the right bundle branch buck. You would expect to see changes here but not as you get out too far to the lateral leads. With the left bundle branch buck you expect to be seeing those more dramatic lateral changes. So this I would not consider to be an abnormal finding. There's no ST elevation here but there are ST signal changes. All right. Does this meet your rule? So left bundle branch buck, right? So all negative QRS with an up... Do you want me to not go through my criteria then? Okay. With an upright T-wave in V1 and then all upright QRS complex in V6 and in lead 1 with a negative T-wave. And this could be RSR prime or it could be all entirely upright. But those are the classic criteria for left bundle and it's obviously wide. It's probably four boxes long. So at this point you're not going to say anything else about ST segments. So ventricular pace rhythm. Of course you all know that that not only widens your QRS but it interferes with your ability to interpret ST segments and T-waves. So as long as the pacer spikes are obvious enough to detect them. I've seen EKGs before where you see maybe this teeny tiny little spike in one lead and then no other leads at all. So especially in a lot of our obese patients or COPD patients it can sometimes be more difficult to tell. So you want to make sure that you're looking at all the leads. In this one it's very clear there's an atrial spike as well as a ventricular spike. So you want to make sure that you're looking everywhere and you see that this is clearly a ventricular pace rhythm at which time you can't say anything or you should not say anything. This is one of the biggest causes of it. Yeah and I can imagine a lot of it maybe from artifact because you're you're rushed. I mean there's so much going on. You're trying to try to get a good quality EKG is not always easy. And so if there's a lot of baseline artifact you could see where a very tiny pacer spike like this one right here could very easily be missed. So it just goes to the whole preparation and making sure that you're getting good quality tracings. Patients who have other pathology can have a lot of changes in their EKG as well and the purpose of this one is just to show you one of those examples. Any type of intracranial event whether it's a stroke or a hemorrhage in the brain can cause significant SD segment changes not only ST elevation, ST depression, T wave inversions. This is an example of a subarachnoid hemorrhage where you see these deep wellans type T waves like I showed you earlier in someone who has a prox LAD lesion. So again you're stuck at this point unless you have focal neurologic findings and then you're going down another pathway but you may very well see changes like this in somebody who has absolutely no cardiac problems at all but from some other pathology. The other non-cardiac pathology that can lead to this is abdominal pathology so like acute pancreatitis somebody who has acute belly that type of thing can lead to these changes as well. But again these are typically depression and T wave inversions but you can see ST elevation too with intracranial events. So this is an example of someone who's got some LVH so let's look at the criteria. So you've got 5, 10, 15, 20, almost 25 here 30, 40, 50 but you actually also meet criteria for what? With a wide QRS you can see widening of the QRS with LVH as well as with bundle branch blocks but this looks like a left bundle branch block as well. All negative QRS upright T wave with predominantly or all upright QRS complex in v6 and lead 1 and then obviously the ST segment changes but these irrespective of the presence of the left bundle these are their very classic changes of strain that can occur with left ventricular hypertrophy. I mentioned earlier hypertrophic cardiomyopathy whether it's asymmetric septal hypertrophy or apical that just means the location in the left ventricle of where the genetic abnormality occurs can cause a lot of ST segment changes and again you still end up having to go with your clinical judgment and what the EKG shows you but this is a completely asymptomatic patient who has this diagnosis. So you're seeing ST elevation here of 3 millimeters not quite two contiguous leads, v2 is not quite a millimeter but then starting to notice these T wave inversions out in v3 with more dramatic T wave abnormalities like that ischemic looking or wellans type T waves that we saw earlier in v5 and v6 and when your QRS is all run together you don't really need to do the math to figure out that there's left ventricular hypertrophy as well. High lateral leads marked T wave inversions in 1 and AVL and even in the inferior leads. So just an example of a completely asymptomatic person who has an underlying diagnosis. Another example of paracriditis this was one of yours this was a great example of paracriditis it's not always this traumatic you don't need a lot more information after this but look at these huge huge PR segment depressions in reference to the ST segment and if you follow it might be a teeny bit up but I don't even think it's quite a millimeter when you follow that out to the following TP segment and here you can see that the ST and the TP is isoelectric and the PR segment's about one and a half or two millimeters depressed in lead three it's about three in AVF and it's depressed all the way around all the way through the anterior and lateral leads so it can be a global diagnosis as I mentioned earlier but it just doesn't have to be this is a great example of paracriditis. Right yeah so the with paracriditis it's concave as opposed to the tombstone looking ST segments and you're going to have a patient that feels better sitting up their chest starts hurting when they lay back they take a deep breath coughs fees bend over to tie their shoes it gets a lot worse and they like to just stay still every time you hit a bump they're going to be in pain it's that very pleuritic type chest discomfort it's not your classic angina. Another example of paracriditis although not quite as dramatic but you can see PR segment depression in lead two not as obvious in AVF but maybe a little bit a little bit more dramatic in one AVL v6 and then starting to peter out by v5 and v4. Nice example of hyperkalemia so remember the initial change that you'll see is that peaked T-wave as the degree and time progresses the QT first prolonged followed by the QRS and then the PR segment and then ultimately everything just turns into a nice sine wave yeah this is a sick oh I mean very very well maybe but also your medication side effects but yeah I mean typically that's the most common group in which we'll see that that's pretty much it for what I have here this is just the the reminder of the the sad is the ST elevation and then not that you want paracriditis but I guess you're happier than if you had a stemming so all right well thanks for your attention guys