Welcome back to part two of the EKG review. So let's pick up where we left off and talk about ischemia and infarction. So this is one of those must-be-competent areas that you will encounter with EKG interpretation. And with EKGs, as you know, we don't pick it up and read it like a book from left to right. We have to think about patterns and looking at EKG leads in groups. So you must consider the leads in groups as they reflect their coronary supply. And that will help you with your ultimate diagnosis, and it'll help you really nail down what's happening from a pathophysiologic standpoint. So our leads that we should consider in groups would be 1, AVL, V5 and V6 for the lateral leads, which reflect the left circumflex artery, 2, 3, and AVF tell us about the inferior leads or the right coronary artery, and then V1 through V4 are the anterior leads, which tells about the left anterior descending artery. We want to look for ischemia, injury, and infarction, and changes must be present in contiguous leads. So what that means is if I just see a Q wave in lead 3, I can't say there's been an old inferior wall MI unless it's present in multiple leads that are right next to each other. So I'd want to see that in 2 and 3, or 3 and AVF, or even better, 2, 3 and AVF. So I will show you examples of all of those things as we move through. This is a picture just depicting the coronary artery supply, and one thing I want to just point out is that we don't want to forget that those arteries also supply areas of conduction in the conducting tissue in the heart. So in someone with an inferior wall STEMI, for example, they may also present with complete heart block if it's an extensive MI because the right coronary artery also supplies the AV node. In the posterior descending artery, we may see those patients present with a new bundle branch block because there are perforating branches that supply the bundle branches. And then the left circumflex, less commonly, that may give off some sinus node or AV node blood supply as well. The posterior wall is supplied by either the right coronary artery or the left circumflex, whichever one is dominant. So whenever you evaluate a patient with an inferior STEMI or a lateral wall STEMI, we always want to evaluate for the potential of posterior wall involvement, and we'll talk about how we do that. Here's a table putting everything together. The anterior leads V1 through V4, lateral 1 AVL, V5 and V6, and inferior 2, 3 and AVF. Early ischemia is reflected in any of these leads by a T wave inversion. Late ischemia is depicted by ST segment depression. And then an injury pattern, which means there's ongoing infarction, is represented by ST segment elevation. If the infarction has completed itself, I will see Q waves. So you want to get used to looking for all of these things on EKG, and they occur in a pattern typically. The last thing I want to talk about with this slide is reciprocal changes. So reciprocal changes will help nail down your diagnosis of an ST segment elevation. So when I see ST segment elevation, this is only the case where you see reciprocal changes, I will see ST segment depression in the mirror image leads on that EKG. So in the anterior wall, if I have an anterior STEMI, I'm going to see ST segment depression and inferior leads. Same with lateral STEMIs. And then in an inferior STEMI, I'm going to see ST segment depression in the lateral leads. This is very helpful because some people, maybe you're not sure if you are truly seeing ST segment elevation, but if you also see ST segment depression in predictable leads, then you should feel really good about that being an injury pattern. So looking for reciprocal changes has very high specificity, and it has a really excellent positive predictive value for ST segment elevation. So they're important things to look for. Serial EKGs are vital because these changes can happen very quickly. And if you have someone come in with acute coronary syndrome, they may have unstable angina and you don't see signs of a STEMI, but then maybe they get progressively worse chest pain. And now you get a repeat EKG and you see that there's ST segment elevation. So anytime we see changes in either the patient's symptom pattern, or if you start seeing these sorts of changes on your EKGs that you're evaluating patient, maybe in the emergency department, these are vital because it could completely change the way you treat your patient. And of course, these things will affect the overall prognosis of your patient. So we start off with a T wave inversion as a first sign of ischemia that we can see anyways on EKG, because we know that those pathophysiologic ischemic changes happen long before a patient even starts developing symptoms. Then we see ST segment depression. And so you always want to be careful to evaluate where is my actual baseline here? So the baseline, if I try and take my pen and draw a line right across there, you want to evaluate where's my baseline. And then I can measure in small boxes. So one small box is one millimeter, and I can measure how many millimeters that is below baseline for ST segment depression. I can do the same thing with ST segment elevation, measure in boxes or millimeters above the baseline. And then if there is an infarct, that tissue has died, that has become scar tissue. And now I see Q waves because it doesn't depolarize. All the electrical vectors are pointing away from that. Reciprocal changes, as I mentioned, high positive predictive value of a STEMI, and it can really help you feel confident in your diagnosis. So the primary change is the ST elevation and the reciprocal change is ST depression. And that happens in predictable leads. So for example, acute anterior wall injury, ST segment elevation in V1 through V4, and ST depression in 2, 3, and 8VF. So let's look at some examples of these things. Anterior wall ischemia, in this example, I can look at V1, V2, V3, and V4. And so not much going on there in V1, but when I look here at V2, V3, and V4, it's almost like I take my fingers and I reach up to the end of that QRS complex, and I just kind of dip it below baseline. So I'm going to measure this in millimeters or small boxes below baseline, and this is consistent with anterior wall ischemia. So I'm certainly going to want to be obtaining serial EKGs on this patient to see if there's a progression. Anterior wall injury is often referred to as tombstoning because these segments here in V1, 2, 3, and V4 kind of look like tombstones. So same concept, if I take kind of the end of that QRS complex and just lift it up off the baseline, that is ST segment elevation, and I can confirm that by looking for those reciprocal changes in the inferior leads, 2, 3, and AVF, ST segment depression below baseline. An anterior wall infarct, so this patient, this was a patient that had an anterior lateral wall, MI, and so you can see these Q waves all the way across the precordium, and I wanted to show you this example too because this is a great example of what we call poor R wave or lack of R wave progression in this case. So normally, if you think about as electricity moves through the heart and goes across the precordium over from the base to the apex, I should see the vectors changing a little bit. So I should see the QRS complexes initially being negative in V1 and V2 because electricity is moving away from those leads, and then it should gradually become more positive as I move to V4, V5, and V6 because at that point, those leads should see electricity moving towards them. So that's normal R wave progression. Generally negative QRS complex V1, V2, by V3, V4, it's kind of as much positive as negative, and then it should be more positive in V5 and V6. So people that have had anterior lateral MIs, we have a changing in that R wave progression. It's not normal as you can see in this example. Sidewall injury here in one, AVL, and really extending all the way over to V2, we have significant SC segment elevation in those lateral leads, and I see reciprocal changes in the inferior leads, 2, 3, and AVF with SC segment depression. Inferior injury, I see SC segment elevation in 2, 3, and AVF, and then there's reciprocal changes here in one, in AVL, where I have SC segment depression. When someone has completed an inferior wall MI, you'll see Q waves here in 2, 3, and AVF. So it doesn't go up, the QRS doesn't go up, the very first deflection is negative, so I call that a Q wave, 2, 3, and AVF. Now posterior wall injury, this is one of those, sometimes I like to call these kind of a rockstar diagnosis, because if you pick up a posterior wall injury, it shows that you've really done your homework, and you're really evaluating that EKG in its entirety, and most importantly, you're hopefully going to positively affect the prognosis of your patient, because you're going to pick out something that means there's a little bit more extensive injury involved. So with a posterior wall injury, an isolated posterior wall injury is not very common. Usually what happens is we see that in relationship to a right coronary or a left circumflex lesion, and so the typical 12 lead EKG does not give us a look at the posterior wall. I can put leads back there and evaluate that, but if you don't have that available, or if you're not able to do that quickly, because obviously this is someone who's not in good shape, you can look for reciprocal changes in the anterior leads. So the mirror image of the posterior wall is the anterior wall. So I can look for reciprocal ST segment depression in the anterior leads. So in this example here, I can see that there's ST elevation in 2, 3, and AVF, and I see reciprocal ST depression in 1 and AVL. So remember, patients are either right coronary or they're right or left dominant, depending on whether the right coronary or the left circumflex wraps around and supplies the posterior portion of the heart. So in this case, it looks like this person has a large right coronary artery that probably wraps around and supplies the posterior portion of the heart. So they have some posterior involvement, which tells me that there's an extensive ischemic process going on. So if I look at V1, V2, in this case, it really kind of extends throughout multiple leads, but typically you look at V1 and V2 and look for ST segment depression, and you'll see it kind of has this really characteristic appearance where again, it looks like I just dropped that ST segment down below baseline, but then it just kind of slowly swoops up. So there's something called a mirror sign. So if you take this, if I were to print off this EKG and I flip it over and I hold it up to a light, or you can take the EKG and hold it in a mirror, which is probably not super convenient for wherever you're working, but you can take this, flip it and hold it up to a light. And what you'll see when you look at the back of that EKG is V1, V2, and V3. It'll look just like classic ST segment elevation. And that confirms your finding of posterior wall involvement. And that's someone that you're certainly going to want to watch a little bit closer. Everything else can be classified as ventricular hypertrophy, atrial enlargement, and specific clinical correlates. So you can read about these things in your EKG text chapters 13 and 14, which go over specific findings of how you can diagnose or diagnose voltage criteria for ventricular hypertrophy and other clinical correlate findings like hypothermia, electrolyte abnormalities. So I strongly encourage you to quickly read about this, those things, so you're well prepared for practice. Let's talk about supraventricular arrhythmias, which is as an electrophysiology PA is always my favorite topic. And I love evaluating these things on EKG because it's kind of like a puzzle that you get to piece together and you have to look very closely for clues to help you figure out what's going on with your patient. So as I mentioned in the electrophysiology topic, supraventricular arrhythmias, it's kind of an umbrella term. Lots of things fall under that. But from a rhythm standpoint, we're typically talking about atrial tach, AV node reentrant tachycardia, and AV reentrant tachycardia. Those are our three classic PSETs. So when you see an EKG like this, and you'll notice if we go through our steps, we say the rate is fast. So rate, too fast. Rhythm is regular. And then part of my rhythm step is to evaluate the P wave and its relationship to the QRS. And I cannot readily see a P wave here. I can't see a PR interval. And so when that happens, I can simply stop and I can say, this is SVT. And there are other things that you can do then at that point to try and figure out what's going on with the patient. Now, it's OK to simply say this is SVT and offer a differential diagnosis. But sometimes there's other things that we can do. So if we can see a P wave and figure out where that's at, then that makes our job a whole lot easier. In order to do that, you can maybe, if you're in the hospital, you can go look through telemetry. So monitor their telemetry from overnight, or that morning, or that evening, and try and see if you can find periods of where that rhythm starts and stops because if it starts and stops abruptly that implies some type of a re-entrant mechanism and oftentimes you may even be able to see what's going on when that rhythm starts and stops and that can help you with your diagnosis. But as you'll find out a lot of times we we aren't able to figure out exactly what's going on and that's when we just need to know what do we do next. So if you can find initiation and termination of a rhythm that oftentimes will help you really narrow down what's going on. So here's an example this this was a patient that I was evaluating in the office and they had a pacemaker and they were having this repetitive non-sustained atrial tachycardia and so I wanted to try and catch it on EKG and this is a great example of initiation and termination because it's slow so it's really easy to see. So I'll call your attention to the rhythm strip down here and so we'll see a normal beat and a normal beat and then you'll see that looks like it's starting to get a little faster. So right here this beat kind of comes in early and then I'll see that they're off and running with this atrial tachycardia and so you'll see that p wave almost kind of disappearing in the t wave there and then it starts to slow again and terminates right here and they actually come back in with a paced beat from the atrium. So this is an example of initiation abrupt initiation abrupt termination of an atrial tachycardia that's non-sustained and you can see how that starts and stops. Other things you can do SVT if one of patients in SVT is you can try vagal maneuvers so have them bear down and what we're trying to do there is slow conduction in the AV node increasing vagal tone. Adenosine is another option for how you can do this. So a narrow complex identifies a supraventricular origin that passes through the AV node. Adenosine will block temporarily in the AV node which will slow the ventricular rate and can be a very helpful diagnostic tool because when the ventricular rate is so fast it obscures what's going on in the atrium so I can't see the p wave but if I can slow that ventricular rate a lot of times I can see exactly what's going on in the atrium. So it can help differentiate between things like atrial flutter and other types of SVT. Clinically this is very important because I want to know from a risk stratification standpoint if my patient has atrial flutter because then I need to think about anticoagulation and a clinical pearl would be in general any any rhythm that terminates with adenosine because it can also be therapeutic not just diagnostic is likely to be amenable to catheter ablation because that tells me that that rhythm requires it utilizes the AV node either to initiate or maintain that arrhythmia and if that's the case then it's that means there's an extra limb there somewhere that I could probably find with an electrophysiology study and ablate. So let's look at a couple examples of patients that were in SVT and were given adenosine. So if I just showed you maybe two seconds of each one of these rhythm strips I couldn't tell you what that rhythm is all I could do is give you a differential diagnosis of maybe two or three things. They both look the same but in both cases the patient was given adenosine and so what you'll see here is when I temporarily block in the AV node I see these nice flutter waves just marching on through because adenosine doesn't do anything to the atria so my atrial rate just keeps going but it blocks in the AV node and it's temporary you can see that come back here. Now adenosine is not usually going to terminate atrial flutter as it does not in this example. Down here this patient had some type of a I think this this patient ended up having an AV node reentrant tachycardia and what happened was we gave the patient adenosine and it terminated so terminated the rhythm so this was not only diagnostic it's diagnostic because I when I block within the AV node I see there's nothing else going on there but it's therapeutic because it terminated it and now I can see a sinus beat come in here and here okay so that's why that's how adenosine can help you. We discussed AV reentrant tachycardia as well and the importance of a delta wave so what happens in AV reentrant tachycardia is if the patient is normally conducting as usual down the AV node and then an extra beat comes in a PAC comes in because that's oftentimes how all of these reentrant arrhythmias start so a PAC comes in it blocks at the AV node but then it's going to slip down that accessory pathway and the accessory pathway and the AV node both they conduct antegrade and retrograde so that impulse slips down the accessory pathway and then it's going to go right up the AV node and that's how we have our loop tachycardia. Same thing can happen though if the patient is conducting normally down the accessory pathway in sinus rhythm a PAC comes in it blocks at the accessory pathway and it goes down the AV node and then it goes to retrograde up the accessory pathway and that's how I initiate my tachycardia. So here's another example on a 12 lead of a pre-excitation so I see let's say let's look at lead v4 and v5 are great examples here so I see a very short PR interval and a slurring in the F-stroke of the QRS so when I see this this means that that person in sinus is conducting very nicely down their accessory pathway so if they were going to have an arrhythmia initiate it may look like this. So that PAC comes in and it blocks at the accessory pathway but it goes down the AV node and then comes right back up the accessory pathway so I'm going to call your attention here see if you can pick this out with me. I know that it's going down the AV node because it's a narrow QRS so that's why we call this orthodromic means they're conducting down their AV node and then at the terminal portion of the QRS I can see a little inverted P-wave and so what that is is that's retrograde activation so the QRS tells me about normal ventricular activation and then that retrograde P-wave tells the inverted P-wave there tells me about retrograde atrial activation going back up and so that's you can actually see this cycle happening so it's pretty neat. So there are some types of AV node re-entrant tachycardia that can look the same so if you are able to see something even if you don't know what it is you say I don't know that looks a little funny I'm not sure what's going on there but let's look into that a little bit further and then you can figure out exactly the type of tachycardia they're having. What's really helpful too is if you've got a patient like this try to find an EKG of them in normal sinus rhythm and then you can really look and evaluate for those little nuances that are different. Atrial fibrillation is the as we said the classic irregularly irregular rhythm and so we see this fibrillatory baseline with no clear P-waves in between QRSs that are happening very erratically and unpredictably. Another can't miss diagnosis you can't miss atrial fibrillation because those patients are at increased risk of stroke. Same with atrial flutter. I wanted to put this example in to show you too that remember atrial flutter isn't always regular so those QRSs are oftentimes irregular as well and so you can see in this case it's it's not really following a pattern it's an it's irregularly irregular but then my next step is always to look at my P-wave and I can see that sawtooth flutter wave pattern confirming this is atrial flutter. Ventricular tachycardia is defined as a run of three or more PVCs and oftentimes this is a macro ranch circuit that's around abnormal tissue in the ventricles that's from when oftentimes we're going to see this patients that have had an MI patients that have a cardiomyopathy and they can develop VT as a result of that abnormal tissue. We want to make sure we time this and know how long it's going on for because if it's greater than 30 seconds we count we call that sustained and remember that wide complex tachycardia in the setting of coronary disease is assumed ventricular tachycardia until you prove it's not. Look for AV dissociation which is hard to find if the rate is very fast and then always note that the VT is monomorphic or polymorphic because polymorphic VT brings to mind a few additional things like long QT syndrome. So here's an example of a little slower VT where you can pick out that AV dissociation that I'm mentioning here. So I can see this little P wave here and I can see another one here and there's another one here. So that is called AV dissociation. I see P waves that are occurring independently of whatever the QRS is doing. So wide complex tachycardia with AV dissociation you feel really good about calling that ventricular tachycardia. There are other criteria you can use to define ventricular tachycardia that are gone over in detail in your book but some of those things would be of course a wide QRS. You might notice that the there's what's called positive or negative precordial concordance and that means that all the QRSs in the in the precordium they kind of have a similar appearance. So in this case we're kind of positive there's a very strong positive concordance across there across the precordium. So there are other things you can look for but if you see AV dissociation you're going to feel really good about calling that ventricular tachycardia when it's wide complex. Ventricular fibrillation is hard to miss. So with ventricular fibrillation we lose those components. I can't say here's a Q and R and an S or a T. We lose all of those components because now the ventricles are just kind of quivering and there's no meaningful cardiac output. So that's a good example of a VT and a T. I wanted to end our EKG session by going over a few high-risk EKG findings. So there's something called Wellen's syndrome which tells you about a high-grade LAD lesion and it has a characteristic appearance on EKG. So what's interesting about Wellen's syndrome is these patients a lot of times they'll present and they'll have a history of very classic angina. So maybe you've got a guy who was running in a 5k and he had horrible crushing chest pain and he's telling his wife about it after the race and he says well I feel okay now. And as wives and girlfriends and mothers typically do we say I really think you should probably go get that checked out. So you convince the guy to go to the ER even though he's feeling fine no problems and then you get an EKG like this. So these people will kind of transiently reperfuse but then they progress again to ischemia later. So it's a very high-risk EKG finding that often occurs in a pain-free state. And so what you'll see is we have these deeply inverted T waves here in the precordial leads V1, V2, and V3 anterior precordial leads. And there'll be kind of this positive deflection and then a negative deflection so a biphasic component to that T wave but they deeply inverted terminal portion there. So that's a classic finding in Wellens. And so we don't want to send that person home. We want to make sure we treat them appropriately. Next is high-grade AV block. So high-grade AV block we talked about clear indications for pacemakers like third degree AV block, Mobitz type 2, patients that maybe have highly symptomatic other types of heart block may qualify for a pacemaker. But high-grade AV block is another one of those sort of umbrella type terms but two to one AV block is something that I see a lot in electrophysiology. So here where this patient is dropping every other QRS complex. So we have a P wave and nothing after it, a P wave and a QRS, P wave nothing after it, P wave and a QRS. So they're dropping every other beat which means that's a very unstable rhythm. So this is someone high-grade AV block. We want to make sure we evaluate that person for reversible causes and then typically they end up needing a pacemaker. And lastly is long QT syndrome. I talked to you about the QT interval and how we can measure that. The QT interval is a little bit difficult to eyeball and get just right. But one of the tricks I do is I find an RR interval. So I mean by that is here's an R wave and here's an R wave and I'm going to look and see where is that where does that QT fall in between there because that QT interval should be less than half the RR interval. And if it's not then I should think about a prolonged QT. So what's challenging is when there is a prolonged QT what happens there is I'm prolonging the ventricular repolarization phase and so everything just occurs a little slower so it's very sluggish to come back up to baseline and it can be difficult to say exactly where that ends. So what I try and do is draw a diagonal line from the tip of the T wave up to baseline and that is where I can say it ends. So this patient this patient was on an anti-arrhythmic drug Sotalol and had some renal failure issues and presented with some near syncope and this was a presenting EKG with a long QT interval and then they ended up having short runs of polymorphic VT as a result of that. So you can see here the long QT and anytime I prolong that refractory period then I can I prolong that relative refractory period and that's when if there's a strong enough stimulus a PVC falls there and they can have ventricular tachycardia that is typically polymorphic as a result and that's what happened in this case. So that concludes our EKG lecture. I hope you find found this helpful. Here are some references that I used when preparing the lecture and I have some articles here in case you want to read more about some of the things that we discussed. Thank you.

ischemia

infarction

EKG interpretation

coronary supply

diagnosis

EKG leads