Hi, and welcome to our next offering in our series, Electrophysiology for the Cardiovascular Advanced Practice Provider. Our topic today is EKG interpretation. I have some readings here for you to check out. EKGs are something that you probably have a baseline level of comfort with, so my intention here is to try and take that to the next level. In your EKG textbook, if you feel that you need a refresher on some of the basics, please read over some of those early chapters in the book so that you feel like you're caught up to speed. I want to talk about things that I see a lot in electrophysiology, either things that we get consulted on a lot or just some discussions I have with colleagues on a regular basis, things that providers maybe feel a bit less comfortable about, and I want to try and take your skills to that next level with learning things in a bit more detail that you might not have a great understanding of, so that's my goal with this lecture. We're going to recall a systematic approach to EKG interpretation, and we'll talk a bit more about supraventricular tachycardias and how we can diagnose those on EKG. Supraventricular tachycardia, I want you to feel more comfortable with diagnosing that. Vesicular block, as well as antiarrhythmic medications and their effect on the EKG. Here's a little review, systematic approach. There's lots of different systems you can use to interpret a 12-lead EKG, and there's plenty of different ways to do it, so do what you feel comfortable with. This is a system that I use, and it helps me not to leave anything out. The first thing is to calculate the rate, so we just want to know, is it too fast? Is it too slow? Or is it just right? The most common way I do this is by looking at a standard EKG, I look at the rhythm strip along the bottom, and I count up all the QRSs that are there in that rhythm strip, and I multiply by six. I like this way because it doesn't matter if the heart rate is really fast, really slow, or if it's irregular, I get a very accurate heart rate. You may be familiar with the 300-150-100 method, which is also a really great way to do this. You find a QRS that falls on a thick, dark line on one large box, and then you count over by one large box until you get to the next QRS, and you go 300-150-100, 75-60-50, and that approach is gone over in your book. The next step is evaluate the rhythm. What we want to know here, are the QRSs following a pattern, or are they not? I like to think of it that way because if I know if the rhythm is irregular, I can then think, is it regularly irregular, or is it irregularly irregular? That's nice because now I've got a built-in differential diagnosis. If the QRSs all follow a pattern, and they're predictable, then it's regular. If I know that the rate is above 100, then I can say sinus tachycardia. If I know that the rate is slow, then I can say sinus bradycardia. I can do that by two things. One is establishing that it's regular, and the second step is looking at the P wave. Evaluating the P wave and its relationship to the QRS, this will oftentimes hold the key to my diagnosis. Just because something is regular and fast, it may not be sinus. Maybe it's PSVT. I can tell that by looking at the P wave. If something is regularly irregular, maybe it's something like ventricular bigeminy or trigeminy, or a Mobitz type 1 second degree AV block like wanky block. That can follow a pattern. Whereas if something is irregularly irregular, it's probably atrial fibrillation or possibly a variable flutter. After I establish the rate and the rhythm, now I look at the axis. I want to know really if it's normal left or right, and most of the time, that tells me everything I need to know. However, we're going to take it a step further and learn how to figure out axis in degrees, because that's vital if I want to try and diagnose a hemiblock. That brings me to my next step, block. I want to evaluate the PR interval. Is it greater than one large box, greater than 200 milliseconds? Then there's a first degree AV block. The QRS, is it wider than three small boxes, wider than 120 milliseconds? Now you need to consider the potential for a left bundle or a right bundle branch block. Then finally, the QT interval. The last step is to evaluate for ischemia or infarction. If you're like me, this is probably the place where your eyes go to first. Certainly if someone has ST segment elevation, that's where your eyes should go first. You always want to evaluate for those more subtle changes of ischemia or maybe an old infarction. That's your systematic approach. That's the one that I use when evaluating a 12 lead EKG. Let's move on to our first topic, determining the axis in degrees. The cardiac axis is the general direction of electrical flow through a person's heart. Normally, if I think about the base being up here and the apex being down here, my normal conduction should be like this. If I shift that conduction this way, I have left axis deviation. If I shift the general direction of electrical flow this way, then I have right axis deviation. Determining the axis in degrees, I really only need to look at leads one and AVF. Leads one and AVF create my four axis quadrants, which tell me normal, left, right, or indeterminate, which falls in the ... I'll get my pointer here and I'll show you where those are. This is your upper quadrant where it's an indeterminate axis. Normal axis should be right here between plus 90 and zero. If I look only at leads one and AVF and I think back to Eintobin's triangle when you learned about that, I know that in lead one, lead one is going to be positive at the left and lead AVF, I could think of as having a positive orientation at the feet. As electricity moves towards a lead, that lead will see it appear positive. As it moves away, it'll appear negative. Those are important concepts when you think about axis as well as bundle branch block. If I look only at leads one and AVF and I evaluate the QRS complex, whether it's positive or negative, that's step one. If the QRS in lead one is predominantly positive, then I know the axis is pointing somewhere to the patient's left. That means it's going to be somewhere over here in one of these quadrants. Then I need ... The next step is to look at lead AVF and I want to see where the QRS is there. If it's positive, then I know it falls somewhere down here. Then I look, where do those two overlap? Between here and here, they overlap in this normal axis quadrant right here. For most people, that's it. That's all you need to do is to determine if it's normal left or right. We want to take it to the next step and try to figure out the axis in degrees. For all of us, if the axis is normal, you don't really need to know a whole lot else about it. But if the axis falls in the left or right quadrant, it's possible that that patient has a hemiblock. What I mean by that is the left bundle has ... There's two fascicles. There's an anterior fascicle and a posterior fascicle. You need to determine if one of those is blocked or delayed because that's a type of a conduction delay. If we start combining conduction delays, that can be a bad thing for that patient. We want to make sure we evaluate the EKG in its entirety. Let's look at that a few more different ways. This is our axis wheel a little bit bigger so you can see it. Each lead is assigned a general vector within that EKG. What we're doing when we combine, we say the cardiac axis, we're saying it's the electrical average of all of those vectors and that 12 lead EKG. That's the general direction of electrical flow, which normally we want it to be somewhere in that normal quadrant. We can determine the axis in degrees by, first step, figuring out if it's normal left or right. Then we want to identify the most isoelectric lead. That means the lead that's as much positive as it is negative. The average QRS vector will intersect the most isoelectric lead at a 90 degree angle. Using this figure, we can locate the position of this lead in one of those quadrants and then we move 90 degrees towards it to see what that number is. Let's look at an example. In this EKG, I can look at leads one and AVF. I'll also introduce the two thumbs up method here, which you might be familiar with. We can look at the QRS and lead one and it's positive. The QRS and lead AVF is negative. My left thumb is up, so it's a left axis deviation. You can also remember it that way. That's a quick and easy way to determine axis. I know there's a left axis deviation somewhere. The mean axis is going to be somewhere between zero and minus 90. Then I look and see which lead is most isoelectric. Now, remember, we're not looking at the precordial leads. We're only looking at the limb leads. Lead two is clearly the most isoelectric. It's as much positive as it is negative. I know that the mean QRS vector is going to intersect that at 90 degrees. Here's lead two. I can count 30, 60, 90 degrees and I come up with minus 30. Now I know the axis in degrees. It's very simple to do that. We care about axis deviation because that can give us some additional clinical cues as to what's going on with that patient. If someone has a left axis deviation, certainly that could be from a left bundle branch block. If I've got a delay in conduction on the left side, I will require additional electrical vectors to passively depolarize from right to left. That shifts my general axis to the left. Same concept with an anterior fascicular block, which I'll show you a picture and that'll make more sense here in a minute. Obesity can do this. If someone is very overweight, then their abdominal adipose tissue can push up on their diaphragm and that can force their electrical axis to the left. For right axis deviation, it's kind of the opposite of everything we've talked about so far. Another thing I'll point out clinically is COPD can do that. If someone has big hyperinflated lungs, you think about what a chest X-ray looks like in someone with advanced COPD, their lungs become very hyperinflated and that stretches their mediastinum in a vertical direction. And that also stretches their apex of their heart. So again, it's kind of like you take their apex of the heart, you just kind of pull it down and that shifts over to the right. So left anterior fascicular block versus posterior fascicular block, if we just kind of picture the heart here surrounding this, we got our AV node, here's the right side of the heart, the right ventricle, and here's the left ventricle over here. So the anterior fascicle is located near the anterolateral portion of the left ventricle. So when this fascicle is blocked, there's a delay in electrical activation of that area, which is going to shift the general axis towards that direction. So it causes left axis deviation. And it has to be minus 30 or more negative. So to diagnose the left anterior fascicular block, step one, they have left axis deviation. Now remember, they don't have to have a full left bundle branch block, they don't. So the QRS is not wide enough to meet the criteria for a bundle branch block and the additional criteria we look for with the bundle branch block. But we see left axis deviation and the QRS is often a little wider than it should be because there's a slight interventricular conduction delay. And then what we see is in the inferior leads, they're predominantly negative. There's an RS pattern and the lateral leads are predominantly positive. There's a QR pattern. And this makes sense because of the direction that we're shifting electricity. So let's look at this on a 12 lead. So in this example here, we can see here's lead one and here's lead AVF. And lead one is predominantly positive, lead AVF is predominantly negative. So there's left axis deviation. The next step is to look here at the inferior leads two, three and AVF and I see a nice RS pattern. RS, RS. That's not a Q wave because the first deflection in that QRS is up. And then I look at leads one and AVL and I can see a Q and an R pattern in those leads. So I have left axis deviation plus a shifting of electrical flow and I can diagnose this person as having a left anterior fascicular block. Think of it this way. Think of that cardiac axis. Leads one and AVL are predominantly positive. So they're gonna see electricity moving towards them. Leads one and AVL tell me about the lateral wall. I have a shifting of electricity towards the left anterior fascicle because I'm trying to depolarize passively. So that shifts electricity towards those leads. So the lateral leads will see electricity moving towards them and it looks positive. Just the opposite occurs with the inferior leads but that's down here. Electricity is moving away because it's shifting over to the lateral side. And that's why two, three and AVF are predominantly negative. It's kind of just the opposite with the left posterior fascicular block. So the left posterior fascicle, you can see in the picture here, is located inferiorly and toward the right side of the left ventricle. A delay in electrical activation of this area will shift the axis towards the right. So plus 120 or more positive. So to diagnose the left posterior fascicular block, there has to be right axis deviation. And then the inferior leads will see a QR pattern or they're predominantly positive and the lateral leads are predominantly negative. So in this example here, we see there's a right axis deviation. We see lead one is predominantly negative. Lead AVF is predominantly positive. And I see inferior leads, the QR pattern and inferior leads. So predominantly positive and the lateral leads are predominantly negative. So we can determine the axis in degrees in this one too, if we want, because we can look at which we should. So ABR of all the leads here, the limb leads, that's the one that's as much positive as it is negative. So let's just look back at our picture here. So we know there's right axis deviation. And then ABR is the one that is most isoelectric. So I can go 30 from ABR. I can go 30, 60, 90, and see there I have an axis of plus 120. So it checks out. So that's why we care about determining axis in degrees. Okay. So axis in degrees for fascicular block. But then another thing that you might not think about is when someone comes in and it's always pretty obvious, someone's got a left bundle branch block or someone's got a first degree AV block, but we might not think to look for a fascicular block. And two of the most concerning electrocardiographic findings in the setting of someone with syncope is bifascicular block with first degree AV block and left bundle. So bifascicular block with a first degree AV block and a left bundle with a first degree AV block. So those are two things that we always wanna look for when someone comes in with syncope or near syncope. So studies have shown that patients with a bifascicular block or a left bundle are more likely to have high grade AV block when you do an electrophysiology study and a baseline long PR interval increases that risk, which reflects the advanced conduction system disease. So when you see a patient like this, maybe they're completely asymptomatic, but you wanna make a note of this so you can follow up with them in the future and make sure that there's no progression. So in this example here, we can see this patient has a right bundle branch block. So the QRS is wide, it's more than three small boxes. And I've got the RSR pattern here in V1 and V2. And then in V6, I have an RS pattern. But then you'll also notice that the axis is abnormal in this example. And we've got an RS pattern in 2, 3 and AVF. So this person has significant conduction delays on this EKG, a bifascicular block with a first degree AV block. And this is someone that we're gonna follow a little bit more closely. So we've got a right bundle branch block, a left anterior fascicular block and a first degree AV block. So, and if you can follow my pointer here, I'll show you a quick and easy way to look for a first degree AV block. If I find a QRS that falls on a thick dark line like this one, and then I look at the start of the P wave. If it's more than 200 milliseconds, then I, which I can quickly eyeball that and see that it's more than one large box. And that looks like a first degree AV block. So that's someone that we're gonna watch a little bit closer. The other example will be a left bundle branch block with a first degree AV block. So left bundle pattern here, the QRS is wide, more than three small boxes. And I've got a classic pattern of a left bundle here with the predominantly negative complex in V1 and predominantly positive in V6. And I've got a first degree AV block here as well. So those are two EKGs that you'll wanna follow a bit closer. Maybe you ask them additional questions about medications that they're taking, questions of fatigue, near syncope and certainly syncope. So our next topic is supraventricular tachycardia. This is a common all encompassing term for any rapid arrhythmia that originates above the ventricles. So this could be things like sinus tachycardia. It could be AB node, rancher tachycardia, atrial fib. So lots of things fall in this category. Patients with SVT, we're saying they have a narrow complex QRS. So less than 120 milliseconds or three small boxes. And it's fast. It's greater than a hundred beats per minute. What makes this a bit more complicated if someone has aberrant or slow conduction through the ventricles, and that can result in a wide appearing QRS, which can make the diagnosis more difficult. So when you see someone with SVT, your differential diagnosis is pretty broad at first. But remember what I said about the P wave. We wanna evaluate the P wave and its relationship to the QRS. And that can help us narrow down our differential diagnosis. Your job with SVT is to help you Your job with SVT is to determine, number one, is it dangerous? Number two, can I fix it? Can it be ablated? And then number three, I guess I can add a third thing in there that you wanna ask yourself, how should I treat this? Is the patient symptomatic? Do I need to treat this? Because sometimes our treatment can be worse than the actual rhythm itself. So SVT, identify the P wave if possible. Look for a break or a pause in the rhythm to pick out P waves and note their relationship to the QRS. You certainly don't wanna miss someone with atrial flutter that now you need to evaluate for anticoagulation. Look before and after the QRS and within the T wave. If you have access to an EKG of them in sinus rhythm, this is very helpful to try and pick out subtle changes. So you can look at those EKGs side by side and evaluate for any differences. The next step, find the initiation and termination of the arrhythmia. Look for a gradual increase or decrease in heart rate. That's more consistent with something like sinus tachycardia. If you have a sudden onset and termination, that's more consistent with something like PSVT or paroxysmal supraventricular tachycardia. Identify if the rhythm initiates with a PAC or a PVC. So if you're working in the hospital and you're evaluating someone where you suspect SVT, maybe they've got a narrow complex tachycardia, then look back through telemetry, see what you can find. If you look back all through the night, maybe you'll find a place where it started. And if it starts suddenly and stops suddenly, it implies some type of a potential for a re-entrant mechanism. Whereas if you see them gradually increase their heart rate and you can see a P wave that looks normal that's starting all of that, maybe it's sinus tachycardia. So look at a couple examples here of two different patients. And if you only looked at the first part of each rhythm strip, I would say, you can't say what that is. You can offer a differential diagnosis, but you can't look at that and say exactly what's going on. However, when both of these patients were given adenosine, which is going to temporarily block in the AV node, you can see a significant difference with their underlying rhythm. So in the top example here, now we see these beautiful little flutter waves marching on through. In the bottom example, we actually terminate the arrhythmia. So the arrhythmia gets terminated and we can see pickup, it picks up here with a sinus beat, one and two. So a little clinical pearl, if you see a patient who has an arrhythmia that terminates with adenosine, you want to really think about whether or not that person could be considered for an ablation because a lot of times an arrhythmia that terminates with adenosine means that it requires the AV node to initiate and maintain that arrhythmia. So that means it's usually something that can be fixed with an ablation procedure. Your patient on top there is someone that now you need to think about anticoagulation and risk stratification. PSVT, as the name implies, paroxysmal supraventricular tachycardia, sudden onset and sudden termination. When you say PSVT, what you're saying is it's one of these three things, ectopic atrial tachycardia, AV node reentrant tachycardia and atrioventricular reentrant tachycardia. Those are three things that we would consider. So ectopic atrial tachycardia, this occurs via three mechanisms. There could be enhanced automaticity, triggered activity or micro reentry, which involves a localized area of excitable tissue. Atrial tachycardia, three or more PACs, and we say it's sustained if it lasts more than 30 seconds. A lot of times this involves just one dominant pacemaker that overdrive suppresses the sinus node, remember we learned about that in our previous lecture, to become the dominant pacemaker. The fastest pacemaker will win whether it's supposed to be there or not. So an atrial tachycardia, now you can also have a multifocal atrial tachycardia, but an ectopic atrial tachycardia, as the atrial rate increases, the PR interval prolongs similar to a Wenckebach pattern. The faster the AV node is stimulated, the longer it's refractory period becomes. And as I mentioned in our previous lecture, this is because we want to prevent the ventricular rates from going too fast when the conduction goes through the AV node. The P wave will eventually become buried in the preceding T wave and may not be visible at faster rates. This is why evaluating for the initiation is so important because if you just look at a few beats of that atrial tachycardia, or maybe five, 10 seconds of it, you might not see that, but if you go back and sometimes it's only a couple beats that you can see, but you can really see that P wave come first with a PAC and then a shorter, a longer PR interval after that. And then the P wave will eventually bury usually in the T wave. As the atrial rate slows down, P waves will become visible again as the PR interval returns to normal prior to termination. So here's an example that is, it's pretty slow, but this is a patient that had a pacemaker and they were having repetitive, non-sustained atrial tachycardia. And if you look at the rhythm strip here, this is what's most helpful. Here's a normal beat and here's a normal beat. And you see this one comes in just a little early and that P wave looks a bit different than the other P waves as well. And now you can see that PR interval starts to lengthen a little bit and that P wave really disappears in that T wave before it slows down again. And now I can see that P wave prior to termination. And this patient has a pacemaker. So that's an atrial pace beat and now they're back in normal sinus rhythm. So that's an example of atrial tachycardia. Other types of tachycardias are what we call reentrant. So AV node reentrant tachycardia and AV reentrant tachycardia. And from an electrophysiology standpoint, reentrant circuits have two limbs. So there's two components there. Usually there should only be one. And they require three components, unidirectional block in one of those limbs, slow conduction of an impulse down the other limb, and then a recovery at the block site prior to usually a retrograde transmission of that impulse. So AV node reentrant tachycardia, this is the most common thing that you're gonna see of the PSVTs when we talk about the reentrant mechanisms. So frequently affects middle-aged people, it can occur in any age group. And this occurs because there's a rapidly conducting impulse utilizing two pathways within the AV node. So normally you should only have a fast pathway. So in patients with AVNRT, patients have a dual AV node. There's a slow pathway and a fast pathway. So what happens is a normal impulse goes down the fast pathway, and then a PAC comes in and it blocks at that fast pathway. But it just slips right down that slow pathway and it goes slowly down there. And by the time it gets to the bottom, that fast pathway is recovered and it's ready to go. Transmit retrograde fashion up that fast pathway. And now we have our loop tachycardia. So what happens is your ventricle and your atria, they end up getting stimulated at about the same time. So the ventricles usually are first and then the atria are after, but it occurs so quickly that a lot of times that P wave will be buried in a QRS. But sometimes you can see a little retrograde P wave at the end of that QRS. So it initiates with a premature atrial contraction. The P wave is buried in a QRS, or sometimes you see it at the end. And when initiation and termination are not available, it can be really hard to say what this is. There's a lot of different types of SVT that can look exactly the same. But when you can see a P wave, now you know what the diagnosis is, or at least you can certainly narrow it down to a handful of things. So here's AVNRT. So you're going to look at this and say the QRSs are fast, they're regular, and they're narrow. So this is PSVT. I cannot identify anything in between the QRSs. I can't pick out any P waves. So I can't really say for sure what this is, but I can offer a differential diagnosis of different types of SVT. Here's the alternative form where I can see a little retrograde P wave. That's this right here. And a lot of times you'll see it in the inferior leads, 2, 3, and AVF. Okay, so that's a retrograde P wave that's occurring as the atria are conducted retrograde via that AV node and that extra pathway. The other type is AV reentrant tachycardia, and we also sometimes call this accessory pathway SVT. This involves an abnormal area of conducting tissue outside of the AV node called the bundle of Kent. Electricity spreads from the sinus node through the bundle of Kent and bypasses the AV node on its way to the ventricles. Think of it this way. If you picture the atria, a little pond, and then you picture the electrical impulse, like a pebble, you drop that impulse, you drop that pebble in that pond, and it's just going to ripple out to everything in its path. And that's what happens with these sorts of things. So if there's a pathway in the AV node, and then farther out in between the atria and the ventricles, when you drop that pebble in, and that electricity is just going to spread out, and wherever it gets first is where it's going to go. So sometimes you'll see that being conducted through the accessory pathway, and that's when we see pre-excitation with a delta wave, and sometimes it just goes through the AV node. So with AVRT, you can go either way. We can have electricity going down the sinus node, simulating the ventricles, and then going up the accessory pathway, or we can have the impulse going down the accessory pathway, simulating the ventricles, and going back up the AV node. As you can imagine, if the ventricles are stimulated via an accessory pathway, that will look quite a bit different than if they're being stimulated via the AV node. The key here, which can be confusing until you see it, is that when someone manifests an arrhythmia, the delta wave goes away. So we don't see the delta wave, but the delta wave tells us that they have an accessory pathway, and I'll show you some examples of that. So AVRT is defined by the direction of conduction over the accessory pathway. We call it orthodromic AVRT, which is the more common type, and that's when conduction occurs via the AV node and retrograde via the accessory pathway. So when someone's in sinus rhythm, they may have a concealed pathway. So when someone's in sinus rhythm, then the conduction might be going down the AV node, and then you don't even know they have an accessory pathway. But if a PAC comes in, it can block at the AV node and it can go down the accessory pathway, and now we can have a wide QRS as a result of that. The alternative is if they're conducting normally down the accessory pathway, now I see a short PR interval and a delta wave, I see pre-excitation. A PAC comes in and it blocks at the accessory pathway, but it's going to go down the AV node and then back up the accessory pathway. Now I've got a narrow complex tachycardia that looks a lot like a AV node re-entrant tachycardia, which is also narrow. So that's kind of what I just explained what happens there. So let's look at an example of this with the delta wave. So in this patient, there's sinus node activity. I can see a P wave, but the PR interval is short and there's a slurring in the upstroke of the QRS that we call a delta wave. You can see it better in some leads than others. You see a really nice delta wave here in AVL. This is a delta wave here in three in AVF, and you can also see it pretty nicely in all the precordial leads. So what this tells me is that the sinus node starts the impulse and it's conducting down the accessory pathway. So normal, otherwise everything is normal. This is what it looks like when someone, when a PAC will come in, it's going to block at the accessory pathway, the bundle of Kent, and it's going to shoot down the AV node. So it's going to go down the AV node and then back up the accessory pathway. And look what you can see here, an inverted P wave. So a retrograde P wave. And that makes sense because the ventrals are being stimulated via the AV node. So that's why the QRS is normal and narrow, but then there's a retrograde P wave as it goes back up the accessory pathway to the atria. And now I have my loop tachycardia, which looks like this. Now with antedromic ABRT, much less common, but it can potentially be dangerous because it tells us that that accessory pathway can conduct. And remember the accessory pathway does not have those principles of refractoriness that the AV node has. So that means it's going to go as fast as it can. And in a lot of cases, it doesn't go very fast, but when it can conduct fast and the person say goes into atrial fibrillation and they've got an accessory pathway, that's when people can have a ventricular rate in the upper 200s, 300 beats per minute, and they can have ventricular fibrillation as a result. So that's why we care about this. So antedromic ABRT is just the opposite of what I talked about. So now these patients are going to, their normal connections going through the AV node, a PAC comes in, blocks at the AV node and shoots down that accessory pathway. And as a result, their QRS looks very wide and it looks every bit like the person has ventricular tachycardia. So you don't see this very often, but that's what it can look like. All right. Next topic is atrial flutter. So one of the important things to differentiate from an electrophysiology standpoint is typical versus atypical flutter. And we care about that because typical flutter is generally or typically amenable to ablation. And that's nice because you can knock out that pathway that's not there, that shouldn't be there, that pocket of excitable cells in the atria. And then you can make that patient feel a lot better and you can reduce their risk of stroke as you do it. So with typical flutter, we have energy transmitted from a single circuit. So it's a single circuit. It's bigger than an atrial fib circuit, somewhere in the atria. And it's transmitted in a counterclockwise fashion, typically around the tricuspid valve. So we can see this with negative P waves in the inferior leads, 2, 3 in AVF and positive P waves in V1. So I always think about this, like if I had a clock face and I put the clock face on the EKG, and I'm going to see the hands going counterclockwise. And so what do I have over here? I have leads 2, 3 in AVF. So 2, 3 in AVF, and then I have V1 is going to be up here. So 2, 3 in AVF are going to see that impulse moving away from them. That's why they're negative. And V1 is going to see it moving towards it. And that's why they're positive. It can also be clockwise and that's just the opposite, just the opposite findings. So V1 will be negative and 2, 3 in AVF will be positive. If it doesn't meet one of those criteria, then we call it atypical. So P waves do not follow a particular pattern. There's still those beautiful little flutter waves, but it doesn't follow a pattern. And this tends to behave more like atrial fibrillation. There's more than one circuit. So it's not as amenable to ablation as something like typical flutter. So let's look at an example of that a little closer. So here's your 12 lead EKG. Hopefully you can pick out those flutter waves really nicely there. And then if I make leads 2, 3 in AVF and V1 a little bigger, let's look at what I mean by negative. So I kind of think about which end is more pointed. So of this little circuit, here's a point and here's a point and there's one and there's one and there's one. So that's negative. And V1, you can clearly see that that's upright, positive, positive, positive, positive. So that's what I mean by negative versus positive. And the first couple of times you see typical atrial flutter, you'll really get the hang of it. You'll see it and you'll say, aha, that's what that means. And then it's very easy to pick up once you see that. Here's just the opposite of clockwise typical flutter. So 2, 3 in AVF are positive. Those flutter waves look upright. And then V1, we see those flutter waves as negative. So you can really look like you know your stuff when you pick out a typical flutter. And then atypical flutter, it just doesn't follow a pattern. In this example, everything is positive. And so what you'll often see is you'll get EKGs at different times on that patient and their flutter waves might look different each time you see them. SVT with aberrancy versus ventricular tachycardia. So this is a bit more nuanced thing to learn, but let's say you see a patient with a wide complex tachycardia. Well, in general, especially in someone with structural heart disease, you should assume that that's VT until you prove it's not. That's a good approach. But there are some clues you can look for. And that's what I will share with you today. So structural heart disease, especially LV dysfunction, you've got to treat that as VT until someone proves you otherwise. And this is in part because number one, it's much more dangerous and life-threatening. And VT is much more common than SVT with aberrancy. There are several different criteria you can look for. There's something called Welland's criteria, which has been around for decades. The Brugada algorithm is a little bit newer, but both well-validated criteria and approaches that you can use. So if I were going to pick out a few things from those that you can look at a little quickly and easily on EKG, here's the things that I look for. So the first thing is positive or negative concordance in all precordial leads. So that's something that's more likely with VT. So if you think about your precordial leads, which are placed right along this area, as electricity spreads through there, you should see characteristic findings. And that's what we call that R-wave progression. So normally we see the R-waves being more negative in V1 and V2, and then maybe isoelectric by V3, V4, and then by V5, V6, everything should be mostly positive. And that's because those leads are seeing electricity either move towards them or away from them. If you lose that concordance, then that means that maybe there's an impulse that's coming from somewhere else that doesn't follow that typical pattern that you should see electricity flowing through the heart. Like if someone's got a VT focus, it's somewhere down in their ventricles, it's going to send impulses like this. And you're more likely to see it in that indeterminate axis category, which brings me to my next point, indeterminate axis. So indeterminate axis is something that you are much more likely to see with VT. If you have an old EKG, look at the VT, the VT axis compared to their normal axis. In VT, the axis is generally going to be distinctly different than the axis when they're in normal sinus rhythm, because it's coming from a different place. AV dissociation, if you're lucky to see that, that oftentimes just seals the deal for your diagnosis that that's VT. So with AV dissociation, remember that atria have a great job. They have it pretty easy. It just starts the impulse from the sinus node. And they don't really care what happens after that because they got the AV node there to provide backup, the Purkinje fibers to provide backup. So they don't know what's going on. So with AV dissociation, the sinus node will just kind of send the impulse. And then somewhere along the line, there's that ventricular focus that just starts firing off very rapidly. And so you'll see P waves just march on through doing their thing, almost always slower than a ventricular focus. And then you'll see these QRSs that are occurring very, very rapidly. And so usually you'll see this better at slower rates, but I can see P waves that are clearly not associated with the QRS. And that's the key that you're looking for. QRS duration is wide, and particularly that RS component is very wide. And then VT is much more likely to be regular than irregular. So those are some things you can look for to help you diagnose this. So here's a patient that has a, their heart rate is fast. The QRS is wide. And so at first glance, you might look at this and think, oh, maybe this person has VT. But if we apply some of those criteria that we've just talked about, the very first thing is the positive negative concordance. QRSs are, they're kind of looking positive here and here, and then clearly negative all the way across. So that doesn't really match up. The QRSs are certainly wide. The axis here is positive in V1, is negative in AVF. So it's a left axis deviation. So now you're starting to think, is there some type of a baseline bundle branch block? What's going on here? So when we go through our criteria, even though some of them are helpful, some of them don't really match up. So we're able to find an old EKG and we see this. So let's look and compare. The axis is exactly the same. I still, I continue to lack positive and negative concordance across the precordium. See, there's a kind of a mix of things there. And I see that their baseline QRS is very wide. So this is someone that has an interventricular conduction delay to start. They've got a right bundle branch block, looks like a left anterior vesicular block. So that is what's resulting in this wide QRS. And so when we compare this and we look at this, the general direction of energy flow through every lead really looks exactly the same. And then we can compare these two EKGs to a different patient that truly has VT. And here's a great example of negative precordial concordance. Look at V1, 2, 3, 4, 5, 6. So negative all the way across the QRS. This is what a QRS is are wide and it's very regular. So that's something that can, that can help you as well. So a lot of times you're, you know, that all criteria aren't going to completely match up, but you can take the whole clinical picture into consideration and take, make a nice educated estimation of what you think is going on. So a couple of pictures of AV dissociation. So this one is really slow. We're trying to pick out some P waves. I got a P wave there and a P wave there with some very slow ventricular beats. We're trying to say that those P waves are not associated with the QRS. Not like we see right here with this beat where there's a P wave clearly associated with a QRS before an ectopic beat comes in. If we apply that to a 12 lead like this one, I can and I'm looking at the rhythm strip here. It gets a lot easier to pick that out. And so I can see P waves. Here's a P wave right here. Then I can also see a P wave here and a P wave here. So those are P waves that do not appear associated with the QRS. It doesn't look like this person has some type of a flutter where I can pick out P waves. That's certainly not sinus tachycardia. So if you see things like that, that can be extremely helpful. So AV dissociation is often diagnostic. The other criteria that's often diagnostics are called fusion beats. So fusion beats occur when an atrial impulse is transmitted through the AV node. And this activates the ventricle simultaneous with ventricular depolarization that occurs via an ectopic focus generating VT. So remember the P waves, they do their thing and they go on with their life. So if the VT rate slows just enough that one of those P waves captures intrinsically in the ventricle, and then they go right back to their ventricular focus, you'll see that as a capture or I'm sorry, as a fusion beat. So a fusion beat is when there's kind of a mix of the two. So we have a mix of a P wave kind of capturing in the ventricle, and it occurs really the same time as a ventricular focus is still firing. And it looks like a perfect combination of the two. And so this right here is a fusion beat, this one right here. And you can see how it looks similar, but a little bit different from the ones around it. A fusion beat, you're really only going to see in someone with slower VT though. And it makes sense because of the mechanism of it. We always want to make a note if someone has polymorphic or monomorphic VT. Someone, so here's a sinus rhythm and then the person spontaneously goes into some VT right here, monomorphic ventricular tachycardia before it terminates. And that looks distinctly different from someone with polymorphic VT. So when someone has monomorphic VT, sometimes we think about that as maybe more stable. You'll see that with patients who maybe have a big old previous MI and they've got some scar tissue there. And now we create a re-entrant circuit around that scar tissue. Whereas someone with polymorphic VT, things we automatically want to think about would be ischemia, a prolonged QT, medications that might be prolonging a QT or hypokalemia that can be doing that, and bradycardia. So here's another example of a patient with polymorphic ventricular tachycardia. What you'll see here is often these paired episodes where you've got a normal beat and then a PVC, a pause, a normal beat, a PVC. And then look what happens here. We have this PVC falling right at the end of that T wave because the QT interval is long. We're prolonging that relative refractory period. And now with a large enough stimulus, we can be off and running with this polymorphic VT. And that's exactly what happens here in a patient with bradycardia and this pause-dependent torsades. Brugada pattern is a rare but important pattern to look for in EKG. This is a type of a long QT syndrome, which is thought to be due to a mutation in a cardiac sodium channel. Someone may not never even know that they have a brugada pattern, but this is something there are a handful of things I always look for when I'm evaluating a patient with syncope, and this is one of them. So in V1 and V2, sometimes into V3, which you'll see is an RSR pattern, which mimics an incomplete right bundle branch block with ST segment elevation. So if you look at it real quickly, you might even think it's ST segment elevation, but it has a very distinct appearance that doesn't look like anything else. The clinical manifestation of this is sudden cardiac death from ventricular fibrillation in patients with structurally normal hearts. So genetic defects similar to that, which causes long QT syndrome, and here we see V1 and V2. We have an RSR, and then look at that ST elevation off baseline. Very classic in V1 and V2. It's like you took that J point and you just picked it up off the baseline there with an RSR pattern. Okay, antiarrhythmic effects on the EKG. In electrophysiology, this is a big part of our job, and it's something that you should be aware of in cardiology or whatever practice you're working in. If you're evaluating patients who are routinely receiving antiarrhythmic drugs, we want to get in the habit of looking for certain things on their EKG. So we see patients usually every six months to have an EKG to make sure that there's nothing deleterious that's happening over the course of time. So antiarrhythmic medications will cause a change in those action potentials to suppress arrhythmias and disrupt those reentrant mechanisms, but sometimes that can be a bad thing. So sometimes we can go a little too far with those effects, or if they're on additional medications that can do that as well. Now we have a combined effect that can potentially be negative. So here's some things that we'll look for. So as you recall with this cardiac action potential, we have sodium and calcium influx are responsible for that depolarization and then the plateau phase, and then the potassium efflux causes repolarization, and if we start disrupting that, we shift the action potential one way or the other, and we can see those changes on EKG. So with the class one sodium channel blockers having a moderate sodium channel blockade, the EKG changes might be something like a QRS prolongation, sometimes a QT prolongation, and a widening of P waves, and this is predominantly because of their effect on sodium channels. The other sodium channel blockers, for instance, something like lidocaine tends to have a weaker sodium channel blockade, and so we don't see a lot of distinct changes with lidocaine and maxillitine. With the one Cs, we use these a lot in clinical practice, like flecanide, propafenone, so strong sodium channel blockade, and what occurs here is a prolonged QRS duration and a PR interval. So I will always look for those things, and you should anticipate seeing some degree of this, and that's fine. What you want to make sure is that you don't start with a baseline normal EKG, and then maybe three months later, they've got a large first degree of E block, and now you see them three months after that, and now they've got some type of a, you know, a bundle branch block on top of that. So those are the sorts of prolongations that you want to look for and just be cognizant of and make sure that patients don't have any symptoms. And then the last thing we look for is with potassium channel blockers, and the QT interval is our big concern here. So things like amiodarone, Sotolol, that can prolong the QT interval, and oftentimes things like Sotolol will actually admit the patient to the hospital and monitor their QT interval to make sure, because a lot of times those changes will happen within the first five or six doses, so we monitor them to make sure that we're initiating those medications as safely as possible. So let's look at some abnormal effects. So here's a patient that had flaconide toxicity, and you can see really wide QRS complexes. You start to lose a lot of those normal markers on EKG, like a PR interval, where does that start, the T wave, and so we sometimes will call this like a sine wave pattern, and usually you stop the medication and that will improve. Sotolol on a patient with renal failure, you can see a prolongation of the QT interval, and it has a very characteristic appearance when the QT gets prolonged. So you see how it just gradually slopes back up to baseline. So normally, think about that action potential, the way it happens, we should just enter that repolarization phase and then everything starts all over again, so the ST segment should be coming right back to baseline. When we prolong the repolarization period, that doesn't happen, and we have this gradual sloping back to baseline, which is what I always look for when the QT looks like it's prolonged. Another tip you can look for is if you can eyeball the RR pattern, so the RR complexes, so we look from here to here, and then I want to try and measure where that T wave comes back to baseline. Your QT interval, if you're now, of course now we can look at our computer calculations and calculate a corrected QT, but you can eyeball it fairly effectively just at first glance, and your QT interval should be less than half the RR interval. So here's my RR intervals from here to here, and my QT, I want to measure from where it comes back to baseline, which is going to be right about there, and you can see that that looks like it's long. And here we can see that their QT starts being a little bit prolonged, and we have a normal beat and then a PVC with that pause, and then a PVC coming in, and we're kind of off and running with these abnormal beats here. So we see these runs of non-sustained BT, and you can also see some nice AB dissociation with that. So that's one of the potential problems, is if we prolong the QT interval, that can predispose the torsad to point. And then finally, non-cardiac drug effects on the EKG. The most potentially dangerous effect is a prolongation of the QT interval, and if you think about all the drugs that do this, there's a whole bunch of them. And so for most people, they're fine, they take these medications and don't have any problems, but other people, they may have some channelopathy or some abnormality that we would never know about until we test it with these drugs. So when you put patients on medications, just start, just be aware of the main categories of drugs. So things like, for instance, antidepressants. So let's say you've got someone on an SSRI, and you add something like a macrolide to it. Well, you should be aware of the fact that that can potentially have a bad effect on the QT interval. And then especially if that person is also taking an antiarrhythmic drug, well now we're combining, we start combining things, we increase the chance that we can prolong their QT interval. So be aware of the main drug classes that can do that. So that concludes our EKG discussion for today. Thank you very much.

EKG interpretation

advanced practice providers

supraventricular tachycardia

ventricular block

antiarrhythmic medications

arrhythmias

Brugada pattern

prolonged QT interval