And I'll turn things over to you to introduce Brad. Great. So we welcome Dr. Brad Knight. And we're going to first be seeing his pre-recorded video from last year. And then he's going to join us for a live question and answer session right afterwards. So let's queue up the video. And we're staying right on time to the minute. Just to kind of take a step back, and I think Jeff Winterfield made a great point at the beginning of his talk. This is not a board review course. We're not expected to know everything at the end of this course. But it's a way to introduce you to all these important concepts. You'll see that wherever you do your EP fellowship, everybody does things a little differently, different catheters, different setups, different mapping systems. But the principles are all the same. And once you figure that out, you can work with one attending and work with another attending. And even if the displays are different, you'll figure out that the principles that each person is following are pretty much the same. So what are the causes of supraventricular tachycardia? As a general cardiology fellow, you kind of learn what an SVT is. That includes sinus tachycardia, AV nodal reentry, AV reentry using an accessory pathway, atrial tachycardia. And when you hear the term PSVT, in general, that refers to these three tachycardias. These in the past, and if you look in old literature, were all called PAT, or paroxysmal atrial tachycardias, because they didn't recognize that these were really the mechanisms of most of these PSVTs. Junctional ectopic tachycardia sometimes isn't in that category. It tends to occur in the post-operative state, particularly in pediatric or congenital heart disease patients, or with isoproteinol when you infuse it in the EP lab. Atrial flutter and atrial fibrillation are also SVTs, but we can usually distinguish those or diagnose those on an electrocardiogram and really don't put them in the category of the terminology of PSVT, as is MAT, or multifocal atrial tachycardia. So these are the three main mechanisms of SVT. Those percentages are based on a study that we did nearly 20 years ago on the percentages of these categories when patients came to the EP lab with a diagnosis of PSVT. And so 2 3rds of the cases of PSVT that came to the EP lab were AV nodal reentry. About 1 3rd were AV reentry, and 5% were atrial tachycardia. Nowadays, I would say those numbers are different. There are fewer patients with pre-excitation, or WPW, that come to the EP lab, and there are a whole lot of patients who come to the lab with atrial arrhythmias as a consequence of surgery, maze procedures, and particularly catheter ablation. The first step before we talk about what happens in the EP lab is to look at the electrocardiograms. And I'm realizing this is increasingly a challenge. We have EPIC as our EMR. You can go through care everywhere, and you can read all the reports and everything. But one thing you can't look at are the EKGs, of course. So the only thing that you really care about is like going to see an orthopedic surgeon with all your records, but not the x-ray. So make sure you get the primary data, and you will start to realize how important that is when you get patients referred to you with AFib that once you find the tracing, or VF, that's artifact. So look at the tracings. Let's look at this tracing. This is a patient with recurrent PSVT. You can see a tachycardia that terminates, sinus rhythm with a different PR interval. Move my mouse here. And then resumption of tachycardia here. So is this an atrial tachycardia? And do we have an audience response for this? We may not. I just have them for the workshops. That's OK. It's the only question I really have in this talk. Is this an atrial tachycardia? Is this a junctional ectopic tachycardia? Or is this AV nodal reentry? So again, move this mouse. Here is a tachycardia. There's a P wave following each QRS. There's no P wave here. There's sinus rhythm, sinus rhythm with a shorter PR interval, a junctional beat, and tachycardia. So is this an atrial tachycardia? Who wants to say that? Is this a junctional tachycardia? Raise your hand if you think it's a junctional tachycardia. Raise your hands higher than your head. And is this AV nodal reentry? Good. All right. So it's not an atrial tachycardia because the atrial rhythm is not what's driving this. It doesn't start with a premature atrial beat or an atrial tachycardia. It's tempting to think it's a junctional tachycardia because it starts that way, unlike in the EP lab when we introduced premature atrial beats to engage the slow pathway and induce AV nodal reentry. This is initiated with a premature junctional beat. But it terminates reproducibly with VA block. And so these are important concepts. Look at how they start. Look at how they terminate. Look at transition zones. These are where you're going to find the answers to the diagnosis of the rhythm. So this is AV nodal reentry initiated atypically with a premature junctional beat. And this has been suggested to be more common when patients are treated with digoxin for AV nodal reentry or SVT because it slows the sinus rate and increases junctional automaticity. So these are the three categories that I'm going to put the talk into. And I think it's important when you walk into the EP lab to also think this way. The first thing you're going to do, whether it's looking at intracardiac recordings or pacing, these are considered baseline findings. What are the clues when you walk in the lab that this person is going to have one of those three tachycardias? The second thing after you induce tachycardia, which is really required in most of these cases to make a diagnosis, are what are the characteristics of that tachycardia? And then the third part is what kind of pacing maneuvers do you do during tachycardia? So when you walk in the EP lab and you put catheters up and you record electrograms and you do some pacing during sinus rhythm, what are the clues that patients are going to have one of those different types of tachycardia? One is if they have a dual avenodal physiology. If they have evidence of a slow pathway, as soon as you see that, you're pretty suspicious this person's going to have avenodal reentry. But it's not diagnostic. They might also have an accessory pathway. So what are the clues that they have an accessory pathway? Pre-excitation's an obvious one, but a lot of these patients, their pathways are concealed. They only conduct retrograde. And so what are the clues that they have retrograde conduction up an accessory pathway at baseline? Think about what would you be looking for? You would look for abnormal activation retrograde with ventricular pacing. Whether there's eccentric atrial activation, whether there's extra nodal response to parahysium pacing, and we'll kind of go through all these things. And so what are these baseline findings and how common are they? Again, this is data from a paper in Jack, which I think is referenced later, that we looked at 200 patients with PSVT in the EP lab and how common these observations were and how predictive they were for each of the three diagnoses of avenodal reentry, orthodromic AV reentry using an accessory pathway, or atrial tachycardia. So if you have pre-excitation, which only occurred in 15% of patients in this study, the likelihood you have ORT is 86%. It's not 100%. Those patients can also have avenodal reentry. They also can have the accessory pathway as a bystander, which is unrelated to their tachycardia. So they might have more than one tachycardia or it's a bystander. If the VA block cycle length is greater than 600 milliseconds, it's just another way of saying that there's really no VA conduction when you start pacing. If there's no VA conduction, it's very unlikely that there's an accessory pathway. Now, you might have an isoproteranol dependent or a pathway that's not evident at the beginning when the patient's deeply sedated, but that's quite unusual. The likelihood they have ORT is very rare. But you can have avenodal reentry. Remember, avenodal reentry involves the perinodal structures and a lot of times at baseline, there is no VA conduction. So that does not rule out the likelihood of them having inducible avenodal reentry. Dual avenodal physiology, again, it's present in over half of patients who come to the lab with PSVT, but it's not diagnostic, but it's pretty suggestive. And when you put catheters up and you see clear evidence of a slow pathway, it makes you start thinking this person's gonna have avenodal reentry. Decremental VA conduction is another way of, sorry, this mouse is just jumping all over, is another way of saying that it's unlikely to have a conventional accessory pathway, which does not usually conduct in a decremental fashion. Parahysian pacing is a maneuver, again, we put it in this category, even though it's pacing, it's not a maneuver done during tachycardia, this is a maneuver done during sinus rhythm. I think that leads to a lot of confusion. This is not a pacing maneuver that's in training or anything, this is done at baseline to look for evidence of a perinodal or septal accessory pathway. It takes advantage of the fact that the His-Purkinje system is insulated, as does the other pacing maneuvers of differential RV pacing, pacing from the base versus the apex. And today, we don't have time to go through all these, but I'm gonna kind of highlight some examples of the ones that I think are the most important. In general, pacing maneuvers are more specific than pharmacological maneuvers. You'll see a lot of people wanna give adenosine in the EP lab to determine if there's a pathway, et cetera. It can be useful if you're really struggling to make a determination of whether there's a pathway, but in general, it's not specific enough to hang your head on. So what does pre-excitation mean? It means that the ventricles are excited prior to when you would expect them with conduction over the His-Purkinje system. And it's very important to know what that measurement means. It means the measurement from the earliest His recording. You can see here on the surface EKG, you have atrial pacing with one-to-one conduction and a sudden change in the QRS morphology. And the HV interval, which is the measurement from the earliest His recording to any ventricular signal, typically the earliest QRS on the surface, excuse me. And you can see that the HV interval here is negative. It's minus 10. The His recording is after the onset of the QRS. When there's atrial pacing that results in blocking the pathway, you have an abrupt change in the QRS morphology and the HV interval suddenly becomes normal at 35 milliseconds. Less than 35 milliseconds is in general considered pre-excited, that's abnormally short. So this sounds simple, but you have to make sure you understand the principles here. The local appearance here doesn't change. You're not measuring the HV from the H to this V. It's to the earliest V anywhere, which is typically where the pathway inserts. How do you define a slow pathway? The definition of dual avianodal physiology is shown in this slide. This is from Mark Josephson's textbook. Pablo Dennis, who was at Northwestern, actually was the first to describe this in humans. Just retired, he was a tremendous colleague and we'll miss working with Pablo. But in this nice diagram, what you need to remember is the A1-A2 versus A2-H2 curve. That means that when you introduce a premature atrial stimulus, which is the A1-A2 coupling interval, so you're basically giving a PAC. You have a drive train, which is referred to as A1 or S1 in the atrium A1 and the ventricle V1. The second, the number two, is the premature extra stimulus. And you measure the AH interval and it's going to get longer, it's gonna decrement. But if there are two discrete physiological pathways, you'll get block in one and it'll jump to the other one. And so this definition of a greater than 50 milliseconds jump in the A2-H2 interval is how we define it. It was based on a decrement of 10 milliseconds. We usually come in by 20 milliseconds, which we've shown to be just as sensitive to a jump. Patients can have more than one jump. Patients can have no jump. They can have avianodal reentry and have a subtle difference between the fast and slow pathway. All it means is that they have, you know, the properties of the fast and slow pathway are different enough from each other that it can set up reentry. But most people will have a jump like this. And here's an example of that. Here's 600, 420 is a coupling interval, longer than usual, but you can see that the AH is 150. You bring in the coupling interval of that premature beat by 10 milliseconds and the AH jumps out to 330. And what else do you see here? Label this, this is an echo beat. So remember, blocking in the fast pathway and conducting over the slow pathway is a necessary but not sufficient thing for initiation of avianodal reentry. In this case, it caused block in the fast pathway, integrate conduction over the slow pathway, and then that allowed the fast pathway enough time to recover and go back up. So you have a single echo beat. Bringing that premature beat in any sooner is not gonna help you induce tachycardia. This is now blocking, integrating the slow pathway, and usually it means you have to give some isoproterenol or wake up the slow pathway. Can you, before you go to the next slide, can you clarify for everybody, because I'm not sure everyone can tell, how you know that there is an atrial event superimposed on top of a ventricular event, because everything's happening at the same time. That's obviously what the echo is. It's going back to the atrium. How do you know that? Yeah, so when we talk about atrium ventricular depolarizations, it's really important to look at the electrograms on each catheter at baseline so you really know what's being shown so that when you see tachycardia, you can differentiate these. That's one point. The second point is I try to be a minimalist in the EP lab, and we only have three catheters up at the beginning. We didn't talk much about that, but I start with a hyerodatrial catheter, an RV catheter, and a HYST catheter. We use a mapping system still for these cases, but I don't put in a coronary sinus catheter at the beginning routinely, because then that requires four catheters, typically requires accessing two veins. So I try to keep it simple. If I were to move one of these, I would move one of those into the coronary sinus, which we often do later if you still need to make a diagnosis. But the point is that you need a catheter that clearly shows an A and a V. And so if you look at this, again, we don't have sinus here. You'd want to look at sinus, but you can see with atrial pacing that there's an A, sorry, there's an A, a HYST, and a V. And if there's an A in here, you're not gonna be able to see it. But the hyerodatrial catheter shows a pacing stimulus, atrial capture, and then you can see this has to be an A. There's no ventricular signal coming from here. So that's a great point. And in particular, in the coronary sinus, you'll see an A and a V. And you have to be very careful. A perfect example is when you're monitoring VA conduction with junctional ectopy when you ablate a slow pathway. And you'll hear about that, but when you look for junctional ectopy, that's what is necessary to make sure you're ablating a slow pathway. You can't monitor AV conduction. So you, by default, monitor VA conduction. So you have to have a great atrial electrogram. If you have an A and a V and you get a junctional rhythm, you may not be able to determine that. So it applies to many different scenarios. That's a great question. This is, I think, from the heart rhythm board review course many years ago. So I stole this slide from Hugh Calkins to talk about perihysium pacing. So what is the evidence of an accessory pathway? In general, as Jeff showed, some of the most challenging cases are differentiating AV nodal reentry from a septal pathway. However, this only will help you identify septal pathways that conduct more rapidly than the AV node. So the case that was shown earlier, perihysium pacing probably wouldn't be very useful. The principle is that the His-Purkinje system is insulated, and that if there is no accessory pathway and you pace on the His, I think people, now that we're doing a lot more His bundle pacing, appreciate this physiology a little bit better. You're gonna conduct quickly across the AV node to the atrium, but if you lose capture of the His and capture only the right ventricle, you have to go all the way down to the RV apex to engage the His-Purkinje system and come back up. So it takes a lot longer. So in the red, you're typically not just capturing the His. This is non-selective His capture would be the term we would use now, but you're capturing usually the right ventricle plus the His, or the right ventricle plus the right bundle. And then when you lose His capture and get RV capture only, you'll be able to see this response. Unlike if you have an accessory pathway on the septum, close to your pacing site that conducts faster than the AV node, you'll see that with His capture, you go over the AV node or the pathway or straight into the atrium. But if you lose His capture, you still go over the accessory pathway to the atrium. So that number will be the same. So here's an example of an extranodal response during parahysium pacing. And again, we don't have time to go into all this, but how do you determine if you have His capture? We talk about this a lot more now with permanent pacing, but you can look at the intracardiacs or you can actually look at the surface and usually determine with a wide QRS, you don't have His capture. And when the QRS narrows, you do have His capture. Those are the two patterns you're looking for. You tend to start at a very high output, lower the pacing output, and you'll tend to go from His capture to loss of His capture. And at any lead, you can measure the stem to A. If it's the same, then it is considered an extranodal response, which implies that there's an accessory pathway. And here's an example of His capture. In this case, there's a segment between the stimulus and the QRS. This may be pure His capture. An RV capture only. And the stem to A jumps out, consistent with a nodal response. So this is a maneuver that will come in handy in certain situations in the EP lab. But like all these maneuvers, the more you practice, the better off you'll be. So I would encourage you, even with AV nodal re-entry, you got to catheter at the His, just start pacing at high outputs and look at these response. So try to go through all these maneuvers in every case just so you'll be comfortable performing them. This is a pitfall of that maneuver. You can see narrow QRS is here and wide QRS is here. And you can see three different stem to A times. Here's one, here's two. And then this red one is the same, whether you have His capture or not. And this is when you pace too close to the atrial. You capture the atrium by pacing too proximally at the His. So you want to pace distal where you have a very small or no atrial signal. So you don't get atrial capture. If you get atrial capture, your stem to A interval is going to be very short and it's not going to change regardless of whether you're capturing the His or not. This is another, I think, important concept. It's, I think, emphasized on the boards a lot too, is just retrograde conduction. We talk a lot about Ashman's phenomenon and antegrade right bundle, but there's a lot of retrograde right bundle branch block that occurs in the EP lab, that if you recognize it will be very helpful in making a diagnosis. And so the principle here is that if you have normal AV node conduction without an accessory pathway, and you pace the ventricle, you will get a pacing stimulus here with a His and then an A. So you get retrograde conduction up to the His and to the A. And if you get a retrograde right bundle branch block, it won't go directly up to the His. It'll take longer. So the His will be pushed out and so will the A. So the A is coming after the His. The atrial activation is dependent upon His-Purkinje conduction retrograde. That's different than if you have an accessory pathway and either a pacing beat or a premature ventricular extra stimulus, which is how we typically do this. You'll see that when the His gets pushed out here, the VA doesn't change. So VA conduction is independent of conduction over the His bundle. That's proof that there's an accessory pathway. This is a great, great maneuver. And again, I would encourage you, you don't always get retrograde right bundle branch block with premature ventricular beats, but the more you do this, the more you'll see it. And it's also emphasizes the importance of having a pretty good His recording at the beginning of your EP study. All right, since you didn't see that slide. So the next step is when you've induced tachycardia and you wanna know what type of tachycardia it is. So we're gonna go through a list of tachycardia characteristics, but before I show you, I want you to just think about this. So what are the things that when you induce tachycardia, you can look at? One is how fast it is, right? What's the tachycardia cycle length. We talk about the RP interval and what's catheters up, it's the VA interval, particularly the septal VA interval. And if you can't see it, you can look at other VA intervals. What are the things happen during tachycardia that are useful diagnostically? Yeah, so I think someone said wobble also. So if there's variations in the cycle length of the tachycardia, which tends to occur at the beginning and at the end. It's not always present, but if it's there, look and try to deduce, is the atrial changes happening first, the changes in the AA interval preceding the changes in the his-his intervals? If they are, that tells you the A's are driving the tachycardia and that it's an atrial tachycardia. The opposite is true if it's an avenodal dependent rhythm where the his-his changes are changing before the AA. It's another way of saying that the his and the A are linked or not, because if you think about that, that's really the same concept, or the his and the A linked. But the problem with wobble is sometimes you get compensatory changes in the other part of the circuit, and you'll see changes in both measurements. But it is a useful thing to look for. What else? Just imagine you're looking at an EKG like we did at the beginning. What happens during the tachycardia that might be useful? Bundle branch block. So if you get a bundle branch block, that alone can be useful. If you get a bundle branch block, it can also affect the intracardiac timing. And so if you have a bundle branch block and it changes the VA interval, that can be diagnostic, right? What other things can happen? Hm? Cessation. So termination, how does it terminate? We showed that first example without any intracardiac We showed that first example without any intracardiac electrograms that terminated with VA block. These are useful things to look at to make a diagnosis. What else? The onset. Is the onset dependent upon blocking an accessory pathway? I showed you loss of pre-excitation when we were pacing the atrium. If that loss of pre-excitation initiates tachycardia, it's pretty likely that that block was required to induce and that the pathway is part of the circuit. So these are all the things that can happen. Another one that is very useful is when you have a one-to-one tachycardia and you suddenly lose VA relationships. So you get two-to-one AV block, for example. You know that if the tachycardia is continuing and you have two-to-one antigrade block, the ventricles are not part of the circuit, and that rules out AV reentry. So if you watch long enough and see things happen, you'll often be able to make a diagnosis without having to do any pacing maneuvers. In fact, with AV nodal reentry, that's probably more common than not. So here are the things we talked about. If the septal VA interval is very short, which occurs in about half of the time, it virtually rules out AV nodal reentry. And that cutoff number is in dispute a little bit. In adults, it's about 70 milliseconds. In children, it may be as short as 60 milliseconds. But if you have simultaneous activation of the A and the V, then it can't be an accessory pathway. It can't go over the hysperkinesis system, activate the ventricles, and then go up, retrograde up the accessory pathway. Just to clarify, you accidentally misspoke and you said it rules out AVNRT. You meant it rules out AVRT. AVRT. Yeah, yes. Can we redo that? No, you got it, you got it. Yes, if the septal VA interval is less than 70 milliseconds and the atrium and ventricle are activated simultaneously or in parallel rather than in series, that rules out AV reentry with an accessory pathway. It doesn't rule out an atrial tachycardia that coincidentally is conducting with a PR interval that's equal to the tachycardia cycle length. So that's why I say it's not 100%. And I can show you examples of, at least for a few minutes, it'll look just like AV nodal reentry and you'll discover it's not, it's an atrial tach. Eccentric atrial activation. So if the tachycardia results in earliest activation in the left free wall, that's not AV nodal reentry. If it is, it's almost reportable because it would have to involve some AV nodal structure that's away from the compact AV node. So these things can happen, but that would be super unlikely and virtually, if it's far enough away, rules out AV nodal reentry. If you have termination with AV block, it's reproducible. You have one-to-one AV conduction. It terminates with AV block. Then that has to be an AV nodal dependent rhythm. It can't be an atrial tachycardia. When atrial tachycardia stops, unless it's due to a premature beat or some other change, it's not gonna block in the AV node at the same time it stops. It's just gonna continue and conduct. If the VA time increases with a bundle branch block, that's one of the beautiful board questions. Anything that's got 100% up there, like there's no controversy. And so we'll show a diagram of that, but if you have a left bundle branch block and the VA time increases by more than 20 milliseconds, that's diagnostic of AV reentry using a left-sided free wall pathway, ipsilateral block causing a increase in the VA time. The mere development of a left bundle branch block is way more common in AV reentry. The initiation of AV nodal reentry requires blocking the fast conduction over the slow. So that onset does not stress the hysperkinesis system like it does when you initiate AV reentry. So you tend to not get that bundle branch aberration. There's other reasons too, because AV reentry tends to be faster and you're more likely to get bundle branch block. Is the induction dependent on a critical AH, meaning you've blocked in the fast pathway and gone over the slow? It's probably AV nodal reentry, but there are some accessory pathways that require that long PR interval to initiate tachycardia. Is it really slow? You'll see older patients, particularly older patients that come to the hospital on AV nodal blocking drugs that will have tachycardia cycle lengths of 500 milliseconds. They'll have a SVT of 110 beats a minute. That's usually AV nodal reentry. Something has to be conducting really slowly and it's pretty unusual. It goes over the AV nodal and up a rapidly conducting pathway and you don't get tachycardia cycle length that long. If you have AV block during tachycardia and it continues, that means the ventricle is not part of the circuit. It rules out ORT or AV reentry. And then we talked a little bit about the relationships with wobble, which was not something that we looked at in this study. Here is an example. This is a pediatric case. I show it, I tell you that because there's four catheters in here. You can see a His catheter, a mapping catheter, CS and RV. This is a patient with a regular narrow complex tachycardia and just was brought up, where's the A and the V? Well, if you look here on the CS catheter, that's all A. So during tachycardia, you know this is an A, not a V. Right, sorry, right here. So you have simultaneous atrial and ventricular activation and you have spontaneous termination with AV block. In fact, it slows a little bit before it blocks. What's the diagnosis? It's AV nodal reentry. The VA interval is too short to be AV reentry and it terminates with AV block without a premature beat. It can't be an atrial tachycardia. So a lot of these diagnoses are made by the process of elimination. You're excluding other diagnoses as you go. A question just came up on the previous slides to clarify how you know what's A and V. On this slide? Yeah, sorry, I know you said it, but just to slowly go over that. Yeah, I think if you look at the sinus beat, you can determine that this is all A and that that's a small far-field V. Yeah, got it. I mean, the key is to look for A. So we don't have an HRA catheter in here that only has A. Right. So you can, when A and V are separate like they are in this sinus beat, look at all the catheters we have. Is there any catheter electrode pair that has only A and not much V? And the answer is CS910 is really the only one. On CS78, you have A and V, A and V, A and V. So if they're on top of each other, it's really hard to tell. But in this one, CS910, there's only an A and a very small far-field V. So you can infer that if you were to go back here and you see this signal, that must be an atrial signal because this catheter is only recording atrial signals, not V. Everything else, it's hard to say. Yeah, this would be the only other channel maybe you could say this A looks like that sharp A. And you can kind of, but that's important. Thanks, that's very helpful, I think, because they're still learning how to process all of this stuff. That was helpful. Thank you. So this is diagnostic. You could just go ahead and ablate, but you don't want to. You wanna make sure you reproducibly can induce the tachycardia, that you fully understand what the baseline is before you go turning on the RF and delivering RF because if you don't have a good endpoint, then you're not gonna know when you're done. So the toughest cases are cases you've induced the tachycardia once. You cannot, for avenodal reentry, the fast and slow pathways are so similar, you have difficulty inducing tachycardia and you induce it once, you do a slow pathway ablation, you get junctional ectopy, your endpoints are difficult. So unless you completely eliminate the slow pathway, it's hard to know if you're done. We talked about the effect of a bundle branch block. This is a classic figure from Dr. Josephson's book here. Here's a example of AV reentry using a left-sided concealed accessory pathway. The surface would show this P wave after the QRS. And this is the shortest path, but when you get a left bundle branch block, it has to activate the ventricle over the right bundle, slowly conduct through the myocardium, unlike the His-Purkinje system that takes time. It's also a longer circuit and it gets up to this accessory pathway here, making the VA time long. Now, this is an extrapolation of what you learn on surface electrocardiography is that the tachycardia cycle length gets longer. And that is common and you can see it happens here, right? But what can happen is that the conduction time here gets longer and that allows this to recover and this gets shorter. So you get a compensatory shortening in the AH interval. The tachycardia cycle length may not change. So remember, in the EP lab, you're not looking at the tachycardia cycle length, you're looking at the VA interval. And you're looking at the VA interval from the beginning of the ventricular activation to the A, because this VA interval here isn't gonna change. The local VA interval is not what's gonna change. So let me show you an example. So this is the same patient that had avian oval reentry, now has this inducible tachycardia, the same catheter setup, surface EKG, His mapping catheter, CS, RV, and there is a left bundle branch block pattern with a normal HV interval, so it's not VT, and it narrows and you can see that the VA interval from the onset of the surface QRS to this A gets shorter when the left bundle branch block resolves. So that's diagnostic of a left free wall pathway causing AV reentry, right? So that's step one. Step two is to realize all the other things that can throw you off. One, the tachycardia cycle length doesn't change. And it doesn't change because when there's a left bundle and it takes a while to get to the pathway, the AH is short, it's hard to see, but that's the A, that's the His, and then when the left bundle resolves, the AH gets longer. Here's the A and the His, and the tachycardia cycle length, at least at the beginning, is the same. I'm sorry, this mouse is difficult. Am I the only one with control of this? I feel like someone else is moving it. Yeah, are you running that on a piece of paper or is that on the fabric? So why don't we give you a piece of paper maybe and see if that helps. Yeah, I don't want to point with this because then everybody can't see it. Can someone just pass it? Yeah, just throw me a piece. To see if this works. Yeah. While you're doing that. This is real life. This is getting a mouse to work on a recording system. Speaking of real life, a question came up is that you're saying, well, obviously that's the His, and people are like, huh? I don't think I said obviously. How do I know if that's not the His or that's not the His? How are you deciding here which one is the His? All right, well, it's not a great example. I will give you that. That was not, I wasn't, wasn't my point. And I didn't put the catheters in. This was a pediatric case, but how do you know what's the His? I mean, it's, some of it's, you know, ruling in and out. Here, I'm going to have to, I just can't get that thing to work. All right, so this is a signal, a signal, a signal, and a signal here. So you have to sort out what's the A, what's the His, and what's the V. And part of this is when you're moving the catheter in the EP lab, you can kind of sort that out. But you often have the luxury of looking at other electrograms on your catheter. But this, with a narrow QRS, is the expected time to record a His. It's a discrete electrogram. It's consistent with a His. But there is some noise in there. So I can tell you that, I think that's what the A and the His and the V are. But I can tell you it's not a great example. But this is particularly a challenge with catheter instability during tachycardia. Yeah, I think it's a great point that this is real life, just as you were saying before. The point is, is that because the HV interval is so predictable in most people, unless there's Hisperkinsey disease, which is so unusual to see in an SVT case, if you go to the beginning of the QRS and you go backwards 40 to 60 milliseconds and you see a little blip that's predictably that far in front of the QRS, it's probably the His. So sometimes it is a question, but you say, all right, well, that's too close to the QRS. That's too far away from the QRS. So it's gotta be that one. So it's one of the tricks that you use when signals are not optimal. But it's key. And how do you know sometimes when you're ablating a slow pathway and you see a sharp spike at the end of the atrial electrogram, is it a His? You don't wanna ablate the His. So sometimes you have to do pacing maneuvers to separate these electrograms, to sort out what's A, what's His, and what's V. Just like diastolic potential during VT, pacing will separate these. Oh, but before I finish that, you also, besides that there's no change in the tachycardia cycling, the local VA time doesn't change either, remember? It's from the onset of the QRS to the A. But the insertion site of the pathway, that doesn't care how long it took to get there. It's gonna hit the V and then hit the A, unchanged with a bundle branch block. All right, so what other things can you do when you're still not sure what the tachycardia diagnosis is? You can perform pacing maneuvers. The iconic pacing maneuver in the EP lab during SVT is introducing ventricular extra stimuli during tachycardia at varying coupling intervals. We refer to it as scanning diastole with premature ventricular beats. And the concept is trying to deliver a ventricular extra stimulus during tachycardia when the His bundle's refractory. Because if the His is refractory and you conduct up to the atrium during tachycardia, which is harder to do in sinus rhythm, but during tachycardia, then you know you've gotten up to the atrium over some other means that the His bundle was refractory, you must have conducted up an accessory pathway. And so that's the classic teaching, and I think it's important for you to practice that in the EP lab is giving PVCs with shorter and shorter coupling intervals during tachycardia that are synchronized to the pacing system. However, in the interest of time, I'm gonna talk about just ventricular overdrive pacing, and Jeff showed the case of the value of that. I like this maneuver because sometimes you don't have a lot of time. The tachycardia will initiate and it will often spontaneously terminate after 20, 30 seconds. If you can perform one maneuver, you have one opportunity, then you want to perform ventricular overdrive pacing. And it sounds simple, but you need to make sure that when you start pacing from the ventricle, that you're synced properly and that the first pacing stimulus comes in at a long coupling interval so that you can gradually capture the tachycardia. You can't just blindly turn it on or you may come in randomly and terminate the tachycardia with the first beat. So it's more than just understanding what rate and the response. You have to make sure you've entrained it and that you properly time the onset of pacing. And all the pacing systems are a little different, so you gotta get familiar with how to sense properly, how to synchronize the first beat of your drive train, and how to make sure that it's, which electrogram you're synced to on the recording system. But we tend to overdrive pace at about 20 milliseconds faster or shorter than the tachycardia cycle length, assuming that it's pretty stable and that there's not a lot of wobble. And if you pace, and the tachycardia is avenodal re-entry and you have activation of the atrium and ventricle in parallel, if you pace with a properly timed drive train, you'll initially get fusion and then you'll finally start entraining it and the atrial rate will accelerate and you'll conduct up one limb of the tachycardia and when you stop pacing, it'll come back down the other limb. And so you'll get this so-called VAV or VAHV response. All right, so that's what you would expect with avenodal re-entry. And here's an example of that. You're pacing during a tachycardia cycle length of 320, pacing at 300 milliseconds and you conduct up here to the atrium. And how do you know which is the last beat that was entrained or accelerated? You look at the AA interval here, the pacing cycle length is 300, this coupling interval is 300, the next one's 360. This is actually probably the best measurement, is there a pause after here? You have a VAHV. AV re-entry is the same principle because you have a circuit that involves two connections between the atrium and the ventricle and when you get conduction over the EV node and up the accessory pathway and start pacing, you get fusion. You eventually start to conduct up into the atrium and then when you stop pacing, it comes back down the EV node. So you get a VAV response. And here's an example of that. Ventricular pacing during a narrow complex tachycardia with a pretty long VA interval. You get a V, an A, a HISS and a V. This is in contrast to an atrial tachycardia. Even if you mimic an atrial tachycardia in a patient with dual AV nodal physiology with a pacemaker as we did in this study, you will find that there's only one connection from the A to the V. You'll get block with fusion. You'll eventually, in some patients, not all, get conduction up into the atrium that overdrive suppresses this atrial tachycardia and then when you stop pacing, the atrial tachycardia resumes and conducts. But this retrograde conduction results in block antigrade. So you get a VA, no V, VA, AV response. Sounds simple, but it can be difficult to interpret. And here's an example of an atrial tach. You can do this in the EP lab in the patients on isoprol with sinus tachycardia. So next time you're in a lab and someone has AV nodal re-entry and they're in sinus tachycardia and you pace the V and you don't induce AV nodal re-entry, you'll see a VA, AV response. There's a little better HISS recording for you. The question that just came up is, so is the whole purpose of this maneuver just to rule out A-tach, is that all it does? No, but the response as we just showed, VAV versus VA, AV is. But we've ruled out atrial tachycardia, then we're stuck with AV nodal re-entry or AV re-entry. And so the other observations that we're gonna show you, which Jeff showed very nicely. Do you wanna change where you do your fellowship? You know, just give me a call. We need to look at those. I think that answers the question, right? So, but before we show that, we're gonna talk about other pitfalls of just the VAV response. And I have to wrap this up too. We have pacing here. Now, if you just go left to right, you'll see V, A, AV. But if you look at the beginning, this is a long RP tachycardia where you have conduction over the EV node, antegrade in the fast pathway, retrograde in the slow pathway, giving you a long RP tachycardia. So if you start pacing the ventricle and you conduct to the atrium, it's only gonna get longer, it's not gonna get shorter. So you pace the V, you're not conducting to this A, you're conducting to this A. So it's really when you refer to VAV or VAAV, you're referring to the conduction sequence, not just the pattern left to right. And so this is a truly a V, A, V response. So that's important. And here's an example, just like the one that Jeff showed, where the second AA interval after ventricular pacing is truly the last one that was entrained. Other things can happen. You can dissociate the atrium from the ventricle completely or the ventricle from the tachycardia. Sorry, you can just completely dissociate the ventricle from the tachycardia. That doesn't rule out EV nodal re-entry. The EV node is what's the source of the re-entry. The ventricles are not part of the circuit. If you start pacing and you terminate it, you might think, oh, I can't look at the VAV response. What a waste of time. Let's re-initiate it. Go back and look at what happened. And often you'll see that you terminated it without ever getting to the atrium. If you terminate the tachycardia without ever getting to the atrium, then it can't be an atrial tachycardia, right? In fact, when you're struggling sometimes, pacing very quickly for just two or three beats and terminating the tachycardia and going back and showing you never got up into the atrium is a good maneuver too to rule out atrial tach. Here's an example of A, A, A, A. You burst pace the ventricle and it terminates it without ever affecting the A. These are pacing stimuli. And as we're gonna talk about next to my last couple of slides, you'll also notice that there was fusion when that happened. So not only did you terminate it without affecting the atrium, which rules out an atrial tachycardia, you never had full capture of the ventricles. If you have fusion, there must be integrated conduction over the his bundle. How would you have gotten into the circuit if this is an avianodal dependent rhythm? It can't be. This is not just excluding atrial tach. It also excludes avianodal reentry. So this right here is diagnostic of this tachycardia being AV reentry. How much time do I have? I feel I'm already five minutes over. I'll go through this quickly since Jeff talked about it, but the post pacing interval now, so we talked about ruling out atrial tachycardia now, how do we rule out avianodal reentry versus AV reentry? If the ventricles are not part of the circuit, then the post pacing interval is gonna be long. So if the RV is part of the circuit, it will be short and the number and the cutoff and the studies was the post pacing interval minus tachycardia cycle length is less than 115. If it's longer than that, it's unlikely to be an accessory pathway mediated tachycardia. It's very likely to be avianodal reentry, but it's not as diagnostic. There's subsequent papers have shown that if you have a decrementally conducting pathway, you can get a long post pacing interval minus tachycardia cycle length and the RV can still be part of the circuit. But if it's short, you ruled out, that you've proven that the RV is part of the circuit. This is the original data from that study that Greg Michaud published that the stem to A minus VA cutoff is 85. The post pacing interval minus tachycardia cycle length cutoff is 115. Again, papers have shown it's not quite that clean, but if it's short, if it's less than 115, that's very useful. And then this is my last slide showing this transition zone that Jeff alluded to, which I think when you're dealing with a long RP tachycardia with concentric atrial activation, and you can't tell, is this atypical avianodal reentry or is this a slowly conducting accessory pathway? The best maneuver is to look at what happens when you start pacing and you entrain it. And if you pace properly, as we talked about, and you get progressive fusion like this, then look and find out when the first atrial electrogram is that's pulled in. And in this case, the AA interval went from 280, 280, suddenly 250. Well, was the history fractory here? Well, let's look up here and see if there's complete capture yet. Well, if you start here, the QRS is different. So this all must be progressive fusion. So these Fs depict fusion. I think you called it stable ventricular capture, but, or morphology, but here's full capture with ventricular pacing. So there's fusion here. You've accelerated the atrial rate with fusion. And if you've ruled out an atrial tachycardia, then this has to be AV re-entry. This is a great, great maneuver to do in every case you have. And we're back. And we are live with Dr. Brad Knight. Thank you so much for joining us. I want everyone to first take advantage of the survey questions on your screen. So give us some feedback. So again, we can tweak our content for future years. Dr. Knight, thank you so much for joining us. I have some good questions lined up based on the video and presentation from last year. The first I'm going to relay is from Dr. Kumar, who asks, how do we differentiate an AH jump that is long versus a junctional beat? Yeah, that's a good question. I saw that in that list. Let me just first start by thanking you and Mark for doing this. It's a great opportunity to provide educational material. And thanks to Boston Scientific. It's painful to listen to yourself speak, but at least you don't have to worry about people going over time. And I sincerely hope everybody's doing well and healthy during this COVID challenge. So thanks again for doing this. The question at hand is how do we differentiate a jump versus block in the AV node and then a spontaneous junctional beat, which would inherently be premature. That can happen. I think the best answer, there's two issues. One is reproducibility and one is, is it realistic? And there are times where a premature atrial beat can block in the fast pathway and result in a very, very long AH interval. So that can happen, but certainly if it's over 700 milliseconds, that's really unrealistic. So some of it's experienced and then most of it's reproducibility. If it only happens one or two times and you think it's induced maybe by the hiss catheter, that would make it more likely a premature junctional beat. Good question. It's a great question. And I think doing maneuvers more than one time is often the answer to figuring out discrepancies or two possibilities, because if it's the same physiologic phenomenon that keeps happening, then probably it's a real thing rather than coincidence. One question that came up actually also from Dr. Kumar, what happens to the AH and the HV intervals when you're atrially pacing in the presence of an antigrade conducting pathway? Well, a typical AV accessory pathway will have typically a fixed AV interval. So what will happen is that the AH will increase because there's decremental conduction over the EV node. The HV interval will get shorter and the degree of pre-excitation will get greater, but the AV interval will be fixed. And those are all characteristics that do not describe a fasciculoventricular accessory pathway which is coming off below the AV node at the hiss level. And so that would give you a fixed HV interval and a fixed amount of pre-excitation with prolongation of the AV interval with atrial pacing. One question that came up during AVNRT is how would you tell the difference between AV node re-entry with two-to-one conduction versus an atrial tachycardia? Well, AV nodal re-entry can occur with two-to-one AV conduction. It usually occurs at the time of the induction and it's a result of stress on the hiss-purkinje system. The level of blot can be in the so-called lower common pathway below the AV nodal re-entry turnaround point, but it can more typically be within the hiss bundle that's functional. And the fact that it's functional means that if you perform ventricular overdrive pacing, even for a few beats, it will resolve, it will cause correction of the two-to-one conduction and make it one-to-one. So that's a good question. It's interesting because if you have a two-to-one tachycardia, you know it's not AV re-entry. And because AV nodal re-entry is so much more common, it's still more likely to be AV nodal re-entry, particularly if the AV relationship is simultaneous on the conducted beats. Yeah, and that question was from Dr. Talha Nazir. Thank you for that. Next question is a technical one about making measurements. When you're doing this ventricular entrainment maneuver, looking for VAV or VAAV, which signal do you use to assess that first V? Is it the pacing stimulus or what V do you measure from? Usually measure at the ventricular pacing site, which is almost always the RV apex catheter. Yeah, yeah, it would be the onset, I think, of the ventricular signal, which would be the pacing stimulus is usually what people look at in terms of the VA relationship for the most part. I guess a fair question. There can occasionally be latency. There's a pacing stimulus and there's a delay before the myocardial potential. That's uncommon in RV apical pacing in patients with normal hearts. It's more common in the atrium at high outputs up by the SVC or in patients with structural heart disease. A troubleshooting question during parahysian pacing. How can you tell if you're capturing the atrium during parahysian pacing? Is it simply a stim to A time or is there anything else you're looking at? It's a variety of things. There has been a cutoff described in the literature of 65 milliseconds if the stimulus to A is that short or shorter, you're likely capturing the atrium. But the hope is that you're pacing at a site with a very small atrial electrogram. So if there's any question, the key would be to advance the hiss catheter so that you have a large hiss recording or a right bundle recording and you're only capturing the V plus minus the hiss. The other observation would be if, as I showed in that example, there are a variety of different patterns that wouldn't make sense. And so that the stim to A is fixed with loss of hiss capture, but it's still very short and that there's other patterns that are long. That was a question from Dr. Bhullar. Thank you for that. And a question from Dr. Kumar Natarajan. Sorry if I butchered the name. A question is during junctional ectopic tachycardia, what would be your response when you do an overdrive pacing maneuver? Yeah, junctional ectopic tachycardia can happen clinically. It's common in pediatric population. It's common post-operatively. It also can occur when you've done a procedure. In particular, you've done a slow pathway ablation. You're giving now isoproterenol and you get an accelerated junctional rhythm. And the key difference between those two rhythms is whether or not the atrium is conducting to those junctional beats versus spontaneously arising from the AV junction. And so the way to differentiate those two, there's a variety of techniques, but I think the easiest is to perform overdrive pacing from the atrium and sort out whether or not the A is conducting all the way to the next QRS. And I'd have to show you some examples, but there's a nice paper that, I'm not sure who the first author was, but Eric Prostowski was an author on differentiating jet from avian oval reentry. Yeah, good question. Another one that's coming from Dr. Manganiello, can you talk about reproducibility of a jump? Is there an association of having a jump and it says within 10 to 20 milliseconds, and then how do you know if the jump is real or not? So I guess the question is about defining a jump and reproducibility of that. And if you see changes or lack of reproducibility, how do you interpret that? Yeah, so if you deliver an atrial premature beat and bring it in by shorter and shorter coupling intervals, and for efficiency sake, I tend to do that at 20 milliseconds. If you see a jump of more than 50 milliseconds, that's what we use to define discontinuous age curve, evidence of a slow pathway. Now, there are a lot of varieties here, and we talked about how some people might not have a jump. You might also notice differences in vagal tone so that your jump occurs at a coupling interval of, say, 280 milliseconds at a drive train of 600, and then that's not what you see 10 minutes later. It's usually because of a vagal tone and the fast pathway is waking up. You'll get a completely different result when you give isoproterenol. Those numbers will all change. There are patients who can have three nodal pathways or multiple avianodal pathways, so you'll see more than one jump. The final thing I'll say is that if you give an atrial extra stimulus that's very short, you're gonna encroach on the atrial refractory period, and you have to make sure that you're measuring the age properly, and there are times when right before it blocks, you'll get a jump, and so some people don't really include that as a true jump if it's the age interval associated with the last one that conducts. A question came up, a sophisticated one, from Dr. Nadeau-Routier about what cutoff you use when you're distinguishing AV node reentry from AVRT with ventricular overdrive pacing in terms of the post-pacing interval minus TCL in the ventricular channel. When you're adjusting for any AH difference, do you change your cutoffs into what cutoff you use for distinguishing the two? That's a good question. These are EP201 questions, but if you perform ventricular overdrive pacing and you stop, and the next conducted beat, the next AH interval is much longer because it's decremental on that first beat compared to during tachycardia, that will artificially prolong your post-pacing interval. If you correct for that, then your standard cutoff rates would apply, but that is an important correction to make, and that's why sometimes people really just look at the stem to A versus the VA, which doesn't include the AH on the first return beat. A question came up, and this is a little bit beyond the scope of the talk, but sometimes can get confusing when you have actually ventricular tachycardia with two-to-one retrograde conduction versus AV node reentry with two-to-one VA conduction. How would you distinguish those two if in fact the latter exists? Well, assuming the latter exists, which is theoretical that you could, the atrium really isn't part of the circuit during AV nodal reentry, then the question really is how to differentiate AV nodal reentry from VT, and that's largely based on the HV interval during the tachycardia and the other appearances of the QRS. Yeah, absolutely. I wanted to key in where the, I think we've kind of gone through most of the questions, a point that you made in your recorded video from last year, which has to do with fellowship training. And one point to make to the fellows who are attending today and tomorrow is hopefully this isn't only just a learning session for you but in fact an opportunity to virtually at least meet the faculty. I realize it's a reduced program this year, just there's only so much screen time you all can tolerate in three and a half days of sitting in front of your computer is not tenable. But the faculty who we've selected this year are really the cream of the crop in our program. And think about that when you're thinking about future mentoring, whether or not you choose to apply and train at the programs of people, you hear their lectures during this presentation or use these people for resources. Dr. Knight is renowned for his interest and skill in teaching. And I'm sure he would welcome, as would I and the other faculty members, anyone who wants to reach out with questions or mentoring opportunities or things of that sort, even if you're not applying or training in our programs. I just wanted to mention proactively that everybody involved here is really dedicated to that teaching mission. And I'm gonna call in, I think that's it for the questions for the moment. And I'm gonna, I think I say another thanks and turn it over to Dr. Estes and thank Dr. Knight for joining us in the session today. And Dr. Estes and I will sort of close up today's session. Thanks to both of you and thank you to the entire audience. Thank you very much. I wanted to just go over a couple of things, Josh, if we might, in the remaining few minutes, we have just a couple of minutes left. You've been over a lot of the basic concepts as well, but I think it might be helpful to give the audience a sense of when you're approaching, say a routine SBT case, what are the basic fundamental things that you do right at the outset, standard in every single case, and then what are the things that you do right at the outset, standard in every single case before you're getting into these more advanced maneuvers? Yeah, do we still have Dr. Knight on? It's a good question for him, or I'm not sure if we still have him. I'm still on, can you hear me? Give it a shot. And I know that you are a minimalist. Josh advocated for the high radial catheter, coronary sinus, and many catheters. So I think it'd be good for you to distinguish your two approaches. What do you do standardly? Surface EKG, AH, HV, anti-gray curve, retrograde curves. Sure, can you hear me okay? Yes. Good, so what I typically do is try to limit access to one femoral vein and put three catheters in. I routinely put in a catheter in the right ventricle, usually a soft tip, bi-french safe catheter. And then we put in a high right atrial catheter. I usually use a deflectible catheter so that that catheter can be placed in the coronary sinus. And then I'll put a catheter at the hiss. And in most cases, patients have documented tachycardia, and you have a pretty good sense that they're gonna have an inducible tachycardia and that an ablation's gonna be needed. And so if I know that there's a high likelihood of ablation, I will put an ablation catheter at the hiss through a long sheath, usually an SRO. So I'll put a four millimeter ablation catheter at the hiss through an SR0 at baseline. If the patient's pre-excited, Mark, I may think differently. If I think there's a high likelihood we're gonna go to the left side, I may just put in one of those three catheters will be straight into the coronary sinus, typically a multi-electrode catheter. I tend to just, I measure AV block cycle lengths, AV node ERP, and VA block. We don't routinely, but it's probably a good idea to commonly perform ventricular extra stimuli to look at retrograde conduction. And then we perform parahysium pacing from that ablation catheter typically. And Brad, how hard do you work to get a retrograde hiss on your hiss catheter? How frequently do you see it? When is it important? You've mentioned a couple instances where it'd be important to look at the right bundle, hiss activation, and so on. Yeah, well, I think it's a practical question. At the beginning of the case, if the patient has a high likelihood of AV nodal reentry, you start off and you have evidence of dual pathways and you easily induce typical AV nodal reentry. I don't do a lot of these advanced maneuvers that we're describing. Those are kind of part of the toolkit for when you get difficult cases. And as I think I mentioned in the lecture, the biggest challenge is when you have concentric activation and you're not sure if it's atypical AV nodal reentry from an accessory pathway. And you might say, well, why does it matter? Let's just ablate the earliest atrial activation. That does matter because if it's AV nodal reentry, you're gonna often be closer to the hiss than you need to be where you can ablate the slow pathway and sinus rhythm. So that is a critical time to make an accurate diagnosis. And that's what I would do some of these other maneuvers. But you're right, there can be times where you'll do all these maneuvers and you'll still be puzzled. You may get kind of conflicting results. And I think Josh's point's a good one about reproducibility. If you're not sure, do the same maneuver several times until you're confident what the outcome of that maneuver really is. Josh, your view on this. Yeah, I think there are really two different answers. The question is, what can you do in terms of a bare minimum and get the answer you're looking for? And secondly, what do you do in an academic center when you have trainees present? Because they're maybe slightly different. So I do like personally to have four catheters in. I like the idea of having everything in one groin. And there are ways of introducing four small catheters in one groin. But if you're then gonna add an ablation catheter, you might have a fifth access site. But having a high right atrial catheter in addition to a coronary sinus catheter at all times will really help you immediately visually distinguish a retrograde atrial event from one that is coming from the high right atrium, be it sinus or ectopic or whatever. So having all the information at once I think is helpful, both for diagnostic reasons and for teaching reasons. But you certainly can infer things and the more advanced you get, the less information you need to draw a conclusion. When I start out, I like to just make sure everything's plugged in right and everything in sinus rhythm looks appropriate. There's nothing that's gonna confuse you more than having a CS catheter that's connected to the pin block backwards or is not positioned in the way you thought or something dislodged. And then you're in tachycardia and you're going to misinterpret the electrogram. So making sure always that everything makes sense before you start inducing anything or pacing I think is critical. My first maneuver that I do in any SVT is I wanna just see if there's an accessory pathway present. And because in the adult population, we've weeded out most people who have manifest pre-excitation, many of whom are ablated in childhood, concealed pathways are more common. And so I like to do ventricular pacing to begin with, straight pacing or ventricular extra stimulation just to get a sense of at least what the machinery is that we have to deal with in terms of a AV node versus an accessory pathway via conduction opportunity. But realizing that the presence of something, whether it's dual AV nodes or a pathway does not necessarily imply that that is the mechanism of the tachycardia because sometimes you may have a pathway present but have a different tachycardia mechanism. Yeah, excellent. We've got about a minute, minute and a half left. And we just wanna make a comment too about advanced mapping systems, which we haven't gone into this year, but they really are a supplement to the basics that we've emphasized here today. It's most of the time the case that you can deduce the mechanism of tachycardia at its site, not just from the basic maneuvers that Brad's gone over, but also from the entrainment. When you've got a tachycardia and you entrain remotely from it, re-entrant tachycardia that's coming to the left versus the right atrium, you can tell that pretty much just by pacing and training from the right atrium versus the left atrium. And these advanced mapping systems, Carto, Navex, Arrhythmia are all just supplemental. And for the fellows in particular in the EP lab, you need to stick with those basics and recognize the limitations of those mapping systems.

supraventricular tachycardia

SVT

arrhythmias

electrophysiology techniques

diagnosis

treatment

electrocardiograms

tachycardia speed

bundle branch block

pacing maneuvers

interpretation