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EP 101 2020: A Virtual Program for Incoming EP Fel ...
Catheter Ablation of AV Nodal Reentrant Tachycardi ...
Catheter Ablation of AV Nodal Reentrant Tachycardia
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I go back to the conduction system, and we're going to focus on the AV node in particular. This slide was just to remind me to talk about just how different AV node tissue is from His-Purkinje tissue. And I think the best way to make that point is to look at the histology. And I alluded to this a couple days ago. If you look at the histology of the AV node, you're going to see, I won't say disarray, but certainly a lack of organization of the fibers in terms of their direction in stark contrast to the His bundle fibers, which are long and skinny without stroma in between them. So you can imagine the lightning-fast way that signals travel along the His bundle and the Purkinje network in contrast to the meandering, much slower and circuitous way that signals get through the AV node. So understanding the histology actually does help explain the electrophysiology. And you can see why you might be able to get reentry if the AV node looks like this. Here's just the junction between AV node tissue going into His bundle tissue. And this helps me, I think, to have a visual framework when I'm thinking about the electrical properties of different parts of the heart, including the conduction system. You've seen this picture a lot, but I'm going to modify it now and not just talk about the triangle of Koch, which you can now recite in your sleep, but I want to highlight that the AV node, which we've talked about before as being at the apex of this triangle of Koch, right up here where the His bundle penetrates the central fibrous body, it's a little more complex than that in that the AV node, in many people, will have an extension that travels along the tricuspid valve limb of this triangle in front of the coronary sinus ostium. So the AV node, in people who have discernible two components, well, the compact part, the part that we try to leave alone during ablation, is going to be up toward the apex, just on the atrial side of the His bundle. But the slow pathway component is going to extend downward to some degree between the coronary sinus ostium and the tricuspid annulus. Fluoroscopically, these are the catheters that I showed a couple days ago in a routine EP study where you have the high right atrial catheter, the His, the right ventricular catheter, and the coronary sinus catheter. And it's important to know your landmarks when you're ablating. The compact node tends to sit, as I said before, just behind on the atrial side of where you record a His signal, and it'll look like this in both views. Whereas the slow pathway part is going to be extending in the REO downward in front of where the coronary sinus catheter is located, and it's going to be often a little more leftward than where the His catheter is sitting as you park your ablation catheter there. And it's important to recognize these fluoroscopic landmarks if you're using fluoroscopy so that you know that your catheter is positioned away from the blue compact node so you don't injure it during RF delivery. So here using this sort of cartoon is the way you should think about how AV node reentry occurs. So if this is the yellow part on this Netter diagram, which I've now covered in blue, is the compact part of the node, and this extending down is the slow part of the AV node. Here is the scenario where you can set up reentry. We've talked a lot about unidirectional block. This is a basic principle of reentry, whether you talk about AVNRT, atrial flutter, ventricular tachycardia, AVRT, the point being that in order to get reentry, there's always got to be a circuit, which means you can enter the circuit on one side and exit it in another location. And there are two routes to get from that entrance to the exit. And during sinus rhythm, for example, in somebody with two parts of the AV node, the signal is going to be going both down the fast part of the AV node, the compact part, and also down the slow. But the fast pathway, by definition, is going to win. So it's going to activate the ventricles first, and your PR will be normal, less than 200 milliseconds typically. And this part that's happening in the slow component is invisible because this tissue doesn't generate signals on the surface EKG, nor does it impact the PR interval typically. You're going to get a collision of wavefronts during sinus rhythm. If the signal went down both limbs, then when the signal reached the caudal part of the AV node, it can retrogradely conduct up the slow part of the pathway. Maybe I should have made this wiggly to signify slow retrograde conduction. And you'll have two wavefronts meeting each other and colliding, which is obviously not going to facilitate reentry. If you have a very early beat that occurs, it may find both parts of the AV node refractory. And likewise, you can't get reentry going because you have to have unidirectional block, not bidirectional block, which is a terrible term, which is another one of those examples of an EP term that's sometimes used to mean two different things in two different scenarios. I will never say that again on this slide. But the point is that if you don't conduct down either limb of the circuit, obviously you're not going to get anything going. But the way nature has it, the slow part, the slowly conducting part of the AV node tends to recover faster than the fast conducting part of the AV node. So if you have a premature beat, whether we pace or whether it happens spontaneously, that occurs right in that window where the fast pathway is refractory, but the slow pathway has recovered, you can get conduction down only that one limb. And because it takes a long time to travel down that limb, while it's doing so, the fast pathway now is recovered. So when the wavefront reaches this branch point, it will conduct down to the ventricles, but it will also be able to conduct all the way back up to the fast pathway to the origin and reentry gets going. This happens in atrial flutter. This happens in ventricular tachycardia. An early beat that blocks in one of the two limbs conducts down the other and reentry can get going as long as along all parts of the circuit, the recovery time is faster than the conduction time that it took to get all the way around the circuit. If that's not true and that's that concept of wavelength, then the head will catch the tail and you'll have just that one beat and you will not sustain reentry. So some EKGs that many of you are likely familiar with, the top is a patient in tachycardia, the bottom is after termination. And the question with every SVT EKG is where is the P wave? And this is tricky with AVNRT until you recognize that you usually will have simultaneous atrial and ventricular activation during AV node reentry. So you start to look at particular places for the P wave. And if we compare in particular V1 here, if you only looked at this EKG on top, you might think that this is just a little R prime part of the QRS complex. But if you compare the QRS morphology and sinus rhythm, you'll see that that little deflection is absent. You'll also notice in sinus rhythm that the P wave has a particular amplitude and you don't see any evidence of a P wave in the segment before the QRS nor any deformation of the T waves during tachycardia. So all those pieces together suggest that those little terminal blips, known as a pseudo R prime, are in fact the P waves conducting back to the atrium at the tail end of the QRS. So why is it such a short time? And the answer is during this rhythm, as the wavefront travels down the slow, which is the common form of AV node reentry, and reaches this branch point, then you have simultaneous conduction forward down the hisperkinesis system. And you know that that'll take about 40 to 60 milliseconds to get down to the ventricular muscle. But simultaneous with that, you're going to conduct retrograde up the fast, which may be only barely longer than that, to the point where you start activating the atrium. So because in parallel you're conducting forward and backward with the two fast conducting elements, the QRS and the P wave are going to be somewhat simultaneous. How does the AVNRT start? As I said, you need a premature beat that blocks in the fast and goes down the slow, which is another hallmark. If you can catch the onset of SVT with AV node reentry, you will often see, and it was fortuitously caught on this EKG, you will fortuitously see a premature beat that conducts with a very, very long PR interval. Why? Because it's going down the slow part of the AV node rather than the fast. And then when you're in tachycardia, here are those pseudo R primes that if you only saw this, you might think is part of the QRS, but when you compare it with the sinus beat that precedes, you can see it's missing. So that's in fact the retrograde P wave during tachycardia. Well, you might say, well, hey, hang on a second. I know that the AV node decrements, even if you don't have two components. Here's a patient who doesn't have AVNRT, who had a PAC that was caught on an EKG, and you have a long PR. So how long is long enough for me to conclude that it's a slow pathway instead of just decrement down the one part of the AV node? There's a graph for that, and I'll show it on the next slide. Actually, I thought these were in the reverse order. So the point is that when you switch, when you block in the fast pathway and conduct down the slow, you're going to see a sudden jump in conduction time between atrium and ventricle. The next slide highlights it perfectly, but I wanted to show you some intracardiac. So here is the classic atrial program stimulation that you'll do during an AV node re-entry or actually any SVT case where you'll put in a drive train of eight atrial beats in a row followed by a single early atrial beat. In this case, the drive train is 700 milliseconds. The single atrial beat is 590 milliseconds, just a little bit faster than 100 beats per minute on that PAC. I'm going to stop in this talk erasing some of the electrograms because you've seen enough of these that you're going to start learning what to ignore and what to focus on. But I am going to start helping you differentiate atrial from ventricular signals. That was an issue that came up yesterday in some of the questions, and it's one of the hardest things to keep track of when you're trying to see what's happening in the atrium versus the ventricle, especially when those events are simultaneous. So a convention that I'm going to use from here forward when I show these tracings in this talk, I'm going to overlay green bars over things that are atrial signals, and I'm going to overlay purple bars for beats that are ventricular signals. Did I do the purple here? I didn't. I'll do it on a subsequent slide. So here we're pacing in the atrium. These are all atrial signals in the coronary sinus catheter. Here is the his catheter. There is a little far-field atrial signal here. Here's the his potential, and here's the V. And when we pace with that PAC at 590-millisecond coupling interval, here's your AH interval as measured in the his catheter. If we only decrease that PAC by 10 milliseconds just a smidge faster, we now see the PR got much longer on the surface EKG, and the AH got much longer. And then, again, the question is, well, how much is much longer? Because I expected it to prolong because I hit it a little faster and the AV node tissue decrements, and that's where this graph comes in. And we saw this yesterday, but I'm going to go through it in a little more detail. So this graph shows on this axis, the x-axis, how early the PAC was put in. And on the y-axis, what is that AH interval? So here at 100 beats per minute or 600 milliseconds, we put in the A2 beat, and we measure the AH, and there it is. And so then we said, okay, I'm going to ignore the cartoon in the upper left for a moment. I said, okay, I'm going to pace a little bit earlier, and the AH gets a little bit longer because you have decrement in the AV node. Okay, terrific. We're decrementing in the fast. And I'm going to pace a little bit earlier, and it's going to get a little bit longer, and I'm going to pace a little bit earlier, and it's going to get a little bit longer. And as you graph this, you see sort of a pattern. And you can keep going and keep going and keep going, and this is normal decrement in the AV node as I increase the prematurity of that early atrial beat, the A2 beat. And you say, okay, this is fun. Let's keep going. So you decrease yet 10 milliseconds earlier, and this happens. And you say that is not consistent with the rest of the graph. You have a discontinuity in this graph. What happened? Well, this is not normal decremental behavior. This is a sudden change to a much longer time for a very small incremental premature beat. And what happened, of course, here, as you now know well, is we didn't conduct down that same tissue. We blocked in that tissue. This was the effective refractory period of the fast component of the AV node. And we instead conducted down the slow, which was silent until now, but now is becoming manifest. And it's also, by the way, been decrementing, but we haven't seen evidence of that because we're getting to the ventricle through the fast pathway first. But now the fast pathway is refractory. And if we keep going, you're going to see a new line form of dots that shows decrement in the slow part of the AV node. And that makes sense. So this jump, this sudden change in conduction time is what we refer to as a jump. And that's also the point at which you start seeing reentry because you get unidirectional block. You block in the fast. You conduct down the slow. And it's only when you pace PAC faster than this critical interval that you're going to see reentry occur. So we define a jump as a sudden change in the AH interval of 50 milliseconds or more for decreasing by 10 milliseconds the prematurity of the A2. I know you've heard it before, but this is a point that's important to remember. It's going to be fundamental in your SVT cases. Just like on the surface EKG, when you see P waves hanging off the end of the QRS and you know things are simultaneously occurring, there's a signature pattern in the intracardiacs as well, and you've already seen this. When you see this kind of tracing where everything seems to line up, and again, I'm going to highlight the onset here, pacing A1, A1, A2. There's a very small far field A on the His channel. The His catheter was pushed a little further in, so we don't have as much atrial recording. And you see a long AH, which occurred after a jump when this A2 came to this degree of prematurity. And I'll spread it out a little bit. Here is AV node reentry looking at all the catheters, and I'm going to again highlight the His in orange, ventricular events in purple, and atrial events in green. And everything sort of lines up. In fact, the very first thing that you're going to see is the His signal, right? Because the first thing you're going to get to as you're at that branch point at the caudal end of the AV node is you're going to go down to the His. Before you see a QRS, before you get back up the fast pathway to the atrium, you're going to see a His recording. So that's always going to be the first event during AVNRT. And then it's a race. Sometimes you see the atrium before the ventricle. If the fast pathway is super fast and your HV time is a little bit longer, that's okay. And this is why when we talk about entrainment from the ventricle, when we talk about that VAV versus VAAV response, people will often say, well, VA His. If you see a His recording, that means the signal is going down to the ventricles. And because occasionally you can get back up to the atrium a little bit before you actually got down to the ventricles, you don't want somebody to say, well, that's a VAAV, ignoring the fact that the His is in front of that A and falsely conclude that it's an atrial tachycardia. So you'll hear people say VA His, all right, because of that race and sometimes one wins and sometimes the other. There was a question yesterday that came through we didn't answer about what is an echo beat. And I wanted to just highlight that. So here we were doing programmed stimulation, A1, A2, A3, in fact. And there was one, essentially one beat of reentry, one beat of AVNRT. So here's a very long AH to here. Here's the His, gets down to the ventricle, but there's an atrial event that happens here. And it isn't a sinus beat because the HRA is late in contrast to these beats, sinus rhythm, where the HRA is early. So when you have a simultaneous atrial activation after a long AH interval when you did this programmed stimulation, but it's only for one beat, it tells you that that wavefront went down the slow, got down to the ventricles, went back up the fast, back to the atrium, but it met refractory tissue at the top part of the AV node and could not for a second time go back down the slow pathway with the current. This is a situation where the repolarization time, the recovery time took too long for reentry to sustain. So we only had one circuit. It's known as an AV node echo beat. Echo meaning we sent the signal down and it came back up to the atrium once. You can also have AV node reentry go in the opposite direction. And usually that starts in contrast to a PAC starting the common form of AVNRT. You can have a PVC start the uncommon form of AV node reentry. And so here we have somebody on telemetry who happened to have three PVCs. And you can beautifully see on these two PVCs here, notice the different morphology. There's a retrograde P wave. This is lead two up top. A retrograde P with a short VA time and a retrograde P wave that has a very long VA time and then tachycardia starts. What happened? Well, just in the retrograde direction, just as in the anterograde direction, the slow pathway recovers faster. The fast pathway has a longer refractory period. So this second PVC happened at a time that the fast pathway was refractory so it couldn't conduct up with a short VA time. But the slow pathway said, I'm good to go. So it conducted up the slow pathway, giving you a long VA time. But at that point, now the fast pathway is recovered so it goes back down to the ventricle again. Notice the timing of the P waves here during tachycardia. It's, of course, not superimposed on the QRS because now the retrograde limb is the slow pathway. So that pushes the P wave out toward the next QRS. And some people refer to this as the uncommon form of AV node reentry or fast-slow. So meaning you're going down the fast and up the slow as opposed to slow-fast, which is the typical going down the slow and up the fast, if that makes sense. This is what it would look like intracardiac-wise. Again, you wouldn't see things lined up like you do during the common form of AV node reentry. Here is the hiss. Here are the ventricular signals. And then the atrial signal is pushed out. It's in the long RP category because of the retrograde slow conduction up the slow pathway of the AV node. Here's an example of spontaneous termination, which just highlights and reinforces some of the features. There's the pseudo-R prime in V1 and the pseudo-S wave in lead II that are absent in sinus rhythm. Always compare. And you'll notice there's a little deflection right here. There was a premature atrial beat that penetrated into the AV node, got into the excitable gap, and went in both directions and extinguished the wave front, both in the forward and the reverse directions. And the reentry stopped. Let's talk about ablation. So, really, ablation focuses on your knowledge of anatomy. How many times have you heard that? And you'll continue to. You have to recognize where does the slow pathway typically live? How do I get my catheter there? And how do I avoid collateral damage? So, typically, you'll put your catheter right at the location of the slow pathway anatomically. And you know where the compact node is because you typically will have a His bundle catheter in place. And you try to stay away from it, stay low. It's variable how far down below the His catheter, below the compact node, the slow pathway extends. So, where is the safest place to ablate? At the lower end of it. Usually, people will start somewhere at the sort of near the floor, the lower third of the coronary sinus os, which you can't see, but you can surmise where it is based on the location of your coronary sinus catheter. And here's what it looks like in the LAO view. Here's the catheter clockwise torqued against the septum, away from the His catheter up here. And sometimes you ablate further down and you're not seeing the effect you're looking for, which I'll review in a moment what that is. And so sometimes you do have to go up. You have to be very, very careful the closer you get, especially considering, as Dr. Garcia highlighted with his ice images, that the patient is breathing, that the heart is moving. This patient is alive. Things are happening. So, it isn't a static image. And you have to be aware that, oh, I look like I'm fine on flora or I look like I'm fine on my 3D map. They may cough and now you're not fine anymore. So, being stable and being aware that your catheter can move or that the heart can move toward your catheter in a way that puts the compact node closer to where you're ablating is something you always must keep in mind when you're ablating. Many people nowadays will use 3D mapping, but remember it's just a cartoon. It's just an estimate of things. And so you have to be very careful that your map stays loyal to where you actually are and recognize that there are motion eliminating algorithms that are introduced. So, when you see your catheter floating a little slowly up and down, that's not reality. That's after respiratory filters have been applied and movement filters have been applied. If they took those off, you'd see your catheter moving around real time just like you do on fluoroscopy. So, be aware that there can be a lag in seeing your catheter move in terms of the icon. So, being very cautious. If there's ever any question during RF delivery, during avian reentry, just come off RF. You can always go back on. So, I have the same little speech I give to all the lab staff and everybody involved in every avian RT case. If anybody sees anything funny, and I'll describe what funny could be, just come off. If there's any doubt. If I say a word and you don't know what I said, just come off. Maybe I said turn up the energy, but you didn't know what I was about to say and you came off. Rather you come off than not come off if you're going to damage the compact node. So, what does the electrogram look like when you're sitting in front of the coronary sinus? There's usually an atrial and a ventricular component. Usually they're both sharp. There can be a lot of variability. And there's a textbook image that people see and talking about the components of the atrial signal and the ventricular signal. But usually the atrial signal, because you're right near the annulus and the mass of muscle determines the amplitude of signal, the atrial signal is going to be smaller, maybe a third or a fifth the height of the ventricular electrogram, telling you you're sort of right near the annulus. But in reality, here's a composite picture of a lot of the successful locations I've ablated. And you start looking for the classic anatomic location. But sometimes people's anatomy is a little bit different. And you need to be a little more atrial, or you need to be a little more ventricular, or you need to be a little more septal, or even just sometimes even inside the coronary sinus, which is a segue to this slide, which is that AV node reentry is really a family of circuits. What do I mean by that? Everybody's anatomy is different. How does the AV node connect into atrial muscle? How does the coronary sinus musculature play a role? How does it interact with the left atrium, with the septum, with the AV node? And there can be circuits that are not constrained to, in our minds, the fast and slow pathway parts right on the septum. You can have a leftward element of the circuit. And whether that's AV node tissue to some degree, whether that's atrial fibers, there is debate. But it is not in debate that sometimes you need to go more leftward in order to successfully interrupt a circuit because ablation on the right side is not being successful. In this series of 340 patients, 18 of them had early sites that were found in the coronary sinus or in the left atrium. And the successful ablation was performed at this nontraditional location inside the coronary sinus or transeptal in the left atrium. And whether, again, that's because the AV node had some leftward part or whether there was some atrial muscle fiber playing a role, I don't know that it's clear to me or anybody. But that is where successful ablation was performed after failure to ablate on the right side of the septum at the traditional slow pathway component. How did they figure that out? Well, usually these patients had the uncommon form of AV node reentry where the retrograde limb was slow and inserting over leftward, so you actually had the opportunity to map the earliest atrial signal either during pacing, as is shown here, or during the tachycardia itself. So notice, don't look at everything, but look at the highlighted features. So notice on this LAO image, if this is the traditional slow pathway and fast pathway locations, the ablation catheter is in the coronary sinus, more leftward than typical for where you expect the AV nodes to sit. But yet at this location is where the earliest atrial signal was seen during ventricular pacing, and that was the successful site in this one example that eliminated AV node reentry. What do we look for to know that we're actually heating slow pathway tissue? When you heat up the AV node, it starts to fire, and you see junctional beats, preceded usually by a hiss deflection, and then usually that signal will travel forward and backward at the same time. So it looks like that echo beat, but in fact, it's not an echo beat. You're just generating firing in the slow pathway, and it's conducting in both directions at the same time. If you see block, here you see there's four greens and three purples. If you see evidence of retrograde block or anterograde block, you come off, because you might be injuring the compact node. So generally, we like to see during junctional beats an A and a V on every single beat. If you see this, more Vs than As come off. If you see this, a lot more Vs than As, you really come off fast. So these are clues, and it doesn't necessarily mean that you are injuring the fast pathway. You may just have vigorous firing from the slow pathway, and you've surpassed the effective refractory period of the tissue that would have conducted back up to the atrium. But just in case, come off and collect yourself, and sometimes you will accept this, but only after a few rounds when you figure that this is a safe place to ablate, and this is what we're seeing in this patient. So you have to assess each time. And I want to finish with two minutes on cryoablation, if that's okay. Oh, okay. This is very quick. So some people prefer to use cryoablation, and the main reason is that in contrast to RF, which can cause immediate damage, and the damage to myocardium continues for many seconds after you come off RF, in contrast, cryoablation disables cells before it kills them. So you can see an electrical effect before you have cell death, and that time frame can be 30 seconds or a minute even. So you have leeway. If you see something you don't like, come off cryo, and you haven't actually caused permanent harm. The catheter is put in the same location as, of course, you would with RF. I'm going to skip this study. Interestingly, when you apply cryo, when you freeze the tip, you see this interesting characteristic artifact that appears in the ablation catheter that obliterates the electrograms. It looks like this during cryo, and when you come off cryo, it goes away very quickly. The cryo catheter freezes tissue, and as Ed said yesterday, Dr. Gerstenfeld said yesterday, you kill cells with ice crystals piercing the membranes and with osmotic forces changing and bursting cells, et cetera, but you need a longer freeze, usually four minutes with this type of catheter, to create permanent damage. During that time, you can do an EP study. While the catheter is frozen to the tissue, you can let go of it, and you can say, great, at this A1, A2, I used to see a jump where the P wave conducted with a long AH to the QRS. I'm not seeing that anymore. Why? I've eliminated the slow pathway part of the AV node. So now I've actually reached the refractory period of AV node tissue instead of going down the slow. That's a great sign. So I love doing continuous A1, A2 pacing during cryo. If I still see AVNRT inducible, I don't wait the whole four minutes. Come off, you're not in the right place, and save time, and you can go to a slightly different location. So it's nice to be able to assess during the lesion itself if you're having the effect you're looking for. And last point is the reversibility. So here's an example where the PR interval extended way out to 480 milliseconds. The AH extended way out, and we said, oh, come off, and you can see the cryo artifact disappearing. And within 30 seconds, the AH was back to normal, and the PR was back to normal. So it's a very forgiving energy source in this regard. And I'm going to stop there, and we can do some questions. And in the remaining 10 minutes or so, we'll address them. One of the questions that came up from Dr. Brasseria is, is it safe to ablate the slow pathway in patients with a long PR interval? And maybe an extension of that is, what do you do when you have a very long antecrater refractory period at the fast pathway? Maybe you could address those two things. Yeah, what a wonderful question, and a challenging one. So if somebody has AV node reentry, and in sinus rhythm their PR is long, the question is, why is it long? And there are a couple different possible reasons. One is that sometimes the patient is preferentially conducting down the slow pathway, and then you're getting retrograde penetration, also known as concealed conduction, back up into the fast pathway. And so you may see two families of PR intervals. You may see EKGs with a normal PR, and you may see EKGs with a long PR. And in that scenario, where you get sort of caught in this endless loop of going down the slow and concealing up the fast and interfering with the next beat, by simply eliminating the slow, you're going to immediately return to fast pathway anterograde conduction. And you can usually sort that out before you do any ablation by pacing in the atrium at different intervals, putting in premature beats, and just figuring out how A and V are wired. The other possibility, which is more challenging, and in that first, by the way, you should be able to generate a normal PR interval before you start ablating just by timing things. The other possibility is that you can have what's called an electrotonic effect between the fast and the slow pathways. That means that if you're conducting down the slow in a concealed fashion, the fast pathway forward velocity may be impaired, in which case you'll have a PR that is long, even when you're conducting down the fast pathway. And typically that improves when you eliminate the slow, but it is a bit hair-raising to think that you have a long PR baseline, and then you may ablate part of the AV node and you wonder, am I going to be left with heart block or even worse AV conduction? Personally, I actually like to use cryoablation in that scenario, especially if it's a young person, because you have the opportunity to see temporarily when I disable slow pathway before I actually cause permanent destruction of tissue, where you usually have at least 30 to even 60 or more seconds of reversibility time, you can see what happens. And if you see the PR shortens as you're applying cryo application to the slow pathway, then you're in the clear. If you suddenly see heart block, then come off cryo, and you may need to regroup. Terrific. Another question from Dr. Superin, how often in real life do you see specific slow pathway potentials if they exist before RF? What do they represent? How important are they? Should you look them before you ablate? Yeah, the resolution of an ablation catheter, as Sonny so beautifully outlined in his lectures, is not terrific. You have a large distal electrode, especially if you're using cryo, where it's typically a six or eight millimeter electrode. But even with a standard three and a half to four millimeter tip electrode, the resolution is not terrific and the conduction is slow. So the signal that you're going to be recording is sometimes difficult to see and may be obscured by other adjacent signals. So typically it can be hard to see, and most people do ablation based on their knowledge of the anatomy of the AV node, rather than trying to find a discrete slow pathway potential. But if you do both, if you do see a potential that you're convinced is AV node tissue, and therefore it doesn't track with atrial signals or ventricular signals, sometimes each of those can have multiple components and masquerade as a slow pathway potential. If you're convinced and you're in the anatomic right location, then it's a little bonus, but usually we just go anatomically because that slow pathway potential is hard to record. Yeah, a related question from Dr. Superin again, and he says that sometimes the HISS position is very low, meaning posterior relative to CS, particularly in older patients. It is a very small distance between your HISS and where you may want to ablate your slow pathway potential. So what's your approach in this case? Do you ever ablate when you can see a HISS in your ablation catheter? Yeah, the triangle of Koch will be of different sizes in different people and it may be related to age, but often does not. It just has to do with the relative location of the slow pathway, the coronary sinus and the apex of that triangle where the compact node is located. And so it's important to have landmarks when it's a small triangle. And if you are using fluoroscopy as part of the case, which I recommend, especially with small triangles because again, the fluoro will show you real time how much your catheter is moving with the heart and with respirations. Whereas the 3D map is filtered for breathing and for cardiac motion and can give you a lag or misleading appearance of stability. So it should, you know, you use multiple imaging modalities to be sure you understand where your catheter is located and how much it's moving. It's always safest to start as far away from the compact node as you possibly can. So starting lower than you think with RF is always wise. And you'd be surprised how often you may actually see success lower down than you had originally anticipated. You can always move upward toward the compact node. But once you cause harm, it's hard to undo it. So the short answer is start low and move up. And if you're nervous, consider using lower energy, consider switching to cryo ablation, if that's something that you have at your disposal, so that if you do see heart block or damage to the compact node, you can detect it before irreversible changes have occurred. So, Josh, you alluded to using, you know, a mapping system. Many people will routinely use an advanced mapping system for their avian oval re-entry, make a HIS cloud, and look at the most posterior extension of that, and then make sure that they start as posterior as possible, sometimes behind the coronary sinus with their RF. What's your approach? Do you use an advanced mapping system? Do you make a HIS cloud? How do you use an advanced mapping system, NAVX, CARTA, arrhythmia, with your avian oval re-entries? Yeah. So I was trained without using 3D mapping for my avian oval re-entries, because really it's anatomically based and electrogram based for the most part. And again, you have a more real-time reference of where your ablation catheter is compared to other catheters, sitting in particular at the HIS location with the compact node being immediately behind it. I don't think I've ever done an AV node re-entry ablation where I've ablated behind the coronary sinus. It's typically going to be more of an up and down trial and error method between, on that septal isthmus between the tricuspid annulus and the anterior lip of the coronary sinus, usually starting lower down towards sort of five o'clock if you're looking at the coronary sinus from the right atrial perspective. But you can add the additional information, just be aware of the limitations of the 3D map in terms of filtering the location. If the patient moves, your HIS cloud may no longer accurately represent where the current HIS and compact node are located. Another question that comes up because you often have to use a more complex catheter, such as a contact force irrigated catheter. People will say, well, irrigated catheters make bigger lesions. You shouldn't be using that for AV node re-entry. Well, you do have the additional information of contact force, which some people find helpful, especially when multiple catheter shafts are adjacent to each other and colliding. When you're trying to put clockwise torque on the ablation catheter, you may feel force, but in fact, that's the shaft rather than the tip contacting with tissue. So there is potentially added value there and recognize that the lesion size you make is not a function of whether you're irrigating or not. First of all, you don't even have to irrigate. You can put it at just two cc's per minute. You don't want to put it at zero because the holes will clog up. If at some point you wanted to use the irrigation, you may lose that opportunity and have to switch catheters. But it also is basically related to energy. You could ablate with one watt through an irrigated catheter. It's not going to magically make a big lesion. So control how much power you're delivering with the catheter. And you can absolutely safely ablate AV node re-entry using a 3D mapping system and an irrigated contact force catheter. In our hospital, we do the ablation during the tachycardia. Do you have experience with that? Personally, I don't do that. There has been an interesting compilation of EP people from around the world on Twitter who have these types of discussions. And I did hear that practice, not typically in the U.S., but in some other countries as well. And it's been really interesting to see how people are able to do that. Certainly, you know, if you're being effective because the tachycardia terminates during RF delivery, the risk in that scenario is because you're having a retrograde conduction through the compact AV node during tachycardia, you could feasibly interrupt forward conduction through the compact node inadvertently before you're able to do the ablation. And so, you know, if you're being effective, the risk in that scenario is because you're having a retrograde conduction through the compact node inadvertently before you actually terminate tachycardia and cause irreversible harm to the compact node and thereby aid to AV conduction. So it's not been my personal practice to do that. I guess anatomically, if you knew you were in the right place, it could be done safely. And clearly there are people who are experienced with that technique. I personally do it during sinus rhythm or during atrial pacing and not during AV node reentry, to make sure I'm not damaging the forward conduction through the compact node. Terrific. And Josh, the remaining minute or so here, we've got a couple of questions. What about junctional beats with RF? Do you always look for them as a measure of success? How long do you wait afterwards and perhaps emphasize that with cryo, you don't get those junctional beats. Absolutely. Yeah. And sorry that maybe some of my talk was cut off just for the sake of time today as we're replaying the video. Definitely as you're heating conduction tissue, you see junctional beats. So that's an indication that you're heating conduction tissue, which typically you do need to see to be successful, but not always. So the safest thing to do is after every RF lesion is to recheck and see if your slow pathway is still there. And if you are still able to induce tachycardia, even if you didn't see junctional beats, but usually you need to see them. It's with heating tissue that you see those. So with cryo ablation, you don't it is reasonable during cryo ablation to know if you're being successful to do A1, A2 pacing to do atrial burst pacing. And if you see that you are still able to induce tachycardia 30 seconds or more into cryo, you may wish to terminate that lesion for lack of efficacy and move forward. Okay. Josh, I know you're very active on Twitter and in closing here and thanking you, let me just say that for the many, many attendees here feel free to use Twitter to promote the value of this EP 101. Josh is very active on it. And for any questions that we didn't get to, we could certainly use our Twitter accounts to do that. So with that, we're going to take a break for a 10 minutes. We'll be back exactly at 45 past the hour to start up with the next section with AF ablation and Greg shows presentation. Thanks Josh very much. Well done.
Video Summary
Assistant. In this video, Dr. Josh Moss discusses AV node reentry tachycardia (AVNRT) and the electrophysiology behind it. He explains that the AV node tissue is different from the rest of the His-Purkinje system, which can be seen in the histology of the tissue. The AV node has a lack of organization of its fibers compared to the long and skinny fibers of the His bundle. This difference in tissue organization explains the slower and more circuitous pathway of signals through the AV node compared to the fast pathway of the His-Purkinje system. Dr. Moss also discusses the different components of the AV node and explains how AVNRT occurs when there is a reentry circuit between the fast and slow pathways. He describes how to recognize AVNRT on an EKG and how to map and ablate the slow pathway for treatment. Dr. Moss also briefly touches on cryoablation as an alternative to radiofrequency ablation and its advantages in AVNRT ablation.
Asset Subtitle
Josh Cooper, MD
Keywords
AVNRT
electrophysiology
AV node tissue
His-Purkinje system
tissue organization
reentry circuit
EKG
cryoablation
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