Good morning, everyone. Welcome to the last day of the HRS. Welcome to the in-person board review. My name is Amole Ojo from University of Rochester, New York. I have the honor of co-chairing this session along with Dr. John Miller from Indiana University. The board review this year has been divided into three sessions. So this is the first session, which is going to focus on SVT. So we have three wonderful speakers today. We'll be changing the order of presentation because Dr. Mitchell has a flight to catch, so we will be going first. Just a reminder, we will leave the questions to the end of the session. We have a microphone in the center of the room, which can be used. We can scan the QR code to ask questions, or you can use the app to ask your questions. So we have Dr. Mitchell. There's also ARS. Is it the same code? For the ARS questions? Okay, great. Well, welcome. Sorry, I have to get back to the right coast, and that's a long flight, so I've got to make sure I make it to the airport. So I'm going to ask you some questions about tracings, and in this one, this is the question, and most of them will be similar, sort of not a lot of text here, but just sort of what you think this might be. So orthodromic AVRT using a left free wall, septal wall, or septal pathway, slow-fast AVRT, fast-slow AVRT, or focal atrial tach, and here's the tracing. So we can see here, we've got this catheter is in the RV septum, so you can see there is a right bundle probably. Maybe you can also see a little bit of atrial signal here, and then CS, proximal to distal. So this catheter is picking up both a septal A, a hiss, a V, and then something happens in this part of So these are the options again. And this part on the board you have to do yourself. They don't usually provide the measurements, but I think these are the key measurements. So this is 320 milliseconds. That's stable. That's a stable cycle length during the tachycardia, and if you were to measure it, that's one thing you would want to do first, is to make sure that it's a stable tachycardia cycle length, because sometimes other questions on the board could be, interpret this in trainment, except you're not in training, because you're pacing to never captures, or never accelerates the A. There might be a VA dissociation, and it just appears that you're in training, or that the tachycardia can be very irregular. And if it's very irregular, that makes the interpretation more difficult. So in this case we see 320. On the surface we can see the pacing again, and then I'm measuring the atrial signals in the CS. So what do you think about this? Septal. Yeah, so I think, and this is the way the board questions go too. I know John has looked at the metrics for these many times. And at least a good question on the boards is never one that everyone gets right. It's always, there's a mix. So when the majority of the audience gets it right it's probably a pretty good question. And that is correct. Now why? So let's go back and look at this. So we have tachycardia with a stable cycle length. And we see here we begin to pace. And if you do pacing correctly which is to say you begin to sync your pacing to either a surface electrogram. If you're pacing the V that's fine. Or you can pick an intracardiac electrogram to sync to. When you do that and you begin to pace just faster than the tachycardia. So somewhere usually pick twenty to thirty milliseconds faster than the tachycardia. If it's got a little wobble you might want to pace twenty to thirty milliseconds under the shortest cycle length. That can be useful. And then you're gonna interpret, this isn't looking at the end of entrainment because we don't even show you when we come off pacing. But you're looking at this portion, right? So what do we know about these beats? Does that beat look like that beat? Yes. Does that beat look like that beat? No. Why? Because fusion. So there's a wave front coming orthodromically through the AV node in the His bundle system and produces a QRS. And at the same time there's a pacing wave front that's just getting started. So if you time it right it will barely fuse for the first beat and then you'll see progressively more fusion starts to look more like pacing and less like native QRS. All of the ones, so if you follow along here and you look at this beat versus that beat versus that beat. As long as it's continuing to change they're still fused. You know that. At the end they can be fused still because you can entrain with fusion. But you know that these are all fused because that one doesn't look like that one. Or that one. This is fused. That one still looks like it's a little bit different than the other one. And you would put up all 12 leads in the lab to figure that out. But this one right here accelerates. So this is a His refractory PVC. You could also tell potentially there's a little His right here. And the His is probably just after the pacing spike. So you can tell that this is His refractory just by looking at the surface. And now you've advanced the tachycardia. So you know there has to be a pathway present. It doesn't necessarily tell you it's part of the tachycardia, but it usually is. So then you have to look at the activation. And we have in the RV septum the A near the His is the earliest. And then proximal to distal. So that doesn't make sense for a left free wall pathway. So there's a pathway present and it's likely septal of the choices, septal makes the most sense. Does everybody who didn't see that good with that? Almost looks like the cycle before that is also advanced. Yeah. It is a little bit advanced. I made it clear that it reached the tachycardia cycle length at 290. But there was a subtle also advancement. See John Miller has eye calipers that are calibrated to about 2 milliseconds. So he can look at a tracing and see about a 2 millisecond difference. But no he's correct. It actually advanced with this one, but it's very clear on this one. And then these slides will be available. So you can look at these later. But we've already explained pretty much the Okay. So again new question. We're going to look at a termination of SVT. And we're going to try to decide whether this is a left free wall accessory pathway, a parahysenic accessory pathway, right free wall accessory pathway, bystander, or atrial tachycardia. Yeah, okay. So let's take a look at, again, most people got what I believe is the correct answer, and let's take a look at that. So there's a couple things. Look at everything. So if you stopped looking here, you missed something here. And, you know, so you always want to look at the surface. It's a little messy. We have some noise in our lab sometimes, or maybe the patient was moving a little bit. But we see a tachycardia, one-to-one VA relationship. This is, again, the same catheter configuration. We can see a right bundle or a HISS potential here, and we can see atrial signals after the V. We can see proximal to distal CS. And then we see termination. With the termination, we see what? There's some evidence of pre-excitation. And this catheter that's in the septum has a signal that looks pretty early. It's a far-field V, but it lines up. If this is a HISS, it's right at, it's after the delta wave, and there's this far-field signal here that suggests close to the beginning of the delta wave. So this would suggest it's not a right free wall pathway, certainly not a left free wall based on the atrial activation. And so you'd think this is a septal pathway. Why is this not atrial tachycardia? It's not atrial tachycardia because it terminates with AV block. So atrial tachycardia wouldn't, you wouldn't expect it to spontaneously terminate with AV block when it's been one-to-one the whole time. So you'd have to postulate that atrial tachycardia terminated coincidentally with a beat of AV block. Now if this beat had come way early, if you had an atrial beat that came way early, well then yeah, that could terminate in atrial tachycardia. But this is just marching along happily, same cycle length, and suddenly kind of terminates. So you wouldn't expect that at all to happen with atrial tachycardia. Anything can happen once, but you know, on a board exam they're going to show you something that, they're not going to expect you to pick a fortuitous thing. Yeah, could this be a bystander? Possible, but that's not likely, right? I mean, when you have an accessory pathway, it's both antegrade and retrograde, and you have tachycardia, and you have, it's going to be, you know, don't overthink things. Sometimes, and they're asking you for a most likely explanation, don't pick the zebra if there's a horse as an answer. So go ahead and, you know, pick the thing that's most likely, and don't start overthinking. Well, this could be, you know, I know that they're thinking bystanders, they're going to want to trick me with this one. It's not usually the case, right? They're not going to, it's not going to be probably the more esoteric answer when the common answer makes more sense. You agree with that? Get an explanation for your review later, or you can take a picture of it now. I see people putting their cameras up. Okay, this is a one-to-one SVT, was observed after extensive ablation for persistent AFib. Actually had a lot of, had a lot of ablation on the interatrial septum, and this is the tachycardia that ensued after that. So this was inducible after all of that. This is a ablation catheter at the His bundle recording position. You can see a septal A here. Here's a proximal to distal, or high to low right atrial signals, and then these are CS, proximal to distal. Okay, that's your orientation. So where's the most efficient place to pace as a first step to sort out the mechanism of SVT? Would you pace the right ventricle, the coronary sinus, the left atrium, the right atrial appendage, or the earliest atrial electrogram? Again, let's go back, look at that for a second. It's a one-to-one VA relationship, and here's the high array and the septal A, here's the CS. You can pick. Which place would you pace first that might help you sort out this mechanism? Yeah, great. This is like every question people are getting, somewhere close to 60%. That's good. The temptation is, because this is a patient who had a lot of atrial ablation, to think, oh, we've got a very slow form of atrial tachycardia, there's extensive ablation and some flutter, and I'm going to pay somewhere in the atrium to sort this out. But don't forget, what you should always do when you have a one-to-one atrial tachycardia, what looks like an atrial tachycardia, is it could be something else. And this is not that uncommon. I've seen it happen many times, where people have fumbled around trying to figure it out by pacing in funny places and mapping and doing all kinds of things, and they just can't figure it out. And all you really needed to do was pace the right ventricle to see that you get a VAV response, which is not compatible with intra-atrial re-entry. And why does it look so funny? So why does the activation sequence look like it does? Why is the higher A so late? And why is the septal A so late? I don't see it on this tracing as well, but it's out here. It's because they had extensive septal ablation. So you've created a line of block so that as it breaks out, it can, the CS is where you normally expect it to be for AVNRT, right? It's right lined up within the QRS. But these are so late because there's a line of block on the septum that doesn't allow the right atrium and the HISS A portion to get activated like you normally see it, lining up exactly with the QRS. So you can get really fooled by these, but whenever you have a one-to-one tachycardia, just double-check, pace the RV, and that'll give you the answer as to whether you're dealing, maybe you're dealing with a new mechanism. It's really important to remember. And this isn't the only time I've ever seen, this one was harder to figure out, but it is not the only time I've seen that happen. AVNRT in patients with some septal fibrosis is actually pretty commonly induced, so. And again, this is the, showing you the VAV. All of these electrograms, although they sit in funny places because of the line of block, are driven by this paste V. The paste V drives all of these, so this is a VAV response. And again, if you want to, here's some measurements for you later, you can pull them up in the session, or if you want to take a picture, go ahead. Okay, let's do another one. And then you stop me whenever I run over my time. I may have more than we can go through, and I'll stop whenever we're done. So here's a, do we have a focal mechanism of atrial tachycardia, and the ablation catheter is near the source? Do we have a focal mechanism, but the ablation catheter is far from the source? Do we have a re-entrant atrial tachycardia, and the ablation catheter is near or within the circuit? A re-entrant atrial tachycardia, and it's far from the circuit, or overdrive pacing cannot be interpreted? So, again, when you're looking at these questions, you're going to, you can organize them now into kind of two things. Like, first thing you're going to say is, all right, is there something about the pacing that I never captured, or there's something else where I'd look at five as the best answer. So, I never captured. There's something funny about the entrainment. The other ones are trying to sort out, like, do you know whether this is focal or re-entrant? And then, if it is, am I far or near from that focus or within the re-entrant circuit? That's what this is trying to get at. So here's the, again, you won't get calipers on the test. You're expected to do the measurements yourself. And there's calipers on the screen, but I have, obviously here you can't do that unless you're John Miller with his eye calipers. But the pace cycle length is 265, and the tachycardia cycle length is 285. So we can see that I'm measuring this interval here, and it's at the pace cycle length. And then the tachycardia cycle length resumes. Okay? And here's the pacing site right here. So, take a look at that and think about which of those scenarios makes the most sense. 60%, I'm guessing. 70%. Okay, even better. Alright. Audience saw all the important things on this slide. And they are... First of all, you can exclude five because you actually accelerated the tachycardia to the pacing cycle length. There was capture. You would be tempted to think that perhaps there wasn't, because if you look on the ablation catheter, there's actually evidence of fusion on the ablation catheter itself. So here's a little bit of this electrogram that you're capturing, peeking out behind the signal. But even if you don't recognize that, you can see that there's more or less the intracardiac equivalent of concealed fusion. We've got all the electrograms look exactly the same, and you're driving this interval at the full cycle length of the tachycardia. So this is the concept of sort of downstream entrainment, where you're able to see that electrodes very near to where you're pacing have to be driven all the way through the cycle of the tachycardia because there's a wavefront of collision between your pacing wavefront and the orthodromic wavefront that's coming back to the catheter. They collide with a little antedromic coming off the catheter, and the orthodromic wavefront meet and create a line of block and don't allow you to get to these electrograms. So they have to be driven all the way through. And that's what you'd see similarly in VT, right? If you're in an isthmus for VT and you pace, you see on the surface there's concealed fusion. You can see that pretty easily because in VT there's humps and bumps that you can easily identify on the surface. You can't do that with a P wave. It's not high enough fidelity recording to be able to pick up the kind of differences that you need to see. So you can look at a bunch of electrograms in the heart in key places and tell that there's that. Then the second part is, is it near or far from the circuit? Well, it's near the circuit. The post-pacing interval at that site is quite good. And whenever you see this phenomenon, you can split the electrogram at the pacing site into both an orthodromic and antedromic portion. So in other words, this is the, when we blow that up again, this is the orthodromic part and this we made antedromic because we split that electrogram into both antedromic and orthodromic. And the reason that happens is you have a wavefront coming around and just when it reaches your catheter, you launch another wavefront. So you don't give it a chance to reach your catheter completely. And when you're really in a circuit, the bipolar electrode can pick up a little bit of that wavefront coming back to the catheter before you launch the next one. That's why that long fractionated signal gets, you now see antedromic and orthodromic portions of the circuit. And that's actually, if you ever see that, you're in an isthmus probably. And if you ablate, it's going to terminate at that site. That's a very, pretty specific finding. I'll put this up for your review later. Waldo's criteria. It's worth going over. It's worth thinking about to really get in your head entrainment and all of the things about entrainment. There's so many questions that can be tested on the boards concerning entrainment. So the things you're going to want to really concentrate on are retrograde conduction. Those are frequently missed questions. And then also understand entrainment. Really get that concept in your head and you'll be able to get most questions correct. And these are the Waldo's criteria. I'm not going to have time to go through this, but again, you can take pictures and then review this on your own. And this is another example of the sort of downstream effect where you're pacing from the CS here at the distal portion and there's a circuit coming in this direction proximal to distal. But you drive with this pacing stimulus, you're driving all of these electrograms completely through the circuit. And you can tell because they're peaking out behind. It's a very constant relationship. So this is constant fusion. What if I were to pace a little faster? Well, some of these would then become antedromic. The ones back here. This one might become antedromic if I pace. That's progressive fusion. You change the degree of fusion by pacing faster. That's progressive. Constant is this relationship here where you see the relationship between pacing and all the electrograms are completely constant. You know they're fused because why would this electrogram be driven all the way through? If this were a focal source, you would see this electrogram just in front of the pacing stimulus, not behind it. Of course, post pacing interval people probably understand the best of all this stuff. So I won't go through it. Again, you can take a picture of this slide or review this later at your leisure. I know we have five minutes left so I probably have one more. Okay, this is a pretty good one I think. This study is old enough that it could be tested. During an EP study for atrial tachycardia with a cycle length of 371, here it is, so I'm not lying, overdrive pacing is performed as shown in the next slide. This is high RA, this is CS, and this is an ablation catheter in the CTI. The post pacing interval minus tachycardia cycle length from the mid-CTI is plus 75 milliseconds. Based on this information, what is the most efficient next step to determine a diagnosis? Map the right atrium with the high definition mapping catheter or the left atrium and train from other sites in the CTI and train from the mitral isthmus. Find the earliest atrial electrogram and ablate there to see if tachycardia terminates. So-called thermal mapping. I can go back again. In the CTI we get that post pacing. Yes, again, majority got it. So in training from other sites in the CTI is clearly the most efficient thing to do in this case because you need to recognize the CTI is a little funny. You can get misleadingly long post pacing intervals. It behaves a little bit like a VT circuit where you've got kind of connections to the main way the wave front moves through the CTI but there are portions of the CTI that are relatively like blind spots or blind alleys that connect to the actual circuit. So you can get long post pacing intervals. When we did a study years ago we found actually almost 20% of pacing sites had a PPI minus TCL more than 30 milliseconds and sometimes we saw some, I think over 100 milliseconds different and it would make you start doing all kinds of crazy things but what I would say is you just go check the tricuspid annulus and check somewhere in that CTI it's in if it's CTI flutter. So you just have to march along the CTI and you'll figure it out very quickly. It's clearly the most efficient thing to do if you want to rule out CTI flutter and don't want to have to do a map or redo a map. And here from the lateral CTI, just lateral, just slightly away from where we were, we're now out of the blind alley. We can see a normal post pacing for the CTI. Okay, great. I think I'll stop there since I've run my time. Thank you. Applause Thank you Dr. Mitchell for that wonderful overview of the diagnostic maneuvers in SVT. Now Dr. Miller, my co-chair, will be presenting on 8GM recording basics. Thank you Dr. Mitchell for a whirlwind tour of some very important concepts. We're going to do a whirlwind tour of another important concept here. I have ten minutes to talk about electrograms. People have two day courses on electrograms but I'll do it in ten minutes here. I won't have any audience response for this. Yes I will. There was one at the end. Alright, well first of all we have to figure out what is an electrogram. How do we get it? Every recording that we make is fundamentally a bipolar recording. We call them unipolar and bipolar but fundamentally they're all bipolar. When we talk about unipolar recordings it's between two electrodes that typically at some distance from each other an electrode and a ground somewhere that's some distance away. It contains local information plus information from very far away, everything in between those two electrodes. It does have some directional information by convention an R wave in that unipolar electrode means stuff is coming towards you. A QS configuration means everything is emanating from that point. We can use that information. It tends to be relatively widely filtered. The true bipolar, as it may be called it's shortened to bipolar, is between two closer electrodes that tend to be of a little bit more similar size and it's actually composed of the two unipolars respectively but one of them is electronically inverted and so far field stuff tends to be subtracted out, not uniformly, but it's pretty good at that. There tend to be smaller electrodes at a smaller electrode distance so you get a lot of local information that's occurring just underneath that electrode pair. It is directional when comparing two nearby bipoles but you can't tell anything about direction with any single bipole and it tends to be narrowly filtered. Each of them has good points and bad points. A good electrophysiologist will have both of these in their bag of tricks not just the bipolar. Here's how the signals are generated. We have a catheter here we have a signal coming here. The unipolar tip is electrode 1. The band electrode here is unipolar 2 and the unipolar is the composition of those two. Here we have those two unipolar electrograms. They look pretty similar because the wave is attacking those two unipoles from the same direction so they're going to look pretty similar but they're a little bit off in timing. You see this peaks a little bit earlier here than the second one does. When this second one is inverted electronically and subtracted you get this bipolar electrogram that's usually a little bit more less complex, a lot less drift on it and so forth. That's largely because of the filtering. Now how is this important? I'm going to posit that there is a little red dot underneath here I know that because the next slide shows it. There's a little red dot under here. That's where the impulse starts and emanates in a centrifugal fashion here. It's not really the way Hart does because it's anisotropic but for our purposes it'll do. If you are recording from electrode 1 here you see this unipolar electrogram with this sudden QS. It's right on top of the source and it's right at the onset of depolarization. A unipolar at electrode 3, way off over here, sees something from there but it's coming towards it then going away and it's a little bit slurred. It's not quite on it. The bipolar from 1-2 here sees something from each of these electrodes but in that it sees something from the tip electrode that says I'm early. Bipolar 3-4 is later as you'd expect and you can compare these two now. You can't say anything about direction from 1 or anything about direction from 2 but between comparing these two you say it's closer to 1-2 than it is to 3-4. Bipolar 1-6, let's be inclusive no useful information. So we do have to discriminate every once in a while here. It's great to be inclusive but when you're recording everything, you get everything, it doesn't tell you anything that you need to know. Something is under there. Alright, we move the catheter and now we have some different information. There's the red dot as promised and it's still emanating from there. Now our unipolar from electrode 1, not so good. It's got an R-wave on it and the R-wave starts where the impulse starts but it's not a QS configuration. In fact, nothing is. Nothing is right over there. Unipolar 3 is now a little bit better but it's still not in the action. Bipolar 3-4 is now earlier than Bipolar 1-2 was but if you say, oh I just need to pull back my catheter and I'll be there. No you won't because 1-2, 3-4 is not quite exactly where it is. It's closer than 1-2 is but it's not exactly on it. And again, let's be inclusive and we learn nothing from Bipolar 1-6. This is like going in with an 8mm electrode and saying, I'm going to do some precise mapping in here. Sure, go ahead with a cryo-catheter or something like that. Have at it. Unipolar electrograms have certain strengths. This is the directionality, the QS configuration. You can't see that from just anywhere. This is very handy with a ventricular insertion site in Wolf-Parkinson-White, especially right-sided pathways. Site of origin of normal heart focal atrial or ventricular tachycardias. Atrial is a little bit problematic because the signals are so small to begin with. RVOT, LV, muscular, not aortic sinus, valsalva, but muscular VTs is pretty helpful. Not very helpful in scar-based VTs because the signal-to-noise ratio is not to your advantage because the signal is so small. You can also get some information some other information from the unipolar. That's ST elevation. If you look at this, if anybody's done pericardial synthesis with a V1 clipped on, you look for ST elevation, that's injury. When you have a lot of ST elevation with your unipolar electrogram, back off. You're about to meet the other side of that wall there. Perforate or something. When you are just mapping along and see a lot of ST elevation, it means high contact force. It's a cheap and dirty contact force. I tried to correlate them at one time. It's not a great correlation, but it's close. If you don't see any ST elevation, and then if you're doing ablation and you see ST elevation, you've done some damage there. If you see no ST elevation, you haven't had contact. You've not made a lesion there, so maybe you get better contact. It may be a good site. You just haven't had a good effect because you haven't had contact. If you have ST elevation without effect, you've done some damage, but it hasn't worked, so don't be ablate. And finally, the endocardial unipolar map can unmask epicardial scar. We won't talk about that anymore. Bipolar signals tend to be a little bit cleaner. Most people like looking at them. They're less messy, less subject to baseline drift, more useful in scar-based arrhythmias. Far-field information tends to be minimized, not excluded. Polarity reversal between adjacent electrodes indicates there's something happening right in between them. We won't talk about that any further. Here's a PVC that we're mapping. I have all 12 leads of adequate gain to be able to see that there's differences with pace mapping and so forth. A lot of intracardiac recordings. I like to see what I'm doing. Here we have a site that looks pretty good. It's got a QS on it, but the bipolar is kind of a slurred QS, and if we compare that to, I'm sorry, the QS is coincident with the bipolar electrogram timing. It's early. Everything looks pretty good. This might be a good place to ablate. Normal tissue. On scarred tissue, not so good here, because here we have our unipolar electrogram, and we have some early stuff here, reproducible signal here that's somewhat fragmented, gained up, but you don't see any hint of it on the unipolar, so it's not so helpful in that situation. Here it is. Somebody's had a right-sided pathway ablated. Yeah, we've done some damage there, and we don't see any delta waves, so that's good news. If you see this after ablation, you've done some damage. If you see it before ablation, you've got too much contact. If you are pushing around in an area where you've already done some ablation, it's hard to interpret because there will still be some residual ST ablation. Now, the unipolar and bipolar should agree. Unipolar 1, which is where we're going to be ablating from with RF, ablating from the tip, it should be a QS configuration, and with this bipolar, again, I've got a source underneath here. If you ablate there, you're going to get a good lesion, and you're going to get your tachycardia, your focal tach. Now, let's move the catheter here a little bit, and you see the bipolar 1-2 looks exactly the same here. It's because I made it that way, and it actually is that way. So, if you have the catheter here, and you get a bipolar 1-2 that looks great, that may not be very good because the unipolar is way off over here. Let's ablate there and see what happens. That bipolar looks so good, but it turns out not to be so good because we're not ablating with that second electrode, which is contributing to the bipolar. So, when you're looking at a focal tachycardia, make use of this unipolar electrogram. It can help you out a fair amount. These should agree. Here we have a situation where we have a bipolar that is a little bit early. The unipolar QS, not quite so early. In fact, the proximal is a little bit better of that electrode pair. And when we move the catheter just a little bit, we have a much nicer clean bipolar and unipolar, a little bit overlapping here. That agrees, a good sight, and let's go for it. Now, that's great when you have normal electrograms. When you don't have normal electrograms, there's trouble. The loss of conductive elements means lower signal amplitude, disrupted conduction due to SCAR, meaning delayed signals, interposed late potentials, split potentials, by definition 30 millisecond isoelectric interval between components, fragmentation, lavas, all kinds of havoc. So, in a normal electrogram, we're seeing this sheet of activation going, lots of cells being activated once nearly simultaneously. Nice, clean electrogram. We can argue about whether it's the peak, the baseline crossing, the nadir, most rapid dBDT, it doesn't matter, you're going to be 3 milliseconds off one way or another. With SCAR tissue, it has to propagate through all this stuff, fewer conductive elements, lower amplitude electrogram, fractionated, all that stuff, bad business. So, here we have a cartoon of some different electrogram types. We have a split electrogram here, we have a diastolic quarter low conduction going through it, doesn't always work that way, but in this case it will. And we have an electrogram, an electrode that's perpendicular to its action here. We have a wavefront coming along this way, it's going faster along the side, so we get this component, then we get this component in here, a split electrogram. That same tissue, when interrogated from a different direction here, looks very different. It's got this fragmented, because we're propagating along here, and seeing all these things going on here. Same tissue, same beat, everything. But it looks different because of the way of electrogram, of wavefront approach. That's the lava theory. So here we have another one, where we have just block recording on both sides of this, conduction velocity is very similar, you have a pretty normal looking electrogram. Here we pace from one direction, and the wavefront has to go around, record some from here, some from the other side, a split electrogram. Again, the same tissue is being recorded, it just depends on the direction of wavefront approach. Now, here is some complex recordings here, the difference between near field and far field recordings, I'm labeling the stuff that's with the blue in near field as near field, the red is going to be far field, you recognize by virtue it's being low amplitude, kind of slurred, and so forth. If you want to argue about the timing of any of these, go for it, you're going to be off by 5 or 10 milliseconds, not a big deal. Pick any electrogram, any deflection, you'll be right. These guys, not so much. And you can gauge near neighbors here by saying, well, there's a fractionated signal, a repetitive signal in this bipole here, that's not represented on the proximal, just a few millimeters away, this must be a local recording, it must be a real thing. And it is, in fact, the case. So I have one question here, this is a 53-year-old man, an atrial septal defect for surgical repair, I'll just give you the answer on this one, because we won't have much time. So what we have here is a person who's had surgical repair of an atrial septal defect, and he's had palpitations only for the last few years, and the best site with extensive atrial mapping is shown over here, and it's got, this is a big QS on the V here, but it's got a little QS here, it's just a little bit earlier, and you see this is a burst of tachycardia, another burst of tachycardia. Each P wave looks the same here. So the answer here is to recognize this as a focal tachycardia, very unlikely to be reentry at this time, so you wouldn't attempt entrainment. You wouldn't perform pulmonary vein isolation. This is a focal tachycardia. And you're at a site in the right atrium that looks good, so you'd go ahead and ablate at this site, and we'll just go ahead and ablate at this site. So this arrhythmia is in bursts. All the P waves look the same, signifying a focal mechanism, not scar-related, despite us having an ASD repair. Sites that are 20 to 30 milliseconds prior to the P wave and have a unipolar QRS are good ablation candidates. You won't find a mid-diastolic potential anywhere. It doesn't exist. PVA isolation is not relevant because you've got a good site here. So in summary, Mr. Chairman, bipolar recordings differ substantially from their unipolar antecedents. Unipolar recordings, often neglected, still have value. Bipolar and unipolar recordings work together, providing complementary information that's helpful during mapping. And the effect of extensive scarring on wavefront propagation gives a variety of abnormal electrogram configurations. Ongoing research in this area is still important and working. I thank you very much for your attention. Thank you. Thank you, Dr. Miller, for that wonderful presentation. Our last speaker for this session, but not the least, is Dr. Miles from the University of Florida, who will be presenting on tachycardia diagnosis through cardiac devices. Thanks for the invitation. I emailed John to ask him what I should present in this talk, and he said he really didn't care as long as I was on time. So you guys wave a flag or something if I'm not on time. We're going to talk about electrograms that you get out of devices and what types of arrhythmia diagnostics you can do from those. We're going to talk about atrial fibrillation, try to distinguish it from other rhythms, atrial tachycardia, atrial flutters, AV node reentry or AV reentry enter into the differential at times, and certainly with devices, ventricular tachycardia enters into the differential. Now, we utilize similar concepts in this differential diagnosis as you do during EP studies, except you have limitations. You don't have a His bundle. You don't have a surface electrocardiogram to look at the QRS, and it's very difficult to do purposeful pacing maneuvers. You certainly can't do that when you're pulling up interrogations from the past. You might be able to do a little bit of fooling around with the pacing if you have an ongoing arrhythmia. But just like the EP lab, some of these findings definitively will establish a diagnosis. Some of these findings will exclude one diagnosis but won't tell you what the diagnosis actually is. And some findings are suggestive but not diagnostic of the tachycardia mechanism. And in those patients, you need to try to summate that type of information to decide what you're dealing with. So this is what we commonly get from a device. We get atrial electrograms. We get ventricular electrograms that are either near-field, for example, tip-to-ring, and ventricular electrograms that are far-field. And that can be several things, but commonly might be tip-to-can or coil-to-can, something like that. You also get a marker channel, which is what the device thinks it sees, and that's very important to try to correlate the electrograms to the marker channel to see if the device is seeing what you're seeing on the electrograms. This analysis can be performed either via stored electrograms or real-time electrograms. So what's the differential diagnosis? Well, the first thing we usually do is, are there more A's than V's? And if there are more A's than V's, that's usually an atrial tachyarrhythmia. An exception that we'll talk about in a little bit would be a double tachycardia. If there are more V's than A's, that's usually ventricular tachycardia with some rare exceptions. The caveat, though, is sometimes the device may not be recognizing all the A's or V's, or it may be throwing in extra A's and V's. So electrogram dropout and undersensing from low-amplitude electrograms and blanking phenomena may cause undersensing, and electrogram oversensing, for example, T-wave oversensing and other types of oversensing, can also confuse the device. So this is just an example of more A's than V's. This is garden variety atrial flutter. Every atrial flutter wave is sensed by the device. There's 2-to-1 AV conduction. A nice graph of that 2-to-1 AV conduction. No one, including the device, would argue that that's atrial flutter with 2-to-1 conduction. This is an example of ventricular tachycardia. There's complete VA dissociation. There are more V's than A's. We're going to talk about morphology later. This device actually, by these checks, thought that this near-field electrogram was a match to sinus. But luckily, the VA dissociation would be picked up before the discriminator by morphology, and this would be recognized by the device probably as VT. Here's an episode of non-sustained VT with retrograde WinkyBok. All of a sudden, the V's start first. There is VA conduction, but not 1-to-1 VA conduction. The last V is followed by an A, and as we'll talk about in a minute, the morphology changes. So this is VT with incomplete VA dissociation. Now, if you have a tachycardia that's 1-to-1 with a 1-to-1 relationship, that's more problematic on the differential diagnosis. And how do we make that differential diagnosis? Well, one, you can look at an onset. A sudden onset of a tachycardia suggests an atrial or ventricular tachycardia rather than sinus tachycardia. Gradual onset suggests sinus tach, but does not exclude an ongoing atrial or ventricular tachycardia that gradually accelerates and crosses the line of detection. Secondly, we can look at stability. Irregularity favors atrial fib over ventricular tachycardia or the organized atrial tachycardias. And this is an example of equal A's and V's that gradually accelerates to cross the line of detection, and using onset criterion and maybe some other criteria, VTVF detection was withheld by the device for a presumed sinus tachycardia. Here's an example in a single-chamber ICD of gradual onset that then crosses the line. This could be either sinus tachycardia or an atrial or ventricular tachycardia with warm-up. The patient does receive ATP in this situation because of a non-match of the far-field electrogram. So I don't know what this patient really had. It might have been sinus tach with some sort of aberration or an atrial tach with some sort of aberration. The ATP did not terminate the tachycardia. Irregular rhythms are usually atrial fib, but irregular VT can occasionally fool stability criteria. And here's an example of more V's than A's, VA dissociation, but the V's are pretty irregular. VT can be particularly irregular near its onset or near its termination. Thirdly, we look at electrogram morphology. You can do that either visually or the device may have stored an electrogram for comparison. Good morphology match favors SVT. Poor morphology match favors VT. The limitations of the morphology match, though, are that far-field matches are much better than near-field matches. Aberration during tachycardia can screw things up and make the morphology a non-match, even in an SVT. Don't compare paced QRS morphology to the morphology during the tachycardia. So when you see a morphology change during the tachycardia, look back at the sinus rhythm morphology that you were looking at. Make sure it's not a paced morphology. And post-shock electrograms are sometimes all you have, but they're very distorted and cannot be used for discrimination. Here's an example in the same patient of an atrial tachycardia. It starts with an A, it ends with a V, and the morphology is very similar to sinus. As opposed to ventricular tachycardia in the same patient, it starts with a V, there's VA dissociation, and this morphology is very different from that during sinus rhythm. This is an example of VT with retrograde Winkiebach. Note that the electrogram morphology difference during the VT. We know this is VT because of the VA dissociation, or the incomplete VA dissociation. But note that the electrogram in the near field is not as different from the sinus electrogram as that in the far field. And we'll see some examples where the near field electrogram really isn't very helpful. You can't compare the morphologies in this patient because of bi-V pacing and tachycardia. These morphologies look different. They probably are different because this is VT with VA dissociation, but you can't use morphology criteria because these are paced electrograms over here. Limitations of near field electrograms I've already mentioned. This is a near field match in a patient with VA dissociation. So this is VT, but luckily the VT was identified due to the VA dissociation, ATP was activated, and sinus rhythm was restored. This is a patient of mine who has about 20 or 30 ATP terminations a day because he doesn't want his accessory pathway ablated, but he has Dannen syndrome and a cardiomyopathy. So he has an ICD. The morphology criteria doesn't recognize the difference between the narrow QRS during SVT and the wider QRS during sinus rhythm and constantly gives ATP thinking it's ventricular tachycardia. He's left this alone because the ATP first run always terminates his PSVT, his AV reentry, and he's happy, but he gets a lot of ATPs every day. The fourth thing we look for in a one-to-one tachycardia are the AV relationships during tachycardia. Each company has a proprietary algorithm. It's not my role to go through those. They're helpful, but they're not perfect. For example, if the RP is greater than the PR, that suggests sinus or atrial tachycardia, but that's not always true. A stable simultaneous A and V may suggest or at least bring to mind it could be AV nodal reentry, which is a common arrhythmia. And if you have an ongoing arrhythmia, it might even do pacing manipulations or give adenosine looking for real-time responses such as VA block during the tachycardia or the type or pattern of termination. So we ask, are the A's driving the V's or are the V's driving the A's? Does it start with an A or a V? Does it terminate with an AV, which favors atrial tachycardia, or does it terminate with a VA, which favors VT, but more rarely could be some sort of SVT such as AV nodal reentry or orthodromic AVRT with anterograde termination? You look for cycle length wobble. Is the AA cycle length variation followed by a similar VV variation, as it would be in an atrial tach, or does VV variation drive AA variation as it would in a ventricular tachycardia? Can one find transient AV or VA block during tachycardia somewhere else in the patient's tracings and assess the effects of spontaneous PACs or PVCs on the tachycardia? You can also assess ATP attempts at tachycardia termination just like you do with entrainment in the laboratory. For example, ATP termination of tachycardia without advancing AA intervals excludes an atrial tachycardia. ATP that advances the AA interval to the ATP cycle length but doesn't terminate the tachycardia, you can look for VAV or VAAV patterns, as the previous speaker spoke about, to try to differentiate SVT mechanisms. But remember, VT will often have a VAV pattern at termination. In the lab, you know it's not VT, but with the device, VT may still be in your differential diagnosis. And a ventricular fusion beat, just like Greg showed you earlier on one of the lab examples, a ventricular fusion beat early in the ATP run that advances the AA interval suggests either orthodromic AV reentry or maybe VT, but it excludes AV node reentry in atrial tachycardia. So here's an atrial tachycardia. It starts with an A, terminates with a V. Morphology is different between the tachycardia and the sensed sinus rhythm electrograms. Here's an atrial tachycardia that starts with an A, ends with a V. It's almost surely an atrial tach, but we can't compare morphologies because these are all ventricular pace morphologies. Unless the device has stored a previous sinus rhythm non-paced morphology. This is VT with one-to-one conduction. It's initiated by a V, it terminates with an A, and it has the appropriate morphology change, all suggesting ventricular tachycardia instead of an atrial tach. Here's initiation by a V with termination with an A. So it meets those criteria for a ventricular tachycardia. Only thing we have is a near-field electrogram, and the near-field electrogram is a match. No far-field electrogram is available. So this is how a near-field electrogram for morphology can lead you astray. This is an example of wobble in the tachycardia cycle length. Notice that atrial wobble drives ventricular wobble, meaning that this is probably an irregular atrial tachycardia, not an irregular ventricular tachycardia. This is a patient that had a one-to-one tachycardia that was thought by the device to be ventricular tachycardia. ATP was delivered and a shock was delivered, and the patient wasn't very happy with this. But in the same patient, as we look back at the interrogations, we saw areas where the tachycardia looked the same in the atrium, but there wasn't one-to-one anagrade conduction, convincing us that we had to do some reprogramming to keep that patient from getting another shock. Now here's a patient that we suspected AV node reentry. A PAC starts tachycardia with near-simultaneous Vs and As, and we had the privilege in that patient of having an ATP run actually advance the AA intervals, and we could map these AA intervals through. We knew which A went to which V. We knew that that ATP didn't stop the tachycardia, but it ended with a VAV, and this A couldn't have come from that V, so this ATP made the diagnosis of AV node reentry in this patient very likely. And in addition, in the same patient, a PAC actually terminated the tachycardia probably by entering the anagrade slow pathway, and resulting in termination of the AV node reentry. Here's a patient that starts with a V, has one-to-one VA conduction. ATP that advances the AA interval ends in a VAV pattern, but we know from the onset that this was a ventricular tachycardia. So this is just to remind you, if you don't know like you do in the lab, that it's not a VT, a ventricular tachycardia can have a VAV pattern from an ATP run. What about single-chamber devices? Well, in those, discrimination is limited to onset, stability, and morphology. Remember that even a dual-chamber device is limited to these same three discriminators if a double tachycardia is going on, that is atrial fib and ventricular tachycardia. Also remember that any tachycardia detected in a patient with known complete heart block or an intact previous AV node ablation has got to be ventricular tachycardia, and that's usually very useful in the differential diagnosis. So here's a single-chamber device, non-sustained VT, sudden onset, sudden offset. We have far-field and near-field electrograms but no atrial electrograms. Morphology is different from sinus rhythm, sensed morphology. This is non-sustained ventricular tachycardia. This looks the same, but it's a little bit irregular. The comparison beats that we have are all paced, so you don't have morphology criteria, you just have onset, sudden onset, sudden offset, and unless the patient has known AV block, you can't tell from this tracing whether this is VT or an atrial tachycardia because you can't use the morphology criteria. This is a single-chamber device, sudden onset, regular. Electrogram morphologies do not match. Gets an appropriate ATP. Terminates tachycardia. This is another patient with a single-chamber device. One-to-one, well, you don't know whether it's a one-to-one tachycardia. You have a near-field electrogram and a far-field electrogram. The electrograms are a very good match, and so therapies are withheld. It's probably sinus tachycardia or an atrial tachycardia. Double tachycardia. Simultaneous atrial and ventricular tachyarrhythmias. In these, we have to look to see, is there any consistent relationship between the regularity of the atrial rhythm and the regularity of the ventricular rhythm? Is there a sudden change in the rate or the regularity of the ventricular rhythm? And is there a change in the electrogram morphology? So here's a patient with a double tachycardia. Sudden onset, regular rate, differing morphology than this irregular QRS over here. This is ventricular tachycardia during atrial fibrillation. Double tachycardia. AV relationship is not consistent. This is another patient where the AV relationship is not consistent. The near-field morphology match is good, so it's misclassified as an SVT until, at the end of this tracing, notice that the atrial tachycardia terminates, the ventricular tachycardia continues, and therefore that reveals, as you go back here and look at it carefully, that this was an atrial tachycardia and a simultaneous ventricular tachycardia. Now, how about oversensing and undersensing that might cause misdiagnoses? We have crosstalk sensing in both atrial and ventricular lead, atrial and ventricular electrograms on the same lead, T-wave oversensing, lead fracture, EMI, external noise, and we have various reasons for undersensing, and we'll just show some examples. Here's atrial oversensing due to sensing both A's and V's in this atrial lead. So these V's are represented by relatively large electrograms in the atrial lead, and here's a little graph that results from something like that. This patient would be reported out as having a lot of atrial fibrillation or atrial tachyarrhythmias when he actually does not. Here's an example of T-wave oversensing. Here's the A sensed, the V sensed, and the T wave that's sensed. This T-wave oversensing gives a very characteristic railroad track-like pattern on the interval graph. And the algorithms that the device people have come up with are pretty good at recognizing T-wave over-sensing and withholding therapy if they think it's a T-wave over-sensed arrhythmia. So notice that there's a regular alternation of cycle lengths in the T-wave over-sensing patients. Here's a patient that was under-sensing every other atrial flutter wave. And this is actually pretty common. Every other flutter wave ends up in a blanking period and isn't seen by the device. So instead of mode switching, this device is trying to track every other flutter wave, causing basically a paced tachycardia. And here's an example of that type of tachycardia that, with a little bit of alteration in the AAV relationships, it begins to sense all of the atrial components. It mode switches. And instead of two-to-one tracking, you now have the mode switch type of ventricular pacing at a normal rate. This is an example of atrial under-sensing during atrial fib. The atrial electrograms are very small. You even have intermittent atrial pacing because it doesn't recognize these atrial electrograms. And this can be problematic in the clinic if you're trying to estimate the patient's atrial fib burden. It'll underestimate the atrial fib burden. And it's also hard to figure out in clinic whether periods where the device says the patient's not in atrial fib, the patient might really be in atrial fib. And so it's hard to tell whether the patient is persistent atrial fib, you need to do a cardioversion, or paroxysmal atrial fib, you need to do some other drug or ablation intervention. Here's an inappropriate mode switch due to noise on the atrial lead. This can also lead to false a-fib burden data when you're trying to evaluate the patient's atrial fib burden. So this is a atrial lead fracture causing a mode switch. Worse than an atrial lead fracture is a ventricular lead fracture in a defibrillator patient. I think we'll just leave it that this patient wasn't very happy with this. Here's some external noise that was picked up on the day of surgery. Notice that you can see it in both the atrial and the ventricular leads. So the characteristic of a lead fracture versus external noise is you usually see a lead fracture in one lead. You usually see lead noise in both leads. Here's an example of a colonoscopy where the patient periodically would get bradycardic because you have noise in both leads from some sort of cautery that inhibits ventricular pacing. One thing that I've run across several times is that sometimes you can see noise in one lead and not the other, and you think there may be a lead fracture. But when you look at the gains, the ventricular lead is not gained up to match the atrial lead gain. And when you have someone give you equal gains on both the atrial and the ventricular leads, now you begin to pick up noise not only in the atrial lead but in the ventricular lead, making you think that this is probably EMI, not lead noise. Although I will have to say we picked up a two-lead crush injury to both leads the other day, fooled around with this, saw noise in both leads, and had to do a lot of arm manipulation, actually showed eventually that both the atrial and the ventricular leads in that patient were crushed. This patient, I think, had external noise. Also, I want to point out that EMI is more easily seen on far-field electrograms than it is on near-field electrograms. So if you have a type of device where it's not easy to gain up the ventricular gain to the equal to the atrial gain, you might be able to see the noise on a far-field electrogram. I want to say a word about pacemaker-mediated tachycardia. Pacemaker-mediated tachycardia is a V-paced tachycardia. So if you have a V-sensed tachycardia, it's not PMT. So we'll often get a request from the house staff, is this PMT? But it's a V-sensed arrhythmia. If it's V-sensed, it's not PAT. In what you think is PAT, it's important to try to differentiate a PMT. It's important to try to differentiate PMT from an atrial tachycardia with one-to-one tracking. PMT stops when atrial tracking modes are disabled. Atrial tachycardia does not. And PMT most commonly is caused by an atrial non-capture, or a PVC with a retrograde A that's then sensed and triggers the next ventricular pace beat and repetitively initiates PMT. So here's an illustration of the onset of PMT. There's a PVC that conducts retrograde. The patient doesn't see that because of a blanking, a PVARP, and paces the A, which is still refractory and doesn't capture. The next V, the paced V after that paced attempt at pacing the A, that paced V goes back to the A. It's now sensed, paces the V, goes back to the A, sensed, you're off and running on pacemaker-mediated tachycardia. The offset in this particular patient was a PVC, a spontaneous PVC that was early enough that it did not conduct back to the atrium, terminating the PMT and back to an atrial, an AV-paced rhythm. Here's an example of pacemaker-mediated tachycardia terminated by the pacemaker's PMT algorithm. The pacemaker thinks this is PMT, so it extends the PVARP on this last time so that this atrial sense falls in a refractory period and it A-paces here. There's no V-pace after this A sense. PMT is extinguished. On the other hand, here's a similar patient. Atrial tachycardia is thought to maybe be PMT, so the device does the same type of manipulation. It does its PMT algorithm. This last sensed A is not, does not drive, does not prompt ventricular pacing, but you still get a V sense and the atrial tach continues. So that's how you make the differential diagnosis between PMT and an atrial tach. Notice also that not all of these are ventricular paced. Pacemakers can, pacemakers and defibrillators can induce proarrhythmia. There's certain algorithms that may result in pauses for ventricular prematures that may be ventricularly proarrhythmic. And certain atrial pacing features during refractory period issues can actually probably initiate atrial fib in some patients. Here's an example of a pacemaker algorithm that's designed to prevent, designed to minimize ventricular pacing in someone with right ventricular pacemaker. It creates a pause by allowing AV block to occur. And this was a patient that was prone to pause-dependent arrhythmias. Patients who are prone to pause-dependent arrhythmias shouldn't have algorithms in that allow long pauses. Obviously, we've all seen ATP be proarrhythmic. ATP here turns ventricular tachycardia into ventricular fibrillation, prompting a shock. Here's competitive atrial pacing. This patient is being sensor-driven. It ends up that the sinus A ends up in the refractory period after pacing, is seen by the device but ignored by the device, which then tries to pace shortly after. And this occurs repetitively over and over and over again until finally this particular patient went into atrial fibrillation, probably from this pacing algorithm. This is an example of a similar phenomenon, competitive atrial pacing. You have atrial pace by V-pace. You have a PVC. Probably there's a PVARP extension algorithm on to prevent PMT. So this A was seen but is ignored. It then paces after that with a very short interval and probably started the atrial fibrillation. And don't ignore other iatrogenic events. So I'm just going to show three examples. Here is a patient who got a TAVR and had VT on the day of the TAVR and comes back to us and we say, oh, my goodness, this is a pacemaker. I don't know whether this is a pacemaker or not, but this is a pacemaker and the patient had VT and what are we going to do? But we look back and this was the day that the patient had the TAVR and they did rapid right ventricular pacing during deployment of the valve. With a temporary catheter. With a temporary catheter. So it was picked up by the device as VT. Here's an example where the device was on during an EP study. So you get all this stuff. It looks like the patient has some funny VA dissociated pacing going on here. Then the patient's in tachycardia. Then the patient gets ATP and is back in sinus rhythm. And if you look at the graph, here's the sinus rhythm. Here's the one, two, three, four, five, six, seven, eight beat drive train. Here are the prematures. Here's the ventricular tachycardia. And here's my assistant pacing the patient out of the ventricular tachycardia. And it popped up in a clinic interrogation a little bit later. So it's probably a good thing to turn that off when you're in the EP lab. As it might be good to turn the diagnostics, now luckily we had turned therapies off but hadn't turned the diagnostics off during this RFVT ablation, making a interval graph that looks like something my grandchildren would make and all of this artifact. All right, so John, am I within time? You're fine. Yes, you have time. Thank you. Thank you, Dr. Miles, for that excellent overview of tachycardia diagnosis through cardiac devices. Now it's time for questions. So we have the microphone in the center of the room. Anybody with questions can come up. And we can also ask questions through the app. OK, Dr. Miles, there's a question for you through the app. Are devices nominally set to discriminate SVT versus VT by morphology match via near field or far field EGM? Well, I'm not a super device expert. And as you know, the morphology is part of that trio. And some of the device companies, you can actually choose which of the trio or all of the trio or none of the trio to program on. So that's one thing that's done. In a lot of the devices, only the near field is included in morphology. And that's why several of the examples up there were near field. Those of you who know devices, John, is there a way of toggling back and forth in some of these devices between near field and far field electrograms? Some of them there are. And some of them are hardwired to only go with the near or far. So you might ask your rep for each device what they use, whether they can use one, the other, or both. You also would need to turn on some of the diagnostics. It's frustrating to see somebody who's had an episode and they have an atrial lead, but they didn't have a stored atrial electrogram during that episode. So making sure that when you go back in or have your device rep help you with designating atrial channel as being recorded. It saves battery. They like to save battery. But you also need a diagnosis. But we all hate that device that has that abridged electrogram. What do they call that? The summed electrogram. The summed electrogram. Boy, is that awful. So I think that that was designed to save battery. But I think another month or two of battery drain is worth having good electrograms. It's very frustrating. If it lasts long enough, you'll actually see the electrogram split out. But if it isn't, it's just marker channels. All on the same line sometimes. And sometimes you have to choose whether you want the V's to be displayed, electrograms, or the A electrograms to be displayed. So luckily, gradually, those devices are reaching ERI and we're getting rid of most of them. Thank you. Any questions from the audience? OK, we have another question here. It says, would you recommend turning off MVP algorithms on all patients on class 3 antiarrhythmic drugs to minimize proarrhythmia risk? Yeah, so our policy has been anyone that you're worried about pause-dependent arrhythmias, either somebody that you know has had them in the past. And I think it makes every bit of sense not to allow pauses that I showed in a patient with drugs that prolong the QT. You know, most of the algorithms now, you don't have to allow complete non-conduction. And so I think that that's what's mostly turned on in our office. I don't know about yours. But we don't use the MVP very much in people who are going to really have AV block. Yeah, that's what we do as well. We basically program the maximum AV delay that you want to allow before the patient will kick in. Those are all the questions online here. Any questions from the audience? Yeah, you can use the microphone. Thank you. And this is Dr. Harvey. I'm the electrophysiologist at the Bakersfield. When you program the ICD, when you program the ATP particularly, do you still do this in a ramp or only the burst ATP to prevent the ventricular arrhythmia, that ATP-induced tachycardia that he mentioned? The burst ATP versus the ramp, is there a difference there? The choice of using burst ATP or ramp as a means of decreasing the likelihood of an atrial tachycardia? No, this is ventricular tachycardia. For ventricular tachycardia termination, when you program it, we used to program both the burst and the ramp. But I got all the literature that the ramp can cause the induced more of the atrial tachycardia that the ramp can cause the induced more ATP-induced tachycardia. So is it true or just I'm just wondering? It's true. In my experience, anyway, ramp is more likely to terminate an arrhythmia, but also more likely to get you in more trouble. So that's why most default is burst first. And some don't even have an option. Well, you have an option for ramp in practically every device, I think. But it's a secondary thing that you have to choose to do. I think that's correct. Yeah. And one thing to throw out, certainly I think those of us who've been in the lab for a long time know the faster you pace, the more chance you're going to accelerate the arrhythmia. And the ramp is more likely to do that than the burst. The devices do come out of the box with a relatively long R to first beat of the ATP interval. And that's something that means that by 8 or 10 beats, you've barely fused four beats or five beats. You really don't have much of a burst. So one thing I think might be a little safer than adding a ramp if you're having trouble terminating the tachycardia is to make the sensed R wave to the first ATP a little tighter. Instead of being 90% or so where it might come out of the box, make it 70%. That way, more of your burst actually gets full capture of the ventricle and may be more likely to get into the circuit. I've felt, without any evidence, that that was a little less proarrhythmic than going to the more aggressive ramps and things like that. And they almost always have 8-beat drive. And if you do the math, and it comes on at 87% or 84% of tachycardia cycle length, and then does it at, again, 87% or 84% of the tachycardia cycle length, you may, if you're pacing the right ventricle, you may leave a left ventricular source completely unaffected with an 8-beat drive. But if you do 10, 12-beat drive, you're much more likely to get over there and affect it. Thank you. Any other questions from the audience? Hello. This is Dr. Hasib from Pakistan. I have a question. We use ATP to terminate overdrive ventricle tachycardia. Why cannot we can use atrial overdrive pacing in pacemakers to terminate atrial fibrillation or atrial flutter? So between the echo and a little bit of deftness, it was, why don't we use atrial ATP to terminate VT? To terminate atrial fibrillation or flutter through pacemakers or devices. Oh, OK. So if I understand your question correctly, our pediatricians especially love to put in devices that have atrial ATP for their congenital patients with atrial fibrillation. Their congenital patients with atrial tachs. And there are automatic algorithms that you can get in some devices that will try to terminate organized atrial tachs or maybe atrial flutter with atrial ATP. And there's a literature on trying to activate this automatically in atrial fib patients with the theory that maybe at some times of day or intermittently, it's organized enough that you might stop atrial fib with anti-tachycardia pacing. My gestalt is it's not particularly successful. We don't do it very much, but I do think there's a role for atrial anti-tachycardia pacing in select patients. Some devices, pacemakers and or defibrillators, have automatic ATP as a choice. Some don't, but you can certainly do commanded ATP with practically all of them. Some older pacemakers can't go rapidly enough with commanded pacing. Medtronic had this AT500 for some time back in the early 2000s. And these things would drain their battery like nobody's business because they keep on repetitively trying to pace into atrial fib. And sometimes it works. Like, one out of 1,000 times it works. And you think, oh, I've got it. But it's hard to tell whether that would have stopped anyway. Thank you. OK, our time is up. Thank you to all our speakers. And thank you to everybody in the audience for attending. This concludes the first session of the board review this year. The second session will focus on ventricular arrhythmia and will be starting in about 15 minutes. Thank you.

HRS

SVT

Supraventricular Tachycardia

board review

arrhythmia

electrocardiograph

tachycardia diagnosis

unipolar recordings

bipolar recordings

cardiac devices

atrial fibrillation

ventricular tachycardia

Q&A session