Greetings, this is John Miller with Core Concepts in Electrophysiology, and we'll have some workshop questions for you in workshop number nine. Here we go. These are my disclosures. First question. A 38-year-old man comes to the hospital because of palpitations. Tracing during the palpitations is shown. Adenosine is given in 6, 12, and 18 milligram doses, enough to actually, and given properly, such that symptoms of shortness of breath, chest discomfort are produced, but the arrhythmia persists, which is the following. It's a most likely diagnosis for the abnormal rhythm. Supraventricular tachycardia with aberration. Antedromic reciprocating tachycardia. Reentrant ventricular tachycardia related to the left posterior fascicle or focal ventricular tachycardia from the posterior papillary muscle. Here's the ECG. You can review it, think on it, mull it over, ruminate on it, whatever you want, and your choices, and join us back when you have your choices. The correct answer is ventricular tachycardia of a reentrant nature related to the left posterior fascicle. It's a long way of saying posterior fascicular tachycardia. Now, I don't like that term because that might mean a focal tachycardia. This is not. This is reentry. To say it correctly, you could say it's verapamil sensitive ventricular tachycardia related to the posterior fascicle, which it usually is, sometimes it's not, so it's a mess. ECG pattern looks kind of like aberration. There's some problems with that. The RS ratio in V6 is not very good for that, but you don't know that the leads are correctly placed. The right rabbit ear is greater than the left rabbit ear, except where it's not. In V2, it's not. The airway transition at RS complexes, but the RS is relatively short, so this has several criteria pointing to supraventricular rabbit ventricular tachycardia. The pattern in AVR and the V6 ratio, the small Q and big R in AVR and the V6 RS ratio, and even V1, yeah, the right rabbit ear is taller, but there's no S wave that descends below the baseline. This is an RR prime, not really an RS, as it descends below the baseline. These are not aberration patterns, and furthermore, the tachycardia didn't respond to adenosine, and you say, well, they didn't give it properly. Well, I said they did. He had symptoms. He had these dreadful symptoms that people have when you get them to spread for medication. AV nodal reentry, anything that involves the AV node really should terminate or show AV block. Atrial tachycardia should show AV block. Nothing happened. The precordial airway pattern is not very good for pre-excited tachycardia with these RS complexes out in V6, and so it appears to be VT. Now, we have two VT choices. One is posterior papillary muscle. One is the reentrant Purkinje related to VT, and reasonable clues to that are the presence or absence of Q waves in 1 and V1. Papillary muscle quite often have a Q wave in V1 and not in V1. Contrarywise, the posterior fascicular tachycardias have a Q in lead 1, but not in V1. So this fits best with that, and we'll take a look at some other things. So this is most consistent with the reentrant posterior fascicular VT. All right. We'll go on to the second question here. Let me just go over a little bit at the end of that. One clue to differentiating the rapamyl-sensitive posterior fascicular related VT, reentrant VT, from papillary muscle is what happens with Q waves in leads 1 and V1. Papillary muscle VTs quite often have a Q wave in V1, build Q wave, and not in lead 1, whereas the Purkinje related reentrant ventricular tachycardia, posterior fascicular related tachycardia, have a Q wave in lead 1 and not in V1 exactly the way they have. So these features all taken together are most consistent with this posterior fascicular related reentrant ventricular tachycardia, rapamyl-sensitive, et cetera, et cetera. Question number two. A 39-year-old woman has episodes of tachycardia at two different rates. Some are associated with mild palpitations, others with near syncope, despite being in a similar setting. Based on the figure, the most likely tachycardia diagnoses are, one is atrial tachycardia, or it's atrial tachycardia and using two different avianotal pathways. Avianotal reentry is present in both of these tracings. Atrial tachycardia in one of them, avianotal reentry in another, or atrial tachycardia in one and orthodontic reentry for the other. Here they are. Slow one on the left, fast one on the right. Same individual, different times, two different rates, and maybe two different tachycardia. So check it out, make some measurements if you care to, or just take a wild guess. It's one of those four things and rejoin us when you have your answer. The answer is it's avianotal reentry in both cases. Careful inspection will show that these are the same atrial rates, but the ventricles are exactly twice as, half the rate here as they are over here. And right in the middle here, you see this really odd deflection. That's not any kind of a T wave, that's a P wave, and it's a really narrow P wave. And so this is two-to-one conduction in avianotal reentry. This is an individual who has one-to-one conduction and two-to-one conduction. Most often you see a big hiss potential on the conducted ones and block below this in the non-conducted ones. Sometimes you don't see a hiss and sometimes that is the lower common pathway block. Most of the time it's probably blocked below this, but it's initiated response to medications and so forth. So think of this when you have two different tachycardias in a person, two different rates of tachycardia, one is exactly half of the other. Look for that little P wave between QRS complex. The reason this is so narrow is if you think about it, if you've got sinus rhythm and a normal P wave is maybe, let's say 80 milliseconds. Let's say half of that is right atrium and half of that is left atrium. So you propagate from right atrial source, sinus rhythm across the septum 40 milliseconds, another 40 milliseconds to get to the lateral left atrium, you're done with P wave. What if you're coming up the middle and activating both atria simultaneously, 40 milliseconds there, 40 milliseconds there, it's the same 40 milliseconds. So it's a really narrow P wave. The narrowest you'll find are the septal P waves. All right. So there's the answer to that. Question number three, 37 year old man with palpitations and lightheadedness comes for EP study and attempted catheter ablation. He's had three prior failed catheter ablation attempts. ECG during an episode is shown in tracing 3A and intracardiac recordings in tracing 3B. Based on the recordings, you conclude that the rhythm is AV nodal re-entry with lower common pathway block, sinus rhythm with 1-2 AV conduction, junctional tachycardia with right front branch block and right posterior fascicular block, fascicular tachycardia from the left anterior fascicle, or re-entry within the hysperkinesia system, anterogradially down the left anterior fascicle and retrogradually up the left posterior fascicle. That's a lot. Here's his ECG. And I should say that this is from the lab. So these four beats are the same as these four beats are the same as these four beats are the same as these four beats. So it doesn't go from this beat to this beat and stutter along as these four beats are the same representing all 12 beats. This is the intracardiac tracing. And I've taken both pieces of information to get the correct answer here. So here we have ongoing tachycardia. You can make your choices and come back to us back to the presentation when you are set. I'm set. This is fascicular tachycardia from the left anterior fascicle. This is a focal tachycardia. We have in this tracing, well, we had on the surface ECG what looked like left anterior fascicular block. We had a right bundle pattern and we had a left axis deviation. Or it could be, I'm sorry, it looked like left posterior fascicular block and right bundle ranch block. On our ECG, we had, let's just go back to it here. We have right bundle ranch block, pretty narrow QRS complexes and a rightwards inferior axis suggesting posterior fascicular block. Or it could be emanation from the left anterior fascicle giving right bundle ranch block and left posterior fascicular block appearance. Now on the intracardiac recordings, we have some interesting findings here. Tachycardia is going along here and along here. And then we have these narrow QRSs here. Now if this were junctional tachycardia with right bundle ranch block and left posterior fascicular block, a premature in the atrium or an atrial complex sinus beat that it conducts should have the same QRS pattern if it really is conducted through the conduction system that has right bundle ranch block and left posterior fascicular block. Here, we have a pretty normal QRS when we have an A that is perfectly timed to fall in. This is A being dissociated here. There's another A there, another A there. And this one also conducts with a narrow QRS. Therefore, this cannot be junctional tachycardia with aberration along the way or fixed conduction defect. If it's reentry within the hysperkinesis system, a fully captured narrow QRS complex should conduct down both fascicles, whichever fascicles are involved, and interrupt the pathway because it's going down both pathways. And the returning impulse has to be coming up with light. So the arrhythmia continues here. So it can't be that. If it's avian ovary injury with lower common pathway block, we would see more A's than B's, not more B's than A's. Sinus with one to two conduction, OK, that's possible except for what happens with this narrow QRS complex. All the complexes should look the same when they're conducted. And you should have exactly two QRSs for every P. It's not that here. That's particular tachycardia is the best answer. There's the hystere and there. And there's a little retrograde hystere. I wouldn't pick that out of the ground. But in judging when we were pacing along, that seemed to be the best candidate for a retrograde hystere potential. Now, if it's coming from the anterior fascicle, it's not going to take long to get to the hystere. So it's going to be before the QRS just like this. All right. Now, part two of this question, this is not, this is just a workshop. This is a simulation. This is not the way it is on exam. You don't get part two and part three of questions on the examination. Overdrive pacing in this patient is performed from the right ventral during the arrhythmia for 20 cycles at different cycle lengths. The same ventricular arrhythmia resumes after each pacing run has concluded. The paced cycle length used and the interval to the first complex of the resumed arrhythmia are shown as followed in this very small table here. So the faster you pace, you get different intervals from the last paced complex to the first returned PT complex. And so the faster you pace, it actually takes longer for the tachycardia to resume. The most likely arrhythmia diagnosis based on this information is focal automaticity, micro-reentry within the left anterior fascicle, triggered activity due to delayed action depolarization or triggered activity due to early action depolarization. join us when you're ready with your answer. The answer is focal automaticity. This is a nice example of everything that should be a focal automatic source. We have overdrive pacing. This is at pace cycling 450. We get a return cycle over here at 615. I'm superimposing the last two cycles of overdrive pacing and the first cycle of what comes back in blue here, aligning everything with this last stimulus here. So the pace cycling is a little bit faster because the blues are a little bit earlier here, 430 milliseconds. And then the return cycle, first beat of resumed tachycardia is pushed out a little bit. Here is the last two cycles of pacing at 410 milliseconds. And you see that the red is further out still. This is overdrive suppression of focal automaticity. The faster you pace, the more overdrive suppression there is. The longer you pace at the same cycling from the same site, the more the degree of overdrive suppression. Now, with delayed after depolarizations, you might expect to see overdrive acceleration. So the next return cycle comes back sooner than anticipated because it's constantly loading with the faster rate. Reentry should have a fixed return cycle. It shouldn't vary like this. I'm not sure what would happen with early after depolarization related tachycardia. I just don't know what would happen with that. But this is a characteristic feature of focal automaticity. Here is some ablation site possibilities. This is a really good site here. You look for the very earliest electrogram that you can find out here. Those pretty fast conduction is pretentious to milliseconds make a difference. So this is, if this is the best you could find, OK, I think you should do better than that. This is not so good here because the proximal is actually earlier than the distal. And here, the distal is great. It's kind of a fragment. It's way out front here. And ablation there was successful in this case. There's ablation. You get some overdrive or some heat-related automaticity. And it fires off a little bit. And then it goes back to sinus rhythm. This is the final ECG sinus rhythm of AV conduction, no bundle. Now, here's some tips on mapping of these guys here. Here we have an aortic valve, left bundle, anterior fascicle, septal fascicle that's there, the posterior fascicle, mitral valve here. Looking at it kind of from a paleo view here. So left valve. All right. Let's say we've got a focus that's there in the anterior fascicle, as was in this case here. And let's say we have done extensive mapping. And we have found the site out here in the periphery of the left fascicular system, where we have a fascicular potential during tachycardia. And it's 22 milliseconds before the QRS onset. That's pretty fine. Let's ablate there. Let's see what happens. Well, if you ablated that site, the peripheral site out there, you have no effect on the BT. It just doesn't care because you weren't anywhere near it. But no harm done to the QRS complex in sinus rhythm. Once you get rid of it. You're trying to get rid of the BT. All right. Here's another site over here. Let's say, oh, it's 28 milliseconds per year. Why didn't I find that before? That's great. There's a blade there. See what happens. Yeah. All right. It's proximal to where your actual impulse formation was from, and it doesn't have any effect on the BT. You get the focus is merely turning away over here. But now, if you get rid of the focus, you are bought into left anterior fascicular. OK. That happens on a lot of ECGs, but that would be it. Right? That would be it. Let's say you find a spot down here. That's only 15 milliseconds before. Now, I'm not sure why you would be happy with a site that's 15 milliseconds before. If sites that are even earlier than that were not successful, I don't know. I wouldn't do it. But let's just say you did. So this is on the other fascicle, the posterior fascicle, and you can't do any better than that. It's getting kind of late. So OK, let's wait and just see what happens. All right. So again, you're not on the focus, so you don't have any effect on BT. But now, you got left posterior fascicular block excited. That's a really rare thing to get left posterior fascicular block, because it's your most reliable, most redundant fascicle of all. You just don't see left posterior fascicular block on XCGs very much. When you see it, it's trouble, because that's your last stand, your most sturdy pillar. And it's already been knocked out. So anything that happens to the others, you're in trouble. Oh, and by the way, we already did have stuff happen to the others, didn't we? We had left anterior fascicular block. Now, we got left posterior fascicular block. That's basically left lateral brachial block. Congratulations. Great job. But if you find this spot here, this 38 milliseconds, it's not very far from these other things. But tiny is a little bit better. Or it is pretty far from these things. But conduction is so rapid that you spread from there so rapidly that 5 milliseconds, 10 milliseconds can be a significant difference, a significant distance. We'll start back here a little bit, Scott. OK, congratulations. You just got left bottom branch block. Super. Now, if you get to this site over here, the actual site is 38 milliseconds. That doesn't seem like that's much of a difference. But conduction is so rapid in the Purkinje system that it can get from point A to point B that are pretty far separated pretty fast. So the timing difference may not be very much. 10 milliseconds between these two sites. But that's larger than an RF application. So you can't get lucky with this. You have to be right on the spot. It takes a lot of very careful meticulous mapping, finding that site earlier than which there is nothing. So if you ablate here, you get termination of ET and no effect on the surface adhesions that we had in our case. All right, in the summary of this question, vesicular VTEs, tachycardias may be re-entrant, or as in this case, focal. Overdrive pacing can differentiate these two things. You either have fusion, you have a constant return cycle with re-entry, or you have overdrive suppression and no fusion with focal tachycardias. It's important to determine whether the arrhythmia is junctional with bundle branch block, or vesicular block, or a vesicular rhythm. Easy to sort that out in most cases. Base the atrium or see what happens during the sinus rhythm that is dissociated. Correct targeting in the focus with very meticulous mapping, very careful mapping is critical for eliminating it and not causing unwanted collateral damage to other areas that are innocent and bystanders along the way. Here's question number four. 53-year-old man who had an atrial septal defect repairs teenager has had palpitations for four years and representative tracings of these palpitations are shown in figure one or directly above. He undergoes mapping. The best site with extensive right atrial mapping is shown in its highest septum in figure two. At this time, you should ablate at this site, attempt entrainment at this site, map the left atrium for mid-diastolic potential, ablate the left atrium on the opposite side of the septum from where you're making these recordings, or perform pulmonary vein isolation. Tracings, think about it, turn me off, fine, doesn't matter to me. Come back, you'll be back when you've got your answer. The answer is ablate at this site. Why? Well, the behavior of this is burst of atrial tachycardia. All the P waves look the same. This is probably a focal process. Yeah, he's had an atrial septal defect repair. Yeah, he's got scar in his atrium. Yeah, an atriotomy. This is not the behavior of reentry, this is the behavior of focality. And thus, a site that's maybe 20 or 30 milliseconds prior to the P wave and has a unipolar QS configuration in the atrial aspect of the recording is probably a pretty good choice. There is no such thing as mid-diastolic potential in focal tachycardia. So you can go to the other atrium, you go to the other ventricle, you go to their brother-in-law, it doesn't matter, it's not there. And you can't entrain a focal tachycardia. So attempting entrainment doesn't make any sense. Having the left atrium to find a mid-diastolic potential that doesn't even exist, that doesn't make any more sense either. Blading at the left atrium on the opposite side, you're going to get better than this, really? You're going to find a better site than this? And PV isolation, what? What was in your coffee today? That doesn't make any sense either. This is not atrial fib, it's not an atrial tach coming from a pulmonary vein, it's coming from here. Thank you for your attention. Hi, this is Greg Michaud from Vanderbilt in Nashville. Welcome to Core Concepts in EP and Board Prep. This is workshop nine. Case one, a 56-year-old patient with recurrent persistent atrial fibrillation after prior PBI and CTI. Radiofrequency ablation complains about increased dyspnea with exertion. He had a normal LVEF prior to ablation. He is referred for redo ablation. He's been taking a PIXA band by his report. Which of the following is the most reasonable next step in his care? TEE prior to the redo ablation procedure to evaluate the left atrial appendage. Intracardiac echo during redo ablation procedure to evaluate the left atrial appendage. Cardiac catheterization to determine if he has stiff left atrial syndrome. CT scan, proceed directly to catheter ablation without pre-procedure testing. So I would argue CT scan is the best option. So what are we thinking about in this clinical scenario? Well, one is increased dyspnea with exertion after his a-fib ablation. There's a couple of things that come to mind immediately there. Well, stiff left atrial syndrome is something to consider, but honestly, with someone having a normal left ventricular ejection fraction, a simple PVI procedure, there's no reason to suspect that PVI alone would create stiff left atrial syndrome. That's usually associated with a lot of ablating, particularly the anterior wall of the left atrium. Could he have heart failure or something else? Sure, but this seems to be related to the ablation procedure itself. And what are the possibilities there? Well, one is that he has pulmonary vein stenosis, and that's something we always need to consider. And one of the reasons I get CT scans when patients have had prior pulmonary vein isolation procedures, particularly if I haven't done it, I've not seen pulmonary vein stenosis in the patients I have done in the last 15 years, but I think the, certainly we see it from time to time. So it's a good test to get, and that would answer the question. The other thing to think about is maybe as a phrenic nerve injury. Now you could potentially diagnose that on physical examination. You could also diagnose it on a CT scan. The scalp films would show the elevated right hemidiaphragm and would diagnose that as well. So a CT scan would really help with the two most concerning complications from the initial procedure. I'll leave this for you to look through. And this was his CT scan. So clearly his increased dyspnea may be from this pulmonary vein that's severely stenosed. So how do you manage this? One thing is I didn't take him for another ablation procedure, at least not right away. I sent him to my colleague who does pulmonary vein stenting. So what he did was went in and wired the left superior pulmonary vein and put a stent there. We then did a follow-up CT scan months later to determine it was open and patent. We also determined that that lung field was not dead from this pulmonary vein stenosis. So stenting it was probably the right thing to do. And actually the patient felt better from the stenting alone, but was still having paroxysmal atrial fibrillation. And when we brought him back, we found that the pulmonary veins were not completely isolated. Obviously we made sure we came out far from the pulmonary veins. And obviously if this vein is isolated, there's no reason to go near it and ablate it. In which case, we I think had touch up under the left inferior a little bit and some spots around the right, which were not stenosis. So the important point here is, I think you can do another ablation following pulmonary vein stenosis. I wouldn't want to do it before. And then if there are other veins that are stenosis, you want to stay particularly wide around those veins so you don't worsen the pulmonary vein stenosis. And then avoid ablating around any veins that are already isolated obviously. That's not a good idea. Case two, patients referred for SVT recorded on telemetry strips while in the hospital shown in figure one. What is the most likely SVT mechanism? Avianodal reentry, orthodromic AVRT, sinus tachycardia followed by high degree AV block, junctional tachycardia, or atrial tachycardia. Here's the strip. Tachycardia here. Something else here. You can think about it for a minute. I'll pause in that strip. And then show you what I think is the best answer, avianodal reentry. So why is it not these other things? Let's take a look. So here's the explanation. And like the last case I showed in, or not the last one, but a case I showed in a different workshop, nature sometimes provides us the EP study necessary to make a diagnosis. In this case, nature is mimicking an attempt to overdrive atrial pace during SVT. And we can see there's a stable cycle length. So here we've laid down calipers and we put out marching calipers. If anyone, I have no interest in this financially, but there's a program called EP Calipers. David Mann, M-A-N-N, is the creator of this. And it's available. You can buy it for minimal amount of money that allows you to do this. And I find it really useful. I use it all the time in PowerPoint presentations to try to measure things. You can calibrate it to the particular tracing you're looking at. So, you know, the absolute value of the caliper, and then you can throw out. Mark, there's a lot of interesting features. I have no interest in doing this, but I know many of you are probably wondering, you know, what kind of caliper system are you using here to do this? And that's the answer. So in this case, we've thrown down a caliper with the measurement. This tachycardia is very stable, pretty slow, but stable at 561 milliseconds. And then something happens. First of all, there's a little star here that shows you there's a P wave. How do I know it's a P wave? Here's a QRS without a P wave, because the P wave's in front. This looks like sinus rhythm or sinus bradycardia. The P wave is in front now. So I know it's not at the end of the QRS. And if we look at this QRS here, we can see the P wave tacked on to the end of a very narrow QRS. You can also see it in the other one. So here's an inverted P wave at the end of this QRS and an upright P wave. So this would probably mimic an inferior lead. This would mimic probably a V lead. I don't know what these leads are actually, but it doesn't matter. Here we have termination of the tachycardia, but something happens before that termination. What do we see? We see a P wave come early here. It's marked by the asterisk. And this little caret marks another P wave. So how would we interpret this? Well, what we need to know is, does this P wave do anything to this QRS? And the answer is no. If you look at the calipers, they're marching along, This QRS is unperturbed by this first PAC, but the next QRS is not. So this PAC affects that QRS, not this one. This is the same sort of thing you would do if you were trying to determine, is this AVNRT or a junctional tachycardia? You'd pace the atrium and see where you affect the QRS. So if this, we were starting to pace during AVNRT in an EP study and we saw this A affected this QRS, we'd call this an AHA response. It's a delay, but this is the one affected. So we had an AHA response that caused delay. It's not an AHA response. So the next PVC blocks in the path, in the antigrade slow pathway. So this one delays it and this one blocks. You could say, well, maybe this PR is conducted. I think this is a pseudo PR interval. This P does not conduct to this QRS, but blocks antigrade. This is a very long PR interval because this PR is a little shorter than sinus rhythm PR. After this period of tachycardia, you wouldn't have expected a P wave to conduct with a short PR like that. It would be longer or at least as long as in sinus rhythm when it's bradycardic, but it's not, it's short. So this is a pseudo PR interval and this P wave blocks to the QRS. So you've now probably diagnosed AV nodal reentry, right? First of all, you have a relationship of the QRS and the P wave, it's simultaneous. That can't be ORT. This is too short a VA time to be ORT. It's not junctional tachycardia because this, you had this behavior where you went down the slow pathway to affect the tachycardia and terminate it in the slow pathway. That wouldn't have been expected with junction. You would have to get into the junction first. And we didn't pull this beat in. We did it from over a slow pathway, delayed it. So I think this other thing about AV block, no, there's one-to-one relationship between the P and the QRS throughout the tracing, except for this one beat probably where this P wave blocks. This is not high degree AV block. So AV node re-entry can be diagnosed. That's ruled out by a short VA. This doesn't look like sinus tachycardia. There's not high degree AV block. It's not junctional tachycardia. It's very unlikely to be atrial tachycardia with this relationship. Could we say a hundred percent? No, but given the other findings here, it's much more likely to be AV nodal re-entry. In fact, there was a paper Brad Knight did. And when you had this relationship of QRS to P wave and all the cases that they looked at, atrial tachycardia was not a part of the mechanism in any. So just statistically, this is much more likely to be AV node re-entry with these findings. Again, I'll pause on the explanation if you want to read it. Okay. Move on to case number three. The following tracing was obtained from a patient following catheter ablation for persistent AFib. The multipolar catheter labeled A to E is within the left atrial appendage, which of the following lesion sets is most likely to produce such an atrial activation pattern? Pulmonary vein isolation alone, PVI with additional line of conduction block from the left inferior pulmonary vein to the lateral mitral valve annulus, PVI with additional line of conduction block from the right inferior pulmonary vein to the mitral valve annulus, PVI with additional line of conduction block from the left superior pulmonary vein to the anterior mitral valve annulus, PVI with additional line of conduction block between superior pulmonary veins. So I think everyone would recognize these particular lesion sets, hopefully. Roof block, anterior mitral block, anterior mitral block close to the appendage. And what atrial activation pattern do we see? It's this one. So this is in the appendage. This is high right atrium, coronary sinus, and left atrial appendage. What do we notice about this tracing? It gives us the answer to this. Well, we notice that it's a very late timing of the left atrial appendage. So how do we get a very late activation of the left atrial appendage? Which lesion set produces that? Well, it's PVI with additional line of conduction block from the left superior pulmonary vein to the anterior mitral valve annulus. That gives you a line just in front of the left atrial appendage. We had seen another question in a workshop where we saw a line like that that wasn't blocked and the left atrial appendage was not late. In this case, it is blocked. So there's very late conduction to the left atrial appendage. How does that work? Here's the explanation. And it shows that the left atrial appendage is normally activated through right to left conduction and sinus rhythm over Bachman's bundle. So normally you'd expect the left atrial appendage to be somewhere in here, somewhere around the mid coronary sinus perhaps. But what we see here is it's conducting all the way through the coronary sinus before it reaches the appendage because it has to go posterior around the mitral annulus to get to the appendage. It's a line of block here. There's no way Bachman's bundle can't reach this because it's blocked all the way from the left superior pulmonary vein to the mitral annulus. And now conduction has to go all the way around the annulus posterior and lateral to reach the appendage. So it's always going to be after coronary sinus activation. If the activation is before coronary sinus activation completes, then this line is not blocked or there is no line here that prevents that wavefront from coming. This wavefront is tough. A lot of people don't like it because the left atrial appendage is so late it may predispose to potential dysfunction of the left atrial appendage. And it's also not hemodynamically all that beneficial potentially because the left atrial appendage is contracting in the QRS here. But sometimes nature kind of presents us with this where there's a huge scar along the anterior wall of the mitral annulus and this is very late anyway. And so sometimes just completing this line may be the answer to mitral flutter. Now, other lines. So a line like this doesn't prevent Bachman's bundle conduction which comes right to left through here. So Bachman's bundle inserts up here. This would allow conduction. This line cuts off Bachman's bundle. A posterior line obviously wouldn't also cut this off. Activation would proceed here to the left atrial appendage unimpeded. You haven't done any ablation here. All the ablation is done on the posterior lateral side. Pulmonary vein isolation alone also wouldn't do anything particularly to delay the left atrial appendage. So let's move to case four. Also known as case five. So this is a 20-year-old female with palpitations and SVT, came to the EP laboratory for possible catheter ablation. During the EP study, she had spontaneous episodes of SVT at 580 milliseconds, which accelerated to 430 milliseconds in isoproterenol. Figure one, panel B shows overdrive pacing of the tachycardia from the high right atrium. The most likely SVT diagnosis is AVNRT, junctional tachycardia, orthodromic re-entry, septal atrial tachycardia, right atrial tachycardia. Here are the tracings. Panel A showing the tachycardia seen in the lab. And panel B showing overdrive pacing from the high right atrial electrode here. We have his bundle recording. We have right ventricular apical recording. So how would you interpret this? Well, I think this is one of those zebras again, where the 20-year-old patient comes in with something that you don't expect, and that's junctional tachycardia. And why do we say that? This would be most likely AVNRT in the vast majority of patients, but unless you do a maneuver like this, you're not going to be sure. And ablation of the slow pathway region, right inferior extension of the slow pathway would not fix this problem. You can ablate away. It's not going to happen. The site of origin of junctional tachycardia is usually much higher than that. It's actually a difficult ablation to perform. Often we do it with cryo if it's absolutely necessary and really symptomatic, but we would, in a case like this, probably go back and try to spend more time treating her with drugs rather than risk AV block by trying to ablate junctional tachycardia in her. Why do we know this is junctional tachycardia? Well, because the atrial overdrive pacing shows an AHA response. The atrial pacing here, the last H and V driven at the pace cycle length is clearly this one, right? Pace cycle length, QRS to QRS, same as that. This is the last one driven. So that H is the last one driven. A-H-H-A. So this, you've shown convincingly that you overdrove junctional tachycardia and not AV node reentry. Now, sometimes these patients have both. So it's worth trying to sort out whether this is the only tachycardia she has. It's possible she could have both AV node reentry and junctional tachycardia. So one option would be to get rid of the AVNRT and leave behind the junctional tachycardia. But if this is the only arrhythmia she has, and in her case it was, we elected to leave this behind from an ablation standpoint and then try drugs to treat this so that we didn't put her at risk of AV block or at high risk for AV block. You know, going into the procedure, often we're telling patients the risk of AV block is minimal. The chance you will walk out with a pacemaker is minimal and you wouldn't want to do that, have exposure to that much higher risk of AV block without having a long discussion about that first in the 20-year-old patient. So this was a really important maneuver to perform in her. Here is the answer that you could for case four, otherwise known as case five. The tracing you know, suspicious for AVNRT and this is the explanation for why it's not. And here's the figure showing what I pointed out with my mouse. The AH is being driven. So this A is driving this H because this HH is at the paced cycle length. And then it comes back with this H and A. Here's the real case five. A patient is admitted to the ICU following an anterior wall MI and the following is recorded on telemetry. What is the most likely explanation? Two forms of VT are present on the tracing. Two to one atrial flutter is present and becomes one-to-one with bundle branch block aberrancy. Sinus tachycardia is present followed by SVT with bundle branch block aberrancy. Two to one atrial flutter is present followed by ventricular tachycardia. Two to one atrial flutter is present followed by artifact. Here's the tracing. I'll pause on this, give you a moment to look. Note that there's a pulse ox tracing as well. And I think the best answer is going to be two to one atrial flutter followed by ventricular tachycardia. So how did I come to that conclusion? Well, here's the explanation. Okay, let's take a dive into this tracing a little bit. So I think atrial flutter is present. There are, if you subtract the QRF, in your mind, you can see two flutter waves for every QRF. So this is highly suspicious for two to one atrial flutter. And it could be sinus tachycardia, I guess, but these P waves don't really look like sinus P waves. And there's two for every one QRF. So I think the left side of the tracing is flutter. Now, the question here is, did this flutter go one to one suddenly? And the answer is no, because this right side of the tracing would have to be then double the ventricular rate of the left side of the tracing, or periods of one to one interspersed. This is a new rate, 300 milliseconds, faster than the left rate, but not double. So this is not a multiple of the flutter rate here. And we do see other cases where, we saw this recently in the hospital where we were able to obtain the tracings of someone who had underlying heart disease and you worried about VT because they saw a wide complex tachycardia, but we were able to see that developed right bundle branch block, and they went from two to one, clearly to one to one, exact multiple of the flutter rate. So it's worth paying attention to that. The flutter rate here is double this rate, and it doesn't go one to one. So that's number one. Number two, the other thing would be the clinical scenario. So the clinical scenario is an anterior wall MI, and someone develops a wide complex tachycardia that's not due to the initial rhythm or a multiple of this rhythm. So the other thing is the first bead of tachycardia looks fused. So it's somewhere between the native QRS, which is narrow, and the wide QRS here. And we can see that that is sort of and it makes sense too, because the first beat comes almost about the same time or just slightly earlier than the native QRS would be expected to come. And so you get a fusion on the surface between VT and the native QRS. Gives you that narrow one, and then off to the races for VT. Could this be artifact? Always have to be suspicious of something like that, but these QRSs look pretty real. And the plethysmography down here suggests that there was a change in the rhythm. So there was stable plethysmography here, some respiratory variation probably, but then despite this being a regular tachycardia, not all the beats are being perfused as one might expect with ventricular tachycardia. If this were artifact, there shouldn't be any change in the plethysmography really, unless the plethysmography had artifact as well. But I think this plethysmography, pleth tracing is pretty clean, doesn't look artifactual. So I think we can go back and look at this and see that this is not two forms of VT. It was a narrow complex with two to one. Atrial flutter at the beginning, it didn't look like sinus tachycardia. It wasn't bundle branch aberration because it didn't become two to one, and it was an artifact. Thank you. Welcome to core concepts in electrophysiology and board preparation. I'm going to do workshop number nine, and I'll go over the questions and give you plenty of time to work on the answers. Here are my disclosure of relationships. The first case is a 25 year old woman who presents with her first episode of syncope and palpitations. She's on no medications. There's a family history of sudden cardiac death. The patients presenting EKG is shown in tracing one. This is tracing one. The question based on this tracing is which is true about this patient. Auditory stimuli are a common trigger. Exercise likely triggers syncope, choice B. Choice C, ANC2 mutation is likely present. Choice D, the patient's QT shortens during exercise. So use that electrocardiogram to come to a conclusion. The correct answer is QT shortens during exercise. So the basis of this question is a recognition of the morphology of the QT interval and the three most common types of long QT. The patient's history suggests an inherited arrhythmia. The ECG is consistent with long QT syndrome. The ECG shows a long isoelectric segment, and this is most consistent with long QT3, which is due to a sodium channel mutation or a mutation in the SCN5A gene. Auditory stimuli are not common with long QT3, but are common with long QT2. Exercise, particularly swimming, exacerbates long QT1. ANK2 mutation causes long QT4, which is associated with AFib and bradycardias. The QT fails to shorten in long QT1, but may shorten in long QT3 with exercise more than in controls. Since the patient has not been treated and the family history is not felt to be predictive of sudden cardiac death with long QT syndrome, an ICD is not generally indicated as first-line therapy. However, in the presence of such a long QT interval, it is appropriate in the setting of syncope to recommend an ICD. This slide illustrates the ECG patterns seen in the different types of long QT. Long QT1, as shown on the top, they're normal proportions. Long QT2, which is a decrease in IKR. You will see a bifid, or notched, but low amplitude T wave, and long QT3 is characterized by a long isoelectric ST segment, as shown in the following case. Case two. A 68-year-old man had a biventricular ICD implanted one month ago. He comes back today after noting no improvement in heart failure symptoms. Interrogation of his device, which is shown in the first tracing, tracing 2-1, shows 99% LV pacing with a V-to-V, or an LV-to-RV offset of zero milliseconds. The patient's interrogated thresholds in clinic today are LV two volts at 0.5 milliseconds, RV one volt at 0.5 milliseconds. The programming change to result, or that could result in improvement, the so-called fix is A, increase LV pacing output, B, pace the LV first, C, reposition the LV lead, or D, echo-guided optimization of the AV intervals. So let's go ahead and let you think about that. First, I'll show you the EKG. On the left side, we see bi-V pacing. On the right side, in the middle panel, we see RV pacing, and on the right panel, we see LV-only pacing. So bi-V pacing, RV pacing only, middle panel, LV pacing only, the far right panel. Please go ahead and think about those choices with respect to the EKG tracing. What would make this patient show an improvement in heart failure symptoms? So I'm gonna go ahead and show you the answer. The correct answer to this question is pace the left ventricle first. So the critical observation is if you look at the far right panel as shown here, you can see the stimulus artifact and you can see there's an isoelectric interval of at least 80, almost a hundred milliseconds from the stimulus to the QRS onset. This is seen in approximately 5% of patients with LV pacing and that is market latency from the stimulus artifact to LV capture. The appropriate therapy therefore is to make sure that there is LV pre-excitation and fusion of the wave fronts from the left ventricle and the intrinsic conduction system or the right ventricle. The surface EKG is critical. If one looks at the surface EKG with bi-ventricular pacing, there is minimal evidence of LV activation. No little Q or big Q in limb lead one or AVL and R is greater than S in B1 and B2 and normal or left axis deviation in the frontal plane. Latency to LV stimulation and LV pacing, thus we have to activate the LV earlier to get fusion and to allow the left ventricular, and to allow the left ventricular excitation to contribute to the total ventricular activation. We do not need to increase LV output. The LV output is okay and the same rationale for not needing to shorten the AV interval. Increasing the LV output will stimulate a little additional LV myocardium, but also markedly deplete the battery. So again, these are the EKG signatures that indicate adequate bi-ventricular pacing. Pay specific attention to a QS complex in B1, changing with activation of the LV to a small R, big S or big R, big S or big R, little S or monophasic R wave. And we'd like to see at least something similar to that in B2. So this is an example of a paper where you can see a patient who is an excellent responder and a patient who responded poorly to BIV. And the high responder, we see big R waves in B1, in RS in B2 and a big QS in limb lead one. And here in this non-responder or low responder, the R wave did go to the QS, but we have minimal R wave in B1 or B2, suggesting minimal LV contribution to activation. So this is a good opportunity to discuss troubleshooting CRT non-responders. It is important to do three things. Make sure the patient is an appropriate choice. That is, make sure the QS is at least 130 milliseconds. We prefer sinus rhythm. Left bundle patients are preferred, they respond the best. And you wanna make sure there's a high percentage of LV pacing. You wanna optimize CRT delivery as shown in this and make sure the patient's heart failure is being optimized. For example, if the patient has moderate to severe MR, you may have to fix the MR as well as get LV pacing. These are the most common causes of CRT non-response you see demonstrated on this slide. And of course, in CRT non-responders, it may be worthwhile to try to optimize AV timing, optimize LV-RV delay. If they're in AFib, ablate the AV node to optimize the percentage of BIV pacing. You wanna look at the LV localization and you wanna make sure for sure the patient has some electrical dyssynchrony. This is a table from a paper in Jack looking at factors that predict an ideal response to CRT. And they're shown in the table and you can work your way down through the table to figure out how best to predict which patients will respond to CRT and what you can do to maximize the CRT response. We've already talked about a lot of these factors, but this is another table summarizing them. On case three, case three, a 66-year-old male is seen in the emergency department complaining of his device shocking him while he was working in his woodshop. Patient's history is significant for primary prevention ICD, ischemic cardiomyopathy, EF at 20%, atrial fibrillation, diabetes, and class one heart failure. Patient has a sub-QICD implanted in 2012. No DFTs were tested at the implant, doing an LV thrombus, and the following data was obtained from the device interrogation. Here's the data from the device interrogation. This is a data from the patient's subcutaneous defibrillator. You see how the device is programmed. You see the patient had a shock delivered. An episode was treated. And here you see the patient's recording from their sub-QICD. You see the delivery of the shock, and then the recording after it. This patient received a shock because of A, myopotential over-sensing, B, air entrapment in the header, C, T-wave over-sensing, D, ventricular tachycardia, and E, supraventricular tachycardia. Here is the tracing. Okay, the correct answer is C, T wave oversensing. Let's go over the differential diagnosis of inappropriate shocks from a subcutaneous ICD. Starting off with C, this is by far seems to be the most common cause for inappropriate shocks in subcutaneous ICDs. Is a consistent pattern of oversensing, long, short intervals that correlate with RNT waves, as I said, is the most common cause of inappropriate shocks with subcutaneous ICD. B, air entrapment, typically you see some sort of baseline offset pattern. A, myopotential oversensing, no low level noise at baseline, no R to R interval variation and not reproducible with isometrics. C, SVT, atrial fibrillation with RVR. The ventricular rate is consistent with regular RR intervals of 400 milliseconds. That is not indicative of AFib with RVR. And you know the rate cutoff is at a higher rate than 150 beats per minute. So here's an example of a sub-QICD with appropriate therapy for ventricular tachycardia. With here you can see appropriate sensing of the tachycardia. Very little dropout. Here you see an example of atrial fibrillation with RVR. And again, very rapid AF that gets into the zone and results in the patient receiving a shock from their subcutaneous ICD. Here's an example in EMI that tricks the device. You can see oversensing in the second panel, which continues here to a greater extent, resulting in an inappropriate ICD shock. Here's an example of a set screw or seal plug issue, which you'd expect to see only shortly after the device is implanted. And you see the variation in noise, which is quite striking. And this finding is almost rhythmic, suggesting air being trapped in and out in these sealing plugs, a shock, and then it sort of goes away for a while. Fairly typical. This is another example of ventricular fibrillation under-sensing due to air entrapment in a patient implanted with a sub-Q defibrillator. And you can see more of a wandering baseline. Here you can see here with loss of a signal, wandering baseline, followed by ventricular fibrillation. And eventually the patient gets a shock. This is a differential diagnosis and treatment of patients with sub-Q defibrillators, management of over-sensing, both diagnosis and management. As shown in the slide, I recommend you study it carefully, particularly for the very limited ways we can manage these patients. Unfortunately, replacement with a trans-menis ICD system may be necessary if an appropriate therapy cannot be prevented by either enabling the smart pass filter or choosing a different vector for sensing. And that will depend upon the ratio of the R-wave to T-wave. Case four, a 25-year-old woman complains of orthostatic lightheadedness, palpitations, tremor, weakness, blurred vision, exercise intolerance, and fatigue. She has never had syncope. Her 24-hour mean heart rate is 80 beats per minute. She underwent a tilt table test. Which tilt table test response would be most consistent with the patient's symptoms? So no syncope. She has orthostatic lightheadedness, palpitations, tremor, weakness. And so which tilt table test is consistent with that? This is A, the head-up tilt table test is shown. Red is millimeters of mercury, B is heart rate, B, head-up tilt test, C, head-up tilt test, D, and E. Which of these is most consistent with the patient's symptoms that I described? The correct answer is C. Let's go over this. Case A illustrates head-up tilt table test in a patient with neurally mediated syncope on mixed cardio-inhibitory and vasodepressor syncope. You may see the decrease in heart rate and blood pressure shown here. Tracing B is a patient with vasodepressor syncope, drop in blood pressure, but not much change in heart rate. The symptoms described in the question are consistent with POTS. The findings are classic, increased heart rate greater than 20 to 30 beats per minute within 20 seconds of head-up tilt table test. You want the heart rate to go up to above 120 beats per minute, but no significant change in blood pressure. As opposed to orthostatic hypotension, where what you see is a prompt or rapid increase in heart rate, but that's associated with a substantial decrease in blood pressure. And here's inappropriate sinus tachycardia. The heart rate increase is typically not postural, but sometimes you may have some immediate increase in heart rate. Obviously, no change in blood pressure. I thought I'd leave you with a couple of pointers for syncope. Vasovagal syncope and recurrent syncope, treatment should be maneuvers, such as counter maneuvers to prevent syncope, such as squeezing your legs together, salt plus fluids, fluterocortisone, or also known as Florinef, Midranine, which is the alpha receptor agonist, and a pacemaker when refractory to conventional therapy. Syncope in a patient where they show your rhythm strips showing sinus nodes slowing with sleep is a normal finding. The P2P prolongation of night preceding a pause is not the cause of syncope and does not mean a pacemaker's indicated. Syncope with specific triggers, such as when the doorbell rings, should indicate long QT type two, for example. Syncope with exercise and imaging shows mid-cavity obstruction. You should think about hypertrophic cardiomyopathy and therapy is now secondary prevention in an ICD. Syncope in a patient with a prior MI and mildly depressed CF, let's say it's 45%. The next step would be to perform an electrophysiology study. Syncope in an EP study showing infrahiscient block, you need to make sure it's pathologic versus functional before you recommend a pacemaker. Case five, an 82-year-old male with a pacemaker implanted for sick sinus syndrome returns for evaluation of his pacemaker two weeks after pacemaker generator change. He has no complaints. He denies fever, chills, drainage. His white blood cell count is normal. That's what his incision looks like. The most appropriate next step is to proceed with aspiration of the pocket. B, start empiric oral antibiotics and reevaluate. C, schedule for lead extraction in the hybrid OR. D, order blood cultures in TEE to evaluate for vegetations on the leads. And I'll go back to the picture again. Here are the choices. The correct answer is start empirical or early antibiotics and re-evaluate. This comes right from the guidelines. And here's the answer. Patient returns with a suspected CIED pocket infection, there's some erythema at the corner of the incision or stitch abscess localized to superficial aspect of the wound. Within the first 30 days of device placement, without fever or systemic toxicity, this patient had a normal white count, you give a course of oral antibiotics and then you re-evaluate the patient to decide what the next step is. Now case 5B, a 70-year-old male with diabetes, coronary artery disease, status post MI, LBEF less than 30% and previous implanted dual chamber ICD many years ago for sudden cardiac death, underwent ICD generator change for a device that was ERI. The patient takes a PIXIVAN because of a history of AFib, he presents nine months post-op with a swollen ICD pocket, exam confirms a mildly tender and swollen ICD pocket, labs demonstrate a white count of 11,000, a normal C-reactive protein, end CED rate, blood cultures are negative, TEE shows no vegetations. The next treatment option would be A, treat for presumed staph epidermidis infection with oral Bactrim for 10 days, then re-evaluate in one month, B, open the pocket, irrigate copiously and insert an antimicrobial Kyrex pouch or envelope, C, aspirate the ICD pocket with a needle and send fluid for gram stain and culture, D, extract the ICD system and place a wearable external defibrillator until IV antibiotics are completed, or E, discontinue a PIXIVAN and re-evaluate in one month. Those are the choices, let me show you the pocket, here's the pocket, patient's head is up here, feet are down here, here are the choices. The correct answer is D, extract the ICD system and place a wearable external defibrillator life vest until intravenous antibiotics are completed. So the patient likely has an indolent seeding of bacteria at the time of ICD-generated change, which were released from sequester due to local trauma. In vivo studies of cultures taken from ICD pockets of generator change show up to 33% are inoculated with entry of bacteria from the skin and late presentation up to one year from implant is common. Pocket infection is a class one indication for complete system removal. Failure to do so puts that patient at increased risk of death and bad outcomes. Pocket needle aspiration is contraindicated and class three in HRS extraction guidelines. The Tyrex antimicrobial envelope specifically state that the envelope is not appropriate to use for treating a pocket infection. Early antibiotic treatment is often used in practice but only delays definitive treatment and delay in extraction of infected system is associated with increased mortality. Here is the flow diagram again from the guidelines. It's a late pocket infections. So CIED removal, including generator and all transvenous leaves. And then four weeks for Staph aureus, for example. Two weeks for other pathogens but this antimicrobial therapy is in this case delivered. It has to be delivered concomitantly with device and leave removal. Case six, what can you say about this patient's prognosis based on the following ECG? A, the patient is unlikely to have SVT. B, sudden cardiac death is unlikely. C, the risk of progression to complete heart block over five years is 20%. D, the risk of developing a PVC induced cardiomyopathy is high. Here's the 12 lead electric cardiogram. So what can you say to this patient? The correct answer is sudden cardiac death is unlikely. This comes also from the guidelines. This ECG, which was recorded from an asymptomatic young man, shows intermittent pre-excitation from a right-sided bypass tract. Because the PR in front of the narrow beats are long, it is clear that the antegrade ERP of the bypass tract is longer than the sinus cycle length. If this patient developed AFib, conduction of the bypass tract would not be rapid. Also, how do we know it's not ventricular bigeminy? The PP intervals are dead on. This observation says nothing about retrograde bypass tract function. However, an AVRT may be possible. In the absence of symptoms, no intervention is necessary. This comes from the 2012 PACES, Pediatric and Congenital EP Society, Heart Rhythm Society Joint Guidelines, indicate that more invasive EP should be considered when the absolute loss of manifest pre-excitation cannot be clearly demonstrated as it was in this case. And this paragraph goes on to describe what needs to be measured. For the evaluation of asymptomatic patients aged eight to 21 years with WPW, the guidelines recommend an exercise stress test. When ambulatory ECG show persistent pre-excitation, so not, for example, this patient with intermittent pre-excitation. And then they talk about what to do from there. These are the guidelines published. Here's the relevant guideline for this patient. Case seven, a 56-year-old female with recurrent syncopal spells for 10 years is found to have a normal calf. Echo stress test and EP study. The following was observed on a monitor. And here you see what the monitor shows. Okay, what are you going to do? What is the most, the mechanism of this pause is most likely due to A, concealed conduction, B, high vagal tone, C, phase four block in the hysperkinesis system, D, phase three block in the AV node. Those are the choices. That's the electrocardiogram. The answer is phase IV block in the His-Purkinje system. Let's go over this. This is paroxysmal AV block. Paroxysmal AV block caused by a premature atrial contraction, a premature atrial contraction. And what you notice is if you imagine what the HH interval is going to be, what the input is, you can see it's going to be long here after the block PAC. And that results in a longer refractory period for the His-Purkinje system. Paroxysmal AV block follows an APB or PAC that is not conducted, either blocked in the AV node or intra-Hisian block, possibly even phase III block in the proximal His-Purkinje system. AV block occurring in this setting of PP interval slowing, not this case, it's typically vagal. This is PP interval actually speeding up a little bit. The following sinus beat is delayed. This sinus beat is delayed and results in prolonged AV block without an escape related to phase IV block in a more distal area of the His-Purkinje system. Phase IV block is terminated by a junctional escape complex that likely originates in a region distal to the site of phase IV block. The escape complex retrogradely excites the distal His-Purkinje system fibers responsible for phase IV block restoring a more normal transmembrane potential permitting successful subsequent conduction to the ventricle. This suggests the presence of unidirectional anterograde block with preservation of retrograde conduction in the His-Purkinje system region responsible for phase IV block. So this is how it's imagined, phase IV block in the distal His-Purkinje system. And then here it is in the AV node or proximal His-Purkinje system. It's an earlier beat, so it shortens the action potential duration. And then it comes down here and it's refractory. This is basically an example of paroxysmal AV block does not occur by an atrial premature beat that is conducted to the His-Purkinje system, not allowing a long cycle length for phase IV bradycardia dependent block to develop. Okay, a 60 year old woman is referred to you for further evaluation. She has a chromopathy and her EF is 35%. On evaluation in the EP lab, the most likely site of ablation would be A, pulmonary vein isolation, B, an atrial tachycardia, C, a fascicular ventricular tachycardia, or D, a slow pathway. Here's the 12 lead EKG. And you have to choose the best site of ablation based on this 12 lead EKG this patient is referred to you. Trace is a slow pathway. This is the ladder diagram. This is a two for one. One P wave, two QRSs. One P wave, one QRS. One P wave, two QRSs. One P wave, one QRS through the slow pathway. One P wave, two QRSs again. And this is what the ladder diagram looks like. You have conduction down the fast pathway, conduction down the slow pathway with a block up into the fast pathway. Now, slow conduction down and then down both pathways again. Following slow pathway ablation, you just have conduction down the fast pathway shown in green. And I would go back and correct myself. This is conduction down the fast pathway, but it's slowed because this is so premature, so early. So this is dual AV nodal, non-reentrant tachycardia, DAVNNT, single P wave conducting down both the fast and slow pathway. There's a wide disparity of age intervals. Typically these patients lack VA conduction. Typically AVNRT is not inducible because of the very poor, sometimes absent retrograde conduction. It can be misdiagnosed as vesicular or junctional tachycardia. It's a rare, rare cause of tachycardia induced cardiomyopathy. Thank you.

electrophysiology

mitral flutter

overdrive pacing

conduction

tilt table test

syncope

ICD pocket

swollen

prognosis

intermittent pre-excitation

mechanism

paroxysmal AV block