Greetings. This is John Miller with Core Concepts in Electrophysiology. I have some questions to discuss in workshop number three. Here are my disclosures. Right on to the first question. A 23-year-old woman is undergoing catheter ablation for treatment of symptomatic Wolf-Parkinson-White syndrome. After eight seconds of radiofrequency energy delivery at 30 watts delivered near the coronary sinus ostium, pre-excitation gradually ceases as will be shown in the figure. Based on the findings and the tracing I'll show, you should continue RF delivery at 30 watts to complete a full minute, increase power to 40 watts and continue delivery for one minute, decrease power to 20 watts and continue delivery for 30 seconds or stop RF immediately. Here's the figure. You can see RF has been on. There's some disruption of the electrograms here and you see delta waves is gradually going away. Make your choices. Pause the presentation at this point. Look at your distractors carefully. Look at the figure carefully. Decide what's going on. Make your choice and then rejoin us when you have your answer. Hopefully it's the right answer. But the right answer is get out of there. Stop RF immediately. This is an urgent situation. What's going on? We're delivering RF and the delta wave is going away. What's wrong with that? What's wrong with that is that the delta wave goes away gradually because we have accelerated junctional rhythm. Look, here's a HISS. This AH is shorter. Since when does conduction get better? Well, it can, but usually it's because accelerated junctional rhythm. So here's the HISS here. Here's the HISS over here. Okay. When you have a pre-excited complex, when you have a delta wave, it's because you have an atrial beat that conducts down the accessory pathway. Well, the A's are getting closer and closer to these. These are sinus A's here. All of them are sinus A's, but the rest of the A's, the ones that are close to the pathway are getting later and later and later. So they're not having a chance to get down the pathway. So it looks like there is no pre-excitation. There may be a little pre-excitation. There certainly is some here. These two QRSs look very similar and the P wave is well into the QRS here. P wave is a little bit before here. So this is accelerated junctional rhythm. And if it accelerates even more, that could be a harbinger of destruction of the AV node and or HISS bundle, mainly the AV node and complete heart block. So continued energy delivery could give us permanent heart block and then 100% pre-excitation. It does happen, but should not happen. And it won't happen if you are aware of what's going on. Don't just throw up your hands in victory and say, yeah, we got the pathway because delta wave is gone. There are other reasons for the delta wave to be gone, including accelerated junctional rhythm. Stop RF delivery immediately. Doesn't mean that this is a bad site. It could be a good site. So how do you remedy this? You just stop RF. You pull out the cryocatheter. If you think, boy, this is a great site. I got to go here. She doesn't like it. She doesn't like this rhythm. She doesn't like this pathway. I don't know why not, but she doesn't like it and it's got to go. So you can bring out a cryocatheter. That might be a little bit safer, or you could do something else. What I do during AV node and during cases like this is I paste the atrium because I want to ensure that I have good normal AV conduction. If you paste the atrium, in this case, you might see no delta wave. You might see a normal QRS complex because you have AV conduction. You don't know that though. So if you get this, first thing to do is probably just back off. And if you're already set up to do it and you see these accelerated junctions, just paste the right atrium. It's a little bit faster than the junctional rhythm. I wouldn't be futzing with this a whole lot and saying, well, actually, this junction is going a little bit faster than I am. I'm still delivering RF. Get out of there. Stop RF. Measure your accelerated junctional rhythm cycling. Set your simulator to paste faster than that. And you can even be pasting at the beginning of RF delivery. And then you'll see the delta wave go away or not go away or get bigger because you're injuring AV nodal conduction. That's the way to do it, not this way. This way is bad. So there's the accelerated junctions. All right. Question number two, 45-year-old woman with recurrent wide QRS tachycardia comes for EP study. Tachycardia is initiated and extra stimulus is delivered as shown in the figure. Based on the results of stimulation, you conclude the most likely diagnosis is ventricular tachycardia, antedromic atrial ventricular reentry, pre-excited atrial tachycardia, or pre-excited AV nodal reentry. Here's the tracing. Here's a stimulus given during tachycardia. And come back to us when you have your answer. The correct answer is antedromic atrial ventricular reentry. Why is that the case? Well, here's tracing again. What's going on here? We can make the measurements here. The tachycardia is pretty steady at 312 milliseconds beforehand. And then things get messy here. The VB interval that follows from the extra stimulus is actually longer than the rest of these guys. Then we got a shorter cycle, and then it settles down and reverberates. The AA intervals there. This is atrial stimulus that we're delivering. An atrial stimulus during a wide curious tachycardia. The AAs are exactly the same as the VBs, and they actually track the VBs here. So this V, 295 VB, this AA that follows it is 295. This is 320. This is 320. What a coincidence. Oh, I missed one here. We'll come back to that. The VAs in the meantime don't seem to change. So there's AV wobble, but not VA wobble. That means something. This is a high rate atrial extra stimulus during a wide complex tachycardia. We don't see a good hiss here, or do we? Actually, we do see a good hiss. It's right here. It's after the curious onset. So this cannot be orthodontic SVT of any sort. So it has to be either VT or pre-excited tachycardia. The last time I saw a VT affected by a single atrial extra stimulus, well, it hasn't been. I haven't seen it. Maybe I missed it, but I've not recognized it. I've gotten over saying I've never seen that. I say I have not recognized that in the past, or I can't remember having recognized it. So this atrial stimulus captures atrium, definitely, and delays the next curious complex. We know about advancing the next complex. What does it mean when we delay it? Well, it means we're conducting over an accessory pathway that has decremental conduction because we pre-matured it. And it says, I can't take it just now. I got to delay a little bit. And then it gets down to the ventricle. That can only happen with the pre-excited tachycardia. Now, your constant VA intervals along here, despite these changing VB intervals, says that the A is linked to the V. And that can't, it should not happen with atrial tachycardia. If it appears to happen with atrial tachycardia, it's just coincidence because the A's are going when they're going. The V's can come along, or they can not come along. It doesn't matter. And so the VA, AV relationships with atrial tachycardia, it's just irrelevant to the atrial tachycardia. It's doing its own thing. And the ventricle is welcome to come along, or it's welcome to stay home. It doesn't matter. But it's not going to be, the A is not going to depend on what the V says. It's just going to do its own thing. So this excludes, practically speaking, an atrial tachycardia, and therefore pre-excited atrial tachycardia. Atrial activation appearing at the level, earliest at the level of his, when it is here, it doesn't appear to be affected by the PAC at all. So there's some A's that are here in the distal his. They seem to be perfectly fixed here. This A in the higher atrium is clearly brought in, but the A's around here are not. So could this be avian ovary entry? I don't know how you affect avian ovary entry when you don't affect the atrium that surrounds the AV node. That'd be pretty unusual. You'd have to have an odd input to the AV node. It's not around the perinatal tissue. OK, this is an odd tachycardia. That'd be an odd situation. Come on. Is this really real life? Or is this just make-believe? No, that doesn't happen. So the fact that that A is unaffected by this stimulus means we can't have affected an avian ovary pathway. And therefore, if we were going down an avian ovary pathway, and this is really pre-excited avian ovary entry, then there should not be a fixed relationship between the QRS onset and this his. Now, this is a very short VH. When do you get that with a pre-excited rhythm? For the nature of vesicular pathway, that's what this is. So it is anti-drug down the pathway of the AV node. We haven't completely excluded a second accessory pathway as a retrograde limb. It's a very short VA interval here. Pretty odd. You'd have to be very, very fast in septal retrograde limb. Pretty unlike it. It's not unheard of to have a second septal accessory pathway in people who have an atrial vesicular pathway, but most of them don't have that. All right. Question number three. A 49-year-old woman has had episodes of tachycardia that began 17 years ago. Let's see. She was 32. Maybe that helps. Maybe it doesn't. Tachycardia is initiated at the EP study and is shown in the figure. The most likely tachycardia diagnosis is atrial tachycardia, AV nodal re-entry, orthodromic re-entry using a left pre-wall accessory pathway, orthodromic re-entry using a septal accessory pathway. Or you can't tell from the information in there. All right. This is a budget EP study. We have only five surface leads, a hybrid atrial recording, and a timeline. Make your choices. This is tachycardia initiation after a couple of atrial stimulated beats. Make your choices and read files. The correct answer is orthodromic re-entry using a left pre-wall accessory pathway. Okay. Why is this? Okay. What we have here is tachycardia long in here. We got the A's going fast and we got the B's going fast. And so tachycardia is throughout. It's not just a couple of PBCs along here. This is all tachycardia from here forward. The thing to notice here is there's change. What kind of change? Well, there's rate change and there's QRS change. And anytime there's change, there's potential for information. So Dr. George Klein has always said, look for zones of transition where you're going from bundle branch block to not. Back to bundle branch block, is there information there? There's change. Maybe there's not information there, but maybe there is. I love seeing an irregular tachycardia because there's an opportunity for information. What's linked to what? What causes what? Instead of everything just in lockstep, you can't really tell. All right. So here is the surface VA intervals from onset of QRS to this A. We don't have 15 channels of atrium. We got one. And that's all you need. Because here we have this VA of 300 with left bundle branch block. Also VA of 300 milliseconds with left bundle branch block. Measuring to the same A when we have a narrow QRS is only 250 milliseconds. Same here. And with right bundle branch block after a long short here is our short long action is 250 milliseconds. Like the narrow QRS. All right. So prolongation of the surface VA interval with bundle branch block indicates participation of a ipsilateral same-sided pathway, same side as the block, because we're prolonging the path length, the electrical path length. This is diagnostic of not only presence of an accessory pathway, but participation of it if you lengthen not the tachycardia cycle length so much. If it does, that's fine. But you got the AV node in there too. They can be longer or shorter based on whether you have a longer VA or shorter VA. It's really this VA interval that's most important. And it's the surface VA interval, not the local VA interval. And if you record the local VA interval in a case like this, it may not change very much because it could because the pathway is slant. But it may not a whole lot. Because as soon as you get to the coronary sinus, that's where the pathway inserts, however long it takes you to get there, you go up to the A. So it takes a long time to get over there with left bundle branch block, not so long with narrow QRS. And if the right ventricle comes to the party late, who cares? The pathway didn't care about that. It's going to have the CS activation when it ordinarily would with narrow QRS. All right. So there are diagrams that we can show with this sort of thing. It's pretty straightforward. Presence of bundle branch block during SVT is a goldmine potentially. Hopefully it's not fool's gold. It's regular gold. And so make the most of that information. And when it's there, it's a freebie. This is an easy, easy question that a lot of people get this question. All right. Another question. A 33-year-old woman has recurrent supraventricular tachycardia during EP study. The recordings in the figure were made. This is a repeated event. The best interpretation is that orthodromic AV reentry is present. A notophysicular tachycardia is present. Atrial tachycardia is present. AV nodal reentry is present or accelerated junctional tachycardia is present. Wow. A lot of stuff. All right. Here is the end of an episode of tachycardia. Lots of things are going on here. So make your observations on this. Check the possibilities. It's one of those. And then rejoin us when you have your answer. Correct answer is orthodromic AV reentry is present. Okay. Why is that? All right. Here's the same tracing I showed. Now, we have not an induced but a spontaneous premature ventricular complex occurs. Maybe it's catheter induced. And it clearly advances the timing of the next atrial cycle. You can see these are reasonably regular. And this is the shortest one there is. And it occurs after this early V. Now, the HISS was probably refracted. We see HISSes everywhere here. That A is brought in. The V is brought in also. And the next expected HISS with these being regular, the next expected HISS would be about right here. So the QRS onset to that V is really short. If you were stimulating the ventricle and you had a stimulus artifact and you could measure to where your next HISS should be, if it's 40, 50 milliseconds, then probably the HISS was still refractory, because you'd have to get to it and then really through it in order to be able to do anything for the atrium, particularly through the avenote. But this expected HISS, boom, it's just barely at the QRS onset there. So this is a HISS refractory PVC that advances the timing of the next atrial recording. And the activation sequence is not in keeping with the avenote. This is a hybrid atrial catheter that really is not hybrid atrium. We don't see a really good avenotal region, AVJ atrial electrogram, but certainly this activation pattern here is one you would expect to see with a right-sided accessory pathway, not a left-sided, not a septal pathway. A septal pathway should have the A's here and the hybrid atrium and CS about equal timing after it. Here the A in the hybrid atrium is early. So that suggests that it's an accessory pathway. Now the consistency of the VA interval, that's VA relationship along in here, suggests that this is pre-excitation of the atrium with this ventricular extra stimulus and fits best with the diagnosis of orthodromic STD. Now, why is this VA shorter? Perhaps this is going up, but it's not going up this accessory pathway over here. All right, so there's the AA intervals and there's the VA intervals that are just totally blocked in here. This A is brought in here a little bit earlier, but the VA is not brought in. Okay, this is question number five. 28-year-old man has had SVT for several years and comes for EP study after catheters are placed. Preference in pacing is performed. Retrograde conduction in this case, based on this example, is via the AV node only, via the AV node and an accessory pathway, via an accessory pathway only, or more information is needed. Study your tracing and your options are right there. You don't have to go back and forth. The correct answer is that an accessory pathway is not only present, but it's the only means of getting back to the atrium. Why is that? Okay, we have three different PACE complexes as a result of pacing on the same site, your periods and pacing. First one is very wide. The last one is not as wide. The middle one is pretty normal. There's a significant stimulus to QRS interval here. I'm just going to tell you that this is what the person's normal convective QRS complex looks like. It's kind of the HV interval here as well. All right, so we have pure HIS. We have HIS plus V and V only. So we ought to be able to make some inferences here. Well, if you have an accessory pathway, the stimulus to A, when you have ventricular capture, is constant. Because the atrial activation depends on VA conduction, not HIS-A conduction. You can have the HIS, you cannot have the HIS. It doesn't matter to the pathway. But the AV node, you have to get to the HIS. And however you get to the HIS, however long it takes you to get to the HIS, then you can get to the A. So with HIS plus V capture, you are capturing the HIS and here's your VA interval of the HIS. With ventricular only capture, you got to get to the HIS. So you got to conduct down to the right bundle somewhere or the other. Get into the hysperkinesis and then you can go. So the stem to A is longer with pure ventricular pacing than it is with HIS plus V pacing with AV nodal dependent conduction. And if you have a pure HIS capture beat, the stem to A is the same as it is with any type of HIS capture, whether it's contaminated with ventricular capture or not. What do we have here? We have a VA, a stem to A, I'm sorry, with ventricular only capture of 270. With HIS plus V capture, it's also 270. And that suggests it's going up the pathway. All right. Two of these, actually three of these could have an accessory pathway. This does, this does, this could. I mean, you can't say exclusively what's going on, but you know, there's a pathway. All right. This is the funny one here. Why with HIS bundle capture only, you need HIS bundle capture is the stem to A longer than it is in the other coordinates. Well, that is because, and we have a retrograde HIS here and you can see it as plain as day. So this HA is not a real interval. It's a pseudo interval because we're not going from HIS to A, we're going from V to A and the HIS is getting conducted to independent, doesn't matter. What's going on here? Well, if you have retrograde connection of the AV node only here, so atria, ventricles, AV node, HIS bundle, and ventricle, we're simulating in the perinodal region here. If we have a pure V capture, then we're going to get to the HIS sometime and have an HA. If we're capturing the HIS plus B over here, then the stem to A is going to be the same as the H to A, but shorter than the stem to A with ventricular only capture. We're all familiar with that AV nodal pattern here. If you've got only accessory pathway connection or your accessory pathway is much better than a very sluggish AV node, here's the accessory pathway here. When you capture ventricle, whether you have HIS capture or not, when you capture ventricle, it goes over the pathway to the atria, stem to A. If you capture this with HIS plus A, I'm sorry, HIS plus B capture over here in the center where we're capturing ventricle only, it's nice for the HIS to be there. It's nice traveling partner, companion, but it's irrelevant. So yeah, you conduct down the right bundle, back up the HIS, great. Too bad, we already got back to the A by this pathway. So whether the HIS is present or not, it's V to A that matters in this case here for the pathway. What about with pure HIS only? Well, this is like a single bead of orthodromic reentry. We're capturing HIS going down the conduction system and then back up toward the base where the pathway is. So this stem to A is the longest one you'll have, longer than these guys over here because they're getting a head start. This has to go all the way down with this capturing all the way back up. So when you see that, this is especially useful in concealed septal pathways because the atrial activation sequence going up the AV node could be very similar to going up a septal pathway. Have you gotten it or have you not? Well, if you can find a pure HIS capture and it's stem to A is the same as when you have stem to A over here, short, and this stem to A is longer because you got to get to the HIS bundle in order to get back to the AV node, then you're golden. But if you have this situation where the stem to A is actually longer than it was over here, you're host. And you still got a pathway to deal with. Very useful technique. Only you see this in those odd situations where we have only retrograde pathway conduction or very sluggish AV node conduction. We have pure HIS capture. Unusual situation. All right, question number six. 13-year-old girl has had palpitations in light-headedness for two years. She had a ventricular septal defect repaired early in childhood. Her resting ECG shows sinus rhythm of pre-excitation. She was referred for EP study and possible ablation. She's had palpitations before also. So this is baseline recordings. And we see pre-excitation. Hooray. And here's a short HV interval. There. Onset of QRS there. And the HV is positive, but it's too short to conduct. So this is pre-excitation time. All right, how are we going to evaluate this? Well, here's atrial pacing at incremental rates here. A little bit faster. And here's our pre-excitation. Here's our pre-excitation. And here's our AH. It's a little bit longer. All of a sudden, we don't have pre-excitation. We just have right bundle branch block conduction. She had a ventricular septal defect. It's probably ventricular valve. The AH is pretty constant along here. The HV is short here. When we have pre-excitation, the pathway fails there. That'll be good. Here we have an atrial extra stimulus, and the AH interval prolongs as it does in response to atrial prematurity over what had happened during dry feeds here. Ordinarily, when you have a race, who gets to the ventricle first over an AV accessory pathway or over the AV node, if the AV node is delayed somewhat, oh, the AV accessory pathway says, great, I'm in. So it goes, and you have more pre-excitation. But it's not uninhibited by the prematurity. You get more pre-excitation here. We don't. We have the same amount of pre-excitation. And that correlates with the HV interval being constant there. You can see that the HV from H to QRS onset are consistently the same. All right. So based on this information, the findings are most consistent with an atrioventricular pathway, a fasciculoventricular pathway, a notoventricular pathway, or a notophascicular pathway. Think about this to find the tracings and make the choice. The correct answer is a fasciculoventricular pathway. Now, here's a little bit more information. When we pace at 600 milliseconds in the atrium, a single beat of each of these three different conditions here, the stimulus to delta is 115. In this case, the stimulus to delta is 126 milliseconds. If we pace faster still, it's 142. All right. A normal, well-behaved accessory pathway doesn't do that. The stimulus to delta when pacing from the same site should be pretty constant, certainly over the range of pacing cyclings represented here. Very rapid pacing cycling, it's okay. You can have a little bit of delay in the pathway, latency in atrial stimulation, all that's possible, but not over these long cyclings. That's just not plausible. So the fact that our stimulus to delta increases says there's delay somewhere, and it's delay getting to the hits. Once we get to the hits, we make our induction down the pathway, and the HV interval doesn't change along here at all. You can see that here. The HV is constant, and the degree of pre-excitation is constant. So again, this race between going down the AV node and the hystric engine system to activate the ventricle versus who's going to get there first, the accessory pathway, who doesn't care about how fast the patient reads. So when you are pacing faster in the atrium and incurring more and more delay in the AV node, you're putting it further and further and further away from the ventricle, and the accessory pathway is there all the time just hitting it. So your degree of pre-excitation tends to increase with more rapid atrial pacing. Here, it's just staying stuck. This is characteristic of a fascicular ventricular pathway, and this is the sine qua non. This is the exquisite explanation of the fascicular ventricular pathway, a junctional complex, junctional escape. If you've got an AV pathway, you can only have pre-excitation if you have an A before the V. Here, we have a junctional complex with no A in front of it, and yet it's pre-excited like everybody else. Once you get to the hyst, once the hyst fires, either transmitted from above or it fires on its own or you're pacing it, you end up with pre-excitation over this pathway. It's a beautiful thing. So in summary, fascicular ventricular pathways as this was has some unique features. A moderate degree of pre-excitation is present. This is probably either a specific connection from the fascicle, typically it's the right bundle or very distal hyst, going into the muscle, or it's a place where the hyst bundle or the subjacent right bundle doesn't have a full insulative fibrous jacket around it and some of the impulse can escape. Primarily, we have an HB interval right on the surface ECG on the intercardiac recordings, and there's a usually an isoelectric interval between the hyst potential inscription and the local ventricular extragram that's right adjacent to it physically, but electrically, it's probably down the right bundle, down the left bundle, and then back up the septum through the hyst prokaryotic system and muscle to muscle. So it's not the most efficient way of getting to that tissue, but if you have a fascicular ventricular pathway, you can get there early. So it's a moderate degree of pre-excitation. It doesn't vary over a range of paced cycle lengths within reason. You can block in this pathway, as I showed in this case, a little bit on your notebook, you can do it pharmacologically, you can block as well, type one A agents. The HB interval likewise remains constant as a degree of pre-excitation. Even junctural complexes, as I showed, are pre-excited. And typically, these pathways don't participate. They can be a conduit for conduction, again, a pre-excited tachycardia. They don't participate as a regular pathway with a tachycardia. So most of the time, they don't need to be ablated. Pathways that can't ever conduct rapidly enough to result in patient risk don't need to be ablated. Those with intermittent conduction or very, very long refractory periods, even with catecholamines, they can still have SDT, can be pretty slow, but they can't have dangerous pre-excited atrial fibrillation that could result in ventricular fibrillation. And pathways that don't participate in any arrhythmia, such as vesicular ventricular pathways, don't need to be ablated either. This patient, a particular patient that we were discussing, had atrial flutter, and we ablated that. The pathway was unrelated to any atrial arrhythmia or anything that could produce symptoms. So simply ablating this pathway would not have yielded a successful procedure. This window dressing had a cosmetic effect on our ECG. It's actually a worse ECG because it's this big, ugly right bundle branch block pattern. All right. Thank you for your attention. Hi, this is Greg Michaud. Welcome to workshop three in the core concepts in EP and board prep here in Nashville at Vanderbilt University Medical Center. Let's talk about a case in which there are tracings. So during an EP study for SVT seen in figure one, the following response to ventricular pacing is observed. Which of the following is the most likely SVT diagnosis? Atrial tachycardia, AVNRT with a posterior retrograde pathway, slow. AVNRT with a superior retrograde pathway, fast. Orthodromic re-entry, not enough information to determine the most likely mechanism. So here we are, tachycardia. Salient features are surface leads, high to low right atrial electrodes, His bundle electrodes with a small His seen here. Not very easy to see, but it's there. CS prox to distal electrograms and RV electrograms. So this is your baseline tachycardia. Here is the response to, here's an initiation. Could I start at this slide again? Okay, I'm going to take it back to here. And I'm going to, so when I first go to this slide, can we cut and restart? All right. I'm going to just go ahead and 3, 2, 1. Here is an initiation of tachycardia with onset of tachycardia following, at least potentially a couple beats. I think there's enough information to say the most likely diagnosis is orthodromic reentry. This is a little tricky, but I think there's enough information here. And what we need to know is that onset of tachycardia can be interpreted in that there's a VAV response. And we can look at the STEMI VA difference in initiation. So just like you can measure post-pacing intervals, since this tachycardia is quite unstable, post-pacing interval may be a little less interpretable. But the STEMI to VA won't change much because that reflects the retrograde limb of the circuit, which is fairly fixed. All the wobbles coming in the antegrade portion of the limb, which is through the AV node. So here, actually the STEMI VA becomes really useful. And we measure the STEMI VA for that first beat of reentry where we go VAV. We see the VA time is 123 milliseconds with pacing, and it's only 73 milliseconds with measurement from the surface to the earliest QRS. So there actually is information here. This looks like a mess. It looks like there's nothing here that you're going to be able to salvage. But I think this tells you the answer because, as I've said in my SVT lectures, when you have a short STEMI to VA difference, that is very telling. That is almost always associated with an accessory pathway, conduction retrograde. It would be similar to doing the pacing and sinus rhythm and seeing the same difference. So you don't need tachycardia, I think, in this particular instance to say that an accessory pathway is present. Tricky, I know. So case two, ventricular pacing at a cycle length slightly shorter than the tachycardia cycle length is shown in the tracing. What is the most efficient next step? Ablate the slow pathway, repeat ventricular entrainment, and measure post-pacing interval minus tachycardia cycle length again. Look for source of atrial tachycardia focus. Observe SVT response at the beginning of the pacing drive or place PVCs on the HISS. You have options here. This is a particular form of tachycardia that requires some additional work other than measuring a post-pacing interval. The figure we can look at shows a VAV response, and you can eyeball it. It's a long post-pacing interval. It's a long VA versus our VA here, STEMA here time. When we go to do the measurements, we'll see that's the case. The one thing we need to know before we decide that this is a slow pathway conduction retrograde and that we're dealing with AVNRT is that when you have these long VA times, VA longer than 40% of the tachycardia cycle length, a decremental accessory pathway is still part of mix. You'd be tempted to say, based on the post-pacing interval, based on the STEMA VA, the VAV response, this is AVNRT. But there is this one zebra that you need to think about when you're doing these cases. Here's the explanation written, and I'll do some more measurements here to show you why. VA STEMA's difference is 130, suggests AVNRT. Post-pacing interval minus tachycardia cycle length corrected, 170, again, suggests AVNRT. But the VA time is quite long, so is this a decremental accessory pathway? Well, what's the most efficient way to figure that out? Yes, you can put PVCs on the HISS, but you already did this drive, and there's a bunch of HISS refractory PVCs at the beginning of this drive. So wouldn't the most efficient step be just to scroll back and look at the beginning of the drive? Of course, that's more efficient than going back, timing PVCs, and putting them on the HISS. So here we have an example, 360, 360, a very stable cycle length. The very first pace beat that is fused on the surface, we know it's fused, and we know it's HISS refractory, because it doesn't look like pacing, and it doesn't look exactly like tachycardia. There's a change in the morphology suggesting there's collision between a paced wavefront and the wavefront coming over the AV node. So we've got a HISS refractory PVC here. We have one here. We probably have one here. I'm not sure. This could be the first beat that's fully paced, but these are clearly fused. So during that zone of fusion, we see delay, and that's what we might expect with a decremental pathway retrograde. So this is an accessory pathway. It's decremental, and it's participating in tachycardia. We know all of those things. You're not going to delay atrial tachycardia with a HISS refractory PVC. You can't get into an AVNRT circuit with a HISS refractory PVC. So this delay tells you it's actually part of the circuit. Now, this is one of the post-pacing interval minus tachycardia cycle length pitfalls you can see, and for a decremental pathway, STEM-AVA pitfall. So it can be misleading when you have a decremental pathway. The way you can sort out the decremental pathway is, first of all, if it's less than 110 corrected, the post-pacing interval, or STEM-AVA minus 85, then it's a septal pathway, as we discussed in the last case. If it's greater than 110, you're looking at potentially a decremental pathway. Inspect the beginning of the overdrive pacing or put in HISS refractory PVCs to see if decremental pathway behavior occurs. If it doesn't, then you're likely dealing with AV node reentry. Moving on to case three. A 65-year-old man with prior ablation for AFib, including single ring pulmonary vein isolation. An example is shown in figure one. The patient had recurrent atrial flutter prompting a second ablation attempt. The following propagation map was obtained while pacing the distal coronary sinus shown in figure two. Additionally, conduction along the roof was blocked as demonstrated by differential pacing maneuvers. Based on these observations, the atrial flutter mechanism is most likely to be which of the following? A reentrant atrial flutter treated successfully by performing ablation rings around ipsilateral pulmonary veins. A focal atrial tachycardia treated successfully by ablation at the site of the gap or gaps in the single ring. Reentrant atrial flutter cured by closing the conduction gaps or gap in the single ring. A different atrial flutter mechanism should be sought. This is the example of a single ring isolation with one ring around the pulmonary veins and posterior wall. You can see the lesions here. And then figure two shows this propagation map when pacing the distal coronary sinus. I'll play that again. And one more time. Okay. I believe the best answer is a different atrial flutter mechanism should be sought. And here are the reasons. So reentrant atrial flutter involving the pulmonary veins usually, and same thing with reentrant arrhythmia following single ring isolation, usually would require two gaps. In this case, we see a single gap, the roof's blocked, a single gap going into this single ring. There were no ablation lesions back here around the pulmonary veins. So with only one gap in this ring and no gaps around the pulmonary veins like you normally would see, reentry is pretty unlikely involving this particular ring. You see gap to gap flutters around pulmonary veins, not that infrequently. But again, it usually requires more than one gap for that because it has to go in one gap and then back out another to create the reentry. Same thing with a single ring. Would have to go in one gap and then come out another gap to form reentry. Reentry is very unlikely when it spreads out like this to create reentry on the posterior wall that then breaks out of here. Pretty unlikely. There was no ablation on the posterior wall. And he's otherwise pretty normal guy. So it takes away the most likely focal mechanism from here is also possible, but it's a pretty unlikely explanation. So I think the important point here would be patient presents in sinus rhythm. You don't just close this gap and call it a day. You really need to seek out another potential mechanism for atrial flutter. And in this case, there was a local reentry circuit confined to an area of scar on the anterior wall of his left atrium. So, of course, we closed that gap, but we were suspicious that atrial flutter was not going to be involving that single ring. Now, we certainly could have added a fib. He could have had bursts of AT that come out of that single ring just like you would see out of pulmonary veins. But we were very suspicious there must be another mechanism. So we tried hard and induced one. Case four. Figure one shows mapping during atrial tachycardia with the multipolar catheter positioned at the hispundal recording region, which is the earliest activation site mapped in the RA. Which of the following is most likely? Ablation at RA 910 will likely eliminate atrial tachycardia. Ablation on the multipolar catheter at the bipolar electrode labeled pentarray 1516, asterisk, is likely to eliminate AT without damage to the AV node. Ablation on the multipolar bipolar electrode labeled pent 1516, again, asterisk, is likely to eliminate AT but with a high likelihood of AV block. Ablation at that same electrode, unlikely to eliminate AT without damage to the AV node. Or ablation at the same electrode, unlikely to eliminate AT and substantial risk of AV block, which is obviously the worst case scenario. So here are the tracings. There's a caliper here that's dropped from the onset of the P wave to give you a little clue. Here's the multipolar catheter. And here's the electrode in question, 1516. We can see 1314, 1516 are about tied. The thing that we notice is the atrial electrogram is relatively big, so the ratio is probably 1 to 2 or 1 to 3 A to V at this site. There's a hispundal recording, albeit sort of far field. And there's a bunch of other bipolar electrograms, some in the high-rate atrium, probably near the septum, CS prox that are timing isn't all that different. There's almost simultaneous timing all the way down. So this is early, but really not that early. And relative to the P wave, which should be a good fiducial point for the earliest onset, you always want to be pre-P wave at any site you're going to ablate. But 10 milliseconds, that seems a little too short to consider ablation at that site, unless you've absolutely mapped everywhere. Now, this is the septum, so where haven't you mapped? You haven't mapped the left side yet. And the site that's the earliest is in a dangerous location. So not only are you unlikely to eliminate the AT at this site, given it's not that early, but you're also at high risk for damaging the AV node, because it's too near the… You see a hispundal N and A at that recording site, so you're probably at risk of creating AV block. So that's the most… That's probably the truest answer of all these here. And here's the explanation, which I'll pause on and you can read. And finally, when we go to the left atrium and map, we see something that looks like a better site. So now when we drop a line from the onset of the P wave to the earliest site, it's about 30 milliseconds. That's more in the range of what you'd expect. It might be earlier than that, but 30 milliseconds is around where you'd expect to find the earliest atrial activation, at least as a starting point. Now, there's no magic number that always works, but we're always looking for something around 30 or more. Some places, like pulmonary veins, it could be much earlier, 100 or 150 early, because there's decremental conduction out of the pulmonary veins frequently. There's some other features here. Unlike the other site that we were talking about, the rounded onset of the bipolar electrogram, this has a sharp component to the onset of the bipolar electrogram. So that's a much more useful endpoint for looking at the earliest site. So it's not only early, but it's a sharp, near-field looking signal. When we map the left atrium, this was the site of the earliest activation. And unipolar electrograms can be also useful. So here's a look at the unipolar. So this was the bipolar electrogram in question, sharp signals. And then we can look at the unipolar atrial signals and see that there's a QS here as well. And the steepest part of the dvdt kind of lines up with the sharp component. So everything matches up. QS and the bipolar sharp are the most steep deflection in that. We trace it up, actually lines up with the bipolar electrograms. This is a good site to ablate. And this was successful. Thank you. Welcome to workshop three. I'm Bill Stevenson from Vanderbilt University Medical Center. Here are my disclosures. Case one, catheter ablation is performed to treat recurrent supraventricular tachycardia in a 28-year-old female with the Wolff-Parkinson-White syndrome. Ablation is initiated with a solid 4-millimeter electrode catheter with temperatures set to 60 degrees centigrade and maximum power of 30 watts. The tracing is recorded. Which of the following is the best next step? A, increase power to 50 watts. B, stop RF and reassess catheter position. C, continue RF ablation at 30 watts for 60 seconds. D, continue RF and start atrial pacing. And here is the tracing. And you can pause the video, analyze, and select your answer. So the correct answer is to stop RF and reassess the catheter position. So what's happening here is we're in sinus rhythm. We turn on RF. And you see that pre-excitation disappears. The QRS becomes narrow. And what's happening here is we're in sinus rhythm. That pre-excitation disappears. The QRS becomes narrow. Now, that may indicate that you have block in the accessory pathway, which would be a good thing and a reason to continue ablating. However, in this case, if you look at what's happening in the atrium, you see that we have simultaneous A and V emerging. The AV interval shortens on this beat, which looks like a fusion beat. And then it's a narrow QRS on these beats. So there is a junctional rhythm which has emerged. And that's potentially why pre-excitation went away, is that the impulse emerging from the junction propagates down through the conduction system depolarizing the ventricle before the wave front reaches the atrium and can go down the accessory pathway. So this is consistent with ablation near the AV node. And this is an anteroceptal pathway that was indeed close to the AV node. So this is a situation where if you continue RF, you're probably going to wind up with heart block, and the pathway may not be interrupted. And in fact, with interruption of RF energy here at the end of the slide, you can see that immediately we have pre-excitation, though the pathway was not affected. Case 2. Pacing from the right ventricular apex is performed during an induced tachycardia in a 38-year-old male, as shown in the tracing. Which one of the following diagnoses is most likely? A, atrial tachycardia, B, AV nodal reentry, C, AV reentry using a left lateral accessory pathway, D, AV reentry using a septal accessory pathway, E cannot be determined. And here is the tracing. You can pause the video and then select your answer. So, the answer is cannot be determined. So, let's look at this tracing. We have a tachycardia that has a right bundle branch block configuration. There is a HISS deflection that's preceding each QRS complex in the HISS lead, and it's a one-to-one tachycardia with a VA time that is shorter than the AV time, as you see here. So, all mechanisms are possible. Pacing is performed from the right ventricle, and you can see that it accelerates the atrial electrograms up to the paced cycle length, and we have an AV type of response with the last paced stimulus. So, this is then either AV reentry using an accessory pathway or AV nodal reentry. So then we look at the post-pacing interval, and we see that it's quite long, 440 milliseconds, relative to the tachycardia cycle length of 320 milliseconds. A long post-pacing interval is consistent with AV nodal reentry, but does it exclude AV reentry using an accessory pathway? Well, it does not if the accessory pathway is remote from our pacing site in the right ventricle. So, for a left lateral accessory pathway, the right ventricle is not necessarily part of the reentry circuit, particularly when you have right bundle branch block, and you can have a long post-pacing interval from the right ventricle, even though this is AV reentry using an accessory pathway. This figure shows you that same tachycardia with the coronary sinus tracings, and you see that we've got distal to proximal coronary sinus activation consistent with the presence of a left lateral accessory pathway. And here you see a single extra stimulus that advances the tachycardia without changing the activation sequence, which remains early at the distal coronary sinus. So, the schematic at the right shows you what's going on. Here's the reentry circuit with the wavefront revolving down the left bundle through the left ventricle and up the accessory pathway, and we're pacing over in the right ventricle near the right bundle, hence the long post-pacing interval. Case 3. During tachycardia, cryoablation is performed at a site anterior to the coronary sinus os. The tracing is recorded after one minute. Which one of the following is the best next step? A, continue cryoablation. B, continue cryoablation and begin ventricular pacing to monitor VA conduction. C, continue cryoablation and begin atrial pacing to monitor AV conduction. Or D, stop cryoablation and thaw. Here is the tracing. You can pause the video and select your answer. So the correct answer is to stop cryoablation, to thaw. So what's happening here? We're in a supraventricular tachycardia that has a one-to-one AV relationship consistent with AV nodal reentry. You can see that there's a HISS deflection here in front of each QRS complex. And we're freezing just anterior to the coronary sinus os. So in the slow pathway area. So if we cool the slow pathway, how should this tachycardia terminate? Well, the wavefront should go up the fast pathway to depolarize the atrium. So we'd see an A. And then it would block in the slow pathway before it returns to the ventricle. In contrast, what we see here is propagation that occurred over the slow pathway, reached the ventricle, and then block between the ventricular activation and atrial activation. So evidence that the fast pathway is being affected. So if that's the case, then we need to stop and reassess our catheter position because it looks like we may be at risk of injuring the fast pathway. Case 4, a 42-year-old woman presents to the emergency room with atrial fibrillation that terminates spontaneously. She has a several-year history of palpitations. An EP study is performed. During catheter placement, a patent foramen ovale is encountered and a tachycardia is induced. Pacing from the coronary sinus is performed during tachycardia and is shown in the tracing. Which one of the following is the best next step? A, map the activation sequence of the left atrium. B, perform entrainment mapping in the left atrium. C, perform ablation of the lateral mitral isthmus. D, perform ventricular pacing. E, perform pulmonary vein isolation. Here is the tracing. The relation of the catheters to cardiac anatomy in the fluoroscopic image is shown at the upper right. You can see that the distal coronary sinus is electrodes 1, 2. The high right atrium, electrodes 17, 18. You can pause the video and select your answer. So the correct answer is to perform ventricular pacing. So what's happening here? We have a narrow QRS tachycardia with a one-to-one AV conduction and earliest activation at the distal coronary sinus. The long RP interval tends to favor an atrial tachycardia, but AV reentry using a slowly conducting accessory pathway and an uncommon form of atypical AV nodal reentry is also possible. We see the last two stimuli of pacing from within the coronary sinus. Pacing accelerates the electrograms and QRS complexes up to the pacing cycle length. And the post-pacing interval is 310 milliseconds, which is equal to the tachycardia cycle length. So we're in the reentry circuit here. So this could be either AV reentry using an accessory pathway or an atrial tachycardia that is involved in that area of the atrium or perhaps the distal coronary sinus. So we haven't distinguished between atrial tachycardia, possibly a macro-reentrant atrial tachycardia even, and AV reentry. So to make that distinction, the most straightforward thing is to ventricularly pace. Case 5, pacing is performed during supraventricular tachycardia as shown in the tracing. Which one of the following is the most likely diagnosis? A, mitral isthmus-dependent atrial flutter, B, focal left atrial tachycardia, C, AV reentry using a left lateral accessory pathway, or D, atypical AV nodal reentry. Here is the tracing. And this is the same patient that we just discussed. So here is the answer. You can pause the video and select your answer. So this is AV reentry using a left lateral accessory pathway. So here is our one-to-one tachycardia with a relatively long VA time. And pacing from the right ventricular outflow tract, in this case, accelerates all the QRS complexes and electrograms to the pace cycle length. When we come off of pacing, the last atrial electrogram accelerated to the pace cycle length is way over here, indicating this long stimulus to conduction time to that part of the atrium. So this is an AV response. Would be easy to be misled and think it's an AAV response because of that long stimulus to atrial electrogram time. The atrial electrograms of the preceding beat actually fall after the last stimulus. But this is the last one accelerated to the pace cycle length, so it's an AV response. That excludes atrial tachycardia. The post-pacing interval in the ventricle is 380 milliseconds, which is only 60 milliseconds longer than the tachycardia cycle length. That excludes AV nodal reentry as well, although we had already done that in our previous tracing. Case 6. A 34-year-old male undergoes EP study for evaluation of neuroQRS tachycardia. The tracing shows tachycardia initiation, which was reproducible. Tachycardia repeatedly terminates spontaneously after a few cycles. Which of the following is the best next step? A, perform ablation of the slow AV nodal pathway. B, perform ablation at the site of earliest activation on the mitral annulus. C, administer isoproterenol and repeat program stimulation. Or D, initiate tachycardia and administer adenosine. Here is the tracing. You can pause the video, analyze, and select your answer. So the answer is to administer isoproterenol and repeat program stimulation. So this tachycardia keeps terminating is the difficulty in establishing a correct diagnosis. It's a one-to-one tachycardia, and it has a short VA time. But the electrograms are not synchronous. The atrial signals are not synchronous with the QRS. So all mechanisms could be possible from that. RV pacing, however, initiates the tachycardia. And during pacing, the last atrial electrogram that occurs at the pace cycle length is this one. This is an AV type of response, which excludes atrial tachycardia. There are some oscillations in this tachycardia as well. And the VA time is relatively fixed if you measure those. And if you map out the oscillations, you'll see that those are due to changes in the AH interval. Here, the AH diminishing from 370 milliseconds to 260 milliseconds associated with this decrease in the short R to R interval. And then on the next interval, the A to A increases as a consequence of an increase in the AH interval. So the H to H changes are preceding the V to V changes, further excluding atrial tachycardia and telling you that the AV node is somehow an important part of this circuit. However, this could still be AV nodal reentry or AV reentry using an accessory pathway. So in order to make that distinction, it would be very useful to have sustained tachycardia inducible. That can potentially be achieved by administering isoproteranol and getting a sustained tachycardia to allow for pacing maneuvers. Case 7. A 34-year-old male undergoes EP study for evaluation of narrow QRS tachycardia. The tracing shows tachycardia termination, which occurred repeatedly. Which of the following is the best next step? A, perform ablation of the slow AV nodal pathway. B, perform ablation at the site of earliest atrial activation on the mitral annulus during tachycardia. C, administer isoproteranol and repeat program stimulation. D, perform AV node slow pathway ablation and permanent pacemaker implantation. Here is the tracing, and you can pause the video to analyze this and select your answer. So the answer is to perform ablation at the site of earliest activation on the mitral annulus, because this is reentry using an accessory pathway. And this tracing shows some interesting physiology. So the first two beats are wide, followed by two narrow beats, and then the tachycardia terminates. The wide beats are left bundle branch block-like in configuration. In the HIS recording, you see that there is a nice HIS deflection preceding the QRS complexes by an interval that's consistent with left bundle branch block aberrancy rather than pre-excitation. On after the second QRS complex, the next QRS is narrow, and whenever there's a change in the QRS configuration during a tachycardia, during a supraventricular tachycardia, you want to analyze very carefully why that occurred, if you can figure that out, and what effect it has on subsequent atrial activation. And you see here that we have an HH interval of 380 milliseconds. And then on the next beat, when the QRS shortens, the A to A interval shortens to 360 milliseconds from 380 milliseconds. So loss of left bundle branch block aberrancy shortens the VA time, and that's consistent with a left lateral accessory pathway. Then something interesting happens. Following the next narrow beat, there's an A, and tachycardia terminates. Now it terminates by AV block, and the AV block occurred below the HIS. As you see here, this HIS deflection in the breeze all by itself. So this leads one to think, well, is there infranotal conduction disease? The patient had left bundle branch block and tachycardia, and then infranotal block terminated the tachycardia. However, this type of infranotal block is physiologic. You can see that it was a short, long, short sequence of H to H intervals, which set up the block in conduction. And that's physiologic behavior in the HIS-Purkinje system. So during the long H-H interval, the refractory period of the Purkinje system prolongs such that on the next interval, which occurred because the AH interval shortened, that shorter AH allowed the wavefront to arrive early enough to block in the Purkinje system. That AV block terminated the tachycardia, which further indicates that the ventricle is necessary for this tachycardia to continue. So it's AV reentry using an accessory pathway. Case 8. A 28-year-old female undergoes EP study for evaluation of neuro-QRS tachycardia. Figure 9-1 shows pacing from the HIS bundle catheter. And the second figure shows pacing from the basal RV septum during tachycardia. Which of the following is the most likely tachycardia diagnosis? A, typical slow-fast AV nodal reentry. B, atypical fast-slow AV nodal reentry. C, AV reentry using a septal accessory pathway. D, atrial tachycardia. Or E, cannot be determined. Here is the first tracing. So this is parahysian pacing. And then you have a second tracing as well, which is ventricular pacing during tachycardia. You can pause the video, toggle between those, and select your answer. And the correct answer is E, cannot be determined. So during parahysian pacing, you see that we have narrow QRS beats and wide QRS beats, and that's what we need in order to analyze. So the first beat shown at the left is a narrow QRS beat. You can see that there's a stimulus and then an A. The interval from stim to A looks like it exceeds 60 milliseconds. So it's likely that this is not direct atrial capture from the stimulus, but rather capture of the His bundle and then brisk retrograde conduction. On the next beat, we see that the QRS is wide, consistent with loss of capture of the His bundle and the VA time prolongs to 120 milliseconds. So that is consistent with conduction occurring up the AV node during both of these beats, the wide beat and the narrow beat. Now does that observation exclude the presence of an accessory pathway? And the answer to that question is no, because if you have an accessory pathway that has a long VA time, then you simply won't see it. All the conduction will be up the normal retrograde pathway via the AV node if that has a shorter conduction time. So it doesn't exclude the presence of an accessory pathway. So now here is tachycardia, and you see the last two stimuli of a pacing train. This is a one-to-one tachycardia with a VA time, which is shorter than the AV time. And pacing in the right ventricle, we have an AV response. So consistent with either AV nodal re-entry or re-entry using an accessory pathway, and quite a long post-pacing interval, 900 milliseconds with a tachycardia cycle length of 560 milliseconds. So that is consistent with AV re-entry with a long VA time, a slowly conducting pathway, or more commonly, AV nodal re-entry. But we cannot exclude the possibility that this is a slowly conducting accessory pathway. And in fact, that's what this was in this patient. Case 9. A 28-year-old female undergoes electrophysiology study for episodes of tachycardia. During catheter manipulation, a tachycardia is initiated and terminates spontaneously, as shown in the figure. Tachycardia is reinitiated, and the tracing in the second figure obtained. Which is the most likely mechanism of the tachycardia? A, idiopathic interfacicular re-entrant VT, B, antedromic AV re-entry, C, AV nodal re-entry with aberrancy, or D, AV nodal re-entry with a bystander accessory pathway? So here is the first tracing. And here is the second tracing. You can pause the video, toggle back and forth if you need to, and select your answer. So the answer is B. This is antedromic AV re-entrant tachycardia. So in the first tracing, we have wide QRS tachycardia, which terminates. And you can see that it's a one-to-one tachycardia. And then when VA block occurs on the last beat, and the ventricular depolarization does not conduct to the atrium, that terminates the tachycardia. So that suggests that VA conduction is important for the continuation of the tachycardia. And that would be consistent, then, with some sort of supraventricular tachycardia. It's conceivable that the Purkinje system could be involved in a ventricular tachycardia, and that block in the Purkinje system could lead to VA block and terminate the tachycardia. At the two sinus beats here on the right, you can see that the far-field activation on the distal coronary sinus, the V there, suggests that this is quite a short AV interval, and that the far-field ventricular activation actually precedes the QRS complex, consistent with pre-excitation, even though it's really not easily visible in the surface EKG. Now here we are during tachycardia, again, in the second tracing. You can see the tachycardia cycle length is 250 milliseconds. And this shows you the classic method to determine if you're dealing with an antedromic tachycardia. And that is to show that an atrial stimulus can advance the tachycardia at a time when the stimulus would not have been able to get into the AV node. So here in the recording from the high-right atrium, you can see the tachycardia cycle length marching along at 250 milliseconds. A stimulus that falls at this point in time and is delivered here from the coronary sinus does not change the timing of the high-right atrial A, or the A which is recorded here in the HIS proximal electrograms, but it advances the next V and pulls in the subsequent A as well to 230 milliseconds. So that proves the existence of an accessory pathway capable of conducting antedromically. The fact that this reset the entire tachycardia is consistent with AV re-entry. One could also analyze the post-pacing interval in the coronary sinus and show that that's relatively close to the re-entry circuit. Thank you. This is Bill Miles. I am professor of medicine at the University of Florida. And I just have some cases that we're going to talk about. They're multiple choice. And I'm going to show you the choices and I'm going to show you the slide with the case. I might flip back and forth a little bit. I'm then going to pause for a few seconds to let you pause the tape if you want to and look at things more carefully, and then I'll continue with the answers. So I'm not sure how many I'm going to get through, but we'll get started. This is the first case. And in this patient, the HV interval in this patient is the upper limits of normal, is prolonged due to hysperkinesis disease, is normal for a patient with bundle branch block, is short, or cannot be determined because the structure labeled H is really a right bundle branch potential. So this is a little clumsy since we don't have two screens. So I'm going to go back and forth a few times. And again, I think the participants can freeze their tape and look at things. So here's the tracing. Here are the choices again. Here's the tracing again. So freeze your tape and think about what you want to say. Or if you want to cheat, you can just keep going, but I'm going to stop for a few seconds and then we'll talk about the answer. So I think the answer is the HV interval is short. And this was simple if you've been in electrophysiology for a while. But I have so many fellows that have trouble with this that I thought it was worth sticking it in here. So the thing is, the HV measured here is measured wrong. This isn't an HV. The HV is the beginning of the QRS in any lead, the beginning of the H to the beginning of the V in any lead. So you don't measure the HV interval in the His lead. So this HV interval is not 60. You know, the normal HV is 35 to 55. This HV is 30. Because when you drop a plumb line down from the onset of the QRS, the HV is much shorter than it is here. This V represents the ventricular activation of the summit of the right ventricle. We have a left-sided accessory pathway here. You know that because that V is very early in this left lateral lead in the coronary sinus. So you know there's pre-excitation, but the right side of the heart is not activated early. But the pre-excitation is evident if you drop the plumb line. So the HV interval is measured from the beginning of the His potential to the earliest ventricular activation in any lead. It's not measured locally in the His lead. The ventricular activation in the His lead represents basal RV septal activation, which is normally not the earliest site of ventricular activation. In this case, the earliest ventricular activation is the basal left ventricular free wall. That's the circle due to a left free wall accessory pathway. The resultant HV interval is short, and that's the definition of ventricular pre-excitation. Very good. So for some of you, that might have been simple, but I hope it was instructive to others. Here's pre-ablation. Now, post-ablation, we still drop the plumb line at the onset of the QRS, which means that the HV, if you measured H to the V in the His lead itself, you'd still get an HV that's a little bit too long, although it wouldn't be as much too long as was measured on that original slide. Very good. So let's do another case. You are ready to start ablating an accessory pathway. Once you obtain this catheter location in the ablation catheter, you should either A, deliver radiofrequency energy, B, pace the atrium faster to accentuate the delta wave prior to ablation, C, utilize cryoablation rather than RF to lower the risk of AV block, locate this site and several adjacent sites, or move the catheter to another site. And here's the electrograms. So you have the surface tracings, you have His leads, you have proximal and distal ablation, you have a unipolar from the distal ablation, and you have coronary sinus leads. And our lab CS5 is usually near the CSR, CSD is in the more lateral coronary sinus. So let's look at the choices again. The choices are deliver RF energy here, pace the atrium faster to accentuate the delta wave prior to ablation, utilize cryoablation rather than RF to lower the risk of AV block, locate this site and several adjacent sites, or move the catheter to another site. All right, and here are the electrograms. So pause your tape if you want to study the electrograms and the choices. And I'm going to wait for a few seconds and then we'll talk about the answer. All right. So I think the answer is to move the catheter to another site. And hopefully most of you got this. That's because if you drop a plumb line at the beginning of the delta wave on this patient, notice that V1 is upright, 2 and F are down. So this is a left posterior accessory pathway. It's not going to be close enough that you have to change over to cryoablation to avoid the AV node. But look, the distal ablation has almost no A on it. And the unipolar has an R and the rapid decrease in the electrogram is late. So this might be somewhat close, but it's not close enough. The V is not negative. The R wave on the unipolar means that you're not in the right site. So this is a poor site for ablation. The distal bipolar and unipolar electrograms on the ablation catheter do not precede the onset of the delta wave. The distal electrode unipolar electrogram has a large R wave, suggesting the ventricular activation initially comes toward the electrode rather than away from it. There's no A on the ablation catheter, and that catheter might now be too deep in the ventricle. So what is a good site? Well, here's a good site. This site now we've dropped a plumb line from the onset of the delta wave, and we've dropped a plumb line at the onset of the ventricle. I'm not sure whether I can identify a pathway potential here. I certainly can't definitively identify it. But now we have a nice A here, and we have no R wave on the ventricular electrogram, a steep early descent. This is a really good site. So this is what you need to look for. This is why the unipolar electrogram helps you. Those of you who do electroanatomic mapping, the electroanatomic systems give absolutely gorgeous unipolar electrograms. Sometimes they're not quite so gorgeous on some of our more routine mapping systems. This is a much better site. There's a balanced A and V on the distal bipolar ablation lead. The distal unipolar electrogram is pre-delta with a steep descent and no R wave. And note that the proximity of the local A and V electrograms is dependent on the oblique orientation of the pathway and the direction of its activating wavefront. Therefore, the earliness, if that's such a word, of this ventricular activation is actually more important and more reliable for a good ablation site than just the very short local A-V interval. Although many good ablation sites will have merged atria and ventricular potentials, there are sites along the annulus that might have A-V potentials that look like they're merged that are not early and are not good ablation sites. So here during radiofrequency, you can see that the short A-V interval, a few seconds into ablation, markedly and suddenly prolongs. The delta wave disappears. That was a good site for ablation. Very good. Let's do another case. You are performing program ventricular stimulation after ablation of a concealed left free wall accessory pathway. A reasonable next step would be paste the atrium to make sure the delta wave is gone. Give isoproteranol to look for recurrent accessory pathway conduction. Give adenosine to look for dormant accessory pathway conduction. Remap the left free wall or remove the catheters. You're done. So here are the electrograms. We have two panels. We're pacing the ventricle at 600 milliseconds and putting in a ventricular extra stimulus at 420 milliseconds and a ventricular extra stimulus at a coupling interval of 360 milliseconds. Okay. Remember here are your choices. What's a reasonable next step? Paste the atrium to make sure the delta wave is gone. Give isoproteranol to look for recurrent pathway conduction. give adenosine to look for dormant pathway conduction, remap the left free wall, remove the catheters, you're done. Here are the electrograms again. Okay, so go ahead and freeze the tape if you want to look at the electrograms and want to look at the choices and see what you think, see if you agree with me or can argue with me, but we'll pause here. And let's look at the answers. So here's the answer. I think the answer is to remap the left free wall. Now if it's a concealed pathway, pasting the atrium to make sure the delta is gone is sort of stupid. So hopefully you picked up on that. And I'm going to make a case that we can see that the pathway is still there. We don't have to give isoprel or look for dormant conduction and we're not done. So how do you know that? You know that because the stimulus to A is the same with the 420 and the 360 millisecond coupling interval, but you start to see the retrograde hiss move out. If there were no accessory pathway there and you got delay between the ventricle and the retrograde hiss, and you were going up only the AV node, the A would have to move out. So you've dissociated hiss activation from retrograde atrial activation. There's got to be an accessory pathway there. And this is a little bit of a pet peeve because I have some young partners who love to minimize how many catheters they put in and they start pulling the catheters out. Well if you had pulled your CS out, you might miss the fact that that left free wall pathway is still there. If you had kept the coronary sinus catheter in, this is the same patient, I had actually taken out the coronary sinus catheter to try to be more tricky. You can see that that left free wall pathway, that eccentric activation is still there. So VA conduction during the drivetrain is via the AV node, maybe with a slight contribution of the accessory pathway in the most distal electrogram in the coronary sinus. The VA interval does not increase after the more premature ventricular extra stimulus suggesting but not proving accessory pathway conduction. The delayed retrograde hiss in the right panel without VA prolongation dissociates retrograde hiss-purkinje AV node conduction from residual retrograde accessory pathway conduction as demonstrated also by the eccentric activation sequence when the coronary sinus catheter is added. Since these tracings prove residual accessory pathway conduction, there's no need to enhance conduction with isoproteranol or adenosine. So the CS catheter is very useful, but you could have actually figured this out without the CS catheter. And this is just another example, different patient of the same thing. We're putting in earlier and earlier ventricular extra systoles. You can see the hiss move out further and further, but the VA interval stays the same. And in fact, in this example, the retrograde hiss is activated simultaneously with the A, which means you can't be coming up an AV nodal structure in this particular patient. Very good. All right. Well, let's do case four. This patient underwent ablation of a left free wall accessory pathway. Parahiss pacing was performed. A reasonable next step would be remove catheters. The procedure's over. Return the patient to recovery. Map and ablate a right free wall pathway. Map and ablate a septal pathway. Look for additional evidence of successful left free wall accessory pathway ablation. That should actually be, yeah, ablation. Look for evidence of successful ablation. Look for additional evidence. Ablate the rightward inferior extension of the slow pathway. So here's the tracing. This is a parahiss. We're actually, we've actually moved the right ventricular catheter to the parahiss location. So this is actually a hiss catheter from which we are not pacing. And I'm going to actually give you a little more information here. Here are the measurements. And here is a hiss potential. All right. Now we're going to go back. Would you remove catheters? You've ablated a left free wall pathway. Do you remove catheters? Return the patient to recovery. You map and ablate a right free wall pathway. You map and ablate a residual septal pathway. Do you look for additional evidence that your left free wall accessory pathway ablation was successful? Or do you ablate the rightward inferior extension of the slow pathway? Here's the electrogram again. So go ahead and freeze the tape if you're answering the questions. If you need some time to look at both. And I'm going to pause for a few seconds. Okay. Let's look at the answer. Well, the answer is look for additional evidence of successful left free wall success. And the addition of the CS lead, I cheated again, again, some of my partners substitute catheters and don't have a CS lead in at this point, but it really helps you. This is still eccentric conduction coming up the left free wall pathway, but it looks like a nodal response. Why does it look like we get a nodal parahiss response when we still have a left free wall pathway? Well, in this particular case, this is actually complicated. There are two reasons. We're going to go through them one by one. One number one is when HISS is captured, retrograde conduction is a fusion between the AV node and the left free wall pathway. So look at this coronary sinus activation sequence and compare it to this coronary sinus activation sequence. Why do they look different? They look different because the node is capturing the CS5 and maybe the CS4, but the accessory pathway is capturing the distal CS. So when you capture the HISS-A, you get up the node so fast that you fuse between the left free wall and the node, the left free wall accessory pathway and the node. But when you lose HISS capture, the HISS pops out here, the VA goes out because this on the right represents nodal conduction. So this side goes out, but now you have pure left free wall accessory pathway activation. So always look for fusions. When the HISS is captured, retrograde conduction via the AV node fuses with that of the left free wall pathway. This fusion disappears when HISS capture is lost and the STEM-A interval increases in the right-sided leads, despite the presence of retrograde accessory pathway conduction. When performing para-HISS pacing, look carefully for fusion as a clue to the existence of two retrograde conduction pathways and having multiple leads in place really helps. Now what's number two? Well number two is a little more subtle, but also important because look, this is actually pure pathway conduction on both of these before loss of HISS capture and after loss of HISS capture. But the VA changes here also. Why does the VA change when conduction is going over the pathway? Well the second principle is that para-HISS pacing with retrograde conduction via left free wall pathway can mimic an AV nodal response. So this example shows you two fallacies or two pitfalls, I guess I should say, of para-HISS pacing that you need to be aware of. Why is this? Well with HISS capture, the pacing impulse travels down the left bundle branch to reach the left free wall accessory pathway. But with loss of HISS capture, the RV pacing must conduct transeptally to reach the left free wall pathway. No longer goes down the left bundle branch, it has to cross the septum because you're not activating the HISS-Purkinje system and that prolongs the stimulus to A interval. So if you do a para-HISS and you're going up a left free wall pathway, it may mimic a nodal pathway. And I borrowed this beautiful diagram from Eric Krostowski just demonstrating this. When you capture V and HISS, you go down the left bundle to get to this left sided pathway. But when you capture V alone, you have to sort of either go across the septum or get into the bundle branches to get over to the left side and you get prolongation of the VA interval, but it's not going up the node. So keep that in mind. With left free wall accessory pathway, the VA time may be shorter with HISS capture than without HISS capture and may mimic a nodal response. Very good. That's a complicated one. So we have time for more. So this is number five. RV pacing is performed at the same cycle length from three right ventricular sites. What structure is responsible for retrograde conduction? Is it the AV node, a post-receptal pathway, an anteroceptal pathway, a left free wall pathway, or an atriofascicular pathway? And here are the tracings. On the left, we're pacing from the right ventricular apex. In the middle, we're pacing from the post-receptal base. And on the right, we're pacing from the anteroceptal base. What are the choices? You're going up the node, you're going up a post-receptal pathway, an anteroceptal pathway, a left free wall pathway, or an atriofascicular pathway. Here are the tracings. Now this one's going to be a little hard if you don't stop the tape and do a little bit of measurement, because this one requires a measurement. But I thought it would give it away too much if I put the measurement on the question. So we'll look at it in a minute. I'm going to pause. You can stop the tape if you want. And we'll start back in a few seconds. Very good. Well, let's look at the answer. Well, the answer is it's an anteroceptal accessory pathway. Number one, atriofascicular pathways don't conduct retrogradely, so that one's out if you understood atriofascicular pathways. And the measurements I'm talking about are here. Pacing from the apex, it takes 110 milliseconds to get to the right atrium. Pacing from the post-receptal base, it takes 85 milliseconds. Well, if it's shorter getting to the A from the base of the heart than the apex of the heart, there's got to be an accessory pathway. Because if you pace from the base of the heart and there's no accessory pathway, that impulse has to go from the base to the apex or toward the apex of the right ventricle to get into the right bundle branch and then go retrograde. So if the VA from the apex is shorter than the VA from the base, that's nodal conduction. If the VA from the base is shorter than the VA from the apex, this is differential pacing that demonstrates that there's an accessory pathway. And in this particular example, when we were pacing from the antireceptal area, this was an antireceptal pathway, and the VA interval was very short. So we were pacing very close to an antireceptal pathway rather than a post-receptal pathway. So differential ventricular pacing demonstrated that this was an antireceptal pathway, not retrograde AV node. I do put a little asterisk here because you have to be aware that you have to be careful that you're not actually so annular that you're also capturing the atrium, not just the ventricle. But here we knew we were capturing a ventricle only and conducting the atrium. We were very close to the ventricular insertion of this antireceptal pathway. If the stem A at the base is shorter than that at the apex, retrograde conduction is via a pathway. In this case, the antireceptal pacing site is very close to the accessory pathway ventricular insertion. If the stem A at the base is longer than that at the apex, retrograde conduction is via the AV node. The basal paced impulse must travel toward the apex before it can enter the hysperkinesis system to travel retrogradely via the AV node. Very good. Let's do another case, case six. This will be the last case, and I think we have to be a little bit quick. Is this in fact, yeah, okay, we'll do it quickly. I'll have to take you through this quickly. Is this a good ablation site for this antireceptal accessory pathway? And I'm going to skip here because I don't have much time. I'm going to tell you that this is actually not a good ablation site for an antireceptal pathway. Well, let's see why. It's not a good ablation site for an antireceptal pathway because the ablation D is prominently ventricular, which is what we want, but the V on the proximal ablation is earlier than the V on the distal ablation. And so this is not a particularly good site for ablation of this pathway. And one of the reasons for that is that we're recording this pathway right where we're recording his. And you can tell that you have all V in the distal and you have an A and a V on the proximal. And we thought we were just too close to his at this point when we got an earlier V to ablate from this spot. So when that happens, what we often try to do on an antireceptal pathway is to curl the catheter underneath the tricuspid valve. At that point, the atrial electrogram on the distal ablation is very small. The ventricular electrogram is now earlier on distal than proximal and ablation P is all ventricle. On the ventricular aspect of the tricuspid annulus, the his dives into the membranous septum and is less susceptible to damage. The compact node is also less susceptible to damage since it's more atrial than ventricular. And what you do on this particular case, I actually curl the catheter up underneath to approach the tricuspid valve from the ventricular aspect. That's usually what we do. I was just lazy that day. I didn't want to get access from above. But it's actually usually easier to come in from above, curl underneath, and ablate from underneath the valve. So that's the safest way sometimes of ablating an antireceptal accessory pathway that's at the level of the his. And here's an example of ablating from that site. Now we can actually see the his. We can watch for prolongation of the AH interval during the ablation. And we got rid of the accessory pathway. If the QRS gets wider during ablation, stop immediately because this indicates that pre-excitation is increased due to some slowing of the AV node. So I think that's the last case I can get in on my half an hour limit. And this has been enjoyable for me. So I hope it's been enjoyable for you. Thank you very much.

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