Greetings, this is John Miller with Core Concepts in Electrophysiology with workshop number two, My Contributions. Here are my disclosures for your viewing pleasure. Question number one, these are board type questions, so we'll have a STEM, distractors, and usually a figure of these things. A 58-year-old woman with recurrent supraventricular tachycardia undergoes electrophysiologic study. SVT is initiated only with ventricular burst pacing, never atrial pacing or extra stimuli. Results of ventricular overdrive pacing during SVT are shown in the figure. Based on this information, all of this information, the most likely diagnosis is atrial tachycardia, orthodromic atrioventricular re-entry, atrioventricular nodal re-entry, or it's indeterminate, no conclusive findings. Here is the figure. So we're pacing in the ventricle. The last three stimulant complex in the ventricle are shown. Tachycardia resumes over here, and it doesn't have a perfectly regular activation sequence. We're pacing significantly faster in the ventricle. So you have your choices, you have your figure, and that's it. Come back when you pause the presentation. Come back when you have your answer, if you feel bold. And I'm going to go on with the answer here. The answer is dremel, avian nodal re-entry. When in doubt, it's avian nodal re-entry. That's not always true, but it's the most common SVT, so it's not a bad choice. What's going on here, though, that makes this the correct answer instead of just a good guess? Well, we are doing ventricular overdrive pacing during tachycardia, and the key to this solution, to solving this problem, is knowing which of the atrial recordings are associated with the ventricular pacing and which are tachycardia. Now, you'll say, okay, I'm looking for a VAV or VAAV response. Here's a VAAV. VAAV. What does that mean? It usually means atrial tachycardia. Okay. I missed one of these intervals. What is going on in this interval here? Well, if this interval is 280 or 300, then it really is a VAAV. We've conducted retrogradely, and this is 260 from the prior ventricular simulation here. This is a run of eight or 10 cycles here. These are 260. If this is the last one conducted back, and this is the first tachycardia beat, then it really is VAAV. It's atrial tachycardia. If, however, this interval is 260, why is that? Why would that be? Well, the only reasonable explanation is that this stimulus gave rise to this electrogram, and then this one gave rise to that one. This one gave rise to that one. Seems absurd. Too bad. It's true. The post-spacing interval then is 604, if we follow this on. The stimulus to A is not this stimulus to that A. It's this stimulus to the A that results from the stimulation. Not what it looks like, but what it actually is. That stimulus to A there is 380. The VA is 126, and the ... Oh, sorry. That difference there is, what, 154 or so. That's in excess of 125, so this puts us in AV nodal territory, as Dr. Michaud discusses in his presentation about SVT diagnostics. This makes this AV nodal reentry, not atrial tachycardia, and not orthodromic reentry, where those numbers would be less than. Now, it's possible that if you have a slowly conducting accessory pathway, that it'll have decrement in conduction. They don't usually have decrement ... When they can conduct this well, at 280 millisecond cycle length, if you're only pacing at 10 milliseconds, 20 milliseconds faster than the tachycardia cycle length, it would be pretty unusual to have that degree of decrement in there. Not unthinkable, but very, very unusual. The correct answer is AV. In this case, we had an intermediate RP tachycardia. It's not a really long RP. It's not a really short RP. It's in the middle there. These are tough ones, very tough ones. Inducible only with ventricular pacing. That's a little bit odd, but that's a clue that it's probably not typical AV nodal reentry and very, very unlikely to be atrial tachycardia. Wobble in the cycle length can occur within the arrhythmia. It's very, very helpful if you see that, because then you can see what's linked to what. If the Vs shift around, but the As follow them, then you're either dealing with orthodromic SVT or AV nodal reentry, typically going up a fast pathway. If the AV is what's fixed, that's a little bit unusual, but it can be an atrial tachycardia, but the VA interval is all over the place in that situation. It's not real common in AV nodal reentry, but if you've got a slow pathway, that's where wobble occurs. Typically, you would have a fixed VA interval, but a wobble in tachycardia because the AH is prolonging, not the HV. Really rare in orthodromic reentry, it can occur, but it's really, really rare. This is slow, slow AV nodal reentry. We got two ways to have a problem. We got two slow pathways, either or both of which could have wobble. It turns out in this situation, in this particular case, I didn't show you, but in this particular case, there was no clear relationship, no linkage between V and A. The VA was changing, the AV was changing. It's a slow, slow tachycardia. It's a wobble in both of those pathways. The apparent VAAV relationship with ventricular paging during SVT suggested atrial tachycardia, but it's not a real VAAV. It's a pseudo-VAAV. If you know which A follows from the last stimulated V, that's the key here. This takes calendars. I figured out pretty easily. The intervals, then, that you measure appropriately, correctly, indicate you can have a reentry. Slow pathway region ablation eliminated inducible SVT was just one RF application, no big deal. Lessons from this is to take all the data together, not just one part. I saw a VAAV, it must be a major tachycardia. Take all the information and beware the pseudo-VAAV. This is a favorite of those guys and ladies that write the questions for the certifying exam. Make sure you know which is the last conducted interval. It's pretty straightforward if you think of what to measure. This occurs in the entrainment of the trigonometry as well, not just orthodontic. Okay, question number two. A 25-year-old man with recurrent SVT comes for EP study. SVT is initiated and diagnostic maneuvers are performed. Based on the results of stimulation in the figure, you conclude that AV nodal reentry is most likely, AV reentry using accessory pathway is most likely, atrial tachycardia is most likely, or more information is needed. Here's the figure. The maneuver that's performed is a single ventricular extra stimulus delivered during a tachycardia. You can make your measurements, you can think about what's going on, and look at your distractors and come back when you have an answer. The answer is more information is needed. Now, this is a very tricky thing because when that distractor appears on a board exam, it sometimes is just, we couldn't think of another plausible distractor, so we just throw that in there. It's wrong. But sometimes it's right. Don't force your data to provide a conclusion of which it's not capable. Why is it not capable of the situation? Well, we're delivering a PVC during tachycardia. Tachycardia looks regular. I'm not even sure I measured all the intervals. And it is while the HISS is refractory. That's great. Super. There's potential for diagnostic information. It looks like it's a left lateral pathway, doesn't it? Because we got an eccentric activation sequence. I don't have a hybrid atrium here, but we got this kind of a chevron bracketing in the coronary sinus atrial activation at the HISS-A. And I know that that catheter is around the low septal right atrium because it's got the HISS potential. I can't record that anywhere else. That's where it is. Okay. So what we need to then measure is the AA intervals surrounding the extra stimulus. And so they are 360 during tachycardia. I make my trainees measure these intervals first because they're all excited about this interval here that surrounds the PVC. And you're looking for this to be shorter or longer than tachycardia. If you have significant cycling variability, then whatever you're measuring here has to be substantially longer or substantially shorter than any spontaneously occurring interval, because it could spontaneously vary right there and make a wrong inference. That interval is 360. We didn't bring the atrium in. We didn't push it out. Nothing happened. It's as though you didn't even give the PVC. So no information can be derived from this. It looks like a left-sided accessory pathway, but is this definitely not an atrial tachycardia? It could be with slow pathway conduction, anterogradly. Is this definitely not a left-sided exit and avian oval reentry? I can't know that. It's an eccentric activation pattern. It's not definitely orthodontic SVT. Okay. So the hysterefractory PVC has no effect on subsequent atrial activation and therefore has no diagnostic implications. If you advance the timing of it or you delay the timing of the next atrium, if you advance the timing of this next A, it means while the hysterefractory, that means you have some other way of getting back to the atrium aside from the normal conduction system. Therefore, you have an accessory pathway. It doesn't mean it's participating, but you have one. If you make this occur later than it ordinarily would, and the reason that you can't say it's necessarily participating is this concept of, well, if you have a pathway, yeah, you got a pathway because you brought the A and while the hysterefractory, there's no way that can happen, assuming that there's no shorter spontaneously occurring involvement. I'll say that that's the case. Definitely brought it in. No question. Brought it in. That could be an atrial tachycardia or even some odd avian nodal reentry. That's the main act, but you have a pathway that can bring in the timing of atrial activation. All right. So you can't say it's participating in tachycardia. What if you make it occur later than anticipated? Well, if it were an atrial tachycardia or some odd avian nodal reentry, that A should occur unperturbed, just like it does here. But if you make it occur later than anticipated, that can only be because you had an accessory pathway that was participating, and it took its time getting back to the atrium. It had some decremental conduction, and the atrium is waiting for it. It can't continue tachycardia until it gets its signal. Therefore, it's participating in the tachycardia. And the last option here is if you terminate the tachycardia with this hysterefractory PVC, and it doesn't get back to the atrium, that means the ventricle is part of the circuit. The only type of SVT in which a ventricle is part of a circuit is one with an accessory pathway that connects the ventricle or fascicle to some superventricular structure of the atrium or the avian outlet. All right, so the last two of these criteria, delay or omission of subsequent atrial activation following hysterefractory PVC, indicate presence and participation of the pathway of tachycardia. All right, question number three. 24-and-a-half-year-old man with recurrent SVT counts for EP study, SVT is induced, and diagnostic maneuvers are performed based on the results of stimulation in the figure I'll show. You conclude that avian over-reentry is diagnosed, avian reentry using an accessory pathway is diagnosed, atrial tachycardia is excluded, or more information is needed. Okay, here is, this is actually the same patient, and PVC occurs with different timing. Okay, you can observe that, measure it, come back when you're ready. The answer is that atrial tachycardia is excluded. Okay, PVC during SVT, obviously the timing of this atrial activation is brought in, you can see that a mile away, well, we'll measure it. It's shorter, and it's shorter than any other surrounding AA interval. Problem is that this is not during hiss refractions, and I've shown you where the next expected hiss would be. This is, I don't know, 120 milliseconds after the stimulus. Most of the time when you stimulate the right ventricle in somebody with a normal QRS complex, it takes 50, 60, maybe 70 milliseconds to get back to the hiss up the right bundle. And you can, in very rough terms, the stem to H with ventricular pacing is very similar to the HV interval. Why is that? Because you're traversing the same pathway. H, in anterograde conduction, you're going to H to V, okay, 45 milliseconds. With ventricular stimulation, you've got to get into the right bundle somewhere, so there's a little bit of time unless you're pacing right there. And then up the right bundle, it goes about the same velocity of conduction as it does anterograde. So that hiss potential during ventricular pacing is typically going to be before the local ventricular actogram. Sometimes it's buried within it, but it's in here somewhere in the first 40, 50, 60 milliseconds after the stimulus artifact. So this interval here where our next expected hiss is going to be there, there's plenty of time for this stimulus to have gone up and gotten not only to the hiss, but through the hiss and into the AV node. So we don't have good proof of an extra nodal pathway here. Yeah, we prematured the atrial electrogram, it's brought in, but it wasn't brought in because it connected up the AV node, and this is an odd pattern for that. It's connected up the AV node, and we're actually in an atrial tachycardia with an eccentric activation pattern. You don't know for this. How does it exclude an atrial tachycardia though? There's one interval that I haven't shown you here, and it's this one. The prematurity of this atrium here led to delay in the AV node. So the hiss is inscribed, then the HV interval lapses, we make a QRS complex. And if we had an atrial tachycardia that we just slightly prematured here, the chances of it being exactly the same timing after a ventricular event, after a QRS complex, are really, really, really odd, really small. So this illustrates VA linking. Whenever you see a V, however long it takes to get to the V, the A is stuck to it. It's linked. Atrial tachycardias don't do that. So I think based on this, it's very unlikely that there's an atrial tachycardia responsible for this. It would have to be an atrial tachycardia that's coming from the lateral left atrium close to the annulus. I don't see those every day. I don't see those every year. They're really not common unless you're a really high volume atrial tachycardia shop and most of us aren't. Then it has to be connecting down a slow pathway. That's a lot to ask. Then when we paste the V, it has to get up the AV node or something and have exactly the same activation sequence as the atrial tachycardia. That's a lot to ask. Any one of those is really rare. The concatenation of those three is just, come on, man, that's nuts. That doesn't make any sense. So atrial tachycardia is excluded. And there's your explanation a little more eloquently in another box. Okay. Question number four. 45-year-old man presented with wide QRS tachycardia and undergoes EP study. At EP study, the effect of an extra stimulus is shown in tracing number four that I'll show next. There's only one tracing here. It goes with question four. The best interpretation is ventricular tachycardia is present. Pre-excited AV nodal reentry is present. Antedromic tachycardia is present. Orthodromic tachycardia is present or no diagnosis can be made. Here it is. There is a single extra stimulus delivered during a wide complex tachycardia. And you think about stuff and make any measurements you want and pause me. I won't be offended and you can come back with what you feel like. The answer is antedromic tachycardia is present. What is antedromic tachycardia? Most of us call it a pre-excited tachycardia in which atrioventricular conduction is over a single accessory pathway and retrograde conduction in this reciprocating tachycardia, AV reciprocating tachycardia is uniquely at the AV node. It's not down the AV node and the pathway and up something else. It's not down one pathway and up another. There are terms for this. It's pathway-pathway tachycardia. Antedromic tachycardia is a pretty specific term down an accessory pathway up the AV node. So how do we know that that's what's going on? Everything else that's a pre-excited tachycardia is just a pre-excited tachycardia. All right. I have the onset of the QRS complex, I think pretty fairly here. And we look down and yeah, so what? Well, so what is this? Here's a HISS potential. Anybody can recognize that as a HISS potential and it follows the QRS complex. That knocks out orthodromic SVT right away. Yeah, orthodromic tachycardia. It can't be because you have to have a HISS that's before the QRS complex. This is not an operation. So it could be ventricular tachycardia, it could be pre-excited tachycardia, or it could be we don't know what. All right. Let's continue. Here are the VV intervals measured in QRSs and you see 330, 330. It's pretty regular right up until it's not regular. And presumably this stimulus in the atrium has something to do with the next ventricular cycle. Well, as I checked, we can't do anything about ventricular tachycardia with atrial stimulation unless it's bone fracturing. So this is probably a pre-excited tachycardia here. And this next cycle is also delayed. That has importance too. All right. So we've measured the VVs. What causes the VVs and what follows the VBs, all right? Here's the His-His intervals, 330, 330. So this His here, which actually occurs before the stimulus artifact, couldn't possibly be advanced by this. But this next H is advanced by the extra stimulus. And this next H here is longer than baseline by exactly the same amount that the VBs are. So since the His is after the V and occurs at the same cycle length, that means the VH is constant. That means the His is linked to the V, not the V linked to the His. So it's a retrograde His. And the His depends on the QRS complex. It doesn't depend on an AV nodal pathway. It doesn't depend on any other pathway. It is linked to the V. And finally, the AA intervals here, all right? Here's the AAs and the AVJ region right there, right there. This A here is importantly at 330. It is not affected by this stimulus. It's a perinodal atrium. How do I know it's perinodal? Because it's got a His here, all right? Get over it. It's perinodal. That means that there's no way to affect the AV nodal tissue if you don't affect the atrial tissue around it. So this cannot be AV nodal reentry. Otherwise, this His would be at 330. The V can be whatever it is, but the His would be at 330 because we can't alter. We didn't alter this, so we can't alter its output either. So this is going down a pathway that then connects up to the His and back up to the A, antedromal tachycardia. In summary, PAC during QRS tachycardia is delivered when the His is refractory here, and it doesn't affect the septal atrial activation, but does advance the next QRS and His potentials, and thereby resets the tachycardia. The next day, it's brought in, and the next cycles are after. This excludes VT because you can't affect ventricular tachycardia with an atrial tissue stimulus, and it also excludes preexcited AV nodal reentry for the reasons I articulated because you didn't do anything to that next, this atrial electrogram here to have affected the AV node. His after the QRS excludes orthodromic reentry. Preexcited can be ventricular tachycardia. Atrial activation after the advanced V here is identical to the others, and it would be very unusual to have a septal, another septal accessory pathway. Not unthinkable, but far and away the most likely since the HA is constant here, so the BA is constant as well, but the HA is the constant feature that makes an AV nodal activation pattern. Everything is lining up to being down the accessory pathway at the AV node. All right, so questions one through four that we've just been through have a common theme. They're diagnostic maneuvers during SVT. Stimulation during tachycardia can help differentiate one type of SVT from another. It can determine the tachycardia mechanism and or mode of global atrial activation. That is saying whether we have focal emanation or macro reentry. That wasn't the point of what I was talking about here, but it has that capability in broad terms. It can differentiate a good potential ablation site from one that's unacceptable, such as a bystander site. We did see that. Stimulation during tachycardia can confuse the matter, though. All right, make sure the stimulation has an interpretable effect. That is, you did definitely have capture. You did change some aspect of the rhythm. You changed from bundle branch block to knot. You terminated without propagation. You accelerated all the electrograms, the phase cycling, that sort of thing. Make sure that there's an interpretable effect before you go interpreting stuff. Make sure you understand which is the last conducted or entrained electrogram before resumption of tachycardia. We saw that with our reentry case, which is the last conducted to, not the last captured one. The capture occurs at the electrode-tissue interface. Everything that follows from that is conducted to or controlled by the wavefront, the result of the wavefront. It's not captured. It didn't capture the lateral left atrium when you stimulated the right atrium. You controlled it. It didn't capture it, but it captured the right atrium. Make sure you're paced for long enough to control all recordings and at high enough output the capture is definitely present, but not too high because it's not specific results. And I thank you for your attention. This is Greg Michaud. I'm here for workshop number two in the core concepts in EP and board prep course in Nashville today at Vanderbilt University Medical Center. Let's start with case one. So in this particular case, the following is observed during a period of induced SVT during EP study. What is the most likely SVT mechanism? The choices are AVNRT, atrial tachycardia, orthodromic AVRT, antedromic AVRT, or notophysicular tachycardia. Here's the tracing. Of course, you can pause on this and spend as much time as you like looking at it. The salient features are that this catheter is in the right atrium, high RA to low RA. This is His bundle recording catheter and CS catheter proximal to distal. The His catheter does have a His bundle recording on it. So the answer is the most likely SVT mechanism is AVNRT. And let's explain that. First of all, we have a stable atrial tachycardia demonstrated before it terminates. And it terminates with a premature beat. If we go back and look at that, we can see that the cycle ain't stable. There's calipers on the A to A time, and that's stable at 354. And one can see without calipers that on the surface, there's a premature beat that occurs substantially early and is associated with termination, back to sinus rhythm over here. There's a little His bundle potential out in front of this premature beat and actually is earlier than the expected His timing here. And it's narrow on the surface with a slight change in morphology suggesting that this premature beat came from either the vesicular system, or as frequently as the case, the His purkinje recording catheter causes ectopy. This is sort of an unusual termination of an SVT. The AT would not be expected to terminate without premature depolarization of the atrium. So if you've got a PVC or a junctional beat that conducted to the A, it might terminate atrial tachycardia, but this did not. ORT is not really a viable possibility because there's a short VA time in the tachycardia. So if we look at the His A, which is right here, and CS A, you can tell that because when there's no A, these are clearly the atrial signals in coronary sinus. If you just use the coronary sinus electrogram, that's quite early. And then proximal is expected to have a bigger A than distal, but there's an atrial signal in the His catheter as well, and that's quite early. So that VA time is well less than 70 milliseconds, which would make ORT virtually impossible. A notophysicular tachycardia could potentially terminate this way, but it's a rare diagnosis and would be a lot less likely than AV node reentry. So of those two choices, AV node reentry would make more sense. This is the tachycardia cycle lane. So this His beat actually comes earlier than the expected His timing, as I mentioned, and this arrow points out the His A for you. So AVNRT makes the most sense. It's a really unusual termination of AVNRT. You probably wouldn't see this in real life because you don't have catheters in the body, but with the catheters in there and their proclivity in causing premature beats, you might see this. Let's move on to case two. In this case, we're pacing from a catheter positioned at the His recording spot. The following tracing is obtained shown in figure one. What is the most likely explanation for the atrial activation sequence? Number one, atrial activation is a result of direct pacing capture. Atrial activation occurs via retrograde conduction through an accessory pathway alone. Atrial activation occurs through the AV node alone. Atrial activation occurs via retrograde conduction through slow and fast AV nodal pathways. Atrial activation occurs retrograde over an accessory pathway and the AV node. So those are all your possibilities. I know it's a lot to look at, but there is a way to figure this out. So what we're seeing here is parahysian pacing. We're pacing here and capture the His bundle. Here we don't capture the His bundle. We know that for two reasons. One, in this case, the QRS is narrow relative to here, so we've lost His capture in this case, gained His capture here. Second, we can actually see the His bundle recording here. So when we capture the His bundle, it gets pulled into the pacing stimulus and you lose it. When we lose it, it jumps out from the pacing stimulus and it's now retrograde. So the His here is a retrograde His, and it's clearly evident on this catheter when we lose direct capture. The first thing we need to figure out in the question answers is, are we capturing the atrium directly? It's one of the pitfalls of parahysian pacing. You don't want to capture the atrium directly because then you can't interpret retrograde conduction. In this case, we know we're not because the stem to A time in the coronary sinus is sufficiently long, more than 60 milliseconds, to suggest that we're conducting retrograde and not capturing the atrium directly. So that answers that part of the question. That eliminates that answer. Second, now that we know we're conducting retrograde, we want to look at a couple things. One is, does the atrial activation sequence remain the same when you gain and lose His capture? And is the atrial activation time change, or does it change? So here we can see there's a clear change in timing, at least in the high RA and the His. When we gain His capture, we have a shorter stem to A time than when we lose His capture. The His A jumps out, the high right atrium jumps out. We'd be suspicious that this is AV node conduction because when you get a change in activation time coincident with loss of His capture, in other words, you get an increase in it, then that is most frequently associated with AV node conduction. And in this case, that is true. However, there's also a change in atrial activation sequence. If it were purely over the AV node, this sequence should look the same as the sequence, and it does not. You can eyeball it and see that. Here, the His A and the CS procs are timed simultaneously. Here, the His A clearly precedes the CS. So there are two activation sequences and a change in time. That would indicate there are two pathways retrograde. The most likely explanation for that is fusion over an accessory pathway and the AV node. And we can kind of see evidence of that when we throw down some calipers. So when we look at the stem A time to the proximal coronary sinus in this blue caliper, we can see it's 115 milliseconds. The blue caliper here with loss of His capture shows the same timing. So the timing with and without His capture in the coronary sinus is fixed. The timing in the His A and high right atrium is not. So when we lose His capture, we go from nearly 90 milliseconds to about 117 milliseconds at the His A. So there's clearly fusion between two pathways. There's two activation sequences. And the fact that there's a fixed time here suggests there's both accessory pathway conduction and AV nodal conduction. So it's a little confusing, but if you put together all your bits of knowledge you've gained in this course, you should be able to figure this one out. All right. Obviously, you can go back and read my explanation as well. And you can just pause on that particular slide. And I'll give you a chance. There's the slide. So you can pause on that to read my explanation. So case three, the following tracings show a long RP tachycardia at onset and following ventricular pacing 20 milliseconds faster than the tachycardia cycling. PVC's time to occur when the His bundles refractory did not affect the tachycardia. This is not shown. What is the most likely mechanism? Atrial tachycardia, junctional tachycardia, atypical AV node re-entry, or ORT using a slowly conducting post-receptal accessory pathway. Let's look at the tracings. Here's the onset of tachycardia. Here, P waves, P waves, tachycardia begins. There's ventricular pacing. And as we've said here, the pacing was 20 milliseconds faster than the tachycardia. So we overdrive pace it. So tachycardia is 580, ventricular pacing is 560. And we look at this response. If we look at this particular tracing and don't do measurements, we'd be very tempted to say this is atrial tachycardia. Because number one, it begins with an A that looks the same as the next day and it didn't get triggered by a PAC. Most of the time, the PAC would look different than the SVT. In this case, it just starts right up. That would be consistent with atrial tach. And then if you eyeball this, you'd say VA, A, V. But you really need to do the measurements to sort this out. Because this is more likely to be atypical AV node re-entry. Here's the full explanation. You can read it. Pause on it. But I'll also explain here while looking at the tracing. So what we have here is not a VA, AV. But when you actually do the measurements, you can see that this is the key interval. This interval is at the pace cycle rate, not the tachycardia cycling. And now we know how to interpret the VAV response. We know this V drives that A. We know this V drives that A. So now we can call it a VAV response. We can actually see, I think, that there's also a retrograde hiss here when we overdrive pace, which is going to be necessary to get into an AV and RT circuit. For a slowly conducting accessory pathway, we might expect, number one, that the hiss would be driven orthodromically, which it's not here. This HH interval is clearly much longer than the tachycardia, so it's driven retrograde. So that's one piece of evidence against the slowly conducting. The other piece was something that we don't show in the tracing, but the PVCs timed to be hiss refractory had no effect on the tachycardia. In addition, the post pacing interval is very long. The VA stim A is very long. So again, with a decremental pathway, these could be long, but in the absence of affecting the tachycardia with hiss refractory PVCs, not a likely answer. Junctional tachycardia would not expect to have this relationship with the A's to the V's. It would be timed closely to the V or slightly after. So that gives you the answer there. Let's move to case four. Case four. So this is a 68-year-old man with a prior inferior wall myocardial infarction. He presents with dyspnea and palpitations. Baseline ECG is shown in figure one and presenting ECG in figure two. Which of the following statements is most likely to be true? The presenting rhythm is bundle branch re-entry VT. The presenting rhythm is superventricular tachycardia. Presenting rhythm is idiopathic vesicular VT. Presenting rhythm is ventricular tachycardia associated with inferior wall myocardial infarction. The patient has alternating bundle branch block and should be scheduled for a pacemaker. Here's the first tracing. And the second tracing. You can pause on that to look at it more carefully and that to look at it more carefully. And the best answer, I believe, is the presenting rhythm is ventricular tachycardia associated with inferior wall myocardial infarction. And what is the basis for saying that? Well, number one, the baseline ECG shows sinus rhythm with PR prolongation and left bundle branch block. So if the patient were having superventricular tachycardia of any form, one would expect left bundle branch block. That would be the typical scenario. And one would not expect an SVT to have a narrower QRS than the baseline left bundle branch block. So even if someone had alternating bundles, which would be very unusual to have left bundle branch block at baseline and then have SVT with right bundle branch block would be a real rarity. I don't think I've ever seen it, for instance. I think it puts it into the category of very rare. So here we have tachycardia and it's a right bundle morphology. It has a superior axis and it's narrow. So how do you get a narrower QRS during tachycardia than during SVT? Well, if you have a prior infar-wall myocardial infarction and the exit site is near the hysperkinesis system, you can engage that hysperkinesis system early and create a narrower QRS than the baseline. This is sort of the basis for left bundle area pacing. When we go and look at trying to correct left bundle branch block, we screw a lead in near the posterior fascicle in left bundle area pacing, and we might get an EKG that looks something like this. Now, VT circuit can also exit near there and produce a similar thing. Now, whenever you see narrower tachycardia than baseline bundle branch block, that's likely, highly likely to be VT. And we know he has an inferior wall myocardial infarction. The pattern is consistent with that sort of a basal infraceptal exit to that ventricular tachycardia. So I think we've answered that question pretty clearly. bundle branch re-entry would not be expected to have a narrower QRS than baseline. Idiopathic vesicular VT is certainly an option, but you have to look at this patient's substrate prior inferior wall myocardial infarction, so it's much more likely to be associated with that. And the pattern on QRS morphology is also consistent with that. This is not alternating bundle branch block, so that part is a distractor. And again, I'll let you pause on the explanation if you want to read it. And thank you. Workshop number two. These are my disclosures. Case one, pacing from the ablation catheter is performed in an apical LV infarct. Based on the tracing, which of the following is the most likely relation of the pacing site to the VT? Is it in a re-entry circuit isthmus, in an outer loop, in a bystander area, or it cannot be determined? Here is the tracing. And you can pause your video and look at this and then select your answer. So the answer is A, in a re-entry circuit isthmus. So this tracing shows ventricular tachycardia with the surface leads and then the intracardiac recordings, as you see. The first stimulus occurs during the QRS. And then there's a pause where one would have expected the next QRS complex of the VT. And after that pause, there's resumption of a wide beat that could be a paced beat with a clearly different morphology. So it appears that tachycardia has terminated and then we have pacing at the site. But the first stimulated beat doesn't appear to have captured. And this is a well-known phenomena. And what's happening is you're pacing at a site in the re-entry circuit and the stimulus actually does capture. But the stimulated antidromic wavefront is contained by returning orthodromic wavefronts. And in the orthodromic direction in the circuit, the wavefront blocks. So that terminates the tachycardia without the stimulus creating a wavefront that propagates to the surrounding myocardium. So this is so-called termination without global capture. And it's very specific for pacing at a site in the re-entry circuit isthmus. Case 2. Pacing is performed from the ablation catheter in an LV infarct scar. For ablation to target the VT exit, which one of the following should be done next? A, ablate at this pacing site. B, terminate VT and pacemap. C, move the catheter more superiorly or cranially in the infarct region. D, move the catheter more inferiorly in the infarct region. Here is the tracing. And you can pause your video and analyze this and select your answer. The correct answer is to move the catheter more inferiorly in the infarct region. Answer D. So here we have ventricular tachycardia. And the last two stimuli of a pacing train are shown. These stimuli advance the QRS complexes and the electrograms to the pacing rate. There is a change in the QRS morphology during pacing as compared to the ventricular tachycardia. Also entrainment with fusion. The post-pacing interval measured to this electrogram is 710 milliseconds, much longer than the tachycardia cycle length of 580 milliseconds. So this is a bystander site that's outside the reentry circuit. Now which way do we need to move in order to get closer to the reentry circuit exit? And for that, we can compare the QRS morphology during pacing with the QRS morphology of the tachycardia. And you see that during pacing, the QRS in lead 2 has a positive monophasic R wave in 2 and 3, whereas during the tachycardia, the QRS complex is isoelectric to negative. So we have to move lower in the heart to get closer to the exit where pacing would more closely resemble the QRS morphology. Case 3, pacing is performed in a ventricular scar region during VT. Which one of the following is the most likely relation of the pacing site to the reentry circuit? A, at the exit, B, in the circuit proximal to the exit, C, remote from the VT circuit, or D, cannot be determined. Here is the tracing for you to analyze and pause your video and then select your answer. So the correct answer is C, remote from the VT circuit. And here we have the analysis. So ventricular tachycardia with a cycle length of 420 milliseconds is present. And you see the last two stimuli of a pacing train pacing at 390 milliseconds. Pacing accelerates the QRS complexes to the paced cycle length. The last QRS which is accelerated to the paced cycle length is this one, after quite a long delay of 380 milliseconds. If we take that stimulus to QRS interval of 380 milliseconds and go forward to a site where we can see a good electrogram recording on the ablation catheter to distal electrodes and go backwards from the onset of the QRS, 380 milliseconds, it lands at this point in time which is well before any inscribed electrogram. That difference is reflective of the difference in conduction time going from the pacing site out through the exit compared to the time that the exit is activated relative to the wavefront of the tachycardia circuit reaching that site. So those are different. And that indicates this site is not in the reentry circuit. If we consider the post-pacing interval, which is difficult to see due to the recording amplifier here being saturated by pacing, if we look at this signal, well, that's 540 milliseconds after the last pace stimulus. And it doesn't appear that there's anything before that in the adjacent bipole. So this is a site which is outside of the reentry circuit, even though there's entrainment with minimal change in the QRS morphology. These are so-called adjacent bystander sites. You can have a long conduction time between the pacing site and the reentry circuit when you're in SCAR, but yet the wavefronts are not able to reach the surrounding myocardium via paths other than those which are closely associated with the reentry circuit. Case 4. Pacing is performed from the ablation catheter in a ventricular SCAR region during VT. Which one of the following is the most likely relation of the pacing site to the reentry circuit? A, outside the circuit, B, in the circuit isthmus proximal to the exit, C, remote from the VT circuit, or D, cannot be determined? And here is the tracing for you to pause the video and analyze. And then select your answer. The answer is B. This site is in the reentry circuit isthmus proximal to the exit. So we have ventricular tachycardia, a cycle length that's oscillating a little bit between 480 and 500 milliseconds, but relatively stable. The last two stimuli of a pacing train at a cycle length of 470 milliseconds. The pacing accelerates the QRS complexes to the paced cycle length, and all of the electrograms as well are accelerated to the paced cycle length. When we come off of pacing, the interval at one tachycardia cycle length, 490 milliseconds approximately, would land here on this electrogram. And we can see that during pacing, we cannot see this electrogram, so it could be captured. We do see this signal during pacing, so this is a far field electrogram, and we don't use that to measure the post-pacing interval. The stimulus to QRS interval is 150 milliseconds. And since we have entrainment with concealed fusion, we can compare that to the electrogram to QRS interval during tachycardia. And you see that that also agrees with pretty much the same point as identified by assessment of the post-pacing interval. So the conduction time from activation at this site until the wavefront reaches the exit from the reentry circuit is about 150 milliseconds, and agrees with the electrogram to QRS interval. These findings are all consistent with a site in the reentry circuit isthmus, 150 milliseconds proximal to the exit. And this is a schematic that indicates what's happening. So here we have our reentry circuit on the left. We're pacing at a site in this isthmus. With the last paced stimulus that captures, we have a wavefront that propagates through the circuit and returns to the pacing site. That's our post-pacing interval, which equals the revolution time through the circuit, which is the tachycardia cycle length. During pacing, the stimulus to QRS interval equals the conduction time from the pacing site out to the exit, and matches the electrogram to QRS interval. Case 5, VT ablation is performed in a 70-year-old male with prior anterior wall myocardial infarction. Pace mapping from the LV mapping catheter is performed during sinus rhythm. The QRS morphology of the induced VT is shown in the second figure. Which of the following best describes the pacing site relation to the VT circuit? A, remote from the VT circuit, B, in the VT circuit isthmus, C, a bystander site, D, cannot be determined. And here are the two figures. On the left, the first figure, which is pacing in the scar during sinus rhythm, and on the right, the 12-lead EKG of the VT. You can pause your video, make your selection. So the answer is D, cannot be determined. So what's happening with pacing in this scar? You see that the paced QRS morphology is very different than the morphology of the VT. If, for example, you consider lead V2 here during pacing, it's a tall monophasic R-wave. But during VT, it's an RS complex, so very different. So is it possible that this pacing site could be in the VT circuit, even though the pace map is very different? Well, it actually can be in the VT circuit. And in fact, pacing at this site, you may get entrainment with concealed fusion during VT because during VT, the wavefronts may be constrained by the returning orthodromic wavefronts. But when you pace in the absence of VT during sinus rhythm, as shown in the bottom right schematic, now the stimulated wavefronts can exit the scar from paths that were not available to them during the VT. And you get a very different QRS morphology. So in scar-related VT, the pace map that resembles the VT occurs when you're pacing somewhere near the exit. You can be in the reentry circuit at good sites for ablation and have a pace map QRS morphology that is very different from that of the VT. So a paced QRS that looks different than the VT does not exclude the possibility that that site is critical to reentry for that VT. And this shows you what we observed when we paced during VT at that same site. We have entrainment with concealed fusion with a post-pacing interval that matches the tachycardia cycle length. You can see that this part of the electrogram is a far-field signal, and there's a little low-amplitude signal at the end, which is what we measured the post-pacing interval to in this case. Case 6, catheter ablation is performed in a middle-aged male with non-ischemic dilated cardiomyopathy and recurrent VT. The endocardial bipolar voltage map with color scale purple being greater than 1.2 millivolts and pacing from the site of earliest endocardial activation is shown in figure 6.1. Which of the following is most likely to lead to abolition of this VT? A, ablation at this site, B, substrate ablation of the entire low-voltage scar area, C, epicardial mapping and ablation, or D, recording right bundle branch activation? So here is the tracing on the left and the voltage map on the right with the pacing site indicated by the arrow. And the voltage map is a posterior view of the left ventricle with the mitral valve indicated here, the aortic valve ring indicated here. And pause the video and select your answer. So the answer is C, epicardial mapping and ablation. So the voltage map is consistent with an area of inferior wall infarct. And we're pacing from in this region. And pacing advances the QRS complexes to the paced cycle length. And the post-pacing interval is about 530 milliseconds. It equals the tachycardia cycle length. However, the stem to QRS is very short. And there's a subtle change in the QRS morphology. If you look at V3 here, you can see that these notches are not quite the same. Similarly, in V4 and V5, just a little subtle difference. So this is consistent with pacing just outside the reentry circuit exit in an outer loop. And that fits with this timing of electrical activation being just after the onset of the QRS complex. Now we're told that this is the earliest endocardial activation site. And we're not in the reentry circuit at that site. There's no other diastolic activity site that was identified if this is the earliest site. So it's likely that we're going to have to go to another surface, to the epicardial surface. An intramural circuit is also possible. And this is what epicardial mapping looked like in that patient. So on the left, you have the epicardial voltage map. And you can see that the extent of low voltage was greater in the epicardium. And this was a VT that allowed for activation mapping. So on the right, you have the activation map. And I will play the video. And you'll see that this is a figure-eight type of reentry with an isthmus and then a wavefront breaking out from the exit region and revolving in both directions. So although endocardial activation looked relatively focal, and there was a point of early activation that was close to the circuit, the entire circuit was really out in the epicardium. And you could entrain the tachycardia from the reentry circuit isthmus out here. And this is an example of that. We have entrainment with concealed fusion, a longish stimulus-to-QRS interval which matches the electrogram-to-QRS interval. The signal is very low amplitude. So it's difficult to know. You could certainly argue about what is a local electrogram here. But you can see that in pacing, we're able to capture. So there certainly is some viable myocardium beneath the site. And ablation abolished tachycardia. Case 7. Entrainment is performed during LV mapping of VT in a 76-year-old male with prior anterior wall myocardial infarction and incessant VT. Which of the following is the most reasonable next step? A, ablate at this site. B, terminate tachycardia and assess sinus rhythm electrograms to guide ablation. C, reposition the catheter and continue mapping during VT. D, move the mapping catheter to the right ventricle for mapping. Here is the tracing. You can pause the video and analyze this and then select your answer. Correct answer is C, reposition the catheter and continue mapping during VT. So we have monomorphic VT and the last three stimuli of a pacing train. And the first step in analyzing any pacing maneuvers during VT is to assess whether you're capturing, whether capture is stable. And you can see that there is a variable interval here between the electrograms and the stimulus artifact. So in fact, the stimulus is marching through and not reliably capturing. So we cannot tell anything about the relationship of the pacing site to the reentry circuit. We simply may not be in contact or we may be in contact over an area that's dense fibrosis. Case 8, a 74-year-old male with prior myocardial infarction and recurrent ventricular tachycardia is referred for catheter ablation. During endocardial catheter mapping, the tracing shown is recorded. Tracing to entrain tachycardia from the ablation catheter at this site is most likely to reveal which one of the following, A, a post-pacing interval that equals the tachycardia cycle length, B, the VT exit site, C, a VT outer loop site, or D, an indeterminate response to entrainment. Here is the tracing, and you can pause the video and analyze this and select your answer. So the correct answer is D, an indeterminate response to entrainment. And the reason is that the VT cycle length is very unstable. You can see that it's oscillating quite dramatically from beat to beat to beat, even though the QRS morphology is really quite stable. So this is a re-entry circuit where either the re-entry path is changing or the conduction velocity is changing. And in that situation, the post-pacing interval is not a reliable indication of the relationship between the pacing site and the re-entry circuit. Thank you. For more information, visit www.ncbi.nlm.nih.gov

ventricular tachycardia

pacing maneuvers

electrophysiological study

reentry circuit

pacing site

bystander site

VT circuit

ablation targets

entrainment

unstable VT cycle length