And I'm going to move forward and introduce the video from last year of Dr. Sam Asravatham. Very fortunate to have him. He's a fixture in this meeting and rightfully so. And he's going to start, we're going to give his talk and then he'll join us for live Q&A right after talking about fundamental EP maneuvers. If we can start that video up, then we'll remain right on time. Thank you. My job is to give you a little bit of taste of the physiology, the physiology foundation, and we'll try to get it all together with anatomy in our evening session. So physiology goes by a synonym in our field. It's called maneuvers. So if you hear this word maneuver, what it is, is you have some kind of arrhythmia, circuit, substrate that you have to perturb in some way, do something. And that something is often pacing, stimulation. And you do that, disturb it, analyze the consequence of what you did. And from your analysis can make very precise judgments of what the arrhythmia is and often where you need to ablate. It's truly the most fascinating field you hear from fellows all the time. When you do it for the first time with an unknown arrhythmia, you do the maneuver, you came to a diagnosis and you were successful. Every time I've seen that look in a trainee's eyes, boy, am I glad I chose this field. That's the time it happens. That's the time it happens. Now there's tons of maneuvers. And one of the things I tell our fellows is if you haven't invented or discovered three maneuvers yourself during your training, you haven't been paying attention. So it's really an infinite number because it's just physiology. It's different takes on physiology. And I'm going to give you just some of the key maneuvers. One of the big ones you'll hear over and over again is you have a narrow complex tachycardia and you pace, you stimulate to mimic a PVC, placing a PVC during tachycardia to try to identify the mechanism of the arrhythmia, PVCs during tachycardia. General rule of thumb, if you have a narrow complex tachycardia and you're not sure what it is, a single PVC will almost always give you a diagnosis. If you have a wide complex tachycardia and you don't know what it is, a single PAC will give you a diagnosis and you should work towards that level of expertise. So what's the idea? So the idea, and you'll hear a lot of terms like pre-excitation index, his refractory PVCs. The idea is if you put a PVC during a tachycardia, you're trying to guess that ventricular beat, how did it get to the atrium? Did it go through the AV node or did it go through an accessory pathway? That's your job. And one of the ways is in a tachycardia like AV node reentry, it's harder for putting in a PVC to get to the atrium. So here you have a narrow complex tachycardia, you place a PVC and then you notice this next atrial electrogram came earlier than it was supposed to. So somehow what you did in the ventricle got to the atrium. Question is, how did it get there? Is it through a pathway or the AV node? Now if it's AVNRT, that AV node is engaged, it's conducting down the AV node and you're fighting from the ventricle to climb back up, it's harder. You have to have a closer coupled PVC, you have to pace faster, it's more difficult. But if you have an accessory pathway conducting retrograde, you pace the V, you easily can climb up that pathway and get to the atrium. So a lot of the maneuvers use this little difference to try and tell you what it is. And you have various systems, indices, numbers to memorize. And what I encourage you is ignore most of things that require memorization of specific numbers. Try to understand the physiology and the signals that you're seeing. That will never fail you. There won't be an exception to just the physiology. So let me give you an example. So here, let's try to figure out what this tachycardia is. So here you see a narrow complex tachycardia. From the ECG diagnosis, you'll say, well, probably some reentrant SVT. But we have to be more specific than that. We have to say, is this a pathway? Is this AVNRT? Is this an atrial tachycardia? This kind of mantra of which of these three it is, you'll repeat over and over and over again in your career. So how do you do that? Well, you have some recordings. You see a HISS bundle electrogram. You see ventricular electrogram. You can always tell the ventricular electrograms because they line up with the QRS. And then you have the atrial electrogram. So we kind of follow it in our mind. We have an atrial electrogram. So that's like a P wave. Gets to the HISS, gets to the V, comes back to the atrium. How did it come back to the atrium? Was it just another atrial tachycardia beat? Was this AV node reentry creating the circuit? Or did it climb up through an accessory pathway? Now you place a PVC. Now this PVC is going to perturb the circuit. And how you know it did that is look at the cycle length, the rate at which you see the atrial electrograms. The cycle length is shorter. That means this A came in earlier than expected. Because of something you did in the ventricle, the A came in earlier. Now what you notice about this PVC is when it was placed, the HISS bundle electrogram was already getting inscribed. Think about that. The HISS bundle is below the AV node. You paste the ventricle. If the HISS already occurred, then if you've come down the AV node and reached the HISS, golden rule of EP, you can't climb up what you just climbed down. So if you just came down to the HISS and you paste the V and you cannot climb up the HISS, how did you get to the A? No mystery. It's an accessory pathway. Make sense? Now if you did climb up to the atrium, now what you'd like to see is, well, I came up quick to the atrium. Look, that next A to HISS is longer. The next HISS to V, the next A to V is changed. By coming up that pathway, I've perturbed the circuit going forward. And we call that resetting the tachycardia. So if I say this in EP lingo, I'll say a PVC placed at the time of HISS bundle refractoriness pre-excited the atrium without a change in the activation sequence and reset the tachycardia. That's just EP speak for saying we have an accessory pathway and the mechanism of this tachycardia is down the AV node, up the pathway. And if I ablate this pathway, then this tachycardia will no longer exist. Make sense? A word about where to pace when you put in the PVC. So here's a little correlation with anatomy. Often you'll see PVCs are placed from near the apex, just for whatever reason. Now when you put a PVC from the apex, it's very hard to know when the HISS bundle is getting recorded. So think about it. If I'm recording by the HISS bundle and I put in a PVC, I have a ventricular activation sequence that climbs up towards the HISS. I also sneak into the right bundle and climb up the conduction system to record the actual HISS bundle. So the HISS bundle recording and the surrounding ventricle get activated about the same time. When stuff gets activated about the same time, that's the enemy. Because then you obscure signals and you're guessing, oh this is HISS because it looks like it. And someone else says no, this is the HISS. But if they're separate, there's no guesswork. So one of the skills in the EP lab is to separate, find maneuvers that separate out interest electrograms. And you'll hear a lot about this, including some very nice examples with Dr. Jackman later through the course. Here's an example of how you can separate it out. You could probably figure this out. Well if I pace from the apex and have two wavefronts at the same time, how about if I just pace from the base? If you pace from the base, the ventricular electrogram of that surrounding ventricular tissue gets inscribed right away. But here's the trick with anatomy is the HISS bundle is insulated. It has a fibrous sleeve. So to actually get from here, ventricular activation, to the HISS bundle, you just can't jump across that insulation. You have to climb down until you have the entrance of the right bundle where the insulation breaks apart and then climb backward towards the HISS to inscribe that signal clearly separate. Now you can see the HISS. If you see the HISS and you put in a PVC, it becomes a piece of cake to say, did I get to the A through the HISS or did I get to the A even though the HISS was just on time? Makes sense? Makes life much easier than memorizing a bunch of numbers. So here's an example here. PVC placed. You see the HISS. You just measure HISS to HISS to HISS. It's all on time. A to A to A. The A comes earlier. And if you make that diagnosis, you say, I pre-excited the A more than I pre-excited the HISS. That's EP speak for saying I did not come up through the AV node. If it isn't the AV node, it's an accessory pathway. Makes sense? Now here's an even more compelling finding. Another rule in EP. Whenever you learn a maneuver which relies on pre-exciting. Pre-exciting means getting to a distant site quicker than the natural tachycardia. You should always remember there will be an opposite phenomenon. By placing a PVC or a PAC, you delay or block some critical limb of the circuit. That's equally important, if not more important, to realize the physiology of what you're observing. For example, you have a tachycardia. Same thing. You have HISS, V, A, HISS, V. So kind of P wave, got down to the HISS, then got to the V. Now you place a PVC and look, I can see the HISS to HISS to HISS is the same time. I didn't touch the HISS, but this PVC stopped the tachycardia and there's no more the next atrial electrogram. Think about that. A PVC stopped tachycardia. A narrow complex tachycardia was stopped by a PVC. The easy way to do that is just go climb up the AV node, make it refractory, and then you'll stop a bunch of tachycardias. AVNRT, atypical AVNRT, pathway related tachycardia because AV node is needed for all of those. But the HISS is on time. HISS is on time means there's no way that this ventricular PVC got to the AV node because the HISS, which is between the AV node and where I'm pacing from, was already engaged. Make sense? It was already activated. You cannot climb up what you just climbed down. So how did this tachycardia stop? It had to affect a limb of the tachycardia that wasn't the AV node. If it isn't the AV node, it's an accessory pathway. So some pathways don't like to be stimulated and pre-excited. If you try to push them, they'll just block. They'll delay. And if you recognize this, you have a diagnosis. There's a pathway. And then you get into the job of mapping, looking at bipolar, unipolar activation sequence, and finding where that pathway is to ablate it. Make sense? Now, if I talk to any of you, you know, maybe 15, 20 years later, actually, I might be vacationing somewhere at that time. But if I do and I ask you, tell me about your tough SVT cases. And I would bet you your top three SVT tough cases from every single person in this room who's starting EP fellowship in July will have an EKG that looks like this. So one of the places where you're tested on your maneuver physiology skills is the long RP tachycardia, where the P wave comes closer to the subsequent QRS. This could be an atrial tachycardia. It could be a pathway-related tachycardia, but just a long conduction time. It could be AV node reentry, where it just so happens, getting back to the atrium from a common point in the circuit takes a long time. It's in these type of cases where you won't see the pre-excitation. When you put in the PVC, his bundle already inscribed PVC stops tachycardia. That's a pathway. And if that pathway can be ablated, this person won't get the tachycardia. Many times, why this is difficult is someone kept waiting to look for the pre-excitation, pulling it in. And hours and hours, they keep trying and then wind up saying, I'm not really sure what this is. Josh, I had a couple of questions. Just for clarification. One question that came up was about the concept of resetting. And the question was, what does resetting mean? Does that not mean that the tachycardia cycle length changes subsequent to the PVC that you put in? So reset. So what does reset mean? So this is not just for narrow tachycardia. It can be for wide tachycardia. It can be for a variety of arrhythmias. So if you have a tachycardia, let's say it's a narrow complex tachycardia, and you put in a PVC. When you put in this PVC, you notice the next atrium came in early. And your first job was to figure out was that through the AV node or through a pathway. And the way you did that is by looking at the His bundle electrogram. Now, when you came up early to the A, if this tachycardia was a tachycardia, ORT, down the AV node, up the pathway. Orthodromic reciprocating tachycardia. Down the AV node, up the pathway. Down the AV node, up the pathway. I put in the PVC. I came in early to the A. That A is going to stress the AV node. It's either going to come quicker to the V, or it'll delay in the AV node and come a little later to the V. But what it tells you is by changing the A, you did something to the next component in the circuit. That's absolute evidence that that pathway you discovered is actually responsible for the tachycardia. Now, you'll say, well, how can you have a pathway that you diagnosed and it isn't responsible for the tachycardia? So Josh used a term there in his talk. He talked about a concept of bystander. Bystander means some pathology, something abnormal exists, but it actually isn't responsible for the tachycardia. So think, one out of every 10,000 live male births is born with an accessory pathway. The folks who are born with the accessory pathway can get pathway-mediated tachycardia, but they're not immune from other tachycardias. If they run, they'll get sinus tachycardia. They could get AV node reentry. They could get an atrial tachycardia. So those folks, the pathway serves as a bystander. It's there, but it isn't responsible for the tachycardia. So in those cases, your PVC maneuver will make the next A come early because you climbed up the pathway to get to the atrium, but it will not reset the tachycardia. The rest of the circuit will just be doing its own thing based on its primary determinant, either AVNRT or atrial tach or sinus tach like that. That is a skill in EP is we have to first understand normal physiology and then we understand how to recognize pathology. But when we recognize pathology, we don't always jump straight away and ablate it. We like to see that there's something good going to happen by ablating this pathology. With pathways, it's not so relevant because if you find a pathway, most of the time, you will ablate it. But the concept of bystander is very important because it shows up in a bunch of other arrhythmias like some types of ablation for ventricular tachycardia where you have to pick your spots. You're just too much to ablate, too much risk if you ablate every single piece of pathology that you find. For example, a challenge for your generation, chronic atrial fibrillation. I would challenge you, a person who's had atrial fibrillation for more than 10 years in a persistent pattern, find me some spot in their atrium that's not pathology. It'll be abnormal. If you don't believe me, send it to me and I'll show you why it's abnormal. That could be histology, it could be an EP tracing, I don't care. How are you going to ablate that whole thing? You can't. So you have to kind of pick your spots. And that's one of the things that you'll learn is diagnosing bystanders versus actual pathology. And one of the concepts that helps us with that is this concept of resetting a tachycardia. But this is a shortcut. Here, if we delay the next atrium, or if we terminate tachycardia by somewhere blocking in that accessory pathway, how do we know we blocked in the pathway? Because the hiss was on time. We did not climb up through the AV node. Here, we don't need to look for reset. Think about that. If you had an AV node re-entry that was going at 200 beats a minute, and you happen to have an accessory pathway, and I put in a PVC and I delay going up that pathway, I come later or I block in the pathway, the AV node re-entry is not going to care. It will still keep doing its own thing. So the fact that you delay or block, that's proof that this pathway is part of the tachycardia. But if you pre-excite, if you come in earlier, you just might be going faster, getting in earlier than the tachycardia. So that one beat may be quicker, but then you don't reset. You just come right back to the same tachycardia. Make sense? Here's another rule about EP that all rules have exceptions and all exceptions have exceptions and that's part of the fun of EP and maybe just for fun when we do the anatomy talk, I'll show you some exceptions to these rules. But the way that you learn those is you first got to have the rule down. You've got to understand the physiology. Zero memorization, it's picturing in your mind and understanding what this is and pretty much you can learn to anticipate some of the exceptions. That's been among the most pleasurable things in my own career is just the thought experiments, is to think what could happen and then you have a case where it actually happens. You just recognize it a little quicker, but that comes from foundation, that comes from understanding the normal physiology. So if I kind of summarize this maneuver, you have a PVC that you're placing in SVT. So think about SVT, narrow complex tachycardia, it's like a black box and you don't know what the circuit is, you're going to perturb it. And the way you'll perturb a narrow QRS tachycardia, high yield, is to put in a PVC. First thing you'll want to know is, did I capture the ventricle? To do anything, after your pacing spike, you've got to see a paced QRS morphology. Then I see, did I get to the atrium? If that PVC get me earlier to the atrium. Now I have to see, did the activation sequence change? Here's another rule in EP. When you do a maneuver, if the sequence of activation, that means where's the first early spot, the late spot, the pattern that Josh showed in that tracing in the CS, coronary sinus, if the activation changes as a result of a maneuver, more than one thing is going on. There's two different ways to get from point A to point B. So when you do the maneuver, you favored one of them over the other. In tachycardia, one was favored over the other. So how you figure that out is the activation sequence change. Some other spot is a little earlier, some other spot is a little bit later. So whenever you see activation sequence change with a maneuver and tachycardia still continues, immediately tell yourself, there's two things here, AV node and pathway, two pathways, three pathways, something like that. Now, if the activation sequence is unchanged, that means I have only one thing I need to diagnose. It's either AV node or it's a pathway. So I look at the retrograde HISS. Is that HISS activated? If that HISS is still on time, it's not advanced, that's an accessory pathway. From V, I got to A, the HISS being on time excludes the AV node. I cannot get to the AV node except through the HISS. Make sense? So then that's an accessory pathway. This is also true if you did advance the HISS, but the amount you advance the HISS is less than the amount you advance the A. So if I did see, I put in a PVC, well, that HISS came in early by 5 milliseconds, but the next A came in by 40 milliseconds. How can that happen? If I'm going through the HISS, that's going to determine how much I can pull in that next A. And in fact, this is probably more important, more common that you'll have to make this call of, did I advance the HISS more or the A more? For that, you got to see the A, you got to see the HISS. How do you see the A? Thousand electrodes in the atrium. You saw many examples there, duo, deca, some halo, all kinds of stuff that you heard some terms about. All are in the atrium. But how do you see the HISS? You have only that HISS bundle recording catheter and you put the PVC near the base so that you have your best chance of seeing that retrograde HISS. Then you say, did I reset the tachycardia? If you did, this is orthodromic reciprocating tachycardia, a narrow complex form of A-V reciprocating tachycardia. But if I didn't reset it, that's how I diagnose a bystander, exists but has nothing to do with the tachycardia. And you still have to figure out what that tachycardia is. Now the next thing you look at is, well, what if I did advance the retrograde HISS and that's the only way I could advance the A. If I advance the HISS retrograde by 20 milliseconds, I advance the retrograde A by 20 milliseconds. What does that tell you? The V to get to the A cares about the HISS. And why would it care about the HISS? Because the way it's climbing up to the A is through the A-V node. Make sense? So narrow complex tachycardia climbing up through the A-V node, not through the pathway is A-VNRT. And little nuance here is in a form of A-V node reentry which is common, the typical form of A-V node reentry, it's very easy. As soon as you climb up to the HISS and you pull in the HISS even 10 milliseconds, you'll pull in the A. But in atypical A-VNRT, you have to do a lot to the HISS. It's not easy. Sometimes 30, 40, 50, I have an example of 60 milliseconds you have to pull in the HISS to get to the A. It's just a little nuance to keep in mind between those two. Then you say, I pulled in the HISS like crazy, 70 milliseconds, and I cannot get to the A. And this tachycardia is just going on and on and on in the same way it always was. What does that tell you about the diagnosis? No pathway and it's not through the A-V node. So what's remaining of our big three? Atrial tachycardia. So that's kind of a positive diagnosis in the sense that you actually are looking by saying that even though I saw my HISS move in by this much, I couldn't do anything to the A. It's an atrial tachycardia. And always, you remember one of the golden rules, if activation sequence changes, more than one thing, real and bystander, fusion, two things, three things are going on there. Now I think what I'll do is just to give you a kind of corollary to this maneuver, I'm going to talk to you about something that I hope you'll do a lot in the EP Lab, parahysian pacing. This will reinforce some of the physiology of this. What's the difference here? PVC in tachycardia is perturbing the circuit during tachycardia. So you've induced tachycardia and now you know and you would have mastered it. If I wake you up tonight in your jail room, as soon as you get up, you'll say PVC placed during tachycardia at the time of HISS bundle refractoriness, pre-excited the next day without changing the activation sequence and reset the tachycardia, that's ORT. I'll bet you you'll say that. But the problem is sometimes when you induce tachycardia, patient doesn't tolerate it very well. They get like hypotensive. It might be non-sustained tachycardia, hard to do the maneuver. Sometimes tachycardias wobble. What the wobble is, is sometimes the rate isn't fixed because tachycardia circuits have multiple components that are accommodating each other. So sometimes they wobble. For an EP fellow in their first day of the EP lab, wobble is your enemy. You don't like this wobble because, wait, how do I do this maneuver? I can't say if I pre-excited or post-excited because the tachycardia keeps changing its cycle length. After the first day, wobble will be your friend because you actually can analyze the wobble. What parts are wobbling? What came early? What came late? And you can make a diagnosis just from the wobble, 100%, even without putting in a PVC. But let's talk about that first day. So now you saw this wobble. You saw hypotension. Without the patient being in tachycardia, can I pace the ventricle and figure out whether I get from V to A through a pathway or through the AV node? Got that? So no tachycardia. Patient is just in sinus, but I'm going to pace the ventricle somehow faster than the sinus rate. And that ventricular pacing, maybe I see it climb up to the A, retrograde atrial activation. You've all seen it with PVCs during ECG. Sometimes pacing the V or a PVC will get to the A, retrograde conduction. Now you have to figure out, is that retrograde conduction through the AV node or is it through an accessory pathway? And there are some many, many ways to try to answer this question. But one of the best to learn early that will teach you about physiology, anatomy, all coming together is a maneuver called parahysian pacing. So parahysian pacing is a unique maneuver where you change the output of pacing. Think about that. When you pace, you can change the rate. That's obvious. You can change the location where you're pacing from. But there are a few maneuvers in the EP lab where you don't change where you pace from or the rate at which you pace. You change the output of pacing. How on earth is that going to be helpful? Well, here's the little piece of knowledge you need from anatomy to understand what makes this possible. And let me give a little alert while I'm doing this, is after I'm done explaining this, I want someone in this room, and I don't mean like Josh or somebody like that. It's someone who hasn't yet been in the EP lab to tell me an exception to where parahysian pacing won't work or can't work. Okay? So alert. Keep that. And there will be a prize for who gets this right. And we'll announce that prize when we do the anatomy dissection later today. So here's the premise. The His bundle is insulated. It's protected so that when sinus beats come down to the heart, to the ventricle, you don't activate the base initially. You activate closer to the apex. About two-thirds the distance to the apex. That's really good that that insulation exists. Because think about it. If you had to squeeze somebody's heart to get the blood out of their heart, where will you squeeze? Would you squeeze by the mitral annulus and tricuspid annulus? That's ridiculous, right? All the blood will get trapped in the ventricle. You'd squeeze from the apex upward. And the only reason our heart does that is because of this insulation. It allows this conduction to get closer to the apex, to start ventricular activation by insulating the proximal part of the conduction system. Now we use that in this maneuver. The idea is if you pace at low output, just enough to capture the ventricular myocardium, and your pacing site is close to the His bundle, parahysian pacing, pacing close to the His bundle, that low output isn't enough to capture the His bundle itself. It's shielding from the insulation is sufficient to prevent capture of the His bundle. Make sense? So at low output pacing, the only thing you're capturing is ventricular myocardium. Now what you do is crank up the output. You pace at high output, so high that now you breach that protecting insulation and directly capture the His bundle. Make sense? But there's no reason you'll stop capturing the muscle. The muscle is easy to capture. So low output you capture muscle. At high output you capture muscle and His bundle. And the key to this type of maneuver is you do something, you make a change, but there's a common element when you make the change and one element that's different. Here the common element is I capture ventricle. The not common element is only with high output pacing I capture the His. So then you say, who cares? Well, accessory pathways are pieces of muscle. If you capture the ventricular myocardium, that's enough to get to the accessory pathway and climb up to the atrium. But the AV node to conduct, it's going to care about whether you captured the His or not. Does that make sense as a construct? So how do we use that construct? Is we say, well, I'm going to pace at high output and low output. How do I know which one was the high output and which one was the low output? If I captured the His, I'm capturing the specialized conduction system. So the QRS will be narrower. So you just kind of glance at this and say, oh, here, this is capturing the ventricle and the His narrower QRS. Here I'm capturing only the ventricle, wider QRS. And then I see how long did it take that ventricular stimulation to climb up and get to the atrium? I'm measuring here from my pacing stimulus to the start of an atrial electrogram here on this catheter. And it took longer when I didn't capture the His. Think about that. It took longer when I didn't capture the His. Means what? It cares about His capture. And what will care about His capture? Accessory pathway or AV node conduction. Accessory pathway piece of muscle doesn't care whether you captured the His or not. But AV node, if you grab the His, then you're quicker to get through the AV node to the atrium. So this tells you that this patient has AV node as the method of climbing from A to V. Does that make sense? Now, on the other hand, sometimes we have some very odd kind of things that will happen in the EP lab where maneuvers like this will literally save the day for you. Yikes. But for example, after a couple of months in the EP lab, you see a tachycardia like this, you'll say, hey, the A and the V are all occurring together. The A and the V are occurring together. How does that happen? And you'll say that's AV node reentry. Because AV node reentry, the way that they're going to get together is AV node is in the center of the heart. If AV node is in the center of the heart, you get to the atrium and the ventricle at the same time. And that creates this A and V at the same time. So AV node reentry. But you'll also look at something that Josh pointed out is the sequence in the coronary sinus. The coronary sinus is placed between the LA and the LV. And some of the electrodes that are deep in the coronary sinus are recording the first atrial signal. So how is that possible? Atrial signal getting recorded somewhere in the middle of the coronary sinus. You'll say that must be an accessory pathway. AV node is in the center of the heart. If it's not in the center, it's out of the sides. It's got to be a pathway. So it's one of those moments in the EP lab where you'll ask yourself who is lying. One piece of information says got to be AV and RT. A and V are together. Another piece of information says that there must be an accessory pathway. So there you do this maneuver. And the idea is you can have all kinds of methods. And we look anatomically why this happens. That even when it's AV node activation, sometimes coronary sequences can be weird or funny. But you do parahysian pacing. So high output, low output. Can anybody tell me is this the low output paced beat or the high output paced beat? Compare it to this one. Very good. Wider, low output. Narrower, high output. And then I look the time it took to get there. When I did higher output, I got there quicker. Higher output, I got there quicker. Higher output, I breached the insulation of the hiss. Cares about the hiss. Cares about the hiss means AV node. So however weird that sequence looked, it's AV node dependent conduction. Another way other than just comparing do I have a wider or narrow beat is you can actually see is there's something that looks like a hiss. If I capture the hiss, narrower beat, it's hard to see that hiss bundle signal because it's part of that capturing paced beat artifact. If I can see it, it means it was released. So that can be also useful. Like look here. Forget looking at the QRS. Just look here and see if you can guess which is high and which is low output. This is the hiss bundle recording catheter. Here I don't see anything reliably like a hiss. Here I see it released. Why do I see the hiss? Because I didn't capture it. That's going to be my wider beat. And look, whether I captured the hiss or not, I got to the A at exactly the same time. Right? Exactly the same time. Means what? Capture hiss, don't capture hiss. But I still get to the A the same way. Doesn't care about the hiss. And what is it that doesn't care about the hiss? It's an accessory pathway. So this funny looking activation sequence is an accessory pathway. Make sense? Now, if you try to put this together, you have to start learning maneuvers with some maneuver. And I would urge you to master these two maneuvers first. That is PVCs during tachycardia. You'll do it a lot. The physiology is straightforward. Once you have it nicely, you'll get a diagnosis very easily. And the second is parahysian pacing because you don't change location or rate, which introduces a lot of vagaries of ventricular conduction, and it's a nice one. It's a little hard concept to get, but if you get it really well, some of the other maneuvers to make the same diagnosis will make it easier for you. So let's look at how some of those rules come together. So we did high and low output pacing. And we recognized because if I have a narrow QRS and I can't see the hiss, I've captured the hiss, that's my high output beat. That's my high output. The wider QRS, maybe I see that hiss released, that's my low output beat. And I compare the two. As always, you see, did the activation sequence change? Why do we look at that? Because if the activation sequence, the atrial activation, which electrode early, which late changes? Remember, two things are going on. There may be two pathways, pathway and AV node. But if the sequence doesn't change, you have only one diagnosis to make. It's either AV node that's responsible for VA conduction, or it's an accessory pathway. And then how do you make that change? You say, well, did by me going from high to low output and vice versa, did it get longer with the wider QRS? When I didn't capture the hiss, did it get longer? If it did take longer to get to the atrium, when I cannot capture the hiss, I'm not directly getting to the hiss. I have to go to the ventricle, climb up the hiss, and then come up to the atrium, that's AV node. If it doesn't care whether you capture the hiss or not, it's exactly the same time to get from V to A, that's an accessory pathway. Very straightforward diagnosis. But if the activation sequence changes, it means there are two things going on. Now, first couple of days in the EP lab, you're forgiven if you just say two things going on. But after that, you can actually figure out what those two things are. You look carefully at all the atrial electrograms and see which ones didn't change and which ones did. The ones that came later with the wide QRS, those areas of the atrium are activated via the AV node. The ones that didn't change, those areas are activated via the accessory pathway. So you not only can say there's fusion, but you'll get it. You have to make sure you're capturing, you have to watch out for some caveats, like did I capture the atrium by mistake rather than the hiss bundle that I'm trying to capture and release. And you'll learn how to do each of those. But if I summarize just physiology approach to maneuvers, you'll see from a very early stage that as you learn EP, you'll always be learning some element of each of these foundations. There'll be anatomy, there'll be physiology, there'll be the engineering, physics aspects. In maneuvers, in maneuvers, we are focusing on physiology. It's the fun part. It's the detective part of electrophysiology. So you have something, you don't know what it is, it's an unknown, and then you perturb it by doing something. We talked about one thing during tachycardia and one you can do when there isn't tachycardia. There are literally hundreds. These are common ones and good ones to start learning from. You put in the PVC, you see if it captures. The key is what did I do to the hiss? So you record the hiss, you strategically put your pacing catheter in the V at a site where it's easy to see the hiss, and you just make a very simple calculation. Was that hiss just coming on time? And when I put in this PVC, I got to the A earlier? If so, I have a pathway. And by doing that, did I reset, did I change the subsequent elements of this circuit? Make it earlier, make it later, change it. Then I've diagnosed that pathway exists and it's part of the circuit. It is responsible for the tachycardia. We talked about a couple of nuances. Sometimes you never get early to the A. You may come late or you may even block in the tachycardia. Analysis is the same. Did I do anything to the hiss? Nothing to the hiss and I stopped the tachycardia, I delayed the tachycardia, I slowed the tachycardia. From the V, the only way I could do any of those if it wasn't involving the hiss and thus the AV node, it's a pathway, it's an accessory pathway. Sometimes you have to make this diagnosis when the patient isn't in tachycardia. So there we have a lot of maneuvers. One that we went over is parahissian pacing, unique maneuver where we change the rate. And you'll already see the coming together of the foundations. To understand the physiology of parahissian pacing, you had to know some anatomy. You had to know that there was insulation around the hiss. Dr. Jackman, Dr. Gonzalez who came up with this maneuver, there's no way they would have thought of this if they didn't know that anatomy already. And you also see signals, activation sequence, type of catheters, recording signals, all coming together. And that's the way that you should do it, going through these three days, these few days and also through your career. Every time you learn an anatomy fact, ask yourself the consequence with engineering or physiology. And same when we learn physiology as well. I'll stop there. Thank you for your attention. Thank you. You gave last year and taking time out of your busy schedule to participate in the questions and answers. And a number of questions came in. I'm gonna kind of group them here a little bit. Sam, I'm assuming you can hear me okay. But one of the initial questions that came in at the very beginning of the talk, which I think is worth spending a minute on here is how do you determine if there is VA conduction? Which electrograms are the most important to pay attention to? This question came in from Dr. Garg. Mark, I'm unable to hear you. I'm not sure if you can hear me. Sam, I can hear you. And my audio should be on. Okay. Yes, Mark, we hear you. Okay, Sam, can you hear me now? Sam, I can see you and I can hear you well. I hope you can hear me. But the question I'm answering is how do you determine if there's VA conduction? What electrograms do you pay attention to? So really it doesn't matter. The things that you want to try to figure out while ventricular pacing is going on is, is there VA conduction that reaches the atrium? And second is, which is the area of the atrium that's activated first? So if you have, for example, a three catheter study and you just have a ventricular pacing catheter, a HISS catheter, and an atrial catheter, you can just look at the atrial catheter to first say, is there VA conduction? Then once you determine if there is VA conduction, then you want to look and see if it's earlier on the catheter in the high right atrium or any other catheter that you have in the heart, like the HISS bundle catheter or a coronary sinus catheter had you placed it in. Where it can get confusing is if there is VA block and there's an ongoing atrial rhythm, sinus rhythm or something else, then when you are looking at ventricular pacing, you'll see some atrial electrograms. And what you have to figure out is if those atrial electrograms are following the ventricular pacing or are they in an independent rhythm? This also is pretty straightforward because usually they're going to be a different race, but where you have to be a little cautious is if there's ventriculoatrialwenkebach. So if the ventricle to atrium is decrementing, you might mistakenly think that this is just sinus rhythm that has nothing to do with ventricular activation. So if I draw a quick picture here to explain this situation, so if we have ventricle here, we're pacing here, we have a catheter here in the high right atrium, maybe a Hispanodal recording catheter, possibly a coronary sinus catheter. You pace here and you see just no atrial activity, you have no VA conduction. If you have atrial activity, then you want to know is it because of your ventricular pacing or is it just an underlying atrial rhythm like sinus? So there you look for a relationship, one to one, B to A, or you can follow a VAwenkebach, the atrial rate changes when you do ventricular pacing. Now, I saw another question that brought up the issue of eccentric versus concentric atrial activation. And when can you be sure this is not AV node? How deep in the coronary sinus? First of all, in general, I like to avoid using the term like concentric and eccentric. What it means in common use is like if on the coronary sinus catheter, your electrodes that are at the ostium are earlier than any other electrode. So that's where this term concentric eccentric comes from. Why you have to be a little bit careful is you may have another site on the septum like the fast pathway exit of the AV node. That's actually the earliest site. But if you're only looking at the coronary sinus catheter, from the fast pathway, you might enter into the coronary sinus somewhere in the middle, giving this pattern that looks eccentric. And if you make an equation in your mind, eccentric means pathway, you could get confused with that thinking. So it's good to remember like what's actually early. And the key places you want to look at is something on the right free wall, like a high right atrial or right atrial appendage catheter, something on the left free wall, so mid or distal CS, and two catheters on the septum. Proximal coronary sinus, the usual site of exit of the slow pathway input to the AV node, and something just behind the hiss, which would be the usual site of exit to the fast pathway for the AV node. Now, there's another question here that says with parahysian pacing, if you find that the pathway is far away from your site of pacing, could you mistakenly think that there is no accessory pathway when there is an accessory pathway? So here, the thing to remember that's important is parahysian pacing is a method to find out whether a specific activation sequence in the atrium is AV node dependent or pathway dependent. So in other words, if you pace from the atrium, from the ventricle, and you saw a sequence that said early activation is somewhere over here, and you have a doubt, is this AV node and my CS is just at the ostium, even though I'm thinking it's a little bit inside, or could that be a posterior septal accessory pathway? So that particular sequence, when you do parahysian pacing, high output and low output. If at high output, you find that your activation with that same sequence comes earlier, but at low output, when you're only capturing the ventricle and you have to go get into the conduction system and then climb out is later, then that sequence is AV node dependent. On the other hand, high or low output, if you get that activation occurring at the same time with the same activation sequence, that's an accessory pathway. So in other words, you define the mechanism for that sequence of activation. If that pathway was just transiently blocked, or you're pacing at a rate where all the conduction is through the AV node, then you won't get that activation sequence. You'll get another activation sequence, which would be different from when you conduct through the pathway. And if you do parahysian pacing, you'll define the mechanism of that activation sequence. This is important for early students of electrophysiology to keep in mind. Parahysian is not a way of including or excluding the presence of a pathway. Parahysian is a method of defining the mechanism of a specific activation sequence. If at any time during the case, the activation sequence changes, if at any time during the case, you use isoproteranol, if you're pacing at a different rate, if you're pacing from another site and see another sequence, then all bets are off for the parahysian you did before. You may have to repeat at that rate or that autonomic tone, reproducing the new sequence and contention, the one that you're trying to figure out what the mechanism is, and that will define it. Now, there's another question here that says, how do you differentiate an increase in AH interval is due to concealed conduction into the AV node by a PVC versus atypical AVNRT? So this is definitely not a EP 101 question, but since this is asked, let me explain it to you. So those of you who are new to the field can appreciate what you have to look forward to when you hit EP 701. So here's the question. You have a tachycardia and let's pretend that it's AV node reentry. So you have input to the AV node, output from the AV node and a tachycardia circuit has started. Now, let's say you see a sudden change in the AH interval during tachycardia, perhaps when you're putting in PVCs. So you're putting in PVCs to define the mechanism of tachycardia, and you see an abrupt increase in the AH interval. So a good way to think through a complex phenomenon in the EP lab is to build a construct in your mind, a visual of what actually do we mean by AH during tachycardia. For those of you who remember your calculus days, just memorizing a bunch of formula are of hardly any value, but you understand the geometric basis of what the calculus means. Most of you probably remember it to this day. It's the same thing in electrophysiology. Try to see, picture the mechanism. So here you're picturing retrograde conduction through the fast pathway going in through the slow pathway. The AH will be defined by the second you got out to the A retrograde from the time it took to reach and go into the AV node again, antigrade. Now, if there's an abrupt change, one possibility is now this slow pathway is no longer operative, but instead of tachycardia terminating, you are able to get in through another slow pathway, another pathway to get into the AV node. So the AH increased suddenly. The questioner is asking, is that the only mechanism? Could there be another mechanism? And absolutely there can be many other mechanisms. One of them specifically, when you're putting in PVCs, the PVC may not have reset the tachycardia by getting to the A, but might have critically found an open window to climb up the hiss, get to the AV node, and just make the AV node conduction much more. So it's not the slow pathway input to the AV node that's changed, but the AV node conduction time itself has increased. Another mechanism that can explain this is if you got out of the fast pathway and now needed to take another route in the atrium because of scar or something else in the atrium to get to the same slow pathway, it could now show up as a long AH interval. There's actually even other mechanisms, but many of them you can figure out even by thinking it through, if you understand the physiology and you have a construct of what the tachycardia circuit is and what each of the interval means. Now, the next question that we have here is, it says, could you please explain retrograde right bundle branch block and how it affects pacing maneuvers? So let me put the construct of para-hissian pacing in another way. Forget about the high output, the low output, all of this other stuff. What's the real difference in para-hissian pacing between high and low output? The difference is whether you capture the hiss or you passively activate the hiss via the ventricular myocardium. In other words, you move the hiss. At high output, the hiss comes early. At low output, the hiss comes late. Now, if the atrial activation sequence follows what the hiss is doing, we say this is AV node dependent VA conduction. In other words, if hiss comes early, A comes early. If hiss comes late, A comes late without a change in the activation sequence. Retrograde right bundle branch block is another way of moving the hiss. Except here, what we're doing, so this is the right bundle, the left bundle, right ventricle, left ventricle. We're pacing from here in the right ventricle. If we pace and the extra stimulus blocks in the right bundle, retrograde, then it has to reach the hiss. If it's going to reach the hiss, it has to go to the left bundle and then get to the hiss. The hiss is late. But if the right bundle is not blocked, you have a straight route to get to the hiss. The hiss is early. Para-hissian, you're moving the hiss. Hiss early, hiss late. Induction of retrograde right bundle branch block, you're moving the hiss. Hiss early, hiss late. And if hiss is late, A is late, same activation sequence. It cares about the hiss. It's retrograde VA conduction via the node. If hiss is late, it took you longer to get the hiss, but the A stayed at exactly the same timing, regardless of the fact that the hiss is so much later, you have an accessory pathway. So the interpretation is similar. The difference is how you move the hiss. In para-hissian, it's high versus low output pacing. In retrograde right bundle branch block induction, it's with and without retrograde right bundle branch block. So if I'm seeing the notes there correct, I believe we are just about out of time for the question discussions.

EP maneuvers

arrhythmias

underlying mechanisms

PVCs during tachycardia

para-hysian pacing

atrial electrogram

AV node reentry

accessory pathway

His bundle

AV conduction