slide forward. This is going to deal with basic stimulation protocols and EP evaluations, picking up where we left off in the last video. I'll meet you on the other side and we'll do a Q&A session for both of these presentations. So thank you so much for keeping those questions coming in. All right, let's talk about EP studies, et cetera, and pick up where we left off earlier. I wanted to show first a couple examples of intracardiac recordings. We're going to focus on this catheter here, which is positioned in the HISS position, even though this happens to be a decapolar catheter. Usually we use a quad in that position, but here it happens to be a deca. And I'm going to show you five different electrograms recorded from these five bipoles, just to give you a sense of the field of view and the types of recordings that we're getting in the heart. So you have to, in your head, imagine the AV groove is going to be somewhere around here within this RAO view, the right ventricle being over here and the right atrium being over here. And actually, I'm going to just click and show the next components here. Notice that in just this short distance, we go from a bipole that's recording here on the left, only really atrial signal timed with the P wave. Sorry for my tremor, it's one of my medications. And there's a little far-field signal that times with the QRS, but we're on the atrial side of the annulus, so we're only recording an atrial signal here. But if you go just one pair of electrodes further, we get a smaller A, more V, and now you can see a bundle of HISS recording in between the two. If you go a little further, you see even less A, and you still see a little HISS and a bigger ventricular signal. So just in this short distance, you can see the change in the field of view of the electrograms that you're recording right at the annulus. And further down, you see a right bundle potential and ventricular signal with no atrial, and further down, just ventricular signal and no bundle recording. We talked about being able to measure intervals inside the heart, and just to review this, this is pretty basic, but just to, again, bring everybody up to speed, including those who have not seen these before. Here is just simple recordings from in the heart. The top three are obviously the EKG leads. Anything that lines up with the P wave is an atrial signal. Anything that lines up with the QRS is a ventricular signal, and anything that's in between in the PR segment is neither, and in this case, it's a HISS recording. And this allows us, as I said earlier, to break apart the PR interval into its two components, the AV node part and the HISS Purkinje part. And the only way we can do that is by recording this intracardiac HISS that you can't see on the surface EKG. So, I don't know why I struggle with this clicker. Here we go. As signals travel from atrium to ventricle, of course, you're going to pass through the AV node to the HISS. Now, the AV node is made of tissue where the fibers are not oriented in the same direction. There is stroma between the myocytes. The conduction through the AV node is disorganized and slow and multi-directional, and therefore, even with an intracardiac recording, we don't record a electrical signal of the AV node. We can record atrial signal nearby. We can record the HISS bundle just after the AV node, but not the AV node itself. So, how can you measure how long it takes to get through the AV node? And the answer is, well, if we can take, looking at the picture up here, record the atrial tissue signal from right near the AV node, and we can record the signal in the HISS just below the AV node and measure the timing between them, that's how long it took by inference to get through the AV node. Notice I didn't say that we use the HRA signal. I don't want to know the sum total of time it takes to get from the sinus node to the AV node and through it to the HISS. I just want to isolate the AV node part. So, when we're making the AH measurement, we will do it using the atrial signal that's nearby the AV node in the HISS catheter. So, you measure from the atrial electrogram in the HISS catheter to the HISS bundle recording itself, and that is the time it takes to get through the AV node. How do you measure how long it takes to get from down the HISS Purkinje system? Well, the start is the HISS bundle. The end is the start of the surface QRS, and so that's the HV interval. I didn't really show what I should have done is put a vertical caliper here. The right caliper really should be at the very start of the QRS on the surface EKG. Wherever you reach the ventricle first is where the AHV interval ends. So, these are the standard measurements that are part of every EP study that you should learn to make and the reason why we measure it at those locations, the AH and the HV. Okay, let's look at a few intracardiac recordings to get those who are not familiar with these as much more familiarized and comfortable. I'm showing them in color because for me adding the color element helps organize things and see patterns better, and I will orient these all in the same sequence for the next series of slides. This is what a sinus beat looks like with intracardiac recordings. How do I know it's a sinus beat? Several reasons. If you look at all 12 leads and on the first page of the recording system, you have all 12 leads. Now only three of them are displayed up top. The P wave is upright in lead 1. It's upright in AVF. It's biphasic in V1. It's stretched out, so it's hard to see that shape. So, you could compress it and look at it at 25 millimeters per second, or you could gain up each of these to see the P wave better, but those are tricks that you'll learn to manipulate the EKG. But importantly, if you look at the activation sequence in the catheters as we discussed earlier, high right atrial catheter, his catheter, CS catheter, you're going to see a sequence where the HRA catheter is going to be first during sinus rhythm if it's positioned near the sinus node, which was a really good point that Furman made earlier, which is you can label these however you want, but if they're not in the positions or they're hooked up wrong, then you're going to have misleading information. So, one thing to keep in mind is always be sure that your labels are accurate, your catheters are plugged in right, and they're positioned in the heart where you intend. Sometimes the HRA catheter slips during cardiac motion and breathing, and it falls over toward the his bundle, and you see a his bundle recording on the HRA catheter. It's out of place. But you see the beginning of the signal during the beginning of the P wave is first in the HRA, it traverses the right atrium, you then see the atrial signal in the middle of the heart where the his catheter is positioned, and then it travels right to left out the left atrium parallel to the coronary sinus, and so you see these atrial signals in the CS after that. Why did I number these with CS 1-2 at the bottom and 9-10 at the top? It doesn't seem elegant from a numerical perspective, and many people will reverse it because they're uncomfortable going out of numerical sequence. For me, it makes sense for a sinus beat to go from left to right, top to bottom. So, I position the electrograms, you can shift them however you want, such that 9-10 is on top, so that during sinus rhythm, the beat is in the sequence that is consistent with the rest that's on the page, top to bottom, left to right. I'm just going to grab my other laser pointer. Sorry, one moment. This one is on the Fritz. And then you see the his spinal recording, and then you see electrograms. Notice the far-field electrograms in the CS catheter. The coronary sinus runs in the groove between the left atrium and the left ventricle. Sometimes it rides, it usually rides more on the atrial side of the groove, so usually you see very sharp, nice atrial signals and less ventricular, but sometimes everybody's different, as was said earlier as well. You may see sharper ventricular signals, especially as you get further out toward the great cardiac vein. This venous structure deviates toward the ventricle and away from the groove, so you start to see taller ventricular signals the further out you get. If you pushed it further out the great cardiac vein, you're going to see even bigger ventricular signals. But you know these are ventricular because they line up with the QRS. Yeah, why is there no fragmented signal over the AV node due to anisotropic conduction? Yeah, in order to generate a signal that we can record that is of a frequency that's in our range that we're looking for, and that is of sufficient amplitude, you need to have enough myocytes that are being depolarized in the same direction at the same time to generate a signal that is of sufficient amplitude to record. And in the AV node, because of the slower conduction and the sort of lack of parallel structure of the myocytes, the vectors are different, there are fewer cells being activated in any region at any given time, is I think anatomically the reason that the signal that's generated is just not large enough and simultaneous enough for us to record with our current technology. There may be ways in the future to do that, but with the electrodes we have right now and the amplification and trying to get rid of noise, we just can't record it. So you think the slow pathway potential as you're doing slow pathway ablations may represent anisotropic conduction? So interestingly, I'm not sure personally that I've seen a signal that I'm convinced is a slow pathway signal, but there's no question that in the little isthmus between sort of in front of the coronary sinus and above the tricuspid annulus, this corridor, as we'll talk about tomorrow, that is where the slow pathway is located, it may be that the reason people see this sort of slow pathway potential may have to do with the cells are more aligned or there's more coordination of electrical systole in that area, and maybe that allows us to record it with our electrodes. I don't know if you have... Well, it's controversial. Nobody really knows. Josh will go over it tomorrow, but to get to something non-controversial, two questions. Why do you measure the earliest ventricular activation from the surface EKG? Why is it never measured from the intercardiacs? Yeah, and it can be either. So the point is you're trying to measure the time from the his bundle to the first branch of your his Purkinje tree that hits myocardium. Where is that going to be, and am I going to have a catheter at that spot? Probably not. It may be in the left ventricle where you don't even have a catheter. It may be somewhere in the right ventricle, which is not where your right ventricular apical catheter happens to be positioned. So the chances are low that you're going to happen to have an electrode right at the first place where the Purkinje fibers break out into ventricular myocardium. That said, maybe you got lucky, and you may see a signal in your ventricular catheter just before the surface QRS starts, in which case I would actually measure to that signal. But you want to measure to the first ventricular event, which is usually the very onset of the surface QRS, which really does summate all of the ventricular myocardium, not just the little local areas where our bipoles are sampling. It's a common mistake and assumes particular importance when you're looking at VA times. You always measure it from the first ventricular activity on the surface or intercardiac. It's almost always on the surface. Then finally, so sometimes, let's see, why does Murgatroyd say to measure the AH interval by taking the peak of the first deflection and not the beginning of the atrial signal on the His catheter? So peak versus... Yeah, so fair enough. So that gets into the question of a bipolar recording and really what part of that multi-deflection signal represents local activation time. And truth be told, whoever asked that is spot on, that really the local activation time is the first sharp deflection rather than the onset of the bipolar recording. So you probably should take the sharp initial deflection, not the upslope or the downslope of that recording, but the sharp deflection is really when the wave front is passing between those two electrodes. But you do want to use the signal right in the His catheter so that you're recording local atrium just above the AV node right nearby and not somewhere else. So you're adding in transatrial conduction time into that measurement. So another good, good question. These are terrific questions. They're really important basic questions that a lot of fellows don't ask. So keep them coming. In the CS, when you get a sharp signal on the V, like you don't have here, what does it tell you about the location of your catheter relative to the LV? This is an important concept. It's a great question. And the point remains that sharp signals indicate that the bipole is near that tissue from which you're recording. So if you're recording a sharp ventricular signal, it suggests that that bipole is close to or overlying ventricular tissue. How could that be? Well, there are a couple of different scenarios where you might encounter that. Number one is if you advance the catheter further out the coronary sinus, as I said earlier, to a portion of the coronary sinus great cardiac vein system that is now veering away from the left atrium and toward the left ventricle, now that venous structure is more ventricular. That's one scenario. Another is you accidentally advanced the coronary sinus catheter down a vein branch that branches off of the coronary sinus and heads toward the ventricle, in which case you'd see only ventricular sharp signals and no atrial signal, which is a sign you need to use fluoroscopy or ice and reposition that catheter so you don't perforate or puncture that vein. And a third is that most of us nowadays put a catheter in the coronary sinus from the groin, where we go up to the right atrium, deflect it, and it tends to ride on the roof of the coronary sinus, which is a little bit more atrial. But in the older days and still now, many people will insert from the internal jugular vein a coronary sinus catheter, and then it travels down to the right atrium and travels on the floor of the coronary sinus, which tends to be more ventricular. So you might have more ventricular signal depending on the approach to the coronary sinus. So how do you recognize the right bundle potential? So yeah, I made that mention and I passed over it, but thank you for asking. So we know that in humans, the His-Purkinje system, and in all animals, it tends to conduct at pretty predictable fixed rates. So the H-V interval almost always is in the 40 to 60 millisecond time frame. If you were to record an H-V interval that's short, 25 milliseconds, there are a couple possibilities, as I'm going to review in a few slides. But one possibility is that that's not a His recording. You advanced your catheter further downstream and you're recording a right bundle potential. So it's a right bundle to ventricular timing of 25 milliseconds rather than His. And another clue is, of course, the more you veer away from the annulus, you're going to see no atrial signal at all. So the combination of seeing an atrial signal in the His catheter and measuring an H-V interval that is physiologic in the range that we would expect tells you that it's likely a His bundle recording. If you don't see an A and this interval gets shorter, this is later, suggests that you may have advanced the catheter and you're recording from further downstream, closer to where it exits to the ventricle. OK. Quiz time. So there are two beats on this page. And now from everything we've discussed, you have to tell me what these beats represent. And you can do either beat first. This is the yell it out, don't text it to your iPad. I have to be able to hear it up here to tell you if you're right or not. And I hear murmurings. I hear ventricular retrograde conduction. So which beat are you referring to? The first beat. And that would imply that that beat is a PVC. And why do you say that? So there are several steps. The way I would methodically go through it is the first thing that I would say is the ventricular events precede the atrial events. It sounds simple, but until you start thinking logically like this, when you get into more complex scenarios, you're going to be thankful that you think it through this way. Well, how do I know if I look at this mess here in the hiss catheter, there's two or three different things in there. How do I know that this is not A and V versus V and A? So number one is you look at the surface EKG and you see up here a wider beat than over here. Is that a P wave in front of this? No. How do you know it's not a P wave? Because there's no atrial signals anywhere that line up with that thing. What is that? It's the T wave from the beat that's off the screen because it looks like this thing. And there's no signals that correspond to the T wave on the intracardiac recordings. So number one, and as Furman said, go to the surface EKG or maybe Sam said it. It's very important to appreciate the surface EKG first. So look at this. There's a P and an arrow QRS. There's a wider QRS with no P in front of it. And then you go to the intracardiac recordings. How do I know that these are atrial signals and not ventricular signals? Because they kind of all, it sort of lines up with the V maybe. They're sharp, but I don't know, maybe I went down a branch of the coronary sinus. Maybe it's advanced out to the great cardiac vein. So the answer is you need to compare it with this beat that's a more predictable beat. This is a sinus beat on the right because it looks exactly the same as the last slide. It has the activation sequence. It's earliest in the HRA. It has the AH, the HV. Everything lines up. So it's always helpful to compare a beat to sinus. I would disagree, though, about the activation sequence and the morphology. I think these electrograms do look a little different in their shape, which, you know, is a subtle thing. We'll get to activation sequence in a moment. But the fact that we have sharp signals here that line up with a P wave, that very highly suggests that on an adjacent beat, the sharp signals are also atrial signals. This catheter didn't wildly go to a new place between beat one and beat two. So if you can say with certainty here that these are atrial signals and you see them over here, they're atrial signals there. This gets especially important when atrial and ventricular signals are overlapping, like in AV node reentry, as we'll see tomorrow, like in a PVC that happens on top of a P wave in those types of scenarios. So get used to figuring out what you know and then extrapolate to what you're not sure. So the fact that you see sharp signals here suggests A. Getting to the other point that was mentioned, though, the activation sequence, that's the second part of this question. So that's a PVC. Is this atrial event a sinus beat or is it retrograde activation? I heard people say retrograde activation, and the question is, how do you know that? Because you could have a PVC happen that doesn't conduct retrogradely and there happens to be a sinus beat there. So concentric activation is a term that suggests that in the coronary sinus catheter, you're going 9, 10, out to 1, 2. You're going right to left in that catheter. So in sinus rhythm, everyone agrees that, yes, that's the direction you'd expect the wave front to propagate, from right atrium across the right atrium and across the left atrium. But during retrograde activation, where you have a ventricular beat, paced or spontaneous, that comes up the hisperkinesis system through the AV node, where is the AV node located? Smack in the center of the heart. And then which direction in the atrium does it go? Both directions. It goes left to right in the right atrium, but it goes right to left in the left atrium. The AV node isn't on the other side of the coronary sinus. It's on the right atrial side, septal side, of where your coronary sinus catheter is located. So during retrograde conduction through the AV node, you are also going to get concentric activation in the coronary sinus, because it's going to come up the center of the heart. It's not coming from the right, high right atrium, but it's going to come up the center of the heart, and it's still going to go 9, 10 to 1, 2. So the sequence in the coronary sinus in both cases will be concentric, and that will not distinguish a sinus beat from a retrograde beat coming over the AV node. So I heard that the hiss is coming before it, but that's true in sinus also. The hiss comes before. The HRA is the answer, right? There's only one electrode here that tells you that there's a different activation sequence in this atrial beat compared with this one. Here in sinus, the HRA is early. Here it's late. So this can't possibly be coming from the sinus node, because the electrode pair that's closest to the sinus node is activated late. So this is a retrogradely conducted beat from the PVC through the AV node, and then going in both directions. Yes, it activates the hiss early, but you'd expect that here, and you'd also expect it here. Yes, it's concentric in both cases, but that's the key. Some people do EP studies without a high-rate atrial catheter. Ah, that's one more catheter. It's helpful sometimes, especially early on, all right? So is there anything—I know we went through that in a lot of detail, but I think it's really important as you are building a foundation, and if we don't get through all my slides, who cares? The point here is to just get familiar with looking at these recordings. I'm going to skip that, and I'm going to go to this one, and we'll cover a couple more things, and we won't cover all my stuff, but that's okay. Two beats. What about these two beats, can you tell me? What are they? I hear different atrial activation. The first one is an ectopic atrial beat, and you say that because? Again, it's all about the atrial activation sequence. So the second beat, again, is a sinus beat, which serves as a nice comparison. But what happens first? We have activation over here. So not only can you tell me that this is an ectopic atrial beat, what more can you tell me about its origin? It's from the left atrium. Where in the left atrium? Septum or lateral wall? High or low? And why? That is a great question. Is it the roof of the left atrium or the floor of the left atrium? Lateral. Why do you say that? So there's one, and why would the HRA timing differ whether it came from the ceiling of the left atrium or the floor? But it's higher over on the right side. So it's true that if Bachmann's bundle delivered signals quickly from left to right atrium, but everyone's a little different in how their atria connect. There's another really key point that gets us back to basics. What were you going to say? The A on the HISS is activated before the HRA. The A on the HISS is activated before the HRA, which is not surprising if you have a signal coming from the left atrium to the septum, where the HISS is, and then to the lateral right atrium. So you might see that in either case. Yeah. What do you see about the P wave shape? Here in sinus, AVF has an upright P. Maybe it's sort of upside down. If it's inverted, it suggests a superior vector, which is a really, really good point. Never forget the surface EKG. It gives you additional information that we couldn't get from the intracardiac recordings. We only have five pairs of electrodes on the floor of the left atrium. We don't have any electrodes on the roof of the left atrium for a time comparison, but we have a surface EKG that looks at the whole of both atria. It's a really, really good point. Can you make that same assumption based on the vector of your HRA? No. So these are all bipolar recordings, and you can't say anything about them by their shape, other than the few issues I pointed out earlier in terms of if there's a change, it means the wave front is different, but it doesn't tell you where it's coming from. A negative versus a positive deflection really has no specific directional meaning with a bipolar recording. I'm going to go a little bit faster through a couple slides. Josh, why don't we do this? Why don't we work these through and put the workshops on hold? Because this stuff is really important. This is the basics, and you're doing a great job with it. Take what time you need. Sorry. I think this year I'm even slower and more verbose than usual. If that's possible. Yeah, thanks. I don't know what to tell you. Just give me like a signal that it's time for me to shut up, and then I won't go too much longer, because there's only so much you can absorb in a day. But I do think it is important to try to understand these basics, because you're going to see the rest of this conference, it's going to be these electrograms. And if we don't kind of get these concepts now, you're not going to be able to pick up quite as much later on. I wanted to show, again, the benefit of his bundle recording in the context of surface EKG and intracardiac recording correlation. So here is wanky-bocky. We know this because we see a prolonging PR interval, and then we have a P wave with no QRS, and then after the pause, the PR interval shortens again. And the equivalent of that inside the heart looks like this. And to help you organize, now instead of showing you one or two beats, there's five beats, and what belongs to what. So I'm going to help you. In the future, you won't need any help at all, but if I group them and I show you where the boundaries of each beat are, now you can start to say, okay, well that times with the P wave, that's an A, that's a hiss, that's a V. In fact, I'll help you there too. I'll label the A, H, and V. So notice as the PR is prolonging, what part of the his bundle recording is changing? The A, H interval, right? It's getting longer. And that's, I mean, to you now that's obvious because you know that wanky Bach suggests delay and block in the AV node. How do you know that? You know that because we owe a great debt to the electrophysiologists who used to practice before pacemakers and defibrillators and before catheter ablation existed. So you ask yourself, what the heck did they do with their time? And the answer is they did this all day. They gave drugs and they put catheters to record the hiss bundle and they paced. That was EP. It was unpopular back then because you didn't do very much. But we learned so much from what they did to the point where they are so exhaustively understood how the electrical system of the heart worked that we take it for granted. So when someone says wanky Bach, you say AV node. Why? Because they did this recording and they saw that the A, H interval is the element that was prolonging during a wanky Bach cycle thereby defining the point of slowing and failure at the level of the AV node. And they saw that over and over and over. And similarly, when you had Mobitz 2 block like this, we had a P wave without a QRS that was unpredictable and the QRSs that conducted were wide with fascicular and bundle branch blocks. They recorded this. They saw a hiss bundle there but no V. So the signal got through the AV node, no problem, to the hiss bundle. But then at the distal hiss or somewhere in the Purkinje tree, that's where the point of blockage occurred. And you didn't see it. So now we know if you see a Mobitz 2 pattern, that suggests Hiss-Purkinje disease, very different treatment implications. AV node block asymptomatic? Not urgent, maybe not need treatment at all. Hiss-Purkinje disease, emergency. They could at any point completely fail with their Hiss-Purkinje system and have asystole or a prolonged pause resulting in syncope or worse, and they need a pacemaker. Clickety-click. I'm going to skip this slide because it's sort of redundant. I am going to skip this slide, I think. I just want to see what I have next. Forgive me for passing this for a moment. Oh, yes, because I wanted to discuss pacing. I knew I wanted to get to something. So pacing maneuvers that we do, and Sam talked about this, so I'll go through actually this slide pretty quickly. But we will do pacing maneuvers during sinus rhythm to assess the conduction system and to try, including sinus node and AV connections, and to try to induce arrhythmias. And then during tachycardia, we do it to try to figure out what is the mechanism and location of the tachycardia. Terminology. So we talk about burst pacing, and we talk about programmed extra stimulation, which is abbreviated PES frequently. Burst pacing means that from one pair of electrodes, you're going to deliver a sequence of pulses all at the same rate or the same cycle length. That's called delivering a burst for whatever number of beats. Programmed stimulation is pretty formulaic. Usually people will deliver eight beats at one particular rate, usually 600 milliseconds, which is 100 beats per minute, or 400 milliseconds, which is 150 beats per minute, for eight beats in a row to create a very stable, predictable electrical environment. And then we put in early beats thereafter. And this is what it would look like. There are your eight beats, and you can put in one or two or three premature beats of shorter coupling intervals. The terminology here is the eight beats of what's called drive train are all known as S1, or that's first cycle length, S1, S1, S1, S1. If it's in the atrium that you're pacing, people may call it A1, A1, A1. If it's in the ventricle, V1, V1, V1. When you put in a single early beat, it's called S2 or A2 or V2. And the next one is S3 and S4. Usually people don't do more than three extra stimuli nowadays during an EP study. And you're often doing this to try to provoke an arrhythmia, or look for a refractory period. You're shortening and shortening and shortening the one or two or three extra beats, waiting until you reach a point where you can no longer capture because you've met the refractory period of whatever tissue you're pacing or through which you're conducting. Or you're looking to initiate a reentry circuit by bringing a beat in so that you block in one limb of the circuit and conduct down the other and thereby initiate reentry through unidirectional block, which we'll talk more about tomorrow. There's a concept called sinus node recovery time where you burst pace in the atrium for 30 seconds and you come off and you wait and see how long it takes the sinus node to recover. Nowadays we don't do this too often. Why? Because of sophisticated, easy-access, long-term recording systems. If someone has presyncope or syncope, whether it's with a Holter monitor or an implantable loop monitor or their Apple Watch, we almost always can get a recording of the rhythm during symptom. That didn't used to be the case. They didn't have these long-term monitors to catch events that happened less frequently than once per day. And so you had to do EP studies to try to see, does this person have sinus node dysfunction that may be an explanation for their syncope? Their resting heart rate's 48. I don't know, did they have a pause? Let's pace, pace, pace, pace, pace, come off. Does the sinus node leap right back into action or is there a delay? For example, here in the top, normal sinus node behavior. In the bottom, abnormal sinus node behavior, a long sinus node recovery time. It's a little bit moot. If you can take a recording that someone fainted when they had a long sinus pause, you could reprove it again in the EP lab or you could go ahead and put in the pacemaker because you've recorded simultaneously the problem with their symptoms. Maybe one or two more slides and then we'll call it. Here again is program stimulation in the atrium. We can see the tail end of the seventh of eight drivetrain beats. It's the conducted QRS. This A1 is the eighth drivetrain beat pacing in the atrium, generating a P wave. Here is the first extra stimulus, the A2 at a shorter coupling interval. And I'm going to have you focus on the His catheter recordings. In fact, I'm going to visually erase everything except for one line because that's what I want you to focus on and you will soon learn to ignore things that you don't need to look at right now, but I'm forcing you to do that now. And first things first, what are these electrograms? It's the pacing artifact. So don't confuse that with an intracardiac recording of atrium or ventricle or His or whatever. And you can see it on the surface as well. So that's pacing artifact and you can ignore that. We're doing that on purpose. That's from us. Notice the PR on the surface on the extra stimulus has prolonged. Predictable, yes, the AV node decrements. The faster you hit it, the slower it conducts its normal AV node behavior. Here intracardiac, the equivalent of that, the AH prolonged on that A2 beat, just as you would suspect. The HV did not prolong because you can hit the His-Purkinje system as fast as you want. It conducts at the same speed. It does not have, in general, decremental properties. Your attention. We have a few minutes now to answer questions and thank you so much for having those questions come on in, forgive me if I'm looking aside occasionally to answer them. But before we get to the questions, let me ask for the next evaluation feedback questions for the presentation that we just heard. So that again, we can see if this is on the mark or needs some adjusting. So we'll put those questions up for you guys and please take a few moments to answer them. And as you do so, I'm gonna get to the questions that you've been asking. Again, thank you. Thank you for those. I've noticed three of the questions so far came from Dr. Nieves. He's gonna be our EP fellow who's gonna be starting with us July 1st. So he's sucking up by asking a lot of questions there. Much appreciated, we very much look forward to having you in our program in July. So let me go through some of them. Dr. Nieves had asked on one of his questions, if the CS1-2 electrogram comes earlier than 3-4 or the rest, what does that mean in terms of that activation sequence? That's not what you would expect during a sinus beat. Does that mean that you have an arrhythmia or that the CS catheter is positioned too far? And the answer could be that it's either one of them. So if the activation sequence shows that the distal most coronary sinus electrode is activated before the ones that come before it, that means that the wave front is reaching that bipole first. And that could either be because the beat originated out nearest 1-2 left lateral. So a left lateral pathway with retrograde conduction to that location or a premature atrial beat coming from the left atrium, or as you imply correctly, the coronary sinus is a C-shaped structure that travels in the posterior part of the LA-LV groove and then wraps around anteriorly. And if you were to advance that catheter past the lateral part of the left atrium so that it starts to curve back around on the anterior part of the LA-LV interface, then certainly signals that are coming from the right atrium may reach that CS1-2 electrode before 3-4. So you have to know when you're looking at activation sequence, the exact location of your bipoles, because if your catheter is in one place, but in your mind, it's in a different place, you may come to a false conclusion. A question came up about the squared off morphology of some of the electrode. This was Dr. Unger who asked this question, what is the significance of a squared off looking morphology of electrograms? And that implies that the electrogram amplitude extended beyond the bounds of what you are limiting for that channel. So if you have an amplitude of electrogram that goes beyond the bounds of a particular channel, then it's going to overlap with other channels. But you can clip that channel in the Pruka, the GE product, you can hit the C button and it will clip off the top and the bottom of the electrogram. And you can do that with two levels of clipping. So you can clip it once and then clip it a second time, and that will give it a squared off appearance. So if you see that, look to the left and see if there's a little tiny C that is denoting that the electrogram is in fact clipped. I do that when I'm preparing slides for display so that you don't get confused which signal belongs to which channel. And that's what the squared off morphology means. Thank you for that question. Another question came up from Dr. Jabber about the signal change during RF ablation. Why is there a change in the bipolar electrogram? When you think about near field and far field recordings, near field recordings tend to be very sharp and far field recordings tend to be more smooth or blunt. And as you're killing off tissue in the ablation catheter, which is also giving you a bipolar recording, you're killing off the tissue that is immediately adjacent to your electrodes. And therefore the near field, the sharpest signals are gonna start to go away and you're going to be left with recordings from a little bit further away, the tissue that isn't killed by the, or disabled by the radio frequency energy delivery. So you're going to see a morphology change from a sharper near field signal to a broader far field signal. And that's one of the ways that you can assess whether you're actually making a lesion, making changes in the tissue adjacent to your ablation catheter and mapping catheter. Another question that came up from a great question from Dr. Lawrence. The question was on the slide of a sinus beat. It was noticed that the electrogram in the right ventricular apex recording came earlier than the ventricular electrogram in the hiss catheter. Why is that? Because the hiss catheter you would think is closer to the atrium. Well, why wouldn't you activate that first? And then as the signal sweeps down toward the apex, then you'd see the RV apical electrogram inscribed later. And the answer of course, is that isn't the sequence that the ventricles are depolarized in sinus rhythm. The hiss Purkinje system exists. It's an upside down tree, as you know. So when signals come down the hiss bundle from the AV node, they're going to ramify down toward the apex. So the little twigs, the branches of the tree insert more apically. So the part of the ventricle to be depolarized first is the apical portion. And if you're right ventricular apex catheter, again, it's important to know where your catheters are located before you interpret the sequence of things. But usually it's positioned in the apex of the right ventricle, near where the terminal fibers of the right bundle branch insert into ventricular myocardium. And therefore the right ventricular apex catheter will record a signal before the ventricular signal up at the base where the hiss catheter is positioned, where it's recording ventricular tissue that's far away from the ends of the Purkinje fibers. So on the screen, it looks funny because you're sort of jumping around. So you have all of the atrial activation first, and then the hiss bundle deflection, and then the RV apex, and then back up to the sharp signal in the hiss catheter for the ventricular part of the signal. And that's a normal sequence. And likewise, in the far field signals in the coronary sinus catheter, again, positioned at the base of the left ventricle, usually those will be later than the right ventricular apex deflection for that reason. And this sort of speaks a little bit to what I was just saying. Dr. Sadia asked the question, can you explain the concept of near and far field? And I sort of just went through that. That is when you have signals that are really close to your bipole, you're going to get a higher frequency or sharper signals considered near field. When there is a more blunt or rounded signal, that's considered far field. It's a little bit further away from your bipole, but still within the field of view. And there was actually another question along similar lines. Let me find it, which had to deal, which dealt with the near and far field, the relevance. Let me find it. The question had to do with, which do you, would you prefer to use near field or far field when thinking about timing? And forgive me, I can't find who had asked that question. My apologies. But the point there is that if you're, let's say mapping a focal PVC, a focal PAC, a focal tachycardia at any location, you will have near field and far field signals. And the question is, well, which do you look at? And the answer is, as long as you're convinced that the far field signals also correspond to the same chamber. So let's say you're mapping a PVC and you have a near field signal in your mapping catheter and it's the earliest you've found, but there happens to be a little earlier far field signal. The question is, well, do you ignore it or do you take it? And the answer is it's very relevant because it tells you there's some tissue not immediately adjacent to your bipole, but a little further away that's being activated even earlier than where you're recording your sharp signals. So at that location, the sharp near field signals reflect what's happening immediately adjacent to your bipole. But if you see a far field signal that's even earlier, it means there's something else going on, not right where you are, but nearby so that you can detect it. So it means you need to further refine your mapping by going a little bit left or right or up or down. Or sometimes it's through the thickness of the myocardium. It may need to get, it may be mid myocardial. It may be epicardial. It may be on the other side of the septum. So you have to figure out if there's a way to get your ablation or mapping catheter to wherever it is that you're recording that far field signal. And when you do, it will now appear as a near field signal, assuming it's not mid myocardial and you can actually get your catheter to that new location. And then that would be more likely a place for effective ablation, assuming it's the earliest spot that you have found in total. A question came up about in fractionated potentials, how do we select which deflection to use in terms of activation time? And it's a wonderful question. And there isn't an exact right answer to that because you have to really think about what is the reason for the fractionated signals. You basically have a lot of different things happening with different vectors in the same little geographic space that's all within the field of view of the Bible. In general, we take the first sharp deflection of the cluster, depending on the type of map and what you're doing. If your question is, when did a signal get to this location? The answer is the first sharp electrogram. If instead your question is, what are the delayed signals you wanna make this ILAM map, this late activation map to see in sinus rhythm or during pacing where there are late potentials, you might choose the latest signal because you wanna see where are the areas of slowest conduction that may direct you to where a critical isthmus might be for ventricular tachycardia. So that's a sort of a rigged map asking a different question where you're asking what are the delayed signals? What are the latest signals? Which is different from when did the signal reach this area during the beat that we're mapping or the rhythm that we're mapping, which gives you take the earliest signal. That was from Dr. Margotto, that fractionated potential. The question about, let's see. Oh, Dr. John asked, are systolic and diastolic potentials only relevant when you are in areas of scar? So a systolic potential just tells you that there is an activation signal that happens during the QRS and a late potential or a diastolic potential during tachycardia tells you that you're activating tissue late. And if you're looking for a critical isthmus within scar, usually we're talking about ventricular tachycardia, re-entrant VT, scar-related VT, then any signal that is happening after the QRS during electrical diastole is interesting in that it tells you that there is a delay. It's something that's happening in between the QRSs. And that could either be the critical isthmus that is perpetuating the circuit, or it could be a bystander area. It could be somewhere that's being activated late during diastole, but isn't really a critical portion of the circuit itself. So it's important to recognize diastolic potentials during VT, for example, but it may not imply directly that that is a critical part of the myocardium for the circuit that you're looking to target. To answer that question, you have to do a different kind of mapping, not activation mapping, but entrainment mapping to figure out if that signal is actually within a circuit. We're gonna talk about entrainment in a little bit. Other questions have come in while I was talking. I don't know, Dr. Estes, if you wanted to feed me one or two last, well, we have two minutes left. I may have time for one or two quick questions if you'd like to jump in before I introduce the next video and speaker. Josh, there are a couple of questions that have come in since you started. One is retrograde conduction. Usually if the His catheter, or proximal CS9 and 10 is activated first, you can say concentric conduction over the AV node. Is there a specific area of the CS, for example, five and six, that you'd say eccentric conduction via an accessory pathway, or is it kind of the positioning of the coronary sinus, an important question? Yeah, it is, and I'll answer that, and then we'll move on to the next lecture, and thanks, everyone, for your questions. It could be some of each. So number one, it is important that if you're assessing whether the wavefront is traveling from the interatrial septum out lateral toward the lateral wall of the left atrium, you need to make sure first and foremost that your coronary sinus catheter is positioned with electrodes nine and 10 at the septum. If it's hanging out of the coronary sinus, and so that electrodes five and six are actually at the septum, then it will look like an eccentric pattern of activation, but in fact, it isn't because your catheter is not in the position that you had in your mind. That was an issue that I mentioned earlier. That said, let's say nine, 10 is at the septum, and five, six is early. That may mean that either the AV node has a little bit of a leftward component, usually you don't get as far out or further than five, six if the catheter is correctly positioned, or you have earlier activation coming from further leftward suggesting an accessory pathway. Thank you for that question and all of the questions. I can answer some of them maybe just in text to individuals.

basic stimulation protocols

EP evaluations

intracardiac recordings

field of view

types of recordings

measuring intervals

intracardiac HIS signals

near and far field recordings

pacing maneuvers