Well, thank you, Nishant, and welcome, everybody. This is going to be, hopefully, a fun session we have here that can get us going. Now, several learning objectives for this evening. First of all, to be able to determine whether retrograde conduction is even present or not, and then know and recognize different patterns of retrograde conduction that may exist when conduction is present, and when it's absent, to be able to determine the site or level block, and several of these objectives are what we found over years of being on the American Board of Internal Medicine when we were looking over the types of questions that candidates routinely missed. It was not the stuff that we thought was going to be hard. It was ECGs, reading ECGs, and retrograde conduction were routinely missed on the examination, so I thought it would be worthwhile to look at this survey. Now, I want to also distinguish between the concept of eccentric retrograde conduction and eccentric atrial activation in an atrial tachycardia. I try to get my fellows to describe what they see rather than put an interpretation on it, because as soon as you start saying, oh, that's retrograde conduction, those are retrograde P waves, you put yourself into a little box and you put on some blinders and say, I'm only going to think in those terms, whereas it may not actually be a retrograde P wave, it may be an atrial tachycardia. And finally, I want to try to get us to understand the distinctions between conduction of the AV node versus an accessory pathway. I'm not going to be talking about perihistin pacing today, that's a topic unto itself, but I do want to talk about looking at the hist potential and whether retrograde conduction, when it exists, depends on the presence of an antecedent hist potential, or is independent of it. We'll see how important that can be and how helpful that can be. All right, so it's an everyday event to assess retrograde conduction. Every time you pace the ventricle in somebody who doesn't have atrial fibrillation, you have an opportunity to look at retrograde conduction. It's completely ignored by a few folks who are too busy to pay any attention to this, poorly understood by some, and as Nishant and I have said, answered incorrectly on board exams by an inordinate number of candidates. We have several tools available to us to make this assessment. First of all, the ECG. And don't forget this, it's at the top of all of our tracings in the lab. People zoom in on what's going on in the intercardiac recordings, but there's a lot of information on the surface ECG. And we'll try to tease some of that out a little bit later. His bundle recordings, of course, presence or absence of a hist potential, and also the effect of premature ventricular complex or ventricular pacing on subsequent PR intervals or AH intervals. So even if you don't see a hist, you can infer a lot about what's going on in the conduction system in the retrograde direction by seeing what happens to the PR interval or AH interval of subsequent beats. We also have other atrial recordings available to us, just to help things out. And when we're talking about retrograde conduction, it refers to activation of the atria either during a tachycardia or ventricular pacing. And we ask the following questions. Is atrial activation related to ventricular activation at all, or is there no relationship? If it is related, how did atrial activation occur? It could be over the AV node, hysperkinesis system. It could be over one or more accessory pathways or some combination of these. It can get pretty thorny sometimes. Almost as important as where conduction is is where it is not. Where does conduction fail? Because if you don't have retrograde conduction, it always blocks somewhere. It could be in the AV node. It could be in the hysperkinesis system. It could be in an accessory pathway or, again, some combination of these or all of the above. Now, retrograde conduction may be present. And when we're talking amongst our fellows, I like to get them to think in terms of two different axes. Each of these should be assessed separately because each has their own importance. One is the vertical axis. That is the sequence of atrial activation, concentric, eccentric, whatever. And second is the horizontal axis, that is the timing of atrial activation after a causal QRS. And that can be a short, medium, or long VA interval. Conduction ratios, V to A, are also considered. That is the one-to-one VA ratio. Type I or type II second-degree retrograde block or a complete retrograde block. That's where conduction is absolute, of course. Block when it occurs always occurs somewhere. When you're pacing the ventricle at a relatively fixed rate and gradually increasing, the AV node fatigues. The hysperkinesis system gets better as you gradually pace faster. So gradual change works in the favor of the hysperkinesis system, works against the AV node. Just the opposite with premature stimulation. The hysperkinesis system is not a fan of surprises. So if you give a premature stimulus during a tachycardia, during sinus rhythm, after a pacing run, the hysperkinesis system, its refraction is gauged from the prior RR interval. So if it's presented with a short stem-stem interval, it is likely to block somewhere in the hysperkinesis system. And we take great advantage of that with some of our maneuvers. So premature stimulation in the hysperkinesis system is more likely to block than the AV node. But with fixed rate pacing and slow incremental changes in pacing rate, the AV node is the first to fail. When block occurs, when you encounter it, it may not be permanent. This may be catecholamine-dependent and may awaken latent conduction. If this occurs, it's more likely to help out the AV node than an accessory pathway. The AV node can awaken with catecholamines a dime a dozen. Accessory pathways, if you just don't have any retrograde conduction at the baseline state, chances are there is no accessory pathway with retrograde conduction. There's a handful of cases in the literature where that exists. All right, now this is a representation now off to the intracardiacs of short, medium, and long RP intervals. And this is really, really short. This is the P in the QRS, classically, and have a little bit of a RP interval here. This is a medium RP, and this is a long RP. And I show this because these are all different types of AV nodal reentry in one patient. And she hit the jackpot that day, had all three types of AV nodal reentry. Now, atrial activation in one-to-one SVTs, several different categorizations here. We'll go through these somewhat laboriously. If there is no discernible RP interval, that is, the atrial activation is within the QRS, this is almost always AV nodal reentry. Rarely you could have an atrial tachycardia with conduction down an AV nodal slow pathway, and it just so happens that the atrial tachycardia cycle length is very similar to the slow pathway conduction time, so the P wave sits in the QRS. Unusual conjunction of events, but it can occur. The short RP interval, that is, with the P wave occurring within the first third of the RR interval, or the diastolic interval, is almost always orthodontic AV reentry. It can be AV nodal reentry, either slow-slow, or even anterograde-slow, retrograde-fast in older individuals beyond about 65, 70, 75. The fast pathway seems to lose some of its fastball at that age, so the fast pathway retrograde conduction can appear in the early portion of the SC segment. Atrial tachycardias can also do this when conducted down a slow AV nodal pathway. Intermediate RP intervals, that is, with the P wave occurring in the middle of the RR interval, are more typically atrial tachycardias, slow-slow AV nodal reentry, orthodontic AV reentry with a relatively slowly conducting, or injured, accessory pathway. Somebody who's had a couple of ablations, and so it takes a little bit longer to went through the base of the ventricle and atrium where some wavered ablation has been delivered. That's certainly worth considering. Then long RP tachycardias, where the P wave is in the final third of the RR interval, are an interesting group, some of the most difficult diagnostic studies. These can be atrial tachs, they can be atypical AV nodal reentry, anterograde-fast, retrograde-slow, or orthodontic reentry with a slowly conducting and or decrementally conducting accessory pathway. These are quite interesting as a group. I didn't include junctional tach in most of these because they can just be anything and many of these varieties and are relatively rare. Now having said that, a lot of electrophysiologists don't even want to discuss the RP interval. Number one, it's hard to tell where the P wave is in SVT. I think we can all remember cases where we argued about that and everybody was wrong. With intracardiac recordings, it can be extremely difficult to know whether the tachycardia has a short or medium or long RP interval. It's kind of how many electrodes do you have and how do you categorize it. The differential diagnosis is always the same anyway, as illustrated here. So we have the RP interval, none short, medium, or long. And you can statistically get a characterization of what's most likely or least likely, but you see AV nodal reentry is everywhere here. Atrial tach is everywhere here. And the only thing that's not represented everywhere is orthodromic reentry and you can't have a P wave inside a narrow QRS complex and have orthodromic reentry. But aside from that, any of these can happen. Now to further illustrate this, looking at these four complexes during SVT, where is the P wave? Is there a P wave? Well, probably there's a P wave and you could say, well, there's a little hump here that's not part of the T wave. So it's probably there. It's probably a short to medium RP tach. And well, there's this thing here in V1, that's really not normal. So probably that's P wave. Maybe there's a second one here, tough to know, but this would then be a medium or long RP tachycardia. Okay, well, let's throw in some intracardiac recordings just for the fun of it here. And here they are. And so this is in fact, a short RP tachycardia. I don't see that P wave here too well, but it's a short RP tachycardia. It's also a medium RP tachycardia because the AVJAs are right in the middle there. And finally, it's a long RP tachycardia because of where the timing of the hybrid atrium is. So that is a reason why many electrophysiologists just say, you know, heck with it, don't even bother me with this short, medium, long RP stuff. I think it's useful to think in terms of what your differential diagnosis is and weighting things, you know, prove that it's not this as opposed to having to prove that it is. All right. Well, this is a, from a electroanatomic map, a CT of the heart for an AF case, but it had nice casting of basically all the chambers here. So we're going to look at concentric activation where conduction goes up the septum and goes up the AV node in both directions here. I've removed the ventricles on this side over here so you can see the two atria being activated nearly simultaneously. This gives rise to a very narrow P wave because if it takes an 80 millisecond P wave, 40 milliseconds of that from the right atrium to the septum, another 40 milliseconds traversed over the left atrium. If you're doing those simultaneously at the center, you have a very, very narrow 40, 50 millisecond P wave, easy to hide within a normal QRS complex. An eccentrically activated P wave coming from the left side, it looks like this with that progression. From the right side, it looks like this. Now, this would favor an inverted P wave in the inferior leads, but if you have a pathway that's way up here on the anterolateral anterior wall of the tricuspid anus, you can even have a positive P wave in the inferior leads. Same thing on the mitral anus, a little less common. All right. So here are a few examples of these different activation patterns with a one-to-one relationship. And here's ventricular pacing at a pretty slow rate here. I show you a retrograde hystere. I want to show a lot of these because I think it's a very important tool to have in your toolkit during these studies. So here's a concentric activation pattern. First at the AVJ, fanning out such that the catheter in the high lateral right atrium is activated about the same time as something in the lateral coronary sites. Pretty good rule of thumb. Now, here's an example of eccentric activation on the left side, where we have a left-sided pathway first to be activated. It's pretty reasonably bracketed here. Maybe there's a potential down here, and then it goes to the AVJ and then on across to the right atrium. So the very last thing we see here is the right atrium. Contrast that with an eccentric activation on the right side. And again, we have a nice retrograde hystere potential here. We have another one over here, and this is an eccentric right-sided pathway. You may say, well, this is just sinus rhythm and isorhythm dissociation. Could be for three beads, but as you pace a little bit faster, this tracks right along with it. So this actually was a right-sided accessory pathway in this case with a 14-year-old girl. Now, distinguish retrograde conduction from simply eccentric activation during an atrial tachycardia. For instance, these are two examples of atrial tachycardias. This with an eccentric activation pattern from the left, this with an eccentric activation pattern from the right, and neither of these are retrograde conduction. So that's why I want folks to think in terms of what is the pattern, what does it actually show, as opposed to putting an interpretation on it until you have further warrant to do that. All right. Now that we've talked about the horizontal axis, the VA time, we'll talk about the atrial activation patterns, the vertical axis during retrograde conduction. Concentric activation with the AVJ earliest is highly reflective of going up a fast avianodal pathway, but it certainly can be a septal accessory pathway as well. It's an important distinction, many ways to do that. If coronary sinus osteoactivation is earlier than the AVJ, this could also be going up the avianode, but typically breaking out on the rightwards extension of the avianodal slow pathway could also be, again, a septal accessory pathway, so-called mid-septal, which is actually the only types of septal pathways there are. Atrial tachycardias may manifest with either the AVJ or the CS having the earliest activation. These can come from a variety of areas in the neighborhood. Important to distinguish these one from another. We're not going to spend a lot of time on this today because it's not retrograde conduction, it's an atrial tach. But these can be arising from a perihistion source in the right atrium, coronary sinus osteum, the proximal mitral annulus. They can be left atrial tachycardias in the right superior pulmonary vein, left side of the septum, aortomitral continuity, and they can even be really not atrial origin at all. They can be from the non-coronary aortic sinus valsalva. So lots of different possibilities there. Eccentric activation coming from the left side, that is the mid or distal coronary sinus, is the earliest activation. The lateral right atrium is the last thing you see. Typically these are left free wall accessory pathways, but don't forget about left atrial or coronary sinus atrial tachycardias. And don't forget about avianodal pathways that may be very odd, even going out almost to the lateral wall. I've seen some that are way posterolateral, you'd say for sure that's an accessory pathway. And it turns out to be just a very oddball avianodal, can be fast pathway, can be slow pathway. And finally, eccentric activation on the right side, it is the right atrial recordings first, coronary sinus recordings being the last to be represented during retrograde conduction or during atrial activation, I should say. These are either right free wall accessory pathways or right atrial tachycardias. I don't know of any varieties of avianodal reentry that nicely fit into this. Well, just because you have one pattern of retrograde conduction doesn't mean you can't have a couple. This is a person in whom we're pacing the ventricle at a pretty stable rate here at about 400 milliseconds, 150 beats a minute. And we see this activation pattern here, which looks okay, ABJ first, then it goes to the CSs, almost the straight line here in the CS, that's a little bit odd, propagation shouldn't really look like that, but maybe our electrodes are in a funny location. And then finally, the right atrium. But as you go further along here, there's a shift that occurs. And it turns out that when the ABJ fatigues, as is usually the case, the more rapidly you pace, the avianodes is the first one to bug out and leaving an accessory pathway. It doesn't have to be that way, but it's typically that way. Over here, we have the coronary sinus activations basically unchanged from what they were. And now the ABJ has faded and the right atrium depends on going past the septum for it. So it also goes out. So over here, we were going up the avianode and this left lateral accessory pathway simultaneously. So there's a fusion of atrial activation that gradually changes over here. And by these two complexes, it's fully going up the left-sided pathway uniquely. With faster pacing, as I said, the avianode is typically the one who bails out first. The more recordings you have, the easier it is to be able to make these subtle determinations. If you only had the hyroid atrium, yeah, it's going out a little bit, but the morphology is just the same. It'd be hard to tell with just a single or a couple of catheters in there. This is another patient in whom there's a rather dramatic change in rectivate atrial activation during the trigger pacing. This is kind of reverse concentric here. The ABJ and the proximal CS are the last to be activated, not the first to be activated. So we have the hyroid atrium and the lateral CS being activated first and everything folds in after that. And it turns out that this is a person who has, over here, this right-sided early activation fades at this point. That's not a very rapid cycle, maybe about 700, something like that. This person had a right-sided, I guess she had pre-excitation and retrograde conduction on the right side and a concealed left-sided pathway. Here, they're fused, going up both pathways on this complex as well. And here, only going up the left-sided pathway, there was quite a bit in the lab. Now, I want to look carefully at how you can use extra stimuli to help sort out what's going on. What we're doing here is using extra stimuli to surprise the hysterokinesis system and take advantage of its inability to conduct under certain circumstances. So here we are with fixed rate ventricular pacing, a drive, and then a single extra stimulus, the S2. You see there's a nice retrograde hiss, and the hiss is typically before the local ventricular electrogram. We'll see why that is towards the end of our session here this evening. When you're pacing from the right ventricular apex, it scapes up the right bundle very rapidly and goes slowly muscle to muscle to this muscle that's immediately adjacent to, but not electrically connected to, this bundle. That's why we have a discrete interval between this potential and the local ventricular electrogram during sinus rhythm. But here with premature ventricular stimulation, it's early enough that it actually encounters the right bundle before it's refracted. This is recovered from this cycle over here, remembering that the hysterokinesis system's refracted here, discovered by what happened on the prior cycle, it can't anticipate. And it's pretty lazy, so it doesn't gear up its repolarization for no good reason. So here we catch the first portion of the normal conducting system that this wave front comes to. It's the right bundle. It blocks retrograding the right bundle, goes across the septum, up the left bundle, and then this so-called hiss out the back here. Notice what happens with atrial activation. It also pushes up. So in this case, we have atrial activation that seems to depend on an antecedent hiss. You move that hiss around, the atrium follows. They're linked together. So this hiss to A interval is about the same as this hiss to A interval. This hiss to A interval here may be a little bit longer because you're premature in the hiss one way or another, and by virtue of that, the AV node, so it could sling out a little bit, but it shouldn't in the short. So in this situation, the A follows the hiss with the same or perhaps longer HA interval, and this is indicative of AV nodal conduction. The more premature your extra stimulus, the further in the hiss eventually you'll come to the functional refractive period, and the hiss won't move in anymore. Contrast that situation to this situation here, where again, we have retrograde hisses that have gained up here before the local configured electrogram, one on the extra stimulus that blocks in the right bundle, retrogradedly goes across the septum, comes up the left, and here it is. Big deal. The A follows it. Big deal. That's nothing special. But what is special here is that these are the A's during the drive cycle, and you have this HA interval here, but now we have this HA interval. That's not right. In fact, some of these A's almost start simultaneously with the hiss. So these A's are being activated independently of the hiss, and in fact, this is a concentric activation pattern here. It looks pretty concentric, but now the right atrium and AVJ are slung further out. So this probably had some conduction up the left side of the pathway and the AV node, and now with the hiss going out, we're going up only the accessory pathway here. So that's the atrial activation sequence there versus the earliest atrial activation. Here it is in the AVJ. Here it is now in the distal CS, lateral CS. This is an even more egregious example here in which we have an extra stimulus giving rise to that hiss out the back there, but the A occurs actually before the hiss, so there's no possibility whatsoever that this A was conducting up the hysperkinesis system of the AV node. This is going up an accessory pathway. So you can use extra stimuli during sinus rhythm, during following a slope and triggered drive to your advantage to help tease out whether conduction is capable of going up an accessory pathway or not, even when it may not be so evident during fixed rate pacing. We'll come back to that. So here's this atrial activation sequence, pretty much the same on both the drive beats and the extra stimulus, and the hiss is just totally irrelevant. Here it is before the local V. Here it is after the local V. It's saying, hey, follow me, and the atrium is saying, I don't need to. I've got another way of getting back over an accessory pathway. So there's those hisses in this outline. In this case, the A precedes the hiss, and it is indicative of accessory pathway conduction. Now a trick that you can use, especially with septal pathways in which your activation sequence is going to be very similar, whether conducting over a pretty good AV node or over an accessory pathway, is to use the element of surprise on the hisperkinesis system again, and that is coming from sinus rhythm and giving a relatively rapid burst of intricate pacing. The first few cycles will catch the hisperkinesis system by surprise. Here's a retrograde hiss here, but then on this second complex, the hiss is way out here, and the hiss is over here. In fact, these, we'll come back to that in a second, but by the time you have paced for several cycles, the hisperkinesis system accommodates to the more rapid cycle length of pacing, and it says, okay, now I'm going to repolarize more rapidly, and eventually you start conducting one-to-one. We don't see that here just yet, but the interesting part here is that we have a hiss before an A, and now we have a hiss after an A, and in fact, these complexes here are fused, going up an accessory pathway and turning back around and going down the AV node, and so these are fused with pacing and anterograde conduction for a couple of cycles here. So this is before ablation of a septal pathway pretty near the AV nodal region, and we're, but there's no pre-excitation, so we can't go by that. After successful ablation, so there are those A's, they're independent of hiss activation. The hiss is just kind of doing its own thing, and here's an A again well before the hiss over there, just trying to help out the best it can, but it's still quite delayed. So in this case, retrograde conduction is independent of the hiss, and that indicates the presence of an accessory pathway. That you, if you've done some ablation already during this case, you got more work to do. And now, and we've done some work, we've done some more ablation here, and we're doing the same thing, burst spacing the hiss, trying to get it separated out so we can see it clearly between complexes here and discern whether atrial activation, in fact, depends on the presence of that hiss or it doesn't care about the presence of the hiss. So here's a sinus complex that doesn't count as a retrograde hiss. Here's a hiss out the back, and an A follows it. And here's another hiss before the local B, and A follows it. There's another hiss, so this is two to one, going up to the Hiss-Purkinje system. If we paced for a little bit longer, we'd gradually go to one to one. We wouldn't learn anything, but when we can surprise it and get it to dance around here, you can get it to give you some information about hiss dependence or independence of atrial activation. And in this case now, we have the atrial activation dependent on the hiss, so this is going up the EV node, the pathway has been successfully ablated. Great. All right. Now, so we've been talking about one to one VA relationships. Now we're going to be talking about second degree VA block. We may not have one to one conduction during ventricular pacing. When you have a gradual increase in the VA interval with incremental rates of pacing, and then finally have retrograde winky block, that is indicative far more likely of the EV node than an accessory pathway. There are exceptions to this, but as a general rule, the faster you pace, EV node will gradually increase its stem to A or VA interval, and finally start winky blocking. Accessory pathways can do that, but they're not characteristic. It's more of an all or none, generally all or none phenomenon. That's indicated here. So a minimal increase or no increase in the VA interval with more rapid pacing, eventuating into the point of two to one VA block, is far more characteristics of accessory pathways. But be careful, because EV node fast pathways, especially in individuals who have EV node reentry, can behave exactly like that. It behaves much more like an accessory pathway or normal atrial muscle than it does EV node decamel tissue. Retrograde conduction can also be assessed in response to extra stimuli. We saw a little bit of that earlier with the hiss coming out the back and whether the A is dependent on the presence of the hiss or not. And if you have a gradual increase in the VA interval or the HA interval after extra stimuli, much more likely you're dealing with the AV node than an accessory pathway. Contrary wise, if there's no increase or minimal increase in the VA interval or an HA interval that's shorter than it was on your drive, it's not really an HA interval. That implies that there actually is H going to A, but there's an H and then there's an A and that pseudo interval is shorter because it's not conducting over the hysperkinesis of an AV node that indicates the presence of an accessory pathway. We saw examples of that earlier. I can't stress enough how important it is to have a good hiss potential on your side here and work for this and work to find a ventricular pacing site, a hiss recording site that can give you a decent retrograde hiss. It really helps out in making this determination of whether your atrial activation depends on or doesn't depend on prior activation of the hiss potential and therefore whether it's going up the normal conduction system or an accessory pathway. Here's an example of retrograde AV nodal Winkiebach. We're used to seeing AV Winkiebach with a gradual prolongation of the downstream effect with a constant or slightly more rapid upstream input. Here we're having input from below and seeing what happens on the downstream cycle, which is actually in the atrium. So we have, again, a retrograde hiss coming along here on each complex. And you would say just on the face of it, the fact that we don't have A's on every single B, we're missing them here, says that, yes, we're blocking retrogradely and it's gotta be in the AV node because we got to the hiss. And if you get to the hiss, you can pretty much get through the hiss and present a complex to the AV node. So here, our stemmed A is gradually prolonging until it fails. And then the cycle repeats over here with a shorter and then gradually longer VA interval. We should all be accustomed to recognizing that. I have a couple of examples of instances in which conduction goes one-to-one and then suddenly goes to two-to-one. This is one of those. And in this instance, when we're with one-to-one conduction, the stem to this atrial signal here, 153 milliseconds, when it goes to two-to-one, over here, it's not much different. It's about 149 within the range of error here. So there's minimal increment from your slowest pace cycling to your most rapid cycling where you go one-to-one and then down to two-to-one in the presence of an accessory pathway. They're typically all or none. There are exceptions to this. Almost always there are exceptions to everything, but it's a pretty good rule of thumb that you don't have much increment in the stemmed A, the VA interval, when you're pacing on an accessory pathway until you get down to very close to refractors. Now, this is an interesting case here, where, again, we go from one-to-one suddenly to two-to-one conduction. It's not winky bonking, it's just two-to-one conduction. And there's a little slight difference here because if you look at this stemmed A here, it's clearly longer over here than over here. And they measure out to 193 milliseconds when we had one-to-one conduction, and now it's 159 when it goes to two-to-one. And this type of, this degree of disparity is more typical behavior for an AV noder. In fact, this was going up an AV nodal fast pathway in a moderately mature woman with, older woman, I should say, with a typical AV nodal reentry. She'd had it for years, she finally got tired of it, presented herself for a study, and this is what she had. Now, I want to focus for a few minutes on retrograde block. Boy, this is a downfall on the board exam. People just, for some reason, have a great deal of difficulty at determining whether there is even VA conduction. Sad to say, even some of my fellows on some rare occasions have a difficult time with this. I'm not going to mention any names. And when block occurs retrogradely, it always occurs somewhere. And by and large, with fixed rate pacing, it's in the AV node. In fact, I'll say, I'll say 99%. I'll say more than 99% of the time. 99.5% of the time, maybe more than that. When you have fixed rate pacing and you're not conducting to the atrium at all, the block is in the AV node. So you can look really smart if your attending says, hey, we got retrograde block here, where's the block? You say, well, it's the AV node, without even looking at the thing. You'd be right, except 0.5% of the time. Now, we can be smarter than that. We can know why that's the case instead of just going by the numbers. And what's going on here is that we have sinus A's along in here. There's one hidden in here. There's one there. There's one there. And there's one over here. And we have a PR interval that's normal over here. There's a first stimulated complex doesn't really capture very much. So that's a normal anterograde conduction. Same thing off over here. And when you don't have any retrograde conduction, it's important to recognize this. And there are easy ways to look at this. The A's are regular. Typically, there's a sinus activation sequence if you've got enough catheters, electrodes to look at for that. And the A's are slower than the V's when you're pacing the ventricle. Now, you can also look at your surface ECG. Remember, that's an important tool that we have and say, yeah, that looks like a sinus P wave there. Can't really see it too well in here, but it seems like it may be the peak of that T wave with positive complex, just like it is over here. Now, when you have block in the AV node, a cardinal feature of this is concealed conduction. Everybody knows what concealed conduction is. It's when you have penetration of a structure, most typically on an everyday basis, it's the AV node, conduction into, but not through the structure. And it renders it partially refracted such that subsequent impulses have a difficult time or have no chance at getting through the structure. Most typically, again, the AV node. So here we are coming along. We're pacing the ventricle. We don't have any VA conduction. And look at this. We have retrograde hisses all along the way. So you say, okay, I know what's going on here. We have retrograde hisses. It's getting to the hiss, through the hiss. You say, when you're pacing in a slow rate, the Hisperkinia system is your friend. It conducts faithfully. So if we have a block, it's gotta be in the AV node. Good reasoning, but it's even better reasoning to look at what happens over here. Look at this PR interval, look at this AH interval. It's dramatically longer than it was on either this bead over here or this bead over here, which we use as our golden thieves to look at and say, okay, that's my standard. And I'm gonna evaluate this bead over here as against the standard over here. This is what normal conduction looks like. What's going on here? Well, why is this AH longer? Why is this PR longer? It's because we've had concealed conduction that penetrated into the AV node and rendered a partially refractory, such that the next atrial complex to come down has a harder time getting through. It takes a little bit longer. A common phenomenon in the AV node in both directions, antero and retrograde. So there's that much wider PR, much longer AH. And I wanna illustrate to you that you don't even need the intercurrent recordings. There it is, it's right there. You can tell by this, why is there such a longer PR interval here than over here? It's because we had concealed conduction into the AV node. Very, very straightforward concept. Now, here's something that you're probably not gonna see real often. In fact, I know you're not gonna see it real often because I have about three or four examples of this. I look at the hissing practically every case within thousands and thousands of cases, and I've only seen this phenomenon a few times. And believe you me, I look for it. So here it is. This is retrograde block in the His-Purkinje system. It doesn't even get to the hiss bundle. How can you tell? Well, remember if we are getting through the hiss and into the AV node, we should have some effect on this AH interval. Look, it's just always the same here. We don't have any hisses before or after a local ventricular electrogram. And this is AV or VA block. The A's are again regular. It's a sinus activation sequence. We have a sinus P wave here, and these activation sequences are the same. So I can infer that each of these complexes, the regular as they are, are all sinus complex, the same thing over here. And yet there's no influence of what goes on below that in the ventricle on that AH interval. So if the AH and PR interval are constant, not the PR interval, but the AH interval is constant, or a PR once you stop pacing, or if there's a complex that's through, that means there's no penetration of the AV node, no concealment, and block is before you get to the hiss. Now, this person has a really sick hiss Purkinje system. There's that AH interval. Here it is during sinus rhythm. AH interval is exactly the same. There's been no effect of the ventricular pacing on it. And this HV here is, I don't know, about each one of these is 100 milliseconds. That's probably about 130, 120, 130 millisecond HV interval with left bundle branch block, sick hiss Purkinje system. Maybe some entry medicines have a little bit to do in the mix there as well. But this patient brought a lot to the table himself with a very ill hiss Purkinje system. All right, another way that people stumble on the board exams is retrograde dual AV nodal pathways. These are quite common in the population. Pretty irrelevant. Not too many people use these in any form of a CT scan. And boy, those bad guys on the board exam, I know at least one of them that's in on this broadcast here. They like these questions because they test what the candidate knows. Not so important electrophysiologically, but it tests the mental of the candidate. Now, how do you recognize retrograde dual pathways? Well, they have two different and relatively discrete VA intervals, just like with anterograde dual pathways, you have discrete H intervals or AV intervals. In this situation, you also typically, not always, but typically have two different atrial activation sequences when you're jumping between pathways. AV nodal echoes of an atypical nature that is anterograde fast retrograde slow may occur at the time of switching between one pathway or the other. So the way this works is during slow ventricular pacing, ordinarily activation goes up the fast pathway. And then as you pace a little bit faster or the fast pathway fatigues, and this gives rise to a short VA interval with earliest activation, the AVJ, but as the pacing goes on, the fast pathway suddenly fails and it shifts instead of blocking entirely, it just shifts to the slow pathway. Now, the difference between the fast pathway and the slow pathway is one is faster than the other. That's how it's called the fast pathway. So it conducts rapidly, gets back to the atrium with a short conduction time. When it fails, it reveals the presence of a slow pathway, which isn't only distinguished thereby, but it also has a different atrial activation pattern, most typically earliest activation in the proximal CS, near the coronary sinus ostium. I have a couple of cases where it's just exactly the opposite of that, where the fast pathway seems to exit closer to the CS ostium and the slow pathway exits northward, very unusual situation, but by and large, in the examples I'll show, this is the rule here, fast pathway, AVJ is earliest, slow pathway, CS ostium is earliest. When that shift occurs, since you're blocking in the fast pathway, retrograde A going up the slow pathway, now you can come back down the fast pathway and activate the HISS and actually cause a QRS complex, which may be the same as the baseline QRS complex during sinus rhythm, or it may be fused with pacing, depending on what your pacing rate is and the slow pathway retrograde induction time. So here we are, we're pacing along in the ventricle, minding our own business, nice retrograde HISS here, it's there on all of these complexes. The A's are here on all these complexes also, except for this one, oh, but wait, just wait long enough, and there's another A here. Now, you could say, well, this is just a PAC, you could say it's the sinus complex, well, if you tried to tell me it's a sinus complex, you'd be way wrong because the atrial activation sequence is very wrong for that, the P wave is inverted, remember the surface CCG as well. So here we are conducting along, earliest of the fast pathway, fast pathway conducting with fast conduction time and earliest in the AVJ, then when we block in the fast pathway, all of a sudden we go earliest in the coronary sinus os region, go up the slow pathway, it can turn around in the fast pathway, so we have this long short sequence here, not long shorting like in Ashman's phenomenon, but going up a slow pathway back down a fast and an atypical AV nodal echo. This is not a normal looking QRS complex, it's fused between normal complex and the paced complex over here. So we'll see another example here, where we're coming along at very slow fixed rate of pacing, and this instance here, we again have earliest activation in the AVJ, not many people would call this a fast pathway, this is about a 250 millisecond conduction interval, well, it happens to be fast for this person, because when we continue pacing, it suddenly shifts to the AVJ not being in the earliest, but the CS os now pulling way in, and almost coincident with the AVJ, but a much longer VA time here, and a narrow QRS, in fact, a completely normal QRS because the stimulus artifact occurs after the local ventricular electrogram that it would have tried to capture. So this is an instance of again, retrograde dual pathways with a pretty sluggish retrograde fast pathway, blocks in the fast, goes up the slow back down the fast with a completely normal QRS complex here. Now, when you are pacing the ventricle at a relatively slow rate, fixed rate, and you don't have consistent, don't appear to have consistent ventricular captures, think of a couple of things here, think of the absence of retrograde conduction entirely, and then you have the ventricular pacing run is interrupted by sinus capture beats along the way, if you saw something like this, and there's no VA conduction, you could have a P wave that just happens to occur there and conducts down the ventricle, you could have as here, retrograde dual pathways with atypical labia nodal echoes going up a slow down a fast, this will tend to be highly repetitive because you have three or four cycles going up the fast, it blocks in the fast, goes up the slow, goes down the fast and echo, the next speed starts a cycle again. It is less the least likely possibility for inconsistent ventricular capture is inadequate stimulation output. How many times you try to crank up the output, it doesn't do any good because that's not the problem. This has no chance of capturing here, and it's not because the output is inadequate, the output is just great here, the problem is that you interrupted your pacing drive with these retrograde duals here. Now, a little bit of fun here as we're getting close to wrapping up with retrograde conduction, this is some problems in the hysperkinesis system, retrograding now, we're used to seeing with extra stimuli, the hys out the back, that's great, that's nothing new, but here during our drive beats, the hys is out the back, it's usually in front of the carotid, remember I said, when we are pacing the ventricle, the right ventricle towards the apex, somewhere on the septum, near the moderator band, you get into the right bundle pretty quickly, it skates up the right bundle, a very rapidly hysperkinesis system activates the hys retrogradely, way up front here before conduction goes muscle to muscle to this ventricular activation here, so why is the hys out the back even during the slow drive beats, that acts like there's block in the right bundle already, well, look in our sinus beat, and yeah, there is block in the right bundle already, so there's a proof of truth in electrophysiology, and all is a beautiful thing, and we have some VA conduction here along the way as well, just for the fun of it. Now, here's a diagrammatic representation of what's going on here, this patient over here, I will postulate has a normal QRS complex, normal QRS duration, normal hysperkinesia activation during sinus rhythm, and so when you pace the right ventricular apex, we have our hys in front here, we have our local ventricular activation in the perihysian septum delayed after that, and the reason for that is when we're stimulating there, it goes rapidly up the hysperkinesia system, slowly muscle to muscle, and then activates this other tissue here, and when we have right bundle branch block in sinus rhythm, such as this patient over here, we try to do the same thing, we'll start over here, going rocketing up the right bundle, slowly muscle to muscle, but in this situation over here, we stimulate, try to go up the right bundle blocks, it still goes slowly muscle to muscle, so it gets to the local V here about the same time, but the hys is activated by this long circuitous way, it has to go across the septum, and up the left bundle to get to the rest of the hysperkinesia system, so that's why the hys is out the back there, and you can see that during drive beats, when you have right bundle branch block during sinus rhythm, you see it routinely during close to coupled ventricular extrasthenia in the right ventricle, where you block retrogradely in the right bundle, just like this. Now, a few years ago, the group from Cornell, with their great expertise in use of adenosine, I just gave a bunch of adenosine to a bunch of folks, and said, how can we use this information upfront, beginning of an EP study, looking for diagnostic information regarding NCTs, well, they gave adenosine 12 milligrams upfront during ventricular pacing, and if VA block was present, you didn't have to go any further, if VA conduction was still present, you just jack up the ante a little bit, and pace a little bit more, or give a little bit more adenosine, 24 milligrams, that'll knock out most horses, as well as AV nodes, and then you add a few more people who have VA block, so the total number of people of this 139 who had VA block with adenosine was 97, and almost all of these did not have an accessory pathway, so if you have adenosine-sensitive retrograde conduction, almost never is it an accessory pathway, the exceptions were patients who had an adenosine-sensitive accessory pathway, a little bit of an unusual crowd here, I wouldn't think there'd be that many, but they were in this case, if you have VA conduction, it may or may not be orthodontic SCT to an accessory pathway, another way of looking at it is giving 12 to 24 milligrams of adenosine during a particular pacing, and if a VA block is present with that, it's really, really unlikely to have an accessory pathway, can occur under certain circumstances, and the rest of this is pretty self-explanatory, and I'll leave this to your reading, you'll have this, Dr. Verma's going to post this later, for your further study to choose to do that. Now, just ending up here, a few little straggling tidbits here, you may have retrograde conduction present even when AV conduction is absent, and this is an interesting thing, you go in to put in a pacemaker with somebody who has complete heart block, and lo and behold, they have nice retrograde conduction, just like you can have no VA conduction in somebody who has very robust AV conduction, you can have good VA conduction when AV conduction is absent. Retrograde AV node conduction, rarely accessory pathway conduction, may be absent when you get into the lab and you're first pacing the ventricle, and in those cases, an atrial tachycardia is more likely what's going on if they have an SVT, you can wake up an AV node pretty easily with some catecholamines, maybe five, 10% of patients with documented AV nodal reentry, and whom you can initiate AV nodal reentry with presence of catecholamines, will not have VA conduction in the baseline state, really unusual for an accessory pathway to do that. Retrograde AV nodal conduction pattern is typically midline, but can be eccentric with these oddball pathways going off into the coronary sinus, even pretty deeply into the coronary sinus. And finally, demonstration of a concealed left lateral pathway can be difficult if you're pacing the right ventricle and it skates up the AV node, it's up the hysperkinesis and AV node very rapidly, and you say, well, I don't have a left lateral pathway. Sometimes you may need left ventricular stimulation via transeptal or retrograde access, or sneaking a catheter out of the coronary venous branch and be able to see that, yeah, I do have retrograde conduction of the left system. Sometimes you have to get another catheter into the left ventricle and pace to really be able to assess whether you're at your earliest activation or where a pathway is in the presence of very good VA conduction of the normal system. Here's an example of that, where we're pacing the right ventricle here, and we have a midline activation sequence here, and it's a little funny, I'm just a person who's had a couple of different prior ablation attempts with a left lateral pathway, and so it's concentric activation pattern. But when we pace the left ventricle here through the ablation catheter, you see, yeah, we still got basically concentric, but there's some stuff going on over here as well, and it was still left eccentric activation, and we wouldn't have been able to see that very well at all where we just paced it from the right ventricle. You can say, well, we just paced faster and the AV node fatigue, usually that works, not all the time, and I'm not sure that you wanna pace it 300 milliseconds or 250 milliseconds when you're mapping retrogradually just to show exclusive pathway activation. You may need to do that with right ventricular basal pacing as well. If you've got a very slick AV node, you're pacing the RV septum and a lateral right atrial AV pathway that doesn't affect very well. So in summary, retrograde conduction is important to understand. It may be present or absent. There are different patterns of atrial activation, and they imply different things about what pathway you may be traversing. Don't forget to look at the surface ECG for the P-wave morphology. It can be very helpful sometimes and make or break the situation. Don't, in your mind, retrograde, equate a retrograde P-wave with an inverted P-wave in the inferior leads. That's a description. It doesn't imply a mechanism. It could be an atrial tachycardia. Retrograde conduction has consistent features with fixed rate pacing or slow, slowly faster pacing. The AV node fatigues earlier than the hisperkinesis system, whereas with premature extra stimuli, the hisperkinesis system fatigues more rapidly than the AV node. You can use this to your advantage and make sure you can distinguish between accessory pathways and normal conduction using extra stimuli. Keep an eye on that his. Whether VA conduction is dependent on it or not, it will be your friend. And beware of retrograde dual AV nodal pathways. And I think we may have time for some questions here. Dr. Verma? You have those audience response questions if you'd like to go over. So you stop me when it's time to stop, but we have four questions here. It's question number one. And we have intracardiac and surface recordings of a 34-year-old man who's undergoing EP study for evaluation of palpitations. Our figure shows one of the following. It's multiple choice, so one correct answer. I think everyone should be able to see the poll I put up. Take a look. Take a little bit of time. Maybe while they're looking at that, I can ask you a couple of questions that have come through. Sure, yeah. One was tips for getting that beautiful retrograde hiss that you seem to have on all your slides. Side of pacing or where you put the catheter. It's a combination of where you can record a decent hiss potential during sinus and having that being nice and stable. And then pacing a variety of areas on the septum. Some people favor pacing very basally. I like to pace a little bit more apically, mid-septum or more apically. And it just makes the differential in the conduction time going up the right bundle. It accentuates that physical and electrical distance and makes it much more advantageous, I think, to see that hiss very, before the local ventricular electrogram. Now, if you use very closely spaced electrodes in your hiss recording, it's not such a problem. But with our standard five millimeter space on a quadrupolar catheter, I like to move around the right vendor a little bit and pick a good pacing site and keep it there. We have 35, 36% of people who have voted. It looks like the majority are choosing no retrograde conduction and blocking the AV node. And bully for them, that is correct. And so we see, this AH interval here. First of all, we have regular A's along the way here with the sinus activation sequence. And on the exam, they're not terrible people that write these questions, I can tell you that. But they give you all the information you need and you just need to figure out where to look for that information. So here we know what the PR interval and the AH interval should be with normal conduction. Here it's longer, inexplicably longer. Well, it does have an explanation because we have conserved conduction here. All right, so sinus activation sequence, blah, blah, blah. We've already talked about that. Go on to the next one? Yeah. Okay, I'm gonna pull this out of the way here for a second. Which of these statements concerning retrograde conduction in the above figure is true? And you can see your choices there. And I'm gonna pull this just a little bit off to the side here. So the folks can be pulled off to the side. So folks can see. And then another question that came through on the slide where you had bidirectional right bundle branch block on the premature ventricular extra stim, the H moved out significantly further than at baseline. What accounts for the additional delay there? Yeah, it's hard to know. I think it could be transeptal conduction in that situation because if we already have retrograde block in the right bundle, you would think, hey, it's not gonna take any longer to get to the right bundle. But there are other things interposed in there going up the left bundle. But more than likely it's tissue, the closest to your stimulation site is gonna have the wave front encounter it first. It's gonna have the longest refractoriness. So more than likely it's just transeptal conduction. We could answer that by having a catheter on the other side of the left ventricle and recording the left bundle potential. All right, 66 votes, 70 votes. All right, very good. And it turns out that that wins and there's a good reason for that. It is correct. And you guys either looked at the answers beforehand or you're just ultra smart. What we have here is a situation in which, I'm sorry, in each of these cases, each of these conflicts, sorry about that. Okay, one more time. We have the CSs are exactly the same. The AVJ pushes out. The stem to A is the same in the CSs. So we are connecting up an accessory pathway all the time. And in the AV node with the AVJ a little bit earlier here on other instances. Very good. All right, third question here. Which of these statements concerning retrograde conduction in the above figure is true? There are your choices. We'll have to refresh the poll over here. Okay, we're done. And I'm going to pull that over here again so we can see our electrograms. We're trying to slow down. Oh, boy. It's exciting. Two of the answers are tied. Wow. All right, well, we'll go with what we got. Let me end this. I think they can see the results now. Ooh, just wins with D there. Well, it turns out D is correct. It is going over the AV node and all these complexes. You see that the AVJ here is, there's our hiss out the back, and the A's follow it, but, and there's our earliest activation. We're actually going over a right lateral pathway over here because it's even earlier than our AVJ. That fails on this complex over here, and we're just going up the AV node on that one. So, AV nodes governing activation on all three complexes. We know that because the CSAs are around the same time as they are these A's over here, AVJ. All right, and there's, A is a little hidden here, but if you can see it here, you should have seen it there, but it's in the quiz. All right, last question here. Easy question. A man with documented SVT undergoes EP study. You have the usual differential diagnosis. In the baseline state, without any sedation, he doesn't have any retrograde conduction. With this finding and knowing that he has documented SVT, we want you to rank the possible choices of possible diagnoses in rank order. So, the most likely to the least likely. I'll ask you another question while we're waiting. There was a question on supernormal conduction and whether, I guess, is that a real phenomenon that we see? Well, I'm not sure we see it in real life. We see it in cellular preps occasionally, but I think pretty much any time you are thinking about supernormal conduction as an explanation for a phenomenon that's observed or other alternative explanations that probably fit better. But it's a great thing to pull out of your bag of tricks. There's a gap phenomenon, there's concealed conduction, there's supernormal conduction. If you're really stumped, you can just start doing some word salad, throwing those guys out and maybe deflect some attention from them. Okay. Let's end this one. Boy, you know, you guys are just right on here and you were listening or you already knew this. And I consider my job done because everybody, the majority got all of these right. I didn't have any real good curve balls here. I'll try better next time.

retrograde conduction

electrophysiology study

atria activation

ventricles to atria

patterns of retrograde conduction

eccentric atrial activation

atrial tachycardia

AV node conduction

accessory pathway

extra stimuli