Greetings, this is John Miller, representing Heart Rhythm Society, and I'm going to give a presentation on electrophysiologic foolers. We run into things all the time during procedures that we're not expecting, and I've run into a lot of these on my own, so I'm sharing some of my sometimes sad experience, and hope that you can have a vicarious experience and not have the same problems that I've had in the past. So, we'll start here. There's some road hazards along the way. When we're doing an EP study, we expect to see certain things. They're not always what we get. Second, we may not see what we were expecting, and we may see what we were not expecting along the way. And the good electrophysiologist has to be aware of the possibility of unexpected occurrences and know how to deal with them effectively during a procedure. It's important to always remember to be able to ask the question, what's wrong with this picture, as well as exercising the principle of testing what you don't know by what you do know. That'll get you out of a lot of trouble. So first things first, we have to make sure everything is connected correctly. This is pretty fundamental, but it's pretty important. You can imagine how important it is in certain situations. ECG leads, all catheters securely into their connector blocks. Inability to capture with pacing may not have anything to do with electrode position or contact, but it may have something to do with how it's plugged in. If it's not plugged in all the way, then you may not be able to capture. Pretty frustrating. All connector pins must be securely into their correct receptacles, that's the coronary sinus, halo electrodes. Most systems now are one plug to put in, but in the old days, you might have a coronary sinus with 10 different electrodes to plug in, and we had one that was plugged in by color once. The nurse was new at this and decided it should go by the rainbow instead of 1 through 10. Pretty good. Make sure the catheter positions are correct, what you intend for them to be, because they can change. Coronary sinus catheter or other reference, of course, if you're using a timing reference from the coronary sinus or any other supposedly static electrode and it moves, you no longer have a stable timing reference for activation mapping. Halo catheter, a 20-pole catheter around the right atrium, if that moves, you can get some pretty weird stuff going on. We'll see some examples. Most of our mapping systems enable us to take a snapshot of a catheter position such as if you think it's maybe become dislodged, you can move it back into position and not lose too much ground. Here's an example here, this is a 23-year-old woman with palpitations coming to the EP lab for a procedure. And you see that she's got a delta wave here, a nice delta wave, and it looks like it's probably right-sided here, although it looks like it's probably left-sided here. Does she have two pathways or are the arm leads reversed? This is a simple thing. This is probably the most common abnormality we run into in ECGs and just the stack of ECGs to read, but it can happen in the EP lab as well. People are talking to the patient, trying to put them at ease and not paying as much attention to where the leads go as other connectors go to where they should be. This is a correct position, it really is a right-sided pathway. You see it's a right-sided pathway because the pre-excitation starts before the P wave has even ended. It can only happen if it's a right-sided pathway close to the sinus node and so on. So helpful aids in making sure the ECG is correct. Your sinus rhythm P wave is a great help because in lead one it should be positive. Most of us hang out in sinus rhythm, and if your patient's in sinus rhythm that day and they have a negative looking P wave in lead one, there's a problem. Sinus rhythm P wave in leads two, three and ABF should be positive as well. Does the ECG make sense or is it something around it that just doesn't look right? Answer that question before moving on because you can get really in the weeds. Imagine if you will that you are looking for something that has an inferior axis when it actually has a superior axis because the leads have been placed incorrectly. This is however a problem when sinus rhythm is not present at the beginning of the procedure or it's not a reliable indicator such as the presenting rhythm is not sinus, it's atrial fibrillation, ectopic atrial rhythm, SVT, ventricular tachycardia, or a paced rhythm. Baseline assumptions may be incorrect under certain circumstances such as cardiac malpositionings, extracardia, a left pneumonectomy, the heart's way off on the left side, or prior ablation or surgery. You can't rely on some of these clues. Otherwise, it's a pretty good way of looking at things. Now, here's a person with atrial flutter. You think this is going to be just a standard atrial flutter and you get things connected and say, oh boy, we got a hot one here today. Well, maybe we do, maybe we don't because this is the correct connections of the catheters. This particular catheter has 20 poles on it and two sets of tens. And if you get these reversed, you get some funny looking things. So here was before, here's after making them correct. It's just flipping the connectors so they aren't together. Reversed connectors, very interesting arrhythmia there and not quite as interesting on the right, but much, much easier to deal with when the connectors are properly placed. Also important is the position of catheters. So here is a coronary sinus catheter, here's a halo catheter, looks kind of wonky in the right atrium here and you get some pretty funny looking activation patterns with it. Here, the halo is more appropriately related to the tricuspid annulus and now we have a very familiar looking activation pattern on the halo electrodes. This is a problem that we have from time to time. This is what looks like typical flutter. We have this apparent rotation around the tricuspid annulus here, looking kind of from bottom up here. And in point of fact, this nice activation map here, 260 milliseconds of tachycardia, we have 263 milliseconds covered, that's pretty good. But in point of fact, what this was, as a patient who had had chemotricuspidismus ablation before, block was present and this was actually a left atrial tachycardia entering around the coronary sinus ostium, in which case it ran into obstruction here, propagated all the way around and its cycle length was about the revolution time around, the propagation time around the tricuspid annulus. The importance here is that if you just look at this pattern, you know what's going on here, this is typical flutter, you can touch it up a little bit and you're two hours, three hours later, you're still touching it up because it doesn't terminate, because it doesn't care that you're there, it's a rhythm coming from somewhere else and the isthmus is already blocked. So, don't fall for that. This is pretty common after a flutter ablation. Left atrial tachycardia is organized, tachycardia is flutters, can mimic typical right atrial flutter with the tachycardia cycle length closely approximating the conduction time around the tricuspid annulus. Now, if you were to do something like pacing down here on this side, you would resolve the matter, because here's a situation like that. We have a pacing from one of the electrodes, it's off on the infralateral right atrium, such as about here or so, and you see that this should be in the circuit if it is actually propagation around the tricuspid annulus in this counterclockwise fashion. Instead, we have this very, very long post-pacing interval, almost, well it is almost exactly twice the tachycardia cycle length. This area is not involved in the arrhythmia, so this is not typical flutter, didn't look like it anyway with the coronary sinus electrodes being distal to proximal, but you don't know where that coronary sinus catheter is, how far out it is. All right, moving on to some foolers in the realm of AV conduction. When you're assessing AV conduction, we expect to see winky bach as the pacing rate is increased. Wonderful. Several things can masquerade as winky bach, that is an atrial stimulus not followed by a QRS. The most common is probably not capturing the atrium. If you don't capture the atrium, you're not going to drive a QRS complex, so it's inadequate output, inadequate contact, so on and so forth. Atrial premature complexes can come along and find the avenodal refractory, it's not going to conduct, or it will prevent you from capturing the atrium and not conduct in that regard. Avenodal echoes also interrupt a drive quite commonly. You really can't define winky bach in those situations because it keeps having an avenodal echo along the way. Pseudoconduction can also occur, not pseudobot, but pseudoconduction. You might be pacing the coronary sinus and thinking you're capturing the atrium, but you're actually capturing both atrium and ventricle. This is especially problematic when you're trying to assess how rapidly an accessory pathway can conduct when you're pacing from close to the annulus. Actually capturing ventricle, you'll be pacing down to 200 milliseconds and think, wow, we've got a really crazy fast pathway here, when in point of fact you're capturing ventricle at the same time. Pacing the right atrial appendage or the top of the tricuspid annulus and capturing both atrium and ventricle can occur on that side as well. All right, here's a loss of capture simulating winky bach. If you're just counting QRSs and you say, oops, missing a QRS, that must mean I had winky bach. Well, make sure you have A's along the way here as well. So missing A there, not really winky bach. Getting close to it, but not really there. Here's another situation where we're coming along, pacing the atrium, gradual prolongation of the PR, and in fact, an AV nodal echo here, another one over here. So you really can't define winky bach structure in that circumstance, but it is an unexpected absence of a QRS when pacing in the atrium. Here's a patient who has a right-sided accessory pathway, and we're pacing the atrium here at the lateral tricuspid annulus, seeing how well it conducts, and in point of fact, it seems to conduct really well here. That's almost 100% pre-excited reason for that, because this is atrial and ventricular capture, and we'll see that in a second here. This is atrial only capture in these two complexes with conduction over the pathway, and here is the envelope of atrial activation, in each case, atrial pacing, capturing in all four complexes here in the atrium. But in these complexes, the V's are drawn into the stimulus artifact because ventricle is being captured as well. Here, the V's are separate because they're being conducted to. This isn't a common theme. Are we capturing something or are we conducting to it, controlling it, if you will. There's a person with a left-sided accessory pathway. We're pacing the coronary sinus, same problem arises. So here we are with atrial capturing conduction over the pathway, and here we're capturing both atrium and ventricle. And as I said, if you're pacing crazy fast, and you're conducting, not really conducting, but you're capturing ventricle as well, you think, boy, this is a wild pathway that I've never seen one conduct this well. Now, retrograde conduction, a little pet peeve of mine with my colleagues is not knowing too much about retrograde conduction. Correct assessment of retrograde type conduction is difficult enough in some cases without adding some more confusion to the matter. You have to know what you're actually capturing, especially with coronary sinus pacing. Are you capturing atrium or ventricle or both or neither? Are you pacing at a cycle length that's different enough from the sinus cycle length to be able to know whether you have retrograde conduction or not? In these instances, you may have pseudo-Winkebach with avian otolagos, among other things. So here we are pacing the ablation catheter that is up against the lateral mitral annulus here. And it looks like we have VA conduction. No problem. We got A's all along there. But it turns out that if you turn down the output, you find that we don't really have any VA conduction. This is just capture of the ventricle and the A's are separate here. So make sure that you don't mistake persistence of retrograde conduction over pathway, which this looks like because it's earliest here in the coronary sinus. We need to do more ablation. Well, no, you don't need to do more ablation. You need to turn down the output and make sure you're only capturing ventricle and not atrium there. All right. Here is the dreaded retrograde dual pathways with single echoes here. So we're going up a fast pathway. Don't know it, but we're also going up a slow pathway. Same thing here. Here, we're actually blocking in the fast pathway. And now you see there's a slight change in activation pattern here. The hybrid atrium and coronary sinus are about the same time. The AVJ is a little bit earlier. Here, the right atrium moves out. Coronary sinus stays where it is. And this is a typical up the slow pathway and down fast pathway here. A standard atypical echo here. And this will interrupt your drivetrain and make you think, oh, we have VA block when you really don't. All right. Parahysing pacing. We should do this quite frequently. It's a good technique to practice to make sure you are facile at using it and interpreting it when it really matters. Usually, it doesn't matter a whole lot. But in some cases, it makes all the difference. You need to know what you're doing. So when we're pacing the hist bundle, you can capture any of the following structures in singly or in combination. The hist bundle, the right bundle branch, the right ventricle, or the right atrium. Retrograde conduction during pacing in this region can traverse either or both of the following in the AV node or an accessory pathway. So we got a lot of possible combinations. All right. What we're trying to do with this is separate retrograde septal accessory pathway conduction from AV nodal conduction. It's an ingenious method by Dr. Jackman and Otomo. But it's something that we need to make sure we understand well and not apply it inappropriately. This technique assumes accessory pathway conduction is faster than the AV nodal conduction and that you'll be able to tell them apart with this technique. However, it can't tell you if there's an accessory pathway that conducts more slowly than the AV node. You'll have an AV nodal pattern with that. And then all the time, you have a slower, more slowly conducting accessory pathway that is hidden there. And you think you've successfully ablated it when you actually haven't. You have to exclude atrial capture in order to interpret the results of this correctly here. Here's a couple of cartoons here. I look for the widest QRS. I'm going to say that that's ventricular only and something that's a little bit narrower but not normal is his plus ventricle narrowing it somewhat. In that case, the his is plastered right up against the stimulus artifact because we're partially capturing the his and part of the QRS is governed by that. So here we are pacing in this region here and conducting in both directions here, propagating anterogradially down the ventricles as well as backwards to the atrium here. And in a person who only has an AV node as their retrograde means of conducting, they conduct up the AV node. So the stim to A time here, stimulus to A time is the same as the H to A time because we're capturing the his here. That should mean that when we don't capture the his, the A should follow the stimulus by a slightly longer interval. And if you can see a retrograde his, there it is right there. And this stim to his is going to be the same as the H to his with partial his capture. And the stim to A is going to be the sum of the interval between the stimulus to the his and from the his to the A. This will remain constant here. There is a linear connection in those circumstances. Therefore, the stim to A when you have his plus V capture is less than the stim to A when you have V only capture when you're going only up the AV node. How about a pathway here? Only going up only a pathway. Well, again, there's a wide QRS, narrow QRS. This has some his component to it. So I'm going to say the his is stuck in there and then the A is off over here as you see it. And when we are capturing ventricle with or without anything else, we're capturing ventricle that gives a head start to the pathway. So the stim to A with his plus V is the same as the stim to A without the his because the his doesn't matter in that situation. You're conducting up the pathway. Therefore, the stim to A in his plus ventricular capture is the same as the stim to A with ventricular only capture. And the H to A here is longer with his capture than it is without his capture. Neither of those intervals are real intervals though because we're conducting up the accessory pathway and not the AV node. So there's not really going from H to A in either of these situations. It's a measurement you can make, but it's not a linear measurement. Therefore, the HA with his plus V capture is greater than the HA with V only capture. Now, here is somebody who's had an ablation. So we had the pathway here. We have what I just showed the HA seemingly long, HA seemingly short, but the VA is constant whenever you capture V, you get back to the A at the same time. And then after ablation, now we're going up the AV node only. So our HA is linear and it's a lot longer than any of these was over here. It's a good to check someone with it. All right, here's a person who has a couple of wide beats. They're not terribly wide, but they're wider than these beats over here, which are not normal. So I'm going to say these are ventricular capture. These are his plus V capture. There's a stimulus artifact running along there. So these are his plus V, these are V only. The stim to A is 120 milliseconds here, 190 milliseconds here mentioned hybrid atrium. The HA, however, when you see a his out the back here, as we see in both of these complexes here, the HA is going to be the same as the HA over here. So this is an AV nodal pattern of retrograde conduction. Here's a person who's had an accessory pathway ablated and we're blessed with having a his plus V and a V only in this sequence in the preablation and postablation. So here's our stim to A of 125 milliseconds and the stim to A remains 125 milliseconds prior to ablation. The his is over here. So this his to A is artifactually short. It's not a real interval. However, when we ablate the pathway and we're going only up the AV node, the stim to A is now longer at 225 milliseconds and it lengthens even more when we have ventricular only capture because we have to wait until we get to that his before we can think about getting back to the atrium. So the stim to A is longer with ventricular pacing than it is with his plus V pacing. And the stim to A, his plus V is the same as the HA if you can see that his with ventricular only pacing. So there's that. Then you get situations like this where you're capturing a lot of stuff. Now this, I'm going to just tell you, this is ventricular only. This is his only. Got three complexes with his only here. And then His plus V plus Atrium. A lot of stuff. A little caveat here, this A is probably a sinus complex that's coming in, so this really is not fully retrograde, retrogradely conducted. It's going up the AV node, however, and the rest of these complexes down here. So the stem to A here with V only, 124 milliseconds, with His only, it's 108 milliseconds, and these complexes were also capturing Atrium, Atrium, Atrium over here. So the stem to A is constant at 64 milliseconds, and none of these are helpful at all. You need to make sure you're not capturing Atrium in order to get this right. Here's a few complexes here. We've got a couple of wides, a couple of more narrows here, and V only with a stem to A of 230 milliseconds. Good. Here's the stem to A of His plus V, and it's less. Therefore, this is an AV nodal pattern, because the stem to A, when you have some His captured, is less than the stem to A when you don't have His captured. AV nodal conduction, right? No, not right. This is a problem here, because it is longer with V only, but it's not longer by enough. Only 13 milliseconds separates these. Now, when we have going up the AV node, we're going stem to His and then His to A, that stem to His is usually about your HV interval, sometimes, usually a little bit longer, 10, 15 milliseconds longer than the HV insides, because you've got to get to the right bundle to propagate up things, and you're pacing the ventricle. So we should smell a rat here when we have this His plus V stem to A not quite enough shorter than it is with V pacing only. In fact, this is because we got a left lateral pathway. And when we can see the His here retrogradedly being propagated to the HA is much less than the HA over here with the His plastered up against the stimulus artifact. And neither are really HA intervals. There's no conduction over the AV node in this person. It's all over the left lateral pathway. So these are kind of false intervals here. All right, here's another person. We got a lot of things going on here. We've got a very narrow bead here, His only capture. We've got a very wide bead, V only capture, His only again, and then His plus A. Well, whenever you're capturing A, forget about it. You can't make anything of that. We're looking for conduction to the atrium, not capture of the atrium. So whenever you're capturing the atrium, it nullifies your ability to interpret that particular complex. Here we are with a stem to A of 144, stem to A of 132, when we don't have His bundle capture. And so what is going on here? Well, they're a little bit odd looking. This is a little bit less here than it is over here. It should be the opposite, right? It was going up the AV node. So what's going on? Well, we didn't look hard enough. Here I'm going to draw the drop lines intersecting the hyoid atrial recording. And you see that we have different activation patterns, depending on which bead we're on. Here we have the hyoid atrium and coronary sinus nearly simultaneous. Here the CS is ahead. So this is, and here's a His out the back here. And it's much, much longer than the stem A over here. So what we have in this situation is a reciprocation back and forth of conducting up the AV node and up an accessory pathway. Here is AV nodal conduction, midline activation. This is a slightly right-sided pathway conducting over it, AV node, and can't interpret this because we're capturing atrium under those circumstances. Here's a really important one. When you've been slogging away at a septal accessory pathway, you got rid of the pre-excitation, sigh of relief, pretty snappy, just do a little bit of quick parius and pacing, clean this up, make sure everything's fine. And you see this, we got the stem to A with a long, or a wide QRS, widest QRS of 140. It's longer with, this person has a right bundle range block. I'm sorry, not a right bundle range block, but this is just their narrow QRS here, their normal QRS complex. Now the stem to A is 210. And that repeats 140 and 210, also repeats. What's going on here? Well, this is a pathway that you have not ablated. It's retrograde conduction. Then you can think of this as a single bead of orthodromic SVT. You're conducting down the normal electrical system, his Purkinje system up to the base of the heart, and then finally make an atrial complex over the accessory pathway. So when you've eliminated anterograde pre-excitation in these people, you feel pretty good about it, but that doesn't mean you've eliminated retrograde conduction. This is the test for it, and hope not to see this. But if you do interpret it correctly, patient needs more work here. All right. Atrial flutter. A lot of us do stuff with atrial flutter. It should be a pretty straightforward procedure to ablate, recognize ablates, and assess for the certitude of a cure of the atrial flutter. But you don't really need a monkey wrench in the works trying to figure out whether you have block or not. There are a lot of ways that this can go sideways. First of all, if you've done a lot of ablation in the gaviotric cuspid isthmus, it's difficult to interpret the electrograms. They're very, very low amplitude, smudged out. Sometimes difficult to distinguish block from very slow conduction. In fact, I think there might be situations where it is impossible to make that distinction. You can do some variations in pacing that can help you. I think most of the time, different sites of pacing, certainly different cycle lengths of pacing, because you might have rate-dependent block after there's been some damage in that area. That'll help you out, just pace faster. You can see that it actually is block at faster cycle lengths, not at the cycle lengths that you're doing. There is a case of that where we're propagating along during coronary sinus pacing, and it kind of looks okay. You've been working at this for a while. A third pass on the CTI, please. Won't this go away? Then it looks pretty good. But if you pace fast enough here, you see that we really still had some conduction over here. Now we have block. This won't always show you. Probably about half of the time when I do this, when there's a question of whether there's persistent conduction or not, this test will help you. The other half of the time, it'll look exactly the same over the range of pace cycle lengths. You don't learn anything from that. It may give you some reassurance that, yeah, I think it really is blocked. Here's an instance of somebody who's had a capo cricospinismus ablation, and it's stuck. They don't have any conduction through there. When a fibrillatory wave comes over the dome of the left atrium, it is constrained in its activation between the crista and the tricuspid annulus. There's wave after wave that goes there, and it hits this dead end down at the bottom of it. You end up with this so-called streaming pattern where it kind of looks like flutter, but it actually isn't flutter. It's really fibrillation in the left atrium. You're going in thinking, oh, I'm going to just do a quick flutter ablation here. No, it's a little bit more complex than that. You can be fooled also with a slightly incorrect positioning of a halo catheter if you use a halo catheter. This is an important thing to get right. There are lots of different purposes for a halo catheter. You might want to be able to paste from a bunch of different sites. You might want to be able to record from a bunch of different sites. You may want to make sure it's on the annulus for assessment of flutter ablation, and each has its merits. They may not be the same thing. One position that's good for one thing may not be good for another. Here's one that's got lots of great atrial electrograms. It doesn't look like we've got block here. It looks like a lot of slow conduction. That's not very good news, but if you look at this, here's the QRS complex. We don't really see any evidence of ventricular activation, so probably this catheter is really not on the annulus. It's way back somewhere. You can have a situation where conduction actually gets around behind here and activates the tip of this catheter as opposed to trying to force it to go through the cable for guess, but this was in a catheter block there. Nothing was done here except to give a little clockwise torque on the catheter, and all of a sudden, you see, hey, we do have block. We didn't do any more ablation here, but we got block nonetheless. One of the markers for being in the correct location is to have some ventricular electrograms in the CTI to be able to say, yeah, or on the triguspid angular recording to say, yeah, we're close enough to the ventricle that we can make that assessment. Now, here's a situation in which we appear to have block because your electrodes are not close enough to the site of ablation to be able to make that determination. You don't see anything in this area here because you don't have any electrodes here. What you see is it propagating around this way, and it seems like it's block, but it's actually pseudoblock. Well, contrary-wise, you're going to have this pseudoconduction in which the catheter is, again, malpositioned to posterior, and it looks like you've got a wavefront coming in from the coronary sinus getting to the triguspid angular catheter electrodes and making you think that you actually have conduction through there, and in point of fact, there is a nice block. Way, way back when we were first doing flutter ablation, it seemed good enough to be able to terminate the flutter with RF application, and if we couldn't initiate it, I thought that was pretty good. We terminated it. We can't reinitiate it. Well, a good third of patients had recurrent atrial flutter, and bring them back, and they had the same old flutter ablation again. Well, what was the problem? We didn't actually have block. We didn't understand in the first couple of years of doing flutter ablation that we really ought to strive for a different endpoint than just termination and non-inducibility, but if you try to initiate flutter at an EP study, I mean, you might succeed, but as often, you don't succeed. You know the patient has flutter. They may have come in for flutter, and then they went into fibrillation, and you paste them out of it or something, but you can't get them back into flutter, so what does non-inducibility mean after a flutter ablation? If you couldn't induce it beforehand, what does it mean afterwards? Nothing, so that's why we fell down on that, but since the mid-1990s with the introduction of the concept of establishment and demonstration of bidirectional conduction block, it's been our standard endpoint. Lots of ways of assessing this. You can look for split potentials, polarity reversal of electrodes, electrograms, and electroanatomic mapping can be used to make this assessment. It's a little bit longer process. You can use adenosine, or you can use differential pacing closer and further away from the punitive line of block, and the acronym for the speed. Everybody likes to do these fast. There it is. That's how you do it. All these techniques have some wrinkles, however, so here is the polarity reversal. You see we're going in two directions, a chevron effect here, pacing into coronary sinus. It looks like we got pretty close to block, but not quite, and then these are blocked over here, and you see this reversal of the polarity going from an RS in halo 7-8 to a QR, going from an RS in halo 5-6 to just a QR, and so on and so forth. It's a nice technique to be able to use. You see it's not perfect because we have an RS here and our site RS here as well. Not a perfect technique, but a nice corroborator, especially if you have a limited number of electrodes to use. Electroanatomic mapping can help as well, so here's our line of block here. We have, if we're pacing from over here, the impulse cannot go through because we have block, so it has to traverse around, and you can get your activation mapping during five minutes of pacing. We have our earliest over here. You get this as close into the line of block as possible to minimize any potential for slow conduction through there to fool things, and you can contrarywise pace from over here and show that you have block in this direction also. Here is another method, differential pacing, so we're pacing from a couple of different sites. Site X down here at the bottom of the tricuspid angle is a little bit more lateral at site Y. This is before ablation. You have this chevron pattern going around both directions with coronary sinus pacing, but we're pacing from electrode number three here at site X. The time from X to A is a certain amount, and if you're pacing more laterally or laterally, then you have a Y to A linear conduction, so in this situation where conduction is present, baseline, before you've done the flutter ablation, X to A will be less than Y to A because X is closer to the line anatomically and electrically in this situation. All right, here we have partial block and delayed conduction through there. Here we have this chevron activation pattern again with coronary sinus pacing just like we had before, and now X to A remains shorter than Y to A because propagation is going back in both of those situations a little bit more slowly. They're both longer, but they maintain the same relationship. It's just taking a little bit longer to get over to the line and then through it. Now, here's a situation where we have complete block, so when we're pacing from the coronary sinus, we block in this direction here. It has to go all the way around, so you have a straight line of activations. It's not vertical. It has a little bit of an angle to it, but it's nice and straight and doesn't have a chevron to it. Here, when we're pacing from X in this circumstance on the opposite side of the far side of the ablation line, and then Y a little bit more laterally, now X is electrically further from the coronary sinus electrodes than Y is. It's anatomically closer, but it's electrically further, so the X to A is now going to flip and be greater than the Y to A in this particular circumstance. You can use that to good advantage. Moving on to accessory pathways. Accessory pathway potentials, I think most of us would say, if you can find an accessory pathway potential, that's a very good target for ablation. There are lots of things that look like accessory pathway potentials. Probably, I would wager that most things that have been called accessory pathway potentials in the past by most of us standard electrophysiologists are actually not. They're just signals along the way. Maybe they're atrial lather ventricular, and a lot of stuff looks like an accessory pathway. It could be an accessory pathway. In order to be one, you have to fill certain criteria. It should be present whenever the pathway conducts. That's pretty obvious. That means it should, with anterograde conduction, have the sequence atrium, accessory pathway, and then ventricle with the accessory pathway furthermore occurring, being inscribed before the beginning of the delta wave on the surface ECG. With retrograde conduction, the sequence should be ventricle, accessory pathway, atrium, and the accessory pathway recording should be earlier than any atrium, any piece of atrium you can record. Furthermore, it should be absent, the accessory pathway potential should be, or blocked distally, when the pathway fails to conduct, either with extra stimulation, rapid pacing, or ablation. Whenever we have loss of pre-explantation, it's not always good news. You can have situations where a person, you're ablating on the foreceptal pathway, and you have some narrow QRSs, and they're actually accelerated junctional beats. We'll see that in a second here. So be very, very careful about erasing the jeer when we lose the delta wave. It may be not such good news. So here's this woman here, who's got this WPW, and these may be accessory pathway potentials. They are reasonable candidates for it. It's before the delta wave. It's present at the unipolar recording as well. It is not present after the atrial electrogram here. It's before the, after the A, before the V here. Not obviously present here, but may be present here, and there, and there. So that's kind of old. Not the best recordings, perhaps. Here's a person who was referred to us after several failed ablation procedures, in a couple different places, and you see this here is very interesting. She just had a little bit of a premature beat here from the APJ region, sinus rhythm. A little bit of a premature beat, wasn't that much, and that caused block in her pathway. Here's some pre-excitation, and there's the local for it, and then this is no pre-excitation. In fact, this thing here is not so much the V, it is the accessory pathway potential, and we see it over here retrogradely as well during SVT. It's interposed between atrium and ventricle, whenever you're conducting in whichever direction. It all has to fit those criteria there. Now, here's a person who, a young person who is a cheerleader, doesn't really feel very warm and fuzzy about having a pacemaker, but she's got this septal pathway. So your job is to distinguish the target from a thing that's in the neighborhood, such as the hiss. Here we have this candidate that might be an accessory pathway potential. It fits most of our criteria. It's before the delta wave here. It's discrete, and so when we go along with a burst of pacing, we see it here, again before pre-excitation, here again before pre-excitation, here again before pre-excitation. Here we have atrial electrograms. We're capturing the atrium, but we're not conducting to the ventricle, so an accessory pathway potential should be absent then, okay? It's absent. It's not that complex. Here we have conduction again, pre-excitation, but we know from here that because we have atrial recordings, but we don't have this thing, that it's not a part of the atrium. Important news. And here it is again, and here it is again, but in the absence of a good ventricular recording. So we're actually conducting, blocking the pathway, conducting down the hiss here, and fortunate that we see a HIS right here, but this is accessory pathway. It's not A, it's not B, it's not HIS, it's an accessory pathway. Not always do you have the opportunity to see it as clearly as this. This is just serendipity. We're pacing it at the right cycling, the right output at the right site. And the pathway has the right properties to be able to reveal all this. Here's a person with WPW and a putative accessory pathway potential here. Problem is that it's after the delta wave starts. So here it is, delta wave has already started. I don't think that's probably an accessory pathway. Now this is a left-sided pathway, so you could get away potentially with the blading in this area, because the connection is on the epicardial surface, takes a little bit of time to propagate in from epi to endo, from where you're recording. So you don't have something that's dramatically pre-delta wave anywhere, but still this really should be before the delta wave to call it an accessory pathway. This was an interesting case of a man with palpitations, and it turned out that he had this problem here. You see this signal between atrium and ventricle, and over here, and it turns out that that is an accessory pathway potential in a person who has atrial grade only conduction. So it doesn't conduct from V pathway to A, it conducts from V to A over the AV node, comes down to the A, and then we inscribe this potential here, a very unusual situation. This is important for him because when we're pacing the ventricle, we conduct up the AV node, here's this thing after the A at the ablation catheter, same thing, ventricle after the atrium, and over here, and the initiation of antedromic SVT propagating down the pathway here, indicated by the red line, and going up the AV node and his, down the pathway, up the AV node and his, and on it goes. So this is atrial grade only, and we see it where it should be between A and V. Intervals are a little bit long, this person turns out he's had a prior ablation in the past. Here is someone who's had two failed ablations in the past, the left lateral pathway, and this is a mess. We have ventricular electrograms, they occur during the QRS complex, there's no problem spotting those. We have atrial electrograms, they occur during P waves. But why does all this stuff in here? Is that a chewed up atrial recording, a chewed up ventricular recording, is it accessory pathway, what is it? It's an artifact, you can even dose. So a way to get around that is to do something we'll separate atrium and ventricle. And here is a handy technique to do it, pacing the ventricle at a fixed rate, and then putting in an atrial extra stimulus just early enough to draw the atrium away from its position as a retrograded conducted pathway. And then you'll be able to tell was there something before it that was definitive or not. Here we are, pacing the ventricle, going up this thing, here's an atrial extra stimulus in the midst of this ventricular drive, and the A is now pulled way away, all these big sharp things are the A, all right? So that's the ventricle there again, and the ventricle again over here, atrium again over here, and this stuff is here, but it's not over here, therefore it was not ventricular, because the ventricle is being activated the same way in each of these cases. If it were ventricular, it should be the same thing seen at each point, it's not, therefore those signals are not ventricular, all right? Moving forward, here's a patient who has had two prior failed left lateral pathway ablations, and this is the applying the same principles with anterograde conduction as we did with retrograde conduction in the last figure here. So we have sinus rhythm, there'll be sinus rhythm along in here, and then a retrograded conducted complex. Here is the conducted complex, we don't see any evidence of that smudge business, either between the A and B or after the B, and when we are pacing the atrium and, or have sinus rhythm, just at exactly the right time coming in with the first beat of ventricular pacing. Now we have all this stuff in here, and clearly, there's where the A is, it is not atrial, it wasn't ventricular before, it's not atrial, so what this is, this is all accessory pathway, and been pretty beat up by the prior ablations, but it's still there, and we were fortunate enough to get rid of it that day. Here's another person who's had a couple of failed procedures elsewhere for treatment of avian artery injury. Interesting, how often does that happen? Not often. So here we are, I just pacing the ventricle along here, conducting along, and five complexes of pacing the ventricle, one, two, three of these have an associated atrial electrogram, all right? Easy to tell what's atrium and what's ventricle then. So here we are conducting to the atrium, we see this funny signal here, what is it? And the ablation electrode gets maybe some Vs here, maybe some As, maybe, I don't know. Let's move on. So here we have this potential of uncertain nature, pretty clearly these are Vs over here, these are As here, but what is that? And then on the next complex, we have this thing is still there, but there's no atrial recording up here. So you don't have intraatrial block in a normal person. Why is this happening? Well, because that's not atrial. This signal is not atrial. Conducting here, see the As, don't learn anything, same here, don't learn anything, it's all the same. Now this is very interesting because we have a ventricle, all the ventricles are the same along here. We have ventricle here, ventricular contraction or electrode depolarization, and that signal is not present there, and therefore it's not ventricular. It wasn't atrial, it wasn't ventricular, so these happen to be accessory pathway potentials. That's a very, very good reason to have a couple of failed procedures for abundant reentry, but it was never there. So this was easy pickings for this accessory pathway. Now, you're looking for the delta wave to go away when you have pre-excitation. Great, here's a 30-year-old woman, has delta wave, it's gotta go. So the colleague turns on RF energy and we see the delta wave go away. Hooray, cheer goes up from the crowd. Hold on, there's a problem here. These are not actually have any opportunity to be pre-excited. This one, a little bit pre-excited. This is accelerated junctional rhythm, and all of these are accelerated junctional complexes. We don't know for sure whether we've gotten rid of pre-excitation in this person or not, and it's time to come off RF because you're gonna knock off this bundle and have two problems. You won't have gotten rid of the pre-excitation and you will have gotten rid of AV conduction. Bad idea. So here it is a couple of seconds later. I haven't turned off RF just yet. We at least have retrograde propagation going up a slower pathway here, but AV conduction is not super under these circumstances. In fact, it's pretty lame over here. And a nice accelerated junctional. Don't even have retrograde conduction on this complex here. Big trouble. Are we gonna, is the AV node gonna survive the day? Well, yes. Somebody comes in and says, hey, turn it off, turn it off, turn it off. And in fact, we have a little bit of pre-excitation coming back there. So it's really important to not misinterpret lack of pre-excitation or loss of pre-excitation with a successful ablation. All right, moving on to atrial potentials during atrial fib ablation. When we're doing pulmonary vein isolation, we want to see potentials disappear, entrance block, and I like to see them not be able to propagate into the atrium. Last I checked, that's the pathogenesis of atrial fibrillation propagation from vein into atrium. So that's great that you have entrance block, but you really better demonstrate exit block. That's what I think. That's our societal recommendations, heart rhythm society. If you're recording from too deeply within a pulmonary vein, you won't see any potentials. It'll look like, oh, it's isolated. Don't have to do anything. Just make sure of that. Far field potentials, atrial potentials from elsewhere can masquerade as PV signals, and you keep on chasing after them, thinking, oh, I've still got more work to do in this vein. For the left superior pulmonary vein, these signals come from the left atrial appendage, sometimes from a non-isolated left inferior pulmonary vein, not so often. For the right superior pulmonary vein, your near neighbors are the right atrium and superior vena cava. When you're assessing for exit block, large stimulus artifacts may cause, which is necessary in order to capture some of this tissue in many cases. You may look like you have a potential, but it's actually just ringing of the amplifier in some older systems that don't have good damping, and it can simulate residual PV potentials. Here's an example of a catheter. It's a ring catheter, a little bit too deeply out the right superior pulmonary vein. Looks like we're done here before we even get started. Hooray, we don't have to do anything there. Well, everybody has PV potentials, practically speaking. So if you get in there and somebody's not ever had an ablation of any sort before, and you see no potentials, that's really unusual. You ought to look for them a little more carefully. So just pull back the catheter a little bit. It's a little bit more proximal to the vessel. There they are. Next is the... Okay, so we'll move on to this one here. Bar field potentials can be very vexing in trying to sort these out. I've continued ablating around the left pulmonary veins when they've long since been isolated. That's an embarrassment to think about how long they've been isolated when we're still ablating. Larger signals can be seen from greater distances. So a ventricular signal can be seen from a greater distance than an atrial signal because it's a larger muscle mass from which you might be recording a far-field signal. The frequency content of far-field signals is often but not always more muffled or rounded, quite often but not always. The timing of a putative far-field signal must be consistent with what you think is the source of its signal. It can't be way off in timing or location. And you should only be able to record these in electrodes that are facing the source. So for instance, if you're thinking that you have left atrial appendage potentials that you're recording from the left superior pulmonary vein as residual, they should be only recordable on the anterior surface of the pulmonary vein. Left inferior pulmonary vein potentials should only be on the inferior portion of the LSPV recording electrodes, whatever arrangement you have. Left ventricular potentials should only be seen on the inferior medial portion of the left inferior pulmonary vein recordings. You really shouldn't see them on the left upper because the left atrial appendages are interposed between them. And the right veins are just very far away from the ventricle. Right atrial or superior vena cava potentials can be recorded on electrodes on the rightward side of the right superior pulmonary vein. The right inferior pulmonary vein has no nearby neighbors. So you really, it's hard to attribute far field signals to something that you see recording from the right inferior pulmonary vein. Here's the atrial septum looked at from the right side here, peel it away here, and we'll see the left pulmonary veins, left inferior, left superior pulmonary vein with a ring catheter in the left superior and the left atrial appendage orifice. If you're recording from these electrodes, a potential that could be far field left atrial, if they're, or from here, they could be far field left inferior vein. They can't be anything far field from back here. There's nothing back there that generates a signal. So here we are in sinus rhythm and coronary sinus pacing, got these crazy signals that are still bothering us here. So residual PV potential is a left atrial appendage. Well, with coronary sinus, it's not very helpful, not very informational, not too much courage to be taken from that. But if you pace the left atrial appendage, these electrodes, these electrograms are sucked into the pacing potential stimulus artifact. And you can tell that, yes, those were far field potentials. I don't need to do any more ablation in this case. Here's another example with sinus rhythm, very bothersome potentials that are still there after all the ablation you've done. They don't appreciate it at all, how the work you've done. Pacing the posterior left atrium, not very cheery here, they just all look the same. They are not brought in by the stimulus artifact, but here when we're pacing the left atrial appendage, they are, so that's good news. Here's a recording from the left superior, I'm sorry, right superior pulmonary vein. We are in the process of isolating and you see we're at atrial fibrillation along here. And you see these funny signals that are kind of straggling through here, not seeming to care that the rest of the vein is in this fluttery thing here. All of a sudden, the vein potentials go away, but these things are consistent here. And they could be a separate strand that is not interconnected with the rest of the pulmonary vein network, or there could be a far field signal. You only see these on a handful of the ring electrodes here. And it turns out that these are the ones facing the superior vena cava when we're in the superior vena cava. Subsequently, you see signals that are about the same frequency as the ones that we'd recorded far field before there. So that's what that was. And you can sort that out with some differential pacing here. This is kind of a smudgy signal. These are actually left atrial signals, these are right atrial signals. From the right superior pulmonary vein. So the dictum of sharper signals being near field, duller signals being far field, not holding so well in this situation. It's just the opposite. So these are left atrial and right atrial, red and blue. And here, when we're pacing the right atrial appendage, we see these signals early activated, preceding the ones that are left atrial. And being recorded from the right superior pulmonary vein. So there are those, very straightforward. And here we are pacing, this is sinus rhythm here, with lateral left atrial pacing. These signals persist in the right superior pulmonary vein. His bundle pacing, they persist. We're capturing only atrium there. And pacing in the posterior right atrium, these signals are drawn in considerably. So they may well be far field potentials from the right atrium here. Here is a nice exit block from a pulmonary vein. You see we have sinus rhythm in the baseline tracing up here. Nobody knows that there's something going on in the pulmonary vein until you pace it here. And we have all these nice potentials here that are captured, not conducted. Nice exit block. Now, when you see these, you see there is a certain activation sequence. We propagate from one place a little bit later to something else that's important. Because in a different situation, this is ringing of the amplifiers of an older system, or older recording system. These look like PP potentials here, but in point of fact, they are just amplifier ringing, not a very well-tuned system. And the hallmark of these is their simultaneity. They don't have an activation sequence to them. So all of these are a simultaneous signal along the way, not a complex propagation in one direction or another. All right, here is another example of a combination of those where we're pacing with that same old system. And we have both amplifier ringing, present in all situations, and also genuine capture potentials with no poor propagation into the rest of the atrium. So we have both captured PP potentials as well as ringing artifact here. All right, overdrive pacing during arrhythmias can be vexing in many situations. We use this all the time. We should use this all the time, diagnostically and therapeutically. From a diagnostic perspective, we're trying to distinguish a focal process from usually macro reentry. In the focal processes, overdrive suppression or variable return cycle can occur, and we don't see any fusion during overdrive pacing. In macro reentry, we see both fusion, and in most cases, over a wide range of pace cyclings and number of pace complexes, a pretty fixed return cycle. There's no evidence of overdrive suppression in these cases. From a therapeutic perspective, we're trying to distinguish good ablation targets from bystanders, would-be targets. But there's a lot of potential for foolery in all of this stuff here. You might not capture it all. Well, you're gonna get a great-looking pace match, of course, because it looks exactly like tachycardia. Of course it does, because you never capture anything. But when you stop pacing, you'll be tempted to measure a post-pacing interval. It makes, it's silly. There is no such, there's no inference to be made from it. It's like it didn't occur. You may not be pacing for long enough to control the entire arrhythmia, and therefore, you'll end up with a variable post-pacing interval if you do it. Several times, you'll just think, boy, this is a weird post-pacing interval here. I thought it was gonna be better. Paces at different cycle lengths from the same site or for a different duration. And if you keep getting different numbers, that's either a focal process or you just weren't pacing for long enough to control everything. You're pacing one little corner. It doesn't have anything to do, it never gets to the arrhythmia, to the circuit or to the focus, to do anything to alter it. And so, this is how you didn't do any pacing there. So don't make inferences off of that either. If you choose the wrong electrogram component to these complex fragmented signals when you're measuring your post-pacing interval, you'll end up with some very bizarre conclusions regarding how suitable that site is for ablation. If the post-pacing interval is extremely in excess of the tachycardia cycle length, 40, 50, or more milliseconds, that's probably a bystander site, a spur off to one side, that Dr. Stevenson taught us many years ago. It could be decremental conduction within the circuit. That is, in my experience, quite rare. Fortunately, it's rare. It would be a big problem for us with pacing for a lot of different places if it were not quite rare. On the other hand, you can have a situation where the post-pacing interval is much less than the tachycardia cycling. You're probably capturing too large of an area. So leapfrogging, instead of having a virtual electrode just at the catheter electrode point of contact, you're now actually capturing a much larger field, so sending the impulse forward from basically head start along the way. Here is an example of a very good-looking pace match when we're overdrive pacing ventricular tachycardia. In fact, there's a QRS complex of the actual tachycardia superimposed. Looks great. Why shouldn't it? Because we never were capturing. You can see the stimulus artifact just kind of walking through here. And on a trigger screen, if you use that, I encourage people to do that, you can spot this a mile away. It's so easy to see that you're not actually engaging what you're trying to capture. So the stimulus artifact is just walking on through. Here's another, a little bit more subtle situation where we're pacing during an atrial arrhythmia. we have nice capture here. No question we have nice capture. But here's an envelope of the rest of the atrial signals and you can see that even some of the nearby coronary sinus electrodes are not governed by or controlled by this pacing. Yes, we're capturing, yes, no question. But are we controlling? No, we're not controlling hardly anything. And if you're not controlling the generator of the rhythm, either focus or the circuit, you can't make any inferences about the post-pacing interval. You can measure it, fine, measure it, doesn't make any sense, don't bother with it. So this is controlling a portion of the CS recordings only, but nothing else, and so it's a very meaningless post-pacing interval. The situation with ventricular tachycardia, which electrogram component are we going after? Well, this one was the interesting one here. Nice mid-diastolic, small, nearly isolated mid-diastolic potential. Great, let's go for it. Test it first, see if it's good. And problem here is we're pacing it, we're capturing, everything's fine. Pacing just a little bit faster than tachycardia, but our post-pacing interval here is crazy short. 200 milliseconds, 240 milliseconds shorter than it should be. Why? Are we capturing too much tissue? Not exactly. Stimulus to QRS when we're pacing here is 310, so if you take this over to this portion of the QRS and measure backwards and say, what was it, 310? It's actually, this is what we're going after, this far-field-looking thing, not the near-field-looking thing. Okay, it doesn't follow the rules, but it is what it is right there. So here's our true post-pacing interval. It's a systolic site, it's an inner loop site, because we have concealed fusion, post-pacing interval equals tachycardia cycling, so on and so forth. Everything looks great for an inner loop site. Well, I was interested in this stuff over here. Too bad, it doesn't count because if you see it during pacing, you weren't capturing it. So it ought to be smacked up against the stimulus artifact if you were actually capturing that tissue. Please distinguish between capture, which is something that occurs between the electrode that's in contact with the tissue and the tissue itself, and control, which is everything else that goes around outside of that. So here we have this potential here that's preserved during pacing. It obviously was not captured. Make sure you know the distinction between what's captured and what's controlled. Another situation here, atrial diastolic signals, where nice mid-diastolic signal, gained up at really, really small signal, should be a good spot for ablation. Let's go for it. Well, let's pace first. So I have a superimposition of the atrial tachycardia sequence activation signature. Well, it looks pretty good. Here is where that potential should be over here, and there should be a stimulus artifact up against that. Well, we're not capturing that because if it were, we would have this interval recapitulated here. And instead, there's that potential there, the post-pacing interval, significantly in excess of tachycardia cycling. This is a stimulus to a reference electrogram longer than the electrogram we're interested in to the same reference. This is an atrial bystander. We see ventricular bystanders with some frequency. Atrial bystanders are, fortunately, not very common. I have a goodly number of them because a lot of things are uncommon, of course. And these have nice diastolic timing. You can entrain with concealed fusion. Everything looks great, except that the post-pacing interval is long in excess of tachycardia cycling. This is almost 200 milliseconds, over 200 milliseconds longer. And the stimulus to reference is much greater than that electrogram to the same reference over here. So don't be fooled by this. In VT, you can have problems in patients who don't have structural heart disease. If you're looking for PVCs, quite often there's such long coupling intervals or you've got them on isoproteinol or epinephrine and the PP interval is shorter. So now the P wave is interfering with the beginning of the QRS complex and making you think it either starts earlier, usually it starts earlier. So you also may not be able to fully replicate. If you only have PVCs, you may not be able to fully replicate the QRS complex with pace mapping. When you're pacing in a burst, you ought to try to put in single extra stimuli from the ablation catheter at a coupling interval similar to that of your spontaneously occurring PVC. That can often give a much better match if burst pacing doesn't do it. A QS configuration in unipolar recordings is common, well sought, appropriately sought, but if your impulse is coming from just a little deep in the tissue, it will not have a QS configuration. So don't wait around for a QS. Don't be scoping around all over the place for a QS. It doesn't exist because it's not, you don't see it anywhere. Catheter-induced PVCs can mimic the real ones and they look really, really good. The electrogram characteristics are phenomenal. So you think, oh, I'm gonna ablate here. This will get rid of it. You can maybe get rid of the catheter-induced PVC, but not the one you're going after. In scar-related BT, we, well, occasionally, with catheter mapping, have intermittent potentials, that is signals that don't repeat with every cycle of the tachycardia, usually in faster ones or very, very sick tissue, a lot of amiodarone, so on and so forth. They can mimic really good diastolic potentials. And if your electroendotomic mapping system is only taking a single beat, says sees these potentials there, that's your spot, when it's actually not. Obviously, it's not because the arrhythmia continues every other beat with its absence. You can sort these out with override pacing, make sure that you have an understanding of what's a bystander site versus what's a genuine one. And then some other stuff we have to think about. Here's a patient who has this PVC. And if you drop a line at the beginning of the QRS onset, this is a pretty phenomenally good-looking ablation site. Well, what if that isn't the onset of the QRS complex? What if it's actually over here? What now? Well, it's now. Same electrode. Now it's not a good ablation site, okay? How do you resolve this? Well, we have ways of figuring this out. So here's a P wave that I'm going to move over here and align it with an electrogram that I know is also part of the atrial activation. And you see the beginning portion of all these is tainted with a P wave. And actually, the QRS complex starts about here. And so this actually went from a good to a bad, back to a good ablation site, all in a few seconds here. Here are catheter-induced PVCs. This is a great-looking site here. Look at this. It's phenomenal. The QRS here, the bipolar electrogram just before the QRS onset. What could be better? Phenomenal site. Problem is, it's a catheter-induced PVC. Of course, it's going to look good. The tip electrode where it's banging into something is going to be the earliest activation precede the QRS complex. Whereas these electrograms during the actual PVC, pretty stinko. So you wouldn't want to ablate here just on the basis of a catheter-induced PVC. Get excited about it. It looks pretty good, but don't be fooled. So catheter-induced ectopy. Morphology must be consistent. So if you think it's catheter-induced and the catheter is still there, paste them there. And it'll look exactly like your catheter-induced ectopy and not like your target PVC. The complex is identical to a paste complex. The tip should be the earliest electrogram that you see in the unipolar. If you're monitoring a unipolar, which I suggest you do, we'll have a QS configuration because everything's emanating from it. Here are intermittent potentials during VT. Gained up gnarly-looking electrogram here pretty fast. And when you see this signal and you're looking around for it there, it's not, it's every other beat. This used to be very, very common in intraoperative mapping probably because of air exposure, some cooling of the endocardial surface. We don't see it quite as much nowadays with catheter mapping, but it still does exist. The importance of this is, of course, if you have electroanatomic mapping, it depicts this beat as the one that's gonna be representative of the site. And it said, oh, there's a mid-diastolic potential there. There's a blade there. All right, here is an odd situation where we have a winky-bock of potentials during ventricular tachycardia. I don't have too many examples of this, but it looks interesting. But clearly, these potentials are not involved in the ongoing perpetuation of this arrhythmia because it goes on leaving them behind. They don't seem to have any beneficial role here. Here's another situation similar to what we talked about before. Here's our mid-diastolic potential we're all interested in. And we're not capturing this. We're capturing this stuff over here. And we've talked about this before. I'm not gonna spend any more time on it. Same case. All right, this is a case of what are we capturing here? Pacing for four cycles, same tachycardia comes back, looks like concealed fusion. And where obviously, if you measure the post-pacing interval to the first electrogram you see coming back, it's erroneous, far, far less than tachycardia cycling. Why is that? Well, we weren't capturing this stuff. When you see it, you weren't capturing it. It should be snugged up to the stimulus artifact. So there it is, it was not captured. This is the actual post-pacing interval here from what it was. And we can measure this stimulus to this QRS and gauge it to the tachycardia cycling. And it comes out just fine. Stimulus to QRS 360. And the electrogram to the next QRS 355 or 65 milliseconds less than where the line is over here. And you see that the true post-pacing interval here is, no, that's not, this is a true post-pacing interval, 415, very close to tachycardia cycling. Good site, either just beyond the exit or at the beginning of an inner loop along the way, but not, maybe it's a good ablation site, maybe it's not. But the key is to make sure you understand which is the electrogram to which you should be measuring, not just the first thing you see or the largest signal. All right, again, what is controlled? This is an SVT that we're using overdrive pacing and we're coming along here, pace, pace, pace. And it looks like this is an AVAV, AVAV. And so that should mean that it has a candidate for being a pathway mediated, but not an atrial tachycardia. So actually what happens in this situation is we're conducting not to this QRS complex, but to this QRS complex. It's easy to get this right by noting which is the last controlled complex. So we're pacing at 270. These are 270 here. So this is our last controlled complex. So this is actually an AVA here, if you will. So it's a pseudo-AHHA, and this is just typical old AV nodal reentry tachycardia. Again, very important, especially with atypical AV nodal reentry and ventricular pacing to make sure you understand which complex is controlled and which is not. Here's an example of that. Here we have what looks like three beats of pacing in the ventricle, capturing V, controlling the A. And so this looks like a V, A, A, V. Ah, atrial tachycardia. Now I understand. No, it's not. Because again, what are we actually controlling? It's not this. We're not capturing ventricle and conducting to this. The Vs are over here. How did they get to this atrium? They didn't. So it's actually, this is, the stimulus is capturing ventricle and going here. And this is actually atypical AV nodal reentry. And a pseudo-VA, A, V, not a regular A, V, A, A, V, pseudo instead, not an atrial tachycardia AV nodal reentry. Last couple of things here. There might be things that interfere with your signals along the way. The P waves contaminating the QRS during PBC mapping. We saw an example of that. PACs or PBCs during testing maneuvers that can result in misinterpretation of signals. Atrial or ventricular components that are displaced due to slow conduction or block and showing up in unexpected locations. I didn't think it would take that long to conduct the thing. It is what it is. Reproducibility of findings is critical as it is in all aspects of electrophysiology. And you have to do some detective work along the way to make sure you understand the true nature of a signal. So here we're coming along with the PBC during SVT. The HISS is refractory. That's great here. Here's the HISS. Everything's wonderful. And there's this A here. So we brought in, we have an A that occurs earlier than expected when we have a stimulus that occurs when the HISS is refractory. We have an accessory pathway. Well, hold on. This V is not very early here. In fact, we haven't even disturbed these Vs here at all. We've captured a tiny sliver of ventricle, but haven't affected these here. So if we haven't brought in the V, how do we bring in the A this much? It's 90 milliseconds early from what it should be. This is just a PAC. It happened to occur then. We didn't cause that. Don't make any inferences. Reproducibility of findings is important. Here is another PAC in that same person, same PAC. And it actually terminates the tachycardia. So make sure that you understand what's causing what. Are you influencing this or is it a spontaneous event? Here's another situation. We have a PVC that might be HISS refractory, and we don't get back to the atrium. This should be an accessory pathway, huh? Pretty straightforward. Not so much. So what's happening here is not an A there, but the arrow is indicative of where the HISS should be. So this HISS is not refractory after all. So you can't interpret it anyway as indicating a pathway or not. But the problem is here that this was gradually slowing down along the way here. Sorry, this was slowing down. And it just happens to have a termination of tachycardia, spontaneous termination at exactly the moment you're putting in a PVC. Again, this will not happen time after time. If it's a reproducible phenomenon, you can take it to the bank, but you can't take this. Now, here's another one that's just weird here. We're stimulating the atrium somewhere, and what is the nature of these signals here? Well, they're ventricular, of course, in this octopolar catheter. Well, are they or are they not? Well, it turns out they are all atrial. They occur within the ventricle, but this is just really, really slow conduction through an atrium. We know that because this is an extra stimulus that is followed by the same amount as these guys here. So long propagation time, long propagation time, long propagation time, long propagation time. So these are actually atrial signals. Make sure you understand what's controlled versus what's captured, and test what you don't know by what you do know. There they are. Some miscellaneous things to end up with here. Sometimes you get some fake signals along the way. They look like they're real signals, but they aren't. Contact artifacts between electrode and other metal in the heart. Either another catheter, mechanical valve, a pacing lead can lead to something that simulates an electrogram. You can usually tell them apart. Pump electrical artifacts can simulate a small potential. You keep on ablating. I gotta get rid of this potential. It won't go away. Well, it's a pump artifact, electrical artifact. It's present immediately before, during, and after ablation, and it won't go away with ablation only when you stop the pump, when it stops pumping at a rapid rate. Valve closure artifacts are especially vexing when you're doing ablation around aortic sinuses, valsalva, and reverberation of the valve leaflets may cause a signal, electrical signal that looks like it's a pre-QRS potential during a PVC. So here we are coming along, and somebody with a heart block and pacemaker, and an HLA arrhythmia, and we're banging along here between electrodes. And this is the ablation catheter, and it has contact with something simultaneously. This is on the pentaarray. So this is electrode-electrode contact between two unrelated catheters here, and they're simultaneous. Here's an event where we have the same looking thing, but where is in the same patient, but where is the other electrode that we're bumping into? We don't see it. It's none of the ones represented here. It's a pacing electrode that you don't see. We need to be aware of this and not muck around there too much, or else you might dislodge it. That has happened. Here's someone who has mechanical valve, and you see electrode contact with the housing or the strutting of mechanical valve every so often in the ventricular systole there. There it is each time. We don't see any other catheter with which contact is being made, and therefore it's something else, and it's something in the patient, such as a valve or a pacing lead. This is pump artifact, and we're coming along here. Here are all these nice little potentials here, and we turned on RF here about a second or two before the pump came on to irrigate the catheter, and at the end of this application, you see the end of RF application here and the end of pump over here, and so don't mistake these for diastolic signals that you have to get rid of. Diastolic potentials versus valve artifact. This has been reported by a couple of series here. It occurs at or after the T-wave, after the dichrotic notch of the aortic valve, and this is cartoonish of Jorge Romero's work with the dichrotic notch, and here's this signal occurring. It's a stimulus artifact here, and here's the signal that occurs way off over here. It makes you think that there's something leading to this next QRS complex here. These are those valve artifacts here. What nice-looking signal is that causing that QRS? Is that the signal that we need to ablate to get rid of this PVC? Well, it occurs other places as well as before the QRS complex. I think it's a bogus signal, a valve closure artifact, not a real signal. So in summary, during EP studies, we expect to see some things. These are not always what we get. We may not see what we're expecting. We may see what we're not expecting. A savvy electrophysiologist has to be aware of things that might turn up unexpectedly. Measure twice, cut once, good rule. Look for reproducibility of findings. Whenever the question, what's wrong with this picture, comes up, answer it, and move on. Get a good answer for it, a satisfactory answer that fills all the criteria you're looking at, and move on, and always test what you don't know by what you do know. I thank you for attention, and do well.

electrophysiology

John Miller

Heart Rhythm Society

ECG leads

catheters

AV conduction

retrograde conduction

accessory pathways

pulmonary vein isolation

pacing techniques

signal artifacts

patient outcomes