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Session II: Invasive Diagnosis and Treatment-6154
Use of Overdrive Pacing-Entrainment in Supraventri ...
Use of Overdrive Pacing-Entrainment in Supraventricular Tachycardia
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Video Transcription
Greetings, this is John Miller with the Heart Rhythm Core Concepts in Electrophysiology course. I want to speak for a few moments on the use of overdrive pacing and supraventricular tachycardia. It's often called entrainment. It's not always entrainment. We'll see some distinctions with that. These are my disclosure of relationships as you can read for yourself. Overdrive pacing during supraventricular tachycardia will encompass several learning objectives here. We'll try to understand the principles and uses as well as proper techniques of overdrive pacing during SVT. It's not simply turning on the stimulator and seeing what happens. We'll want to differentiate among responses to overdrive pacing during SVT and their diagnostic implications when they exist. Dr. Michel will touch on more of this on a subject last year. We want to know essential elements of entrainment including how to recognize fusion. This is a core principle with this technique. And finally, understand the importance of unanticipated responses to overdrive pacing such as non-propagated tachycardia termination that has several different manifestations. Overdrive pacing during SVT from either the atrium or ventricle can, doesn't always, but can yield useful diagnostic information. With overdrive atrial pacing, you can see entrainment or not entrainment. Similarly, with ventricular overdrive pacing in SVT, one can see entrainment or non-entrainment responses, all of which have potential information. With atrial overdrive pacing during SVT, one might see fusion of atrial activation. That means entrainment is present. That means macro-reentry is present. The post-pacing interval minus tachycardia cycle length, that difference is an index of the distance from the pacing site to some portion of the circuit. And it's called entrainment mapping when one paces at one site compares the post-pacing interval minus tachycardia cycle length derived from there to that from another site. And you can form a map of this as well. See some examples of that. Fusion may be absent despite pacing many different sites, many different cycle lengths, no matter how hard you try to define fusion in that case, you just can't see it. That is often associated with transient suppression of the arrhythmia instead of actual termination. And then when the arrhythmia resumes, it often warms up. And this is a hallmark of an automatic, focal automatic tachycardia in its purest form. One might see transient acceleration of the tachycardia. This is a hallmark of, but not often seen, manifestation of delayed after-depolarization-related triggered activity as a mechanism of arrhythmia. A fixed return cycle, no matter for how long you pace or how rapidly you pace within reason, signifies micro-reentry when, again, fusion is absent. No matter how hard you try, you can't see fusion. But if it looks like reentry from other perspectives, such as this fixed return cycle with pacing every time you pace, for how long you pace, at what cycle length you pace, this strongly suggests micro-reentry or concealed fusion in macro-reentry that you just can't see where the fusion is. The post-pacing interval minus tachycardia cycling is an index from the pacing site to the focus or exit from this micro-reentry circuit. It doesn't have exactly the same implications as it does in reentrant arrhythmias because this can be dependent on overdrive suppression of the arrhythmia. So you may pace at one cycle length from a site and get a certain return cycle in the focal tachycardia. You may pace at a slightly faster cycle length at the same site and get a different return cycle. It's not a hallmark of reentry, and it can't be used as an index of how far you are from the pacing site is from the focus because you pace at the same site, and it looks further or less far. It doesn't work that way. So you have to be carefully applying that tool. The AHA response is a hallmark of junctional tachycardia. When you overdrive pace during a junctional tachycardia, you get to propagate down to the hiss, wait for the next junctional complex with starting with a hiss, and then back to the A. That's a hallmark of a junctional tachycardia. All these are manifestations of atrial overdrive pacing during SVT. Finally, the AHA response, you pace the atrial. The last thing you see is an H and V. The next thing you see after that is an atrial electrogram. That is an indicator of either an atrial tachycardia AV nodal reentry or orthodromic SVT. It is not very much of a differentiator at all. Entrainment, big topic. Dr. Stevenson will cover this in the ventricle exquisitely. Other speakers will cover it as well. I will cover it humbly here. Entrainment is a technique which can aid in both diagnosis and treatment. It can define the mechanism of tachycardia macro reentry versus other mechanisms. By helping this, it helps you determine the characteristics of the ablation site electrogram, what you're going to be actually targeting for ablation. Automaticity or triggered activity delayed after depolarizations or micro reentry. Most of the time, we're going to be dealing with a late diastolic electrogram. Micro reentry can have a very prolonged diastolic electrogram. It's very site-specific. You may just see something that looks like a focus. In contrast to that, macro reentry, we're going to be looking ideally for a site with mid-diastolic timing. That's very different from a site that you can't get any earlier into diastole than just late diastole, 30, 40, 50 milliseconds before the P wave onset. These are very different mechanisms. It's very important to make this distinction. Do we have a focal process, focal elimination, or do we have macro reentry? Entrainment helps you do this. It also helps validate a putative ablation site or a candidate ablation site and reentrant reentry. Once you've established that it is macro reentry, you can help validate whether this is a good ablation site or not by evaluating the behavior of diastolic impulses in response to pacing, assessing the post-pacing interval versus tachycardia site length, as we spoke of earlier, and assessing the degree of pace match with that of tachycardia that occurs or resumes after the cessation of pacing. How do you do it? Well, entrainment is continuous tachycardia resetting. You can put in a single or double extra stimuli during a tachycardia and see a resetting response. The next cycle occurs earlier, most typically, than it would ordinarily be expected to if unperturbed. With entrainment, it's continuous resetting. You're continuously spinning it around faster each time. It doesn't get a whole revolution completed until it's sped up again from somewhere either inside or outside the circuit. Requirements for entrainment are several. There are four of them. The most obvious one are you start with a stable tachycardia that's been going on for a while. It can't spontaneously terminate or you won't be able to interpret anything. Stable means 15, 20 milliseconds wobble in tachycardia cycling. If it's much more than that, you're going to have a hard time interpreting your post-pacing interval. You can certainly measure it, but what tachycardia cycling do you compare that to? Is it a good site or is it a bad site? The more play there is in tachycardia cycling, the more difficult it is to interpret what happens after the end of pacing. Start with an ongoing stable tachycardia. Overdrive pace at a fixed rate, fixed cycle length, slightly faster than tachycardia for several cycles. How many? Well, the less difference there is between your tachycardia cycling and your paced cycling, the longer you have to pace to make sure all relevant elements of the tachycardia circuit or arrhythmia, since you don't know what the circuit is yet, all electrograms are accelerated at the paced cycle length. If you're pacing from the lateral left atrium, coronary, distal coronary sinus, you need to make sure electrograms from the lateral right atrium are called into the fold by controlled by your pacing before stopping pacing, however long that takes. Second to finally, the same tachycardia resumes upon cessation of pacing. We start with this ongoing stable tachycardia. Overdrive pace for enough cycles to control everything and then stop pacing and the same tachycardia comes back. It doesn't terminate, it doesn't change to another tachycardia. These are absolutely inviolate essential constituents of entrainment, but they are not entrainment. You can do all of these during sinus tachycardia. Sinus tachycardia is an ongoing stable tachycardia. You can overdrive pace from the right atrium, the coronary sinus. You can control all the electrograms during the arrhythmia. And then when you stop pacing, the same tachycardia comes back. That's not entrainment, is it? That's not re-entry. That's merely overdrive pacing during tachycardia. And many, many people mistake and confuse overdrive pacing during tachycardia with entrainment. These are not the same thing. What you need, the absolute sine qua non of entrainment is fusion. All right. What is fusion? Well, fusion comes in several forms. One is so-called fixed fusion where while you're pacing from site A and recording during tachycardia B, you have something, a paced activation sequence or a P wave that doesn't look exactly like pacing and it doesn't look exactly like tachycardia. And each beat during pacing, once it settles out, looks exactly the same. That's not pacing for five beats and each beat looks like a slightly different blend. That's not fixed fusion. Fixed fusion is where all of them, while things are stable during the overdrive pacing, won't look exactly the same. Fixed fusion, an identical blend of pacing and tachycardia at any given pace cycling. Progressive fusion is a variant of this where one paces from the same site at different cycle lengths. And with this, a greater contribution of the paced wave front becomes evident during the overdrive pacing sequence when pacing at faster rates and lesser from the circuit output. If you have these manifestations, you have fusion, you have macroarray entry, now you know what your ablation site should look like. This is important stuff. Now, when we are talking about fusion, we need to make sure that we understand what it is not and what it is. What it is not is mere capture with overdrive pacing. I covered that. It is not overdrive pacing followed by a change in tachycardia or termination of tachycardia, but it is present when, again, one has a clear blend of fully paced and fully tachycardia complexes in front of them. When the stimulus that is resulting in acceleration of the next complex occurs after the previous one has already started, this is a difficult concept. We will see some examples of this. But you can't have that with the focus. The focus is fired. It does its thing. And if you have a stimulus after that, it can't do anything to the timing of the next output from that focus. It is already committed. So that is an indication of macroarray entry and fusion. When there is a graded change in paced complexes seen over a range of paced cyclings from the same site, that is progressive fusion in a different language. When you are pacing from a multi-electrode catheter, such as a tricuspid angular catheter or coronary sinus catheter with multiple electrodes in a line, and you are pacing, there is a wave front that is going upstream to downstream, and you are pacing at a downstream site but affecting upstream electrograms. So it seems like it is not going backwards. The activation wave front is not going backwards, but you are accelerating these upstream electrograms by pacing downstream from them. Again, easier to show than it is to talk about. And we will see examples of these. So if it is important to know what fully paced complexes look like, with this first point, a clear blend of fully paced versus fully tachycardic complexes, how do you know what fully paced looks like? Well, you can know what a fully paced looks like. So when I start a case that I think is going to be reentering more in a sinus rhythm, I get all my electrodes in place, and I pace from a bunch of different sites. And I say, that is what pacing from there looks like. That is what pure pacing from there looks like. That is what pure pacing from there looks like. That is what pure pacing from there looks like. So I have this library of known paced activation sequences, and I can easily compare them then, look back on the log, and click on that, and it will show up on the screen after I have done overdrive pacing from those sites during tachycardia, and say, do I have fusion, or does it look like pure pacing, or does it not look like pure pacing? If it does not, then it is fusion, and it is very, very simple. You can pace very rapidly during tachycardia. That means that it is basically a manifestation of progressive fusion. You have much, much more of the chamber controlled by the paced wavefront than the tachycardia wavefront. It is almost the same as pure pacing, but not quite exactly. Or you can be smart, and you can know what pacing should look like. So for instance, if you have typical atrial flutter in front of you, what you think is typical atrial flutter, with the linear activation pattern on a multi-electrode catheter around the tricuspid annulus, and you pace from the proximal coronary sinus, and the patient has not had any prior procedures, you know what pacing from the proximal coronary sinus should look like. It should look like a chevron pattern in those tricuspid annular recordings. And if it does not look like that, then you have fusion. You know you do, because you know what pacing should look like, even if you have not actually seen it. All right. Here is an example of a cartoon of fusion. Here we have an atrial tachycardia, and it is outputting to a site over here. It is going through a macro-oriented circuit, figure of eight or a double figure of zero here, and here the tachycardia comes along. When we pace from that same site during sinus rhythm, we get a wavefront that comes towards the circuit, may enter the mouth of it, but certainly overwhelms the output of the circuit if it could get through there, through the diastolic corridor. So we have a P wave that is a purely paced in this situation. If we combine those two and say, what does pacing during tachycardia look like, it looks a little bit like this, where we have a wavefront that's entering the circuit, and it gets out of the circuit and collides with the next paced complex coming on over here. So we have now a boundary that occurs between output from the circuit and output from the pacing, and after a few cycles of pacing, this stabilizes, and a stable boundary occurs there, and you could pace for a long, long time, and that boundary will remain pretty fixed. That results in a P wave that doesn't look like either purely tachycardia or purely paced, it's a fusion. So this is what fusion looks like on the surface ECG. You can see it on intracardiac recordings as well like this. This is a case of atrial flutter. I have a fluoroscopic view of the left anterior oblique, and here's this multipolar electrode catheter around the tricuspid annulus, and we have this counterclockwise propagation here that we're all familiar with in the so-called halo catheter, tricuspid annular catheter, and coronary sinus catheter, proximal or distal. When one paces from a site way out over here on the lateral tricuspid annulus, a little bit faster than tachycardia, which is about 240 cycling, pacing at 220 millisecond cycling, we have a propagation forward orthodromically. It looks exactly the same as during tachycardia because this annular catheter is in the circuit, and it goes backwards one electrode pair to collide with the incoming complex from the next one. So all of these guys are at paced cycling, all of these guys downstream here are tachycardia cycling. We'll see other examples of this. Pace a little bit faster from the same site here. Now we see electrograms being propagated back two electrode spaces here, and collision occurs between these two up here, and when you pace a little bit faster, 190 millisecond cycling, the electrodes, three electrode pairs upstream from that are antidromically propagated, and the collision occurs right along here. When you pace even faster, 180 milliseconds, this is about 50 milliseconds faster than tachycardia cycling, 50 or 60. We collide all the way up here, and fortunately we did not terminate tachycardia or fibrillate or something like that. It was a little touchy to do that, but the collision occurs way up here, and yet the same tachycardia comes back. So affixed complexes at any given paced cycle length, but progressive fusion over a range of paced cycle lengths from pacing from the same site, progressive fusion. All right, this is an example of something that Dr. Michaud brought to light that's been in front of us all for all these years. We just didn't perhaps perceive it as such. This is a manifestation of reentry in that when we're pacing from a site that's downstream, okay, so it looks like propagation is going along like this in this tricuspidane catheter. We're pacing from a site that's downstream from some other sites, and yet we're advancing the timing of these electrograms here. This one is at paced cycle length. These are all at paced cycle length along here, and the ones that are orthodromically activated after that stimulus are at paced cycle length, and everything that occurs after that are at tachycardia cycling. So this is our actual post-pacing interval from this site, for instance. There are several practical aspects of doing this overdrive pacing for the intent of training. It doesn't take much talent to do this incorrectly and get some really goofed-up answers, and there are several easy ways to avoid mistakes. One is to make sure you have consistent capture during your overdrive pacing before you start measuring intervals. So let's just hold on for a second and look at the end of pacing. We're all wanting to measure the post-pacing interval. How about we just make sure for the prior 8, 10 cycles that we did have consistent capture and propagation to everything else? If you have one or two non-captured stimulus artifacts, boy, you can run into trouble trying to measure post-pacing interval. You have to pace for long enough to make sure that you have entrainment, and again, as I mentioned earlier, the less the delta between your paced cycle length and your tachycardia cycling, the longer you're going to have to pace to make sure everybody comes into the fold that way. You have to pace slowly enough to only entrain and not terminate tachycardia, but as I said, and also fast enough to actually entrain, and the slower your pace, the more trouble you have at making sure everything, you just have to wait a lot longer to make sure that everything that you're wanting to control is controlled by the paced wavefront. The more recordings you have to be able to evaluate, the easier it is to see fusion or that there is no fusion. In atrial arrhythmias, the P wave is problematic because it's small. It may be very splayed out in scar-related arrhythmias, and there's T waves and QRS complexes and all kinds of stuff on the surface ECG to obscure it. Nonetheless, we have a lot of opportunities with intracardiac recordings. We have 20-pole tricuspid annular catheters. We have digupolar CS catheters, multipolar electrode arrays that we can stash around in each atrium and evaluate the activation sequence during pacing during tachycardia. With ventricular tachycardia, it's just the opposite. You have 12 surface ECG leads. God gave them to us. Let's use them, and you don't have as many intracardiac recordings in many cases. Check electrograms far away from your pacing site to show that you have control. We're going to try to also pace from pretty far away from where you think the action is in order to be able to see fusion. For instance, let's take the opposite situation. Let's say you think it's coming from the lateral left atrium. Don't pace the lateral left atrium and try to see fusion. It should look a lot like tachycardia. Pace from the lateral right atrium if you want to see fusion. Get as much distance between where you think the exit from a focus or the exit from a circuit is and your pacing site in order to enhance your ability to see fusion. Then once you've decided on a place to pace from, check electrograms as far away from there as you can to make sure everybody was controlled before you start making inferences about mechanism. It's good to pace from several sites at the outset of a procedure, as I described earlier, during sinus rhythm when everything is calm. You know exactly where all your electrodes are. You can take a snapshot on your electroanatomic mapping system if you need to and say, I know exactly what pure pacing looks like from this site. When I pace during tachycardia, if it doesn't look exactly like that, I know I've got fusion. It's very straightforward. One corollary to all this is that with one run of pacing, you can diagnose macro-reentry if everything goes well. You can't ever do that with a focus. You have to exclude macro-reentry and you can't positively diagnose a focus just from responses to pacing. You look at and so forth. It's really the absence of fusions. You have to pace from here, from there, this cycle, that cycle. It's really tedious. It's hard. It's a lot easier to find macro-reentry, which is for better or for worse a more common mechanism. Here's a case of an individual who's had a couple of visits to his atria for treatment of atrial fibrillation. He's left with this rhythm here. Interesting things here. This is a very narrow P wave with a very long diastolic interval. The cycle length is about 340, 350 milliseconds or so. There's a really tiny P wave on the surface, ECG. All of the intracardiac recordings seem to line up around the tricuspid anus and the coronary sinus. Slightly distal to proximal activation sequence in the coronary sinus. Everything's all lined up. It reminds you of a focus. Well, okay, it probably is. Let's just test this theory. Let's pace from a bunch of different sites. I've got pacing during tachycardia. This is the last five cycles of pacing during tachycardia. This is a resumption of tachycardia over here. This is pure pacing from this site during sinus rhythm. During tachycardia, during sinus rhythm. Then I'm going to superimpose one of these complexes here during sinus rhythm over one of these complexes over here and see how they match. They match pretty good, as it turns out. We infer from this that there's no evidence of fusion. Therefore, our initial hypothesis that this is a focal process in somebody who's got some scar in their atrium is nonetheless seems to be validated. But you can't diagnose a focus on the response of one run of pacing. You can with my macro reentry if you see fusion, but not if you don't see fusion. You can't say it's not macro reentry just because you don't see fusion with one drive. Let's try something else. Pacing from the distal coronary sinus, same deal. Pacing during sinus rhythm over here with its activation sequence, pacing during tachycardia over here with its activation sequence, and here is a return of tachycardia. Take one of those beads and put it over there, and again, it doesn't look like there's any fusion at all going on over here. Again, we say more than likely a focal process. Great. Just humor me, do one more side here, proximal coronary sinus. Pure pacing from the proximal coronary sinus, pacing during tachycardia and tachycardia resumes over here. What we see when we superimpose those is, ah, they do not look the same in this instance. This is pure pacing. Pacing during tachycardia does not look like pure pacing. There is fusion, so this is macro reentry. Narrow P wave, all the electrograms that we are recording from both atria line up within the P wave. There's no diastolic anything. Sorry, this is reentry. All you got to do now is find out where the diastolic corridor is and ablate that. It was very simple matter in this case. Here's another case here. This is concealed fusion in an atrial tachycardia. We're pacing at 270 milliseconds. The atrial tachycardia is cycling at 310, pacing a little bit faster than I already like to, but it's okay. Here is a complex, one of these atrial tachycardia complexes, I believe this one here, maybe it's this one, superimposed on the paced wave front and boy, they are identical. So there is no fusion here. So you'd say, oh, it's a focus then. Well, no, this is an exception. If you have determined otherwise that pacing from other places, that this is actually macro reentry, that you had fusion. If you're pacing from within the circuit and the path of the impulse from pacing has to follow exactly the same path as a circuit, whether you're in the middle of the diastolic corridor or the entrance, the exit, it looks the same as a tachycardia pacing during tachycardia looks the same as tachycardia. So this is, we know there is a fusion during this. We just can't see it real well. There's sometimes when you can see it, I'll show an example of that as well. So we have entrainment with concealed fusion here, and here's our site that is the post pacing interval measured from the pacing site back to the pacing site. And that compares favorably with tachycardia cycling. The stimulus to pick a reference electrogram is the same as the candidate diastolic electrogram pacing site to that same reference electrogram. This all ends up pretty well. Ablation here should have an effect. It may not have an immediate effect because it may be a broader band than you can just ablate with one RF application here, but this will have an effect. Now, when you have a concealed fusion, sometimes you flip it around a little bit, it's actually sealed confusion here because which one of these electrograms should I measure as my reference for the post pacing interval? Is it here from stimulus to this portion of the electrogram? That's almost the first one that comes back. Well, that's crazy short compared to the tachycardia cycling. Is it this one? Is it this one? Is it this one? Is it this one? Well, we know it's not any of these over here because they were conducted or controlled by the prior stimulus artifact. These are not captured. People talk about, oh yeah, we captured this stuff. No, you didn't capture that. Capture is what occurs at the interface between the electrode that's emitting the electrons and the charge and the tissue that's immediately adjacent to it. Everything else is propagated to or controlled. So these are all controlled here, but they're not captured. So none of these can be candidates for the post pacing interval. It's only this one here that times with a little bit after this guy here that we see in that situation. And it turns out that this has a very good match to the pace cycling as well. This is a case of a repaired congenital heart disease. Here's a young man who has had atrial flutter following a prior catheter ablation. You'd say, well, I guess we got flutter back because it sure looks like flutter. There's a little bit of a pause here between, this is a multipolar catheter of the coronary sinus here. So it looks like there's a little hiatus between where the tip of the tricuspid annular catheter is and the coronary sinus catheter. This is what the electron atomic map looked like around the tricuspid annulus and the LAO projection here. And it looks like we've got propagation, sure enough, in a counterclockwise way here. But when we pace from the infralateral tricuspid annulus over here at this site, which should accelerate all the electrograms around the marigold round here, we see something very different. The propagation is going backwards from here and forwards on the last pace cycling. So this is, we can't say whether this is entrainment or not, because I don't know what pure pacing looks like from here. It could look a lot like this. It probably does look a lot like this. In fact, this electrogram here looks a lot like that electrogram there, but this is clearly not a tachycardia cyclite. None of these are along in here. So this is problematic for there being a peritricuspid reentry. This was not. In fact, it was a source over here on the septal wall. And you can ablate this cubo-tricuspid isthmus till the cows come home and after they've gone out again and nothing happens because this was not CTI clutter. Here's an interesting example here. We're trying to pace along at a candidate site along the mid lateral, intralateral tricuspid annulus in this person with some pretty messed up electrograms. And when we do that, we are not syncing, synchronizing very well here, but the pacing wavefront stimulus artifacts gradually catch up here to the electrograms. And we see something interesting here. We see an abrupt loss of all electrograms. And when we continue pacing, we see things going in a very different direction. What happened here? Well, what happened here was tachycardia actually terminated along the way, right along in here. We don't propagate from this point forward. We propagate all along down here, but we don't propagate from this point forward. We do propagate down there, but this electrogram was not captured here. It occurs just before the stimulus artifact. This is the one that was actually captured and there's a missing array of electrograms right in there. So we're pacing along there. The electrogram, the wavefront stops after here, gets to this point, and we have a stimulus that tries to send it forward, but the tissue downstream from there is refractory, can't conduct the impulse any further. And when you continue pacing from there, it actually is going backwards through this circuit. And this is an indicator that that site where you did the stimulation is actually an extremely important site because it's in the circuit. And you can't have this response from anywhere but within or really, really close to a critical point of the circuit here. This is called a bunch of different things, non-propagated stimulation during tachycardia, termination without global capture. It's not captures without global propagation and so forth. When you see this, you can see this with overdrive pacing. During tachycardia, you can do it with single extra stimuli. Here's an example of that where we're coming along and delivering a single extra stimulus from this site here. It seems to just poof. It seems to be an invisible ray gun that blasts away at the circuit. Now, this is not, didn't ablate anything. This is not a shock. This is a single extra stimulus that terminates the tachycardia without seeming to capture anything. It had to capture some tissues. It's not sub-threshold stimulation any more than this was sub-threshold stimulation. This is super threshold. It captures just fine, but it captured and sent the wavefront along forward here and terminated the tachycardia without any further propagation. This suggests an excellent ablation site in a very small area because your paced wavefront can't have a large area of control. It's within a narrow corridor, critical for tachycardia perpetuation without transmission through which tachycardia cannot continue and therefore it stops right then. It can be seen while attempting to reset the tachycardia with single or double extra stimuli or when attempting to untrain it. This is tricky because you're looking for what happens at the end of pacing. You're not looking for what happens during pacing. Well, I look what happens during pacing now that I've learned about this thing because if I am at a site that I don't know if it's going to be a good site or not, but I see this response, I know it's a great site for ablation. I've just not seen this fail. It's often unexpected. You're not looking for this in most cases. Very commonly overlooked. I overlook it. I look for it and I overlook it. Just get over it and scroll back once you've done a run of pacing and maybe seen something that's a little bit odd. Why did this do this? Look into it a little bit further. Maybe this is what your phenomenon was and you just stumbled upon a great site. Now what happens to me is I find out about this the next morning when I come in and look over the case and okay, how long was it after I found that this occurred during the procedure before I finally came back to this site and decided it was a good site? Sometimes it's an hour. That's just dumb. Look for it when it's live and in color. There's tachycardia determination without propagation. Physiology of this is as follows. We have this, again, figure of eight or double figure of zero circuit here. We're stimulating from a site that's within this diastolic corridor at a certain location, a certain timing during tachycardia. It tries to send the wave front forward, but finds tissue that's refracted downstream. It can't propagate side to side because of refractory barriers. Maybe it's scar. Maybe it's a functional barrier. It can't propagate backwards because the next cycle is coming in or has just occurred. It dies right there and the tachycardia stops with it. Dr. Jane reported on our experience with this just a couple of months ago and all of these we've talked about before. Now, if you continue pacing from that site and your site of stimulation was closer to the entrance to the circuit, electrically closer to the entrance of the circuit than the exit, you'll have an output from the circuit that looks very different than what you were anticipating seeing. It doesn't look anything like the tachycardia did, like the example I showed earlier where we did overdrive pacing. As soon as pacing terminated, the next paced wave front looked completely different, even though it was pacing from the same site. If your pacing site was closer to the exit of the circuit, you will preserve the same electrogram sequence as you had during tachycardia. It'll look like you just reinitiated, which you may have done. Now, many years ago, Dr. Stevenson's group, when he was at Brigham and Women's Hospital, came up with this algorithm for kind of a scouting expedition. I know I have re-entry. Where's the circuit? Is it right atrium, left atrium? It's just an overall 30,000-foot view. If you pace from the high lateral right atrium and you get a post-basic interval that's relatively short, it's probably a right atrial process. You can refine that further by pacing from the proximal coronary sinus. Is it typical flutter? Is it a lateral right atrial process? If the post-basic interval minus tachycardia cycle length is more than 50 milliseconds from the right atrium, it's probably not a right atrial process, probably a left atrial process. You can refine that further into these large buckets of possibilities with pacing at these different sites. It's a pretty easy, straightforward way of getting a broad brush estimate of where things are. Now, another way of doing it is to pace from just a bunch of different sites, the left atrium and right atrium, as I'm showing here. You can construct a truth table with what happens with that. For instance, when you have cavo-tricuspidismus re-entry, pacing from that cavo-tricuspidismus will be in the circuit. None of these other areas will be. Distal coronary sinus is if pacing from the distal coronary sinus is in and proximal coronary sinus is in but not the CTI or the lateral right atrium or the septum, then you're probably dealing with perimitral flutter and so on and so forth. You can refine this, come up with different examples of this sort of thing. Now, treatment mapping is then the process of using post-pacing interval minus tachycardia cycle length pacing from a bunch of different sites to try to figure out how close is my pacing site to critical circuit elements or not. And when you have treatment with a concealed fusion, as I said earlier, pacing from within or very near a circuit, this would be a bystander site or an inner loop that may be a dominant or non-dominant inner loop. If the post-pacing interval exceeds the tachycardia cycle length by a significant amount, 40, 50, 60 milliseconds, that's seen as much as 100 milliseconds, that signifies that the pacing site is in the bystander spur off the diastolic cord. And this is in treatment with concealed fusion. It looks exactly like the output of the circuit. Pacing during the tachycardia looks exactly like the output from the circuit same activation sequence and P-wave, but the post-pacing interval is excessive. That means you're in this bystander loop, important bystander spur. It's an important thing to know because quite often these are far enough away from the main diastolic corridor that ablation there, even though it's a nice, juicy diastolic electrogram, will not have the desired effect. If the post-pacing interval is similar to the tachycardia cycle length, you're within the main diastolic corridor and have concealed fusion. The stimulus to the output somewhere, reference electrogram, stimulus to P is less than a quarter of the diastolic interval from the onset of P-wave, I should say, stimulus to the onset of P-wave. If it's less than about a quarter of the diastolic interval, you're at an exit site. If it's somewhere between a quarter and three quarters of the diastolic interval, you're in the main diastolic corridor. If it's about three quarters or more of the diastolic interval, this is within the diastole, portion down into four plexus, then you're at an entrance site, pretty straightforward stuff. Here we have a putative circuit and the confluence of the KV in the right atrium. Have a little bit of scar there and we got a circuit, again, propagating like a figure of eight here. If you stimulate from this site over here in the high lateral right atrium, it'll take a certain amount of time to get to that circuit, propagate through it, and then back out to the pacing site. That's a post-pacing interval from that site. If you pace from another site, infralateral right atrium, you have to do the same thing, get to the circuit through it, and then back out and back to your pacing site, post-pacing interval from that site. Based on the coronary sinus ostium, same thing goes through. Now, the post-pacing interval in all of these places, as you can see here, is going to be pretty similar. That sort of means that the physical distance from each of these pacing sites to the circuit is going to be very similar, although with naturally occurring barriers, crystal terminalis, fossil valence, things like that, and scar from prior injury, it's a little tough to make that a hard-to-pass statement. But roughly speaking, if your post-pacing intervals are very, very similar, the physical distance is going to be very similar. Contrast that to pacing for just the coronary sinus, whoa, it takes a long time to get over there and back. That's a very long distance from where the action is. Now, if you pace from right in the very center there, then you have a post-pacing interval equals tachycardia cyclin. Now, let's see some examples of this. How do you do this practically? You can do this using an electron atomic mapping system to help just see this visually. So here we are, we're overdrive pacing during tachycardia here. From this site, all the electrograms are accelerated in pace cycling, same tachycardia resumed upon cessation of pacing, blah, blah, blah. When we look at the activation time from this site right here, referenced to the tachycardia cyclin is 220 or so. And here's our actual activation time, whatever that is, 58 milliseconds after the reference electrogram of the coronary sinus. That's just for reference. If you then measure the post-pacing interval, which was in this case 440 milliseconds, tachycardia cyclin is 245, and that's the post-pacing interval minus tachycardia cyclin difference is 195. And you put that in, just manually move your activation cursor over here. This is kind of an artifact or artificial thing, but until this number reads 195 here. Then you can construct an activation map or a PPI minus TCL map that plots on your electron atomic mapping system into something that will look figuratively like this. So the red is the smallest number that you have, close to zero. Purple is the largest number that you have. And so this gradation can say, hey, I'm pretty close to where the action is. Now, importantly here, all of this area here in red is a PPI minus TCL equals zero. Does that mean every site in there is a good place to ablate? No, it doesn't. You can ablate over here and it has no effect whatsoever. You can ablate over here, no effect. If you ablate somewhere in this diastolic corridor, then you've got something. So here's an example of the raw PPI minus TCL map. And then you can cone this down a little bit and say, I just want to see what happens at less than 30 milliseconds. PPI from zero to 30 milliseconds, allowing for that, we usually give that 30 millisecond PPI minus TCL grease period. Say that, yeah, it's pretty close or it's not. So the smaller the PPI minus TCL difference, the closer the pacing site is to the circuit physically and certainly electrically. It can show you sites that look like they are early, but are actually late. A classic example of this is an individual who's had pulmonary vein isolation. They come back with a macroinvertebrate tachycardia and one or more of the veins is not isolated. Very, very slow conduction into the vein can make a pulmonary vein potential that may look like an atrial signal very, very late, so late that it's actually bleeding into the next tachycardia cycling, so late that it can look early. And so you get all these goofy-looking electrograms. Sometimes it's best to just re-isolate the veins first before venturing into trying to do an activation map. This technique can reveal dual-loop tachycardias. Remember that being in the circuit is not the same as a good ablation site, as I illustrated earlier. It's tedious to do this process. It takes 15 or 20 minutes sometimes to do enough sites that you can have a cohesive-looking pattern here. And unfortunately, every time you pace, there's an opportunity to terminate or change the tachycardia, so it does run that risk as well. Now I want to shift gears here a little bit and talk about pacing during a focal tachycardia. Now you can get a post-pacing interval during a... Anytime you pace, there's an interval that follows. And if it's the same tachycardia that recurs, then you've got a post-pacing interval minus tachycardia cycling that you can use. Be careful with it. This is a post-pacing interval in a focal tachycardia. So we're pacing down here in the proximal coronary sinus. Here's our electrograms in the infralateral right atrium here. And when we pace from there, we get a post-pacing interval. It's not exactly the same thing, but this is a stimulus to the first electrogram that comes back, just for purposes of illustration here. 670. Remember that. Now we pace from a different site here along the tricuspid annulus, and it's now 600. That means that if we pace for the same number of cycles and our first stimulus synchronized exactly so we had interacted with the focus or the circuit, whatever it is, exactly the same number of cycles, 20 beats, 40 beats, whatever it is, then you're going to interpret this interval. The post-pacing interval now is less than it was, so we're closer physically to the action in this case. You pace from the infralateral tricuspid annulus, very close to where the earliest electrogram is. Now we've got something that's 560 milliseconds, that was only about 10 milliseconds longer than the tachycardia cycling. So that's pretty good. But you've got to be really careful with that. Because if you pace for too long, or you think you're pacing for 20 cycles, but only the last eight of them actually interacted with the focus, then you've only overdrive suppressed it for eight cycles, as opposed to 20 cycles, which is going to be a different PPI in those cases. So be very careful with that. Here's an example of an AHA sequence during junctional tachycardia. We have junctional tachycardia coming over here. Gosh, this could be avenodal reentry. It could be an atrial tachycardia with a propagation down the slow pathway. But what is it? When we overdrive pace the atrium, we propagate to this site, we propagate to the HISS here. And then we see this AHA response here. Now, if this stimulus led to that, which means that this HISS-HISS is the same as this HISS-HISS, we'd have a different matter. But this was the one that was controlled by this atrial stimulus, not this one. So we have an AHA response, junctional rhythm. Can't see this with avenodal reentry. Can't see this with orthodontic SVT, or certainly atrial tachycardia. Here is what looks like an AHA interval here, right? It looks like an AHA interval during overdrive pacing from the atrium, but actually it's an AHA response. This is of critical importance in real life in making diagnosis in your patient, but also in examination, where you have to know which is the last controlled complex, not the last paced complex, not the last easy to see complex, but the last one that's actually controlled. So the easy way to do this, just measure your output. This HH here, this RR is 270, the same as paced cycling, not tachycardic cycling. So this is an AHA response, and this is actually avenodal reentry. Particular override pacing, very useful technique. We can assess results of pacing and interpret them when we have retrograde conduction during overdrive pacing. A VAV response is seen in orthodontic SVT or avenodal reentry. Dr. Michaud will talk about this in great eloquence in another talk. A VAAV response, so you're pacing the V conducting retrograde late to the A, and then you wait for the next A to occur. That is atrial tachycardia with rare exceptions, unusual forms of avenodal reentry. Typically, it's atrial tachycardia. You may have a pseudo VAV response, that is, if you don't actually have retrograde conduction, it can kind of look like there is, but you can tell that the A's are not accelerated to paced cycling, so there is no retrograde conduction. That is seen in atrial tachycardia. The pseudo VAAV response can be seen in atypical avenodal reentry or orthodontic reentry using a slowly conducting pathway, rarely in atrial tachycardia with a pseudo VAAV. If you measure, again, with retrograde conduction present during overdrive pacing, the PPI minus tachycardia cycling, if it's in excess of 150 milliseconds, and typically the stimulus to A versus the QRS onset to the same H electrogram is greater than 85 milliseconds, this is avenodal reentry. If the intervals are shorter than that, because the pacing site somewhere within the ventricles is closer to being in the circuit than the avenoda is, which is very far away, then you have orthodontic reentry. Certain exceptions apply to that. Those have been very nicely laid out in the literature in the last 15 or 20 years. When the A tree are accelerated in ventricular paced cycle length during overdrive pacing within two fully paced QRS complexes or in the presence of obvious ventricular fusion, you have orthodontic reentry. If it takes longer, more cycles of pure pacing, that means there's no anterograde HISS propagation that controls part of the ventricular activation. It's all retrogradely conducted, but it takes a while to get back to the atrium, maybe three, four, five cycles. That's avenodal reentry because the avenoda is protected by the HISS and whether there's a lower common pathway or not. If retrograde conduction is absent during ventricular pacing and tachycardia, really atrial tachycardia is your only significant option. It's very difficult to see this notificator, notificatory pathways can do this as well, but pretty unusual. Very, very rarely, avenodal reentry with a lower common pathway, in which case you can't see the HISS, you're not propagating the HISS, or upper common pathway where you do see HISS can be present. But I look for these things and I'm not sure I've ever seen one. I've only been doing this for a few years. Here's the VAV response during overdrive ventricular pacing or pacing along the ventricle here. We're conducting backwards to the atrius and eccentric activation sequence, as we talked about with retrograde conduction. That's the VAV and this is orthodromic SCT. Retrograde conduction is present during pacing. The last paced A is followed by a V. The last controlled A is followed by a V, not by another A. It's not a VAV, it's a VAV. This is a pseudo-VAV response. If you're just looking at this casually, you say, okay, paced V, I got an A, I got a V, it's a VAV. Okay. Well, this is not because we have paced cycling at the 320 here, tachycardia cycling at the 360. And it just so happens that all of our A's are 360. We had no retrograde conduction. So be very careful interpreting this, that you do it correctly, otherwise you'll get some really messed up results here. The absence of retrograde conduction invalidates your ability to say that I have a VAV response, which assumes that there is conduction and diagnosis atrial tachycardia with very rare exceptions as even on the way entries with lower compacted or upper compacted block. This is a VAV response. So we're pacing the V here and we have A's that are different during pacing than they are during tachycardia here. This is a high-to-low sequence. This is a concentric activation sequence. So this is a VAV response. Retrograde conduction is present during pacing and there is no intervening V or his between these with the odd type of the upper slow pathway, even though for entry when you can have a block blochius with an A in between here, it's very unusual, but it does occur. There's a pseudo-VAV, wherever there's a real, there's always a pseudo out there and there's even some pseudo-pseudos. Leave that to another discussion, but here's a VA and it looks like it's an AV here, but this is actually a VAH, which leads to the next A. So this is just AV nodal reentry. And the reason is, is probably because there's a lower common pathway here, it gets back to the atrium much more easily if it gets down to the ventricles here. Pretty unusual type of tachycardia, quite often these are a left slow pathway. This is an example where we have the post-pacing interval minus tachycardia cycling and the stimulus to A and the VA. So here's PPI, here's tachycardia cycling. That difference is, there's PPI here, I'm sorry, the tachycardia cycling difference is 275. The S to A minus the V to the same A, QRS onset to the same A, that difference is 250. This is a very long difference here in both these cases, AV nodal reentry, quite easily done. This is an example of a PPI minus TCL indicative of a slow pathway, a slowly conducting accessory pathway, PGRT type. So here's our pace cycling, a little bit faster than tachycardia, PPI minus TCL only 80, stimulus to A minus the electrogram to A only 60, for the AV nodal conduction with the PPI. So this is indicative of a slowly conducting accessory pathway. You could have decrement here if you pace too fast, that would mess up your PPI, mess up both of these. And could fake you into thinking that it was AV nodal reentry. That's important to pace these long RP tachycardias as minimally different from the tachycardia cycling as possible. Here's a post-basic interval minus tachycardia cycling that looks like AV nodal reentry, but because the right ventricular pacing site is so far away from the left lateral accessory pathway, of which this was a case, it invalidates this. So use the tool correctly, interpret it correctly, use it where it can be interpreted correctly, and don't try to over-interpret something that doesn't really lend itself to it. All right, there's several pitfalls with the overdrive pacing and entrainment. It's a great tool. Back to entrainment. There are lots of pitfalls that the most common one that I see is you just didn't capture when you were pacing. You can get some really great pace maps and get some very confusing post-basic intervals because the last cycle didn't capture. So whatever that next electrogram is after the last stimulus artifact is when it is. It just occurs randomly. So don't fall into that trap. If you don't pace for long enough to entrain, it's difficult to make inferences about the post-pacing interval. If you're pacing from a site that's too close to the exit from a circuit or from a focus, the same problem obtains, you really can't see fusion very well. If you're pacing at too high an output, you're capturing too large of an area, then you may be leapfrogging over some tissue and capturing tissue further away from where you think you were capturing and actually get a post-basic interval that's shorter than the tachycardia cycle. That's a little confusing, but it's simply a very simple resolution with this leapfrogging action. You may change the tachycardia to a new morphology, terminate the tachycardia in some way. That was not a trap. You have to be careful of that. You can see an instance in which you're pacing from a bunch of different sites, and a lot of them or all of them seem to be in the circuit. How can they all be in the circuit? Well, maybe they are all in the circuit. And for instance, pacing around the tricuspid annulus, again, all of those sites hugging the annulus are in the circuit. But most of the sites from the tricuspid annulus to the inferior vena cava are in the circuit. That doesn't mean that each one is uniquely a great ablation site that's going to kill the tachycardia. It may take broad bands in both of those situations to eliminate the hereditary. You might find a situation in which no sites meet good criteria, PPI minus TCL is long. Most often, this is with slower decremental conduction in a circuit. Patients have a lot of sodium channel blocking drug effect, amiodarone, lots of scar, congenital heart disease, post AF ablation tachycardia can sometimes do this. Fortunately, it's not a very prominent problem in the vast majority of cases, but it can be vexing in some. Sometimes you have far field capture, capturing more tissue than you intended to, and this leads to this leapfrogging event where you think you're capturing just one point source, but you're actually capturing tissue some distance from that and actually sending the impulse forward from a place further downstream than where you think you were, and your PPI is going to be less than expected. So in summary, a clear understanding of responses to override pacing can be very important for the electrophysiologist when doing ablation. It aids in diagnosis, diagnosing AV and nodal reentry versus atrial ventricular reentrant tachycardia versus atrial tachycardia. It can aid in categorizing the arrhythmias macro-reentrant or foveal emanation, and thereby indicate the appropriate electrogram characteristics for ablation target sites. And it refines a selection of candidate ablation sites, say, is it a bystander, is it the real thing? It's not necessary in all cases. You don't have to do this in every single case, but you have to do it frequently enough that you're facile with these techniques and their interpretation, how to do it correctly, how to interpret it correctly, in order to be able to use this tool when it's absolutely essential. It is absolutely pivotal for success in some cases, and you'll do yourself and your patients a favor by being very good at this. The user must be aware of potential pitfalls in their application. So takeaways from this. Before measuring intervals and making conclusions, make sure capture was present through all of the cycle that you're interpreting. Measure carefully when you do make your measurements. Very slight differences can have very important implications. Make sure you're knowing which of the electrograms was conducted versus controlled versus pacing. So that one example, I showed a very, very fragmented electrogram. Only one of the diastolic components was the one that was actually captured. The others were controlled or conducted to. And beware the pseudo-VEAV. It has been the nightmare of many electric physiologists in the lab. I have a few questions here. 16-year-old man with no prior cardiac procedures comes for an ablation of what appears to be typical atrial flutter. Pacing was initiated during tachycardia, and as I'll show, the last three paced complexes are followed by resumption of the original arrhythmia. I'm just going to posit that we started with arrhythmia, we overdrive paced, and you'll see that there, you'll see the results of the pacing, the stimulated complexes in the same tachycardia resumes. The figure thus demonstrates entrainment of macro-reentry, entrainment of micro-reentry, override pacing of a focal tachycardia, or inconclusive findings. Here's the pacing. So we started with this tachycardia. We did this pacing, and we resumed this tachycardia here. And I'll let you analyze that, and you can turn me off for a moment and then come back. Okay, the correct answer is that it was macro-reentry. Here's an example of what pure pacing would look like or did look like when pacing from the coronary sinusosteum. You'd have no prior procedures, right? So there's nothing that should have disturbed the activation pattern in the tricuspid aneular catheter here. It should look like the chevron pattern if we're pacing during a focal tachycardia from somewhere else. But the fact that we have clear fusion, it didn't look like pure pacing, right? It didn't look like this, and it didn't look like pure tachycardia because the coronary sinus electrodes are going backwards. They're going distal to proximal here. Therefore, pacing during tachycardia doesn't look like either pure pacing or pure tachycardia. Therefore, we have fusion, and thus macro-reentry is diagnosed. Entrainment of macro-reentry is correct. Question two. In the figure I'll show, entrainment of an atrial tachycardia, it shows that the site of pacing is in an outer loop, in an inner loop, in the common isthmus, a remote bystander, or a bystander adjacent to the isthmus. There's the figure. We'll drive pacing during tachycardia, the last three cycles of which are shown, and then the same tachycardia resumes. I'll posit that this was entrainment. And you can rejoin me later. And the answer is in the common isthmus. Why is that? Well, here we are again with the same figure. The tachycardia cycle is 290. We're pacing at 260 milliseconds. All the electrograms are accelerated. The pace cycling, here's an example of one of the pace complexes superimposed on the pacing during tachycardia. We don't see fusion. So this could be a focus, except I told you it's entrainment. Therefore, it's macro-reentry. So where in the circuit are we pacing? All right. The PPI, the stimulus to A, is the same as the electrogram to A. And the post-pacing interval is the same as tachycardia cycling. So this is in the circuit somewhere. It's not a remote bystander. It's not an adjacent bystander. Somewhere in the circuit. Now, if we have exact replication here, there is no fusion, then it is either an interloop or an adjacent bystander, which we know it's not because PPI minus TCL is appropriate, or it's entrance, exit, or mid-corridor. Which is it? If you look at the timing of the electrogram here, it looks kind of entrancy here. It's at the very end of this T wave, maybe the P wave here. It's either entrance or mid-diastolic here. And since the electrogram is closer to mid-diastole and entrance wasn't a choice, this is an isthmus site. So it's mid-diastolic potential. There's no fusion with override pacing from this site. Stimulus to a reference electrogram is very similar to the electrogram to the same electrogram, the pacing site, to the same electrogram here during pacing and during tachycardia. And the PPI is very similar to the tachycardia cycle. This is my last question. The figure, which is overdrive pacing during an atrial tachycardia, demonstrates entrainment at a site within the circuit, at a site without the circuit, outside of the circuit. Overdrive pacing in a focal tachycardia organ results are inconclusive. Here's overdrive pacing during the rhythm. The same rhythm comes back here. Rejoin me now. The answer is entrainment at a site within the circuit. How do we know that? Here's the recordings here. We were pacing a little bit faster than tachycardia cycling. And we have this electrogram sequence here that is very similar to, but not exactly the same as during tachycardia. Here are these electrograms over here. Here they are during tachycardia. Not exactly the same. And therefore, we have a systolic potential. It occurs within the P wave, at the very beginning of the P wave. We have some amount of fusion. And the stimulus to P is very similar to the electrogram to P in the post-pacing interval. It's similar to the tachycardia cycling. And the solution that fits all of these criteria is an outer loop site. And so that is that. I thank you for your attention.
Video Summary
In this video, the lecturer discusses overdrive pacing during supraventricular tachycardia (SVT) and its diagnostic implications. Overdrive pacing is a technique used to assess and determine the mechanism of tachycardia, whether it is macro-reentry or a focal tachycardia. By pacing at a slightly faster rate than the tachycardia, the lecturer explains that if fusion occurs, it indicates an atrial macro-reentry or the presence of a focal automatic tachycardia. The lecturer also discusses entrainment, which is the technique in which the tachycardia is reset by pacing. Entrainment can aid in both diagnosis and treatment by defining the mechanism of tachycardia and validating ablation sites. The lecturer also emphasizes the importance of carefully interpreting the post-pacing interval and differentiating between fusion and pseudo-fusion. The lecturer provides examples and explains the potential pitfalls of overdrive pacing and entrainment. Overall, the video highlights the significance of overdrive pacing in diagnosing and treating different types of tachycardia and emphasizes the need for careful interpretation of the results.
Keywords
overdrive pacing
supraventricular tachycardia
SVT
diagnostic implications
macro-reentry
focal tachycardia
fusion
atrial macro-reentry
focal automatic tachycardia
entrainment
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