Okay, good morning, everyone. Welcome back to the second session of the in-person board review at the Heart Freedom 2025. Again, my name is Amale Ujo from University of Rochester, New York. I have the honor of co-chairing this session along with Dr. John Miller from Indiana University. So this session will focus on ventricular arrhythmia, and our first speaker will be Dr. Knight from Northwestern University. Good morning. I'm glad you're all here on Sunday morning. This is some true dedication. I gave this talk last year. There's not a whole lot different in this topic. We're going to talk mainly about PVC localization. These are my disclosures. I don't think they're relevant necessarily to this talk. So most of this is electrocardiography, you know, trying to use EKG to localize ventricular arrhythmias, PVCs, and ventricular tachycardia. But we know where common sources of these arrhythmias are, and so it's more of an electroanatomic thinking, and you can kind of go through the anatomical areas first and see what the EKG patterns will look like. So these are the outflow tract locations from the right ventricular outflow tract. You know, I recall many years ago this is where they all seem to come from. Now they seem to come from all over the place. But the RVOT is a common place. It's my sense that exercise-induced VT is more commonly from the RVOT than just PVCs. The PVCs seem to be just as likely to be coming from the LV outflow tract. But the RV outflow tract, you can go up to the pulmonic cusps. There's actually some case reports of PVCs arising from the muscle that extends beyond the pulmonic valve, the LV outflow tract, the aortomitral continuity, and the aortic cusps, the left cusp, the right cusp. Technically, the non-coronary cusp is over the atrial septum, so there's no ventricular arrhythmias, but they can be very close to there. The mitral and tricuspid annulus are sources of PVCs. They can be coming from the HISS region and referred to as parahissian PVCs. And then from the ventricular muscle itself, idiopathic ones can be coming from the moderator band, from the papillary muscles, or the septal band in the right ventricle. The moderator band's an interesting location because there's a septal and a free wall attachment kind of moderating the right ventricle, and they can be coming from anywhere along that, and it's a little bit hard to get catheter stability. On the left side, it could be coming from the posterior fascicle, more commonly than the anterior fascicle, and then the papillary muscles themselves, from the post-remedial papillary muscle, more likely than the anterolateral muscle. There are very few epicardial RV targets, but it probably is true. There's plenty of data that patients with ARVC, for example, have epicardial sources that can't be reached through the endocardium. But just in general, most PVCs that are epicardial are arising from the LV summit, and just above there is the AIV, great cardiac vein junction, and then rarely from what's referred to as the crux of the ventricle. But the reality is, excuse me, areas of inflammation or scar from sarcoid, myocarditis, ARVC, can lead to ventricular arrhythmias really from anywhere. If there is scar, it's often from the border of that scar. It can be from inflammatory infiltrates from sarcoidosis or ARVC. So what are the general principles, what I tell our fellows? First thing I look at is lead V1, whether it's VT or PVCs. What's V1? If it's a right bundle pattern, it's coming from the left ventricle. If it's a left bundle pattern, it's coming from the right ventricle. That's a rule of thumb, but that's not accurate in patients with structural heart disease, often patients with coronary disease. Left bundle pattern is the septum, not truly the right ventricle. So if it's a right bundle pattern, it's from the LV, and if it's a left bundle, it's often from the septum. The next thing is to look at the limb lead axis, if it's coming from down low or up high. An inferior infarct VT often is associated with a deeply negative QRS in the inferior leads because it's coming away from there. The precordial concordance in the morphology of lead V6, but I think more importantly, the precordial transition. So once you've looked at V1 and the inferior limb leads, what is the QRS transition across the precordium? And this can be very sensitive to where they put the leads, even when you see the patient in clinic and then they come into the EP lab, they can look like they're different, but it's really highly dependent on lead location. So that's important when you're setting up the patient in the EP lab and you're fighting for skin space with all the patches for your mapping system, try to make sure that those are very accurately placed. But the principle is that if it's all negative, it's coming from the apex, and if it's all positive, it's coming from the base toward the chest leads. And then how that transition occurs, how close it is to the transition in sinus. You know, is it an early transition or a late transition? The earlier the transition, the more it's pointed over to the left ventricle. The QRS duration can be helpful. If patients have no structural heart disease and the QRS is wide or narrow, that can give you a sense of whether there's cancellation of forces because it's coming from the septum and you have a narrow QRS for that reason. It can be narrow because you engage the Hiss-Purkinje system, you know, fascicular reentry. Very narrow QRS patterns are usually coming in some part from the conduction system. Either they're arising from that or they're arising from adjacent to that and engaging the Purkinje system very quickly. Epicardial location, we're always talking about that. There are some general things that you can look at, but the principle is that if you're activating the epicardium, you're far from the conduction system and you get a very initially slow upslope like a delta wave. So there are ratios you can look at, but the idea is that if it's coming from the epicardium, the activation is going to start off initially very slowly. If it's from the septum or free wall, again, if it's from the septum, there's simultaneous ventricular activation giving you a narrow QRS without mid or late notches, but a free wall, particularly right ventricular PVCs, if it's very wide and notched, it's pretty unlikely to be coming from the septum of the RV outflow track, for example. That can be quite helpful. You know, it's nice to have this in mind when you go into the EP lab. You're ultimately going to be mapping these with usually a QRS as your reference point, finding the earliest site, but if you have a sense of where it's coming from, it can help you plan which access you're going to start with. It can help you educate the patient about what the risks of the procedure are. So let's talk about how to identify outflow track PVCs, whether they're coming from the LV or RV. And again, this is not precise and there's hundreds of papers that keep getting published of how to best determine this, but it is useful if you see someone, you're very confident this is from the RV outflow track based on a 12-lead of their VT or PVCs in clinic. I think that you're going to have a much higher likelihood of success and ease of the procedure. If it's pretty clearly coming from the left side, you are going to have to figure out is that from the left cusp, right cusp, under the valve, on top of the valve. So this is, I think, one of the more useful diagrams that Sam Acerbathum published. And if you look at this figure here, do you see my mouse? No. Here. You see? Yeah. So if you look at this figure here, there's a tricuspid mitral valve and the aortic valve and pulmonic valve. Remember, we'll get to this when we look at lead one, but the pulmonic valve is actually closer to the left shoulder than the aortic valve, which is very central in the heart. You think of the, if it's coming from the right ventricle, it's got to be more toward the right side, but actually the furthest to the left is the antereceptal RVOT. But if it's coming from the anterior RV, you're going to get what is correlated here with this number one, a very deeply negative QRS in lead V1. So we're looking at V1. If there's a notch, you see a notch like this, then you're starting to move more toward the aortic valve, pulmonic valve junction, closer to the posterior RVOT, where lead one will start becoming more positive. As that transition becomes more early, you end up toward, here's this pointer. So as this transition becomes more early, you're headed more toward the cusps. So the right cusp, the left cusp, and eventually the mitral valve. This is certainly not pure. There's always some transitions in between here. But I think this is a very useful way to think about it in your head. So, you know, what does it mean that the transition is early or late? Well, it kind of depends on what their transition looks like in sinus rhythm. So this is that concept here. If you look at lead V1 and V2, there's a formula here that basically says, is the transition with the PVC significantly greater than the transition in sinus rhythm? So you can take these ratios and basically, is this transition sooner than sinus? And that can help you lean more toward the left side. The earlier the transition the precordial leads, the more likely it's coming from the left side. So if you're pretty sure it's from the right side, then how would you start going into MAP? Again, the furthest toward the left shoulder is the antriceptal RV outflow tract. And so the anterior septum gives you a pretty deeply negative QRS in lead I that becomes positive as you move more posteriorly. So if you go up and you kind of record a hiss bundle and you keep going up in that plane, so you're on the true posterior wall, you're going to get a pretty positive QRS in I. So if you see this is positive in clinic, for example, that points you toward the posterior RVOT, but also makes you suspicious it's coming from the left side, because that's just on the other side of it. I get excited when it's a deeply negative lead I. You're pretty sure that this is from a place that's easy to get to from the RVOT. If it's on the free wall, you can look at these transitions as well, but it's not as useful and as common. So here's some examples. Here's an example of RVOT-LVOT. The QRS transition, I'm sorry, the inferior axis is pretty similar. What you notice the most is that the QRS transition in lead V2 here is pretty deeply negative and becomes more positive. So the earlier the transition, the more likely it's from the left side. I'm going to stick with this pointer. So here's just an example. I still use a lot of fluoroscopy, but when I'm targeting an RV outflow track PVC that's near the pulmonic valve, I look in this LAO view first and get the catheter tip as far over to the left as possible, toward the left side, close to the aortic valve. And then depending on how anterior or posterior it is, I'll counter clock it, counter clock it toward the anterior septum. That way you have pretty good contact. And then I look REO. So getting this catheter as far over here as possible can be useful. And here's an example of a mid-septal RVOT. You can see that, again, V1, deeply negative. Actually a little bit of a notch there, but it's a pretty late transition. And lead I is not purely negative. It's a biphasic, a little more negative than positive, but it's biphasic. There's a very early activation with minus 30 milliseconds here relative to the onset of the QRS. And so this was the successful target site. There's a lot of other things you can look at, too, just on your recording system, independent of your mapping system. If you're on the target, this should be earlier than the proximal pair. I often also display the mid, the 2, 3 electrodes. So if you're really on top of it, the earliest electrogram on your catheter should be the distal pair. And if it's not, then you can keep going a little bit further. That's V1. That's lead I. And then this was the pacemap in the same area. It's not perfect, but this is the PVC, and this is the pacemap. Lead I's got a little bit more of a positive ratio than the spontaneous PVCs, but you have these kind of characteristic notching when you pace here that you had during the PVC. So this was a successful site. And again, pacemapping can be useful with these types of idiopathic arrhythmias. In contrast to this, RV outflow tract origin, where you can see it's more positive in lead I, but still a late transition. RV outflow tract, very narrow coming from the septum, a single, beats, couplets, but very positive in lead I. And this is not my case, but it's a case that was published when they did angiography showing that there are some cases where these come from above the pulmonic valve. This is pretty dramatic, but here's the pulmonic valve, and this was the target site there. But it also is what the catheter looks like when you're posterior. This is the posterior RV outflow tract. The aorta mitral continuity, there's a little controversy about that term, but basically to me it means you're near the mitral valve. So if you cross the aortic valve and get under the valve and head toward the mitral annulus, you'll often start to record an atrial electrogram that tells you that you're near the mitral valve. It gives you a very positive QRS in lead V1, so a right bundle branch block pattern with tall R waves in the inferior leads. Often a QR pattern in lead V1, an RS pattern in lead I, and you can have this R wave pattern break where it's positive in I, negative in II, VII, and positive again in VIII, just because of where it's coming from. This is a 22-year-old woman who had ventricular bigeminy from, it appears to be, 11 years ago. I hope she's still doing well. This is the onset of the PVC. Again, pretty early activation. The PVC morphology is upright in lead. Sorry, let me get this mouse. The QRS morphology is upright in the pericordium and negative in lead I. But also you'll notice here that there's an atrial electrogram, which you're not going to see right underneath the left and right cusp. You have an atrial signal here and a very early electrogram. And this was the location of the catheter using a retrogradiotic approach. This is not my case, but these are some catheter positions for locations near the junction of the right and left cusp. Just have to remember when you're in this view on fluoroscopy, the catheter has to be facing forward in the RAO view. If it's down here, it can look great in this view. This is the left cusp and this is the right cusp. But if it's away from you and you look in this view, it's pointing in this direction, you're in the non-coronary cusp. So you come here and kind of get this catheter pointed forward and try to map the left and right cusp. And the junction is a common location of the right and left cusp. What about the LV summit? This is technically one of the most challenging places to successfully ablate. But it will give you a right bundle pattern, inferior axis, like most of the LV outflow tract ones do, but it can be epicardial, endocardial, and intramural. This location is bounded by the bifurcation of the circumflex and the LAD, so you can approach this from the endocardium. You can approach this from the coronary sinus and go all the way out the AIV. The challenge is that the vein at that point is number one, often too small to get an ablation catheter out, and number two, often very close to the coronary arteries. So if it's within four millimeters or so of a coronary artery, you have to worry about injury to the coronary artery itself. So there's other approaches. People have actually sent patients for surgery where the surgeon lifts up these coronaries and goes down into that muscle and ablates it. It's very hard to get pericardial access and get to this space because it's covered with fat. Other approaches which are pretty effective, but technically more challenging, is to find a venous branch of the AIV and inject alcohol. So if you're technically able to do that, it's a good way to do that. If you find the earliest site in the AIV, but it's not a place where you can ablate, you can't get an ablation catheter out there, it's too close to the coronary artery, you can go under that and just anatomically get as close to that as possible because it might not be the earliest site on the endocardium, but the earliest site might not be the closest to the origin endocardially. The mitral annulus, I think these are some of the more straightforward cases. They have a right bundle pattern. They're located in the basal left ventricles. They have positive concordance. All of the pericardial leads are positive. And whether they're coming from the anterior or posterior just depends on what the inferior leads are. And we all know what it looks like. It's like the QRS morphology will look like pre-excitation. It'll look like a left-sided accessory pathway. And you'll have an atrial electrogram when you're mapping. The longer the QRS duration, the more it is from the free wall because there's not cancellation of forces. What about the papillary muscles? This is increasingly a common place of origin, the left posterior medial papillary muscle. It's a difficult place to get stability with RF. I think that people are now way more comfortable going transeptal than retrograde for a lot of these PVCs in the left ventricles. So you can get there transeptal and maybe get a little better catheter stability. People have used cryo to get cryo-adherence to take advantage of that. I've yet, but super hopeful to soon use PFA. On a papillary muscle, I think that would be less dependent on, once you get to that spot, you don't have to sit there for a good 40-second RF lesion. But in general, aside from that commentary, the pattern is in lead V1, basically the fascicular, the PVCs arising from the left posterior fascicle are from a pretty similar location. So they're gonna resemble each other. And they're often, I think, confused with each other. But I think the best way to look at it is it's gonna be narrow. The fascicular origin are gonna be narrow because they look like a bundle branch block. They look like SVT with aberration. And so it's a pretty narrow QRS. There is this other concept that when they come from the papillary muscle, not every QRS is the same because of different exit sites. And here's some examples. These are left posterior fascicular VTs. See how narrow these look compared to posterior medial papillary muscles. So again, V1 is a right bundle pattern in all of these. Lead one is pretty similar. And I think the difference really is how narrow the QRS looks and how much it looks like a bundle branch block pattern. This is one published discriminator. There's a Q wave in one, or AVL, should say AVL, may discriminate left posterior fascicle from posterior medial. So a small Q wave here, just like you would get with a fascicular block pattern, you see a small Q wave. So that little Q wave here in lead one in AVL is not present on the papillary muscle, the PVCs. That might be a useful thing to look at. A correlation with electroanatomic mapping, activation maps and scar maps. We're all very comfortable and fortunate to have ultra high density mapping catheters. A challenge for ventricular arrhythmias is the ectopy that a lot of these cause. So I think most of us are more fond of ones with fixed spacing so that the tips of these catheters aren't tickling the ventricle and causing ectopy. I think Dr. Miller's gonna talk about pacing maneuvers. So I'm not gonna spend too much time on this, but we know that for scar-based reentrant, macro reentry, there's often a critical isthmus that's surrounded by borders of block, which in the past were thought to be mostly functional, but I think now are generally thought to be mostly fixed and scar-based. But they can be complex. You can have a single loop of reentry between a scar and a mitral valve. This is, I think, the classic model of double loop reentry with a critical isthmus here, but you can have multiple loops, and I think we've learned, too, that that is a two-dimensional structure that we're looking at when this is a three-dimensional substrate. So a lot of these reentries and substrates involve the epicardium and endocardium. Not sure why I still have this here, but this was kind of exciting for us. This was one of the first VT ablations we did in a patient using non-contact mapping many years ago who ultimately got a heart transplant, and you can see had an LVAB before they got their heart transplant. And you can see the scar, and then you can see the ablation lesions. And if you ever have an opportunity to go look at your lesions in the pathology suite, fortunately, hopefully not a patient who's passed away, but even if they passed away remotely, you can go look and see what the size of those lesions are that you're creating. And this was back when we had a non-irrigated four-millimeter tip ablation catheter. But this was ablation of an inferior infarct. You can see the morphology here is more of a left bundle pattern in V1, and coming from the inferior wall, so deeply negative in the inferior lead, so going away from 2, 3, and AVF. And you can see there's a beautiful mid-diastolic continuous signal there on your ablation catheter, consistent with being in these protected zones where there's diastolic activation leading to slow VT. And then Dr. Miller will talk about this, but pacing maneuvers where you get concealed entrainment, look at the post-pacing interval, et cetera. And this is just the electrolyte atomic map showing that these tend to be from the scar borders. And termination of that VT. There's been a lot of interest, obviously, in how to map these VTs without leaving the patient in VT for very long because they don't tend to tolerate it. The initial VT ablation studies and targets were patients with huge fixed infarcts and slow VT. We now have patients with multiple non-transmural infarcts, advanced cardiomyopathies and heart failure, non-ischemic substrates who have fast VTs and don't tolerate them, so there's a lot of work in how do you identify the substrate for the VT while they're in sinus rhythm. And they're all kind of the same idea. You know, there's scar that's gonna be the basis of it, so you can look at voltage in your voltage maps, what's red on your cardiomap, for example. But that doesn't tell the whole story. There may be scar that results in slow conduction, so fragmentation of the electrogram, something to look for that's not necessarily on your map. You can then look at the activation. And so if the activation slows down abruptly, that's going to be very likely where the slow conduction is that's causing a protected VT isthmus. So this was a study looking at 16 swine with a healed infarct. And the VT critical zone corresponded to a location characterized by a steep activation gradient. So they referred, everybody kind of describes this differently, ILAM will talk about, but a steep activation gradient and very low voltage amplitude during sinus rhythm. So it allows you to identify a reentry anchor with high sensitivity and positivity. In contrast, the voltage and electrogram characteristics during sinus rhythm were not very useful. So looking at the activation pattern during sinus rhythm and identifying zones of slow conduction in sinus rhythm, may identify the substrate for VT. This has been studied in humans, of course, too, and is referred to as ILAM isochronal, the same time late activation mapping. So you're not looking at the beginning of activation, you're looking at the late activation. And this is an example of the distance and conduction velocity as it comes at a high conduction velocity gets much slower. And this little square is blown up here where you run into an area of actual complete block that kind of slows the conduction here, and then there's conduction around that. So this pacing at this site resulted in a pace map that mimicked the VT, which as you know, is not always the best way to look for VT, because if you are pace mapping in sinus rhythm, and this is the VT circuit, and you're pacing in sinus, you may exit out the entrance to the circuit and get a completely different QRS. So just you have to keep that in mind when you're pace mapping. And then what about epicardial substrates? This is just a case from many years ago in a patient who actually had prior cardiac surgery with a mitral valve, a non ischemic cardiomyopathy. And you can see we're on the endocardium and epicardium, and we're able to identify the substrate of the VT and the epicardium that was not existent anywhere on the endocardium. So how do you identify what are epicardial? There's no vector toward the surface lead, right? So if it's from the epicardium, that's very close to your electrodes on the chest wall, so there's nothing pointing toward it, it's all negative. So the QS in lead one, or AVF, can be very useful. And as I mentioned earlier, it starts out very slowly. It mimics a delta wave or ventricular pre-excitation, and people will call that a pseudo-delta wave. And if it's over 34 milliseconds here, these are all kind of cutoff points that you can keep in mind. They're not perfect, but if it's really wide, QRS over 200, it can be epicardial. You also see that, though, in patients who have been on amiodarum for a long period of time. The intrinsicoid deflection, how late before you get an intrinsicoid deflection, if it's over 85 milliseconds. And then the RS interval and the MDI and any precordial lead of 0.54. This is just kind of an exciting early experience we have with epicardial VTs. You can see there's a mapping catheter, an ablation catheter in the pericardial space, and you can see a mid-diastolic potential here where that asterisk is. This is the VT on the surface EKG. And when we started pacing, it terminates, right? We didn't pre-excite the ventricle. This is the ventricular tachycardia. There's a pause here, so the QRS does not come early. It actually comes late. So we terminated the VT with this beat by causing, without causing global capture. We caused localized capture. And then when we captured the ventricle, we actually had a very different QRS morphology as I talked about before. You're not exiting in the same direction as the VT. But it's something that is proof of concept that this is part of the circuit because you terminated it without global capture. I've got six seconds left, thanks. Thank you, Dr. Knight for that excellent overview on PBC and VT localization from ECG. Our next speaker is my co-chair, Dr. Miller from Indiana University, who will be talking about diagnostic maneuvers in VT. Thank you, Dr. Ojo. This is a great session. I'm glad so many people are here trying to buff up their skills at learning about this sort of stuff. Used to be the room was very sparsely populated with people interested in ventricular arrhythmias. We're supposed to talk about entrainment here. Well, what is entrainment? I'll get some terms down first. It is the continuous tachycardia resetting by overdrive pacing, fixed rate overdrive pacing. There are certain requirements for entrainment to be declared. One is you have to start with a relatively stable ongoing tachycardia, can't vary in cycle length very much because we're pacing at a fixed rate and you're trying to interact with a presumed circuit. And if you have a wildly variable cycle length, it makes it very difficult to know what's going on. Then you start overdrive pacing at a fixed rate, slightly faster than tachycardia for a certain number of cycles. I like to go long to make sure I've got control of everything. 10, 20, 30 milliseconds longer, shorter than the tachycardia cycle length. And then the same tachycardia resumes upon cessation of pacing. Now, most people, when I go around the country, most fellows will say, if we've got these, we have entrainment. Bang, we're done. It's a reentrant arrhythmia. And you can do this with sinus tachycardia. Try it sometime. You can overdrive pace during sinus tachycardia, capture all the atrium, stop pacing, sinus tachycardia returns. So sinus tachycardia is reentrant arrhythmia. No, it's not. It's a focal arrhythmia. So the last thing you need to know that you have entrainment is fusion. And there are a couple of different ways of knowing this. There's a thing called fixed fusion where each complex looks exactly the same as its brethren during the pacing run. An identical blend of pacing and tachycardia doesn't look exactly like either. That means you have to pace from far enough away from where you think the exit is from a circuit to be able to make those distinctions. And secondly, there's progressive fusion where pacing from the same site at different cyclings, you get different degrees of fusion. A different boundary occurs between the paced wave front and the tachycardia wave front. So the hallmark of entrainment is fusion. Here we have a tachycardia coming along. We're recording from an area remotely from the tachycardia in this putative figure of eight circuit here. And there's the electrogram there in mid systole. If you pace from that site during sinus rhythm, and we know we're in sinus rhythm because the cycling is slower than the tachycardia, we got a certain wave front that goes into the circuit, but also overwhelms the exit from it so we have no output from the circuit. If you pace from this site during tachycardia, you end up with this beautiful thing called fusion where we have this boundary occurring between a wave front that is driven through the circuit so some output from the circuit is derived, but it collides with the next cycle coming in from the paced wave front here. So when you're continually pacing at this cycling, at this site, when things stabilize out, you have this degree of fusion here where it doesn't look exactly like tachycardia and it doesn't look exactly like pacing. And it will look that way for a long, long time as long as you're pacing. This is a collision of wave fronts. This is not what you want to see. And there's always a guy taking a cell phone picture out here somewhere. I'm going to spend a little bit of time on this diagram here. We have yellow is VT, red is pacing. And you see this is VT at 490 when we're pacing at 400 milliseconds from the RV, or much, much lower. It doesn't matter. We have pure pacing. Now, I've chosen this pacing site. This is a cartoon, of course. But I've chosen this pacing site for a specific reason. We have a right bundle, right axis tachycardia. From where can I pace in the heart to get something as divergent as possible from this? I need a left bundle, superior axis, a left bundle, left axis. So I'm going to pace from the right ventricular apex. That gives me the greatest opportunity to see fusion on the surface, ECG anyway. Here we go. Pacing at 460 milliseconds, faster than tachycardia cycle length. Each of these complexes is a little bit different than tachycardia, a little bit different than pacing. We have fixed fusion, a blend of those. When you stop pacing, tachycardia returns. Pace a little bit faster at the same site, and now we have a slightly different blend here, slightly more looking like pacing. Lead 1 is a lot more positive than it was before, but not quite exactly the same as pacing. So this also is fixed fusion, same tachycardia returns. Pace a little bit faster. It's almost looking like pure pacing here, but not quite. We've still got a little R wave here at the end of the QRFs with pacing. So each of these is fixed fusion, same tachycardia returns, and over a range of paced cyclings from the same site, we have progressive fusion. The beats don't look the same here as they do there, as they do there. Finally, when we pace fast enough, we have antedromic capture of critical circuit components, this guy here. It's no longer there. We have pure pacing. The entire exit has been overwhelmed with a paced wavefront and antedromic capture, and when we stop pacing, sinus rhythm ensues. These are Waldo's criteria all in one. So when we are pacing from this site over here, I showed this earlier, we have the last couple of beats of paced cycle length here, and we're looking at whether we have fusion out. We do here, and if you pace from a site that is actually within the circuit, I'll go back for a second here, we have a post-pacing interval here that is a little bit in excess of tachycardia cycle length because we have time to get to the circuit, around the circuit, and back out to our pacing site again. That's a post-pacing interval. If we're pacing from a site that is actually in the circuit but not exactly in the diastolic corridor, you have fusion again because we're not exiting in the same manner as it was during tachycardia, but now the post-pacing interval is the same as tachycardia cycle length. So we are in the circuit, we're just not in a critical component here. If we move the catheter a little bit, we have now pacing from the diastolic corridor. It has some antedromic control but also sends an orthodromic wavefront, and now we have this mid-diastolic potential and a systolic potential recording on opposite sides of it. There is a zone of concealed fusion here. There always has to be a zone of concealed fusion. It's concealed because you can't see it. If you have electrodes there, you can see it. Now it becomes manifest fusion. But manifest is usually a term regarded for the surface ECG. Okay, concealed entrainment. What is this? It's a term that's bandied about quite a bit. It refers to a situation in which pacing during tachycardia shows no fusion on surface ECG anyway in a patient in whom you have already demonstrated reentry. This is an important distinction. If you have a focal tachycardia and you pace from that site and you say, hey, I have concealed fusion. I must look for a mid-diastolic electrogram. No, no, no. You need to first prove that you have reentry. We see this all the time with atrial flutter. Some genius puts a catheter at the CTI and says, I paced there. It looks exactly like the flutter wavefront, so I'm going to blade here. Actually, it's a focal tachycardia coming from somewhere else and someone who has prior CTI ablation. So you can ablate for a good long time and nothing much happens with that. So we've already determined that we have reentry. And concealed entrainment then means when you're pacing during tachycardia, it looks exactly like tachycardia. And that designates a site that is either within the circuit or attached to the circuit like an adjacent bystander. Okay. That's good to know. In the circuit at the entrance site, exit site, common isthmus, or an inner loop, you could have something that's attached to the circuit. This is an adjacent bystander, a little spur off to the side. Sometimes if you go in with a big enough bazooka, you can ablate that site, even if it's not in the main diastolic corridor and you'll still get it. It's not very precise. But concealed entrainment can also mean it looks like pure pacing, which is a little bit of a different concept here. That would be where you have just exactly the right combination of cycle length and pacing, and when it comes in during the first beat of pacing comes in during tachycardia, such that you're just capturing the exit site, but it is still able to get almost out, and when you stop pacing it comes back again. A little bit of an unusual situation. Pacing during a focal tachycardia can also mimic these findings. Pacing during tachycardia looks exactly like tachycardia or exactly like pure pacing when you're pacing from anywhere else. The difference is whether or not you've demonstrated fusion. Here's a cartoon of Bill Stevenson's old circuit diagram here. If we are pacing, I have a couple of slides on this, so we'll wait until the end here. This is an exit site. Note the timing of the electrogram during tachycardia. This is during tachycardia over here, the last two complexes of pacing in each of these situations. We have now the post-pacing interval. We have the QRS complex looks exactly like tachycardia. We're off at this exit site over here, and the post-pacing interval equals tachycardia cycle length. If we move to the entrance, the electrogram is much earlier during diastole. Way off over here, heading into the diastolic corridor, has a long stimulus to QRS equal to the electrogram to QRS, and the post-pacing interval, again, is the same as tachycardia cycle length. Moving further around a little bit into the mid-diastolic corridor here, we have this nice isolated mid-diastolic potential from over here. Pacing from there, same QRS complex results, same electrogram to QRS as stimulus to QRS, same post-pacing interval as tachycardia cycle length. And then this important little exception here, the adjacent bystander from way off over here, it looks good. It has a long stimulus to QRS. It has a mid-diastolic activation. The QRS looks the same as tachycardia, but the post-pacing interval is too long, and the stimulus to QRS is equally as long, as much longer as the electrogram to QRS. I'm replicating that up here. I didn't replicate it here. This is a remote bystander now, so we're pacing from anywhere else in the ventricle, and you get fusion here, and you get a long post-pacing interval, and the paced complex doesn't look anything like the tachycardia complex. A little bit further, closer into the tachycardia circuit, we have this outer loop site where it has a systolic electrogram. In each case, these have systolic electrograms within the QRS as opposed to diastolic electrograms on the last slide. We have our post-pacing interval equal to tachycardia cycling. That means we're in the circuit. We're just not in the diastolic corridor. It defines an outer loop here. Finally, the inner loop, of which I have very few examples because why would you ever want to pace here? This has a systolic electrogram, not very interesting. The post-pacing interval, however, is quite good, so we're off over here. If you ablate here and it's a dominant inner loop, you may terminate the tachycardia. If it's the only loop, it terminates the tachycardia. You don't have to be in the mid-diastolic corridor. If you have a dominant inner loop and you ablate there, it simply goes around the outer loop then if it's a dual loop. You suddenly slow the tachycardia and think, hey, I'm getting close. You were close, but not quite close enough to be where the action is. Several pitfalls with entrainment. It has to be used properly in order to make best use of it. Some of these, the most common of which occurs, is non-capture with pacing. We get some beautiful-looking pace matches with us. I guarantee it because you never captured anything. If you try to make inferences about your post-pacing interval, it's all over the place. It doesn't make any sense at all because you never captured. Not pacing for long enough to actually entrain. A lot of my trainees are a little timid at first. They want to pace for, oh, three or four beats because you don't want to do anything. Okay, you didn't do anything. You didn't learn anything. You didn't hurt anything either. So pace for long enough to get the answers that you need. Pace for long enough to make sure all potential elements of a circuit are controlled. If you have poor synchronization of pacing, you may terminate the arrhythmia. You may initiate ventricular fibrillation. So it's easy, easy, easy, easy to synchronize properly. I don't want any excuses. It's easy to synchronize properly. Just do it. Pacing from a site that's too close to the exit of a circuit or focus to be able to see fusion. That's why I choose sites that are far away because I like to do things the easy way. I like to see fusion and don't want to have to work at it. You may change the tachycardia, change to a new morphology or terminate the tachycardia. You may not see a return electrogram because it's all saturated for a good assessment of the post-pacing interval. Or you may measure the post-pacing interval to the incorrect electrogram component and get some screwed up answers here. You may not appreciate the significance of a non-propagated stimuli, as Dr. Knight just showed us. A very nice example on the epicardium. Or you may have many sites that meet the criteria. It's a very broad band through which you're entering, or pacing at too high output captures tissue that's further away from what you think you're capturing. So you're sending a wavefront ahead, kind of leapfrogging over tissue, and you get a too short post-pacing interval or some nonspecific results. You might have a bystander or a decremental conduction, all kinds of things. Lots of trouble with post-pacing intervals. You need to be cognizant of these and not just go in there thinking, oh, here's a nice example here. Perfect pace match here. Isn't it wonderful? Too bad we never captured it. And you can recognize this because if you – I don't look at this interval here, the stimulus to QRS. I look at the previous QRS to the stimulus. If that interval is changing, you never captured it. That's easy. Move on. And you can put a notation in the log, don't look at this. But then everybody will, of course. And this is a great match. No wonder. Never captured. Sometimes you have some unexpected results, such as a post-pacing interval less than tachycardia cyclic. This might be pacing at a site that looks pretty good, yields a short post-pacing interval, or you measured the wrong electrogram component to assess the post-pacing interval, and you might not be capturing all of the electrogram or the electrogram component is regarded as a post-pacing interval, but it actually isn't. The non-captured electrogram component used for the post-pacing interval is always wrong because it was conducted to or controlled. If you are actually capturing electrogram, it's in the stimulus artifact. It's subsumed into that. You don't see it. So there are several solutions to this. One is to make sure you're actually capturing. Duh. Second is carefully assess which component is being captured as opposed to which is being controlled by your paced wavefront. Everybody always talks, oh, well, we captured the atrium from the ventricle. I hope not. I hope you conducted to the atrium from the ventricle. If you capture the atrium from the ventricle, that's called a shock, right? That's the only way you can do that. So here we are coming along here. We're pacing in the ventricle at a site that looks pretty good here, this nice mid-diastolic potential, and everything is wonderful. Oops, but the post-pacing interval stinks because the tachycardia cycle length is much longer than the post-pacing interval. Why is this? Well, we were not capturing this component. You can see it over here. If you can see it, you didn't capture it. So we're capturing something else. What is it? The stimulus to QRS doesn't work. The electrogram to QRS, if we measure here, knowing the stimulus to QRS and work backwards, this is kind of the N plus 1 rule here, working backwards we see this component here, which is a systolic electrogram. It might be an interloop site for you. And we were interested in this site over here. We never captured it. Maybe good, maybe not good. Don't know. We just don't have information about that. So the true post-pacing interval is quite good. Interloop site, good match. You could ablate there and maybe something happens. Maybe it doesn't because this is or isn't a dominant interloop. So correct assessment of the post-pacing interval requires knowing which electrogram component was controlled versus captured. Second, simulation during tachycardia terminates or changes tachycardia without apparent propagation. This is one of my favorite things to do during a study. I still put a fist down on the table when I see this, just the most exciting thing. So when you're overdrive pacing at a site that you think is pretty good, you might see a pause in the middle of pacing, and you might just see it out of the corner of your eyes. It's disappearing off the screen. Look at that. It doesn't seem to capture. You may see a major change in the paced QRS morphology, a change to a different tachycardia after stopping pacing or termination to sinus when you've stopped pacing. Now the solutions to this are to look back and see what happened whenever you see these anomalous things going on. Whoa, what just happened there? Just take a second. It takes a second to look back and recognize this and try to reproduce this finding. As Dr. Knight and others have said, anything can happen once, but if you see this reproducibly, you're in very good shape. Here's an example of this similar to what Dr. Knight had. We've been working, working, finally onto this mid-diastolic potential. We're going to be looking for concealed entrainment, great-looking QRS, great PPI, and tachycardia resumes on cessation of pacing pace. So we pace, and the first thing we see is a hole. We see a pause here. And then the next thing we see is something not very welcome at all. It looks completely different. This is a terrible pace match. Move the catheter to another side. I thought this was good, but it's terrible. No, it is perfect. Do not move the catheter. Step on the pedal. You're home. And the reason for this is when you have this macroenterotachycardia and you're coming along and you stimulate at a site here, it can be a single extra stimulus. It can be the nth beat of drive of pacing. You're coming along at exactly the right timing and exactly the right location within these walls of refractoriness that may be functional, may be scar-raised. And you try to send the wavefront forward. It can't go because the tissue ahead of it is still refracted from the last complex. The next wavefront is coming in. The impulse dies right there. So does the tachycardia. If you're pacing from that site and you see this and it's a reproducible phenomenon, you ablate there, and this thing is gone. It has no choice. It's a nice, narrow, protected corridor. There's no escape from it. The wavefront can't go around it anywhere. And if you continue pacing from there, as Dr. Knight had shown, if your site of stimulation is out here and you continue pacing, you end up looking exactly like tachycardia. You may even reinitiate tachycardia and think, oh, I had a good entrainment. And you missed the whole thing because you weren't paying attention. If, however, you're pacing from closer to the entrance here and you have termination without propagation and it's electrically closer to the entrance than it is to the exit, you get a completely different looking QRS complex. So these are the features that tell you this. You have this unanticipated pause in the midst of pacing. This is the most frequent that I see with entrainment attempts here. This pause in the middle. You think, ah, did we just lose capture there for a second? Look back at that. Look back at that. Maybe the golden fleece there. You may see a major change in the paced QRS complex, changing to a different tachycardia morphology after stopping or termination after stopping pacing. Here's an example of single extra stimuli during it. I'm coming along here. I do this just for the fun of it. It's proof of concept as well. I would prefer this rather than entrainment because you don't change to a different tachycardia so easily. But this just terminates without propagation here. And the next sinus and VPACE beat ensues there. On the board exam, I have some insight into what goes on with that. Entrainment is a favorite topic. It kind of separates the good candidates from the less well-equipped candidates. You will see intracardiac recordings of overdrive pacing during VT. I think that's a safe thing to say. It will be asked, where is the pacing site relative to the circuit? Entrance site, exit site, inner loop, outer loop. Is consistent capture present? Those devious people on the exam committee, I didn't do this when I was on the committee, but they do it nowadays. They will have a question where there's not capture. And then you're supposed to say, what's a post-pacing interval? How do I interpret this? Or none of the above. Is entrainment demonstrated? What do you need to do to show entrainment if you haven't shown entrainment with the slide, with the figure that you've been shown? A pause in the course of in the midst of pacing recognized as a non-propagated termination of VT. Correct interpretation of unusual post-pacing interval will be needed. That is, you have a, like the figure I showed, where we're stimulating during VT, attempting to control, to capture a mid-diastolic potential, and instead we're conducting to it. We never controlled it, so know which component to measure. You will have some correlation between electron and atomic mapping and voltage mapping, and you'll have to say, where should I pace? From where is this arrhythmia exiting? Which location will entrainment with concealed fusion be shown? So I have a couple of questions here, Mr. Chairman, and a few minutes left. A 60-year-old man has post-infarct VT. Results of pacing during VT are shown, and the pace site is what? So here are your choices. There's the figure there. Are we voting? Are you? Okay. Well, we'll go ahead. Oh, wait. Now we are voting. All right, the majority say an exit site, and the correct answer is an exit site. It is a late diastolic potential during the arrhythmia here. The match is very, very good. Post-basic interval, very similar to tachycardia cycling, almost not a tachycardia, and we don't have any ECG fusion. Very good. Boy, these folks are on a roll here. We've not stumped them yet in the first session or this session, so it's an exit site. Okay. A 71-year-old woman has post-infarct VT. Results of pacing during VT from what site are shown? Same choices. I'll let you look at that for a second, and then we'll do some voting. OK. Entrance light, very good, very good. So we're pacing at 410 milliseconds. The stimulus decorius is quite long, the same as the electrogram decorius. Don't be fooled by this big electrogram that's in systole. We're actually interested in this thing that is just in the early part of diastole. And you can see, I can't blow this up, but you can see that this component of the electrogram here is the same as this. So this is driven, and you would be able to say from Dr. Michaud's stuff from the prior. It's not showing over there, sorry. This component here is replicated over here. So we're not capturing this stuff here. We're conducting to this stuff. That stimulus leads to that electrogram component, that electrogram component. We're actually capturing this business here. And so the post-basic interval looks good compared to tachycardia cycle length. Entrance site is indicated by an early diastolic signal. Post-basic interval, very similar to tachycardia cycle length. No ECG fusion, concealed fusion. And the stimulus decorius is the same as the electrogram decorius. Entrance site. All right, the next question here, same old stuff here. 68-year-old woman, post-infarct VT, results of pacing during VT from what site are shown? Notice that I do these cases with all 12 leads showing all the time. They are gained up enough to be able to see little notches here and there. And I find that pretty useful. If you have them really gained down or only have three or four, it's easy to show a match or harder to show a non-match. All right, so boating. Super. All right, so this is a nice mid-diastolic central isthmus site, as indicated here. We got this nice site here. We also have this systolic site here, which is on the opposite side of the line of block, on the opposite side of the corridor wall. So it's a systolic electrogram. We're not capturing this, it's being conducted to, but we are capturing this guy here because it disappears during pacing and has all the nice characteristics that we want here. All right, another one. All right we'll vote. You guys think you're pretty smart. You're pretty smart. No, I can't stump anybody. This is great. Okay, very good. So here we have a situation where we are definitely capturing, because the relationship to the prior QRS looks the same. I don't, I can't measure with my caliper eyes this interval here, but I can look at this one pretty carefully. From the end of all the same. So we're capturing. And the QRS looks exactly the same. So concealed fusion, it's either in the diastolic corridor or some portion of it, or it's an adjacent bystander. Stimulus to QRS, very different from the electrogrammed QRS. Nice mid-diastolic potential there. Juicy, but sorry. Post pacing interval is long compared to tachycardia cycle length, and these are the features of the bystander side. They've got to be careful of these guys here. Nice mid-diastolic potential. Don't fall for it. Then again, if you have a big enough blowtorch, you can probably get rid of that and everything else in there, and it won't matter. All right, how about this here? 73 year old man, here's his VT over here, and here's attempted pacing during VT, and it terminates. So what do you do? Do you re-initiate and map another site, increase the output of pacing, lower the output of pacing, or ablate there? And we'll vote. Pedals in the middle, 100%. I love this. This is great. We've never seen this before, I don't think. This is, you know, the way this usually works here. We have this pause in the middle here, and a different complex over here. As soon as I recognized this, I stopped pacing, but it was too late. And that's our good friend, the non-propagated termination. I'm going to skip through a few of these and get to our end here. Entrainment is a very useful tool, but like all tools, you have to use it carefully. You might run into non-capture with pacing, not pacing for long enough, poor synchronization, pacing at a site too close to an exit from a circuit or a focus to show fusion, pacing at too high output to be able to see anything, changing the tachycardia to a new morphology or termination, many sites meet criteria, no sites meet criteria, or an incorrect post-pacing interval measurement. All these are road hazards along the way. And speaking of road hazards, everybody likes entrainment. Thank you very much. Thank you, Dr. Miller, for that wonderful overview on entrainment. Just a reminder, we can send our questions through the app, and we have opportunity to ask questions from the microphone in the center of the room at the end of the session. So our last speaker, but not the least, is Dr. Swedlow from Cedars-Sinai Medical Center, who will be talking about ICD-EGMs and troubleshooting. It's really hard to follow those two acts, and I don't even intend to try. I'm from Southern California, where we think formal wear is flip-flops. I really believe in audience participation, so I want you folks to grab your ARS. I want everybody to answer the questions, because we don't get a count-up here of the number of people who've responded. So when it was 100%, we don't know if it's the five people in the room who actually responded, or if it's 100 people in the room. And finally, anyone sitting over there, if you can't see there, there are plenty of seats here. And I'm more than happy to stop in the middle, because there's always more cases. So with that, you have the QR code, and let's get started. So based on this electrogram in a patient with a dedicated bipolar right ventricular lead, you can conclude abnormal signals are present on which channel. And we have an electrogram here. We show the atrial signal, we show the RV-coiled-to-can signal, and you can read the questions. And I think whenever you're ready to go to answers, we'll give some of them another 30 seconds or 10 seconds or so. And then we'll look at the ARS. Do I advance? Is that it? I'm so sorry. Okay, do we have a, there's no way for you to put up the count of votes, right? So let's think about this. The purpose of this question is to remind you to pay attention to marker channels. Marker channels are vertical lines that denote the sensed event for all manufacturers. That means a marker indicates an event that is sensed on the sensing channel even if you're only shown the shock electrogram. Now here you're shown the shock electrogram and the sensing electrogram, and appropriate sensing means that there's one sensed event for each two cardiac electrogram. Undersensing is identified in a device by having more vertical marks than the number of true cardiac electrograms, and conversely undersensing fewer vertical marks than the number of electrograms. And then the text is obviously proprietary. So with this context, we can see that every time there's a funny looking beat on the shock channel or funny looking abnormal signal here, there is a sensed event on the sensing channel, and I've marked those for you. That indicates that even though the sensing channel is not displayed, there is an abnormal signal on that channel, otherwise you wouldn't have consistent timing of markers with that. So a little bit on the theme of oversensing, because it's nearly guaranteed you'll get some oversense signals on the boards. Everyone has their own approach, and this just happens to be mine. The first question I ask is, do the signals vary with the cardiac cycle, which means you're dealing with a source that is inside the heart, or do they not vary with the cardiac cycle, perhaps with something else, maybe in respiration? If they don't vary with the cardiac cycle, you have two choices. You're dealing with an extracardiac source, or you're dealing with some intracardiac source that has a component that doesn't vary with the cardiac cycle, and that's almost always a lead problem. On the other hand, if you have just one cyclical oversensed event for cardiac cycle, commonly that is some physiologic signal, a P wave, an EVICD, a T wave, an SICD, or transvenous. On the other hand, if you have multiple oversensed events for cardiac cycle, while it's possible you can have more than one physiologic signal sensed, generally you have a lead problem. If you have both oversensing that is cyclical and non-cyclical, it is almost always a lead problem. All right, so let's just do a little shout out, because it's getting late in the day. How about the top left one? What's that? Somebody loudly. T wave oversensing, and you know that because on the sensing channel, if we showed you the shock channel, even if there are weirdly looking signals, you can't tell what the signal is. There is a lower frequency signal alternating with a high frequency signal. This is the QRS, this is the T wave. If you are displayed a highly filtered sensing channel signal, T wave oversensing looks completely different. Some manufacturers show you wideband signals, some show you narrowband signals, and if it's a chopped up signal like this, it is much harder to tell. You should never try and diagnose T wave oversensing from the pattern of intervals like short and long and that sort of thing. Sometimes people do that from marker channels. While that is possible that you'll have alternating intervals, it is not required for T wave oversensing. Down below we have an, I apologize, we have an intracardiac lead problem. This signal doesn't look like anything that you're used to looking at, but it happens on the, but it's there on the sensing electrogram. It is highly repetitive and doesn't look anything like any of the cardiac signals you're used to looking at that are physiologic, and that's what intracardiac lead fractures look like. How about top right, what do we got here? I'm sorry? Louder. If it's wrong, that's even better, but louder. EMI. EMI, yes, okay. And the signatures of EMI is that we have abnormal signals on both multiple conductors in the same lead, right, the RV coil to CAN, and now from the very fast markers here we realize that these are also on the PACE sense channel and on a separate lead, right? So signals on all the conductors on multiple leads has always got to be in an extracardiac source and this would be pretty typical of EMI. And finally, what do we have on the bottom right? I'm sorry? Lead fracture. That is an interesting thought, but I want to point out something about this lead fracture that I'll come to in a minute. When a lead fractures or when a conductor fractures, it is almost always one conductor. So you will typically have signals only on the channels that involve that conductor. On the other hand, and you are right, this is a lead problem, but if you have a breach of the insulation, right, the plastic itself, that's the insulation, is not a source of electrical signals. The electrical signals are generated because abnormal, because unwanted signals are no longer prevented from entering the conductors, and if it is present on the exact same signals are present on two conductors, right, that tells you it can't be a fracture, and it would be extraordinarily unusual, much more likely an insulation breach. So this pattern of high frequency intermittent signals that vary in shape but always come in little bursts, those are very typical of skeletal mild potentials. And this is a typical pattern you might see in a coil-to-can abrasion, and the signal that really makes that point here, and you wouldn't be expected to identify this on boards in 15 seconds for sure, but you notice this abnormal signal? It's different from all the others, right? It's much taller, and this is the signal that's characteristic of two pieces of metal hitting each other. So you can imagine that the cable to the ring electrode is smacking into the can occasionally and making this make-break potential, while the rest of the time it's recording mild potentials. Okay. Oh, I'm sorry? Can I ask a question? Those EMI examples all look the same. I understand why the frequency is all fixed, because it's probably some 60 cycle or a cell phone or something. You can go back. I apologize. Why does the EMI cycle oscillate like that? Ah, so, like, you know, Brad, that is a great, wonderful question. You notice that even though this is 60 hertz, okay, I'm going to go through this quickly, this will never be on board. Ah, okay. This is... It's a common thing to see. Beg your pardon? It's common to see. Ah, it's common on Medtronic devices only with 60 hertz AC. Europeans don't see this. Why is that? And what is the oscillation? It's eight cycles per second, if you count it. This is because even though... That's because Medtronic telemetry signals at 128 hertz, and the signal, the signal, the EMI is at 60 hertz, the beat frequency is therefore the sampling rate minus twice the signal frequency, which is 128 minus 120, which is eight hertz. And so even though you are above the Nyquist sampling limit and can reproduce all the information, you actually see a slightly distorted signal. So if you sample just above twice the Nyquist limit, you always get a systematic distortion. On 50 hertz signals, if you look at European telemetry, the signals are whatever it is, 28, and they're very hard to see with your eye. And most other companies' telemetry are 256 hertz, so you don't see that. This is far more trivia than anyone will ever ask you on boards, but great question. I think you're the only one that knows the answer to that. No, I'm sure that's not true. Okay, so I'm sorry, let me, am I going, oh, here, let's go, let's go on to the next step. Let's go on to something else. What do we have here? Okay. We have an SICD tracing, and I'm not, again, you know, just to go through a number of tracings, I'm just going to go through this a little didactically. We want to ask, is this cyclical, is the over-sensing cyclical or non-cyclical? Where most of the time, there is one over-sense signal right here for each cardiac cycle, right? And let's say over here, and so this is pretty common finding in SICD T-wave over-sensing. Now if we squint, we can see every now and then, there are multiple over-sense signals per cardiac cycle, where there's also a P-wave over-sense, this, you know, this is an exception that violates my rule of one over-sense signal per cardiac cycle is physiologic, and if you have more than one, it's not. But here, it's pretty clearly, you know, that you just got an extra P-wave, and that can happen, particularly in SICD. Down below, I hope you will all recognize these high-frequency intermittent, you know, 80 to 200 hertz signals as more typical. Skeletal myopotentials, also quite common in extravascular ICDs of both types, EVICD and SICD. All right, skeletal myopotentials, again, we notice here, oh, the point I wanted to make here is never depend on alternating intervals for T-wave over-sensing, right? These intervals are pretty constant in sinus tachycardia, the RT and TRs are the same, you pay attention to the alternating signal morphologies. All right, so let's just show, and you won't be expected to go through all this kind of analysis on a single board question, but all the things we can learn from this tracing, right? Not only if we pay attention, here are the real rounded T-waves, right? Many things like this, higher frequency components, are never far-field T-waves, right? So we have some cyclical over-sense signals, and they vary with the cycle, we have some non-cyclical one, that gives us a lead problem, right? And furthermore, there are no abnormal signals on the atrial channel, that further confirms the non-cyclical signals are not coming from outside the heart. So it's coming from multiple conductors and one lead, that makes us think of an insulation problem, right? We've been through that one, and now we ask ourselves, since the pattern is both cyclical and non-cyclical, we know the insulation defect isn't going to be in the pocket, right? It's going to be in the heart. So what could possibly be the source? Well, we know on the coil-to-can channel, the conductor involved can't be the can, it's not in the heart. And we know on the sensing channel, because we know something about lead design, that the helical coil to the tip goes down the middle, that the sensing cables are much closer to the outside, to the shock channel, the ones that go to the ring cable, so this has to be an outer insulation breach, inner insulation breach between this cable and this conductor smacking into each other. And so just to remind you, when we look at the big picture about leads, the conductors are there to transmit cardiac signals, the very weak cardiac signals to the device, the intermediate pacing pulses out from the device to the patient, and of course the high voltage shock pulses only go out through the conductors that have silver in the middle of them. All transvenous defibrillator leads have this type of general design, there's a helical tip to the screw for an active lead, and then some cables depending on the other conductors. The new Medtronic lead that's just come out is a two-cable lead. Both extravascular leads have all cables, just for your interest, because the cables are stronger, we're not going to worry about Brady leads today. And we'll just point out that when we took this lead out, as expected, right, if you look at the area right under the shock coil, you can see that the ring cable has come on up underneath the coil, that the actual inner insulation, that blue stuff that is like Teflon on the coil is actually worn away and filed down and you can see the filers are actually partially filed down from this direct contact here. And while no one will ask you on boards, you can infer a lot from looking at that stuff. All right, so now let's do an ARS question. Which over-sensing electrogram is a pay-sense conductor fracture? We'll give you 10 seconds or 15 seconds to look at the four different channels here, the four different ones here. And I'm sorry that we can't keep these up while you're polled, but they can't poll here, can they? Or do I have to have the ARS thing up to, I have to have it up, all right. All right, so let's take a look. Yeah, right, you won't be asked to do a memory test on the boards. Okay, let's go take a look here and see what we got. We had two candidates, three and four, okay. So let's just go through these one at a time. On the left, right, we have high-frequency signals on multiple leads, right, EMI, same eight hertz, sorry, it's the same company's device, I have to vary them. Here, right, we have alternating morphologies of T-wave over-sensing. Now, I haven't discussed all the differential diagnosis of funny-looking signals that might or might not be lead fractures. And we're going to come to, I'm going to tell you that in this case, the correct answer was electrogram number three. This fine, high-frequency looking, these intermittent high-frequency, very low-amplitude continuous signals like this, at this extremely high frequency, are again, most characteristic of mild potentials. And these would be diaphragmatic mild potentials, and you know, they vary with respiration. I apologize for showing you one that has a tip-to-ring electrogram. Most of you, some of you in the audience, I'm sure know that mild potential over-sense, and the diaphragmatic mild potentials are almost always sensed only on integrated bipolar leads. The one exception to that is the Abbott low-frequency attenuation filter, which also amplifies these things. But this type of low, this type of signal can easily be confused with lead fracture. You probably won't be asked to make this distinction, but I put it up here because I've seen plenty of leads taken out for this funny-looking signal, and if it varies with respiration, it's not a fracture. So, this gets at what are the characteristics we see when there is a conductor fracture. And a number of years ago, I sort of made a list of them, and this is my list. You might have a slightly different one, but the first point is signal, abnormal signals are almost always intermittent, and they tend to vary not, they vary in amplitude, they vary in morphology, they vary in frequency. You know, they're not all the same uniform frequency. Occasionally, and this is not required, but if you see it, it's a helpful hint that there's a lead problem. The signal is so big because it has a make-break potential that it saturates the sense hemp. Some signals are not cyclical, not necessarily all of them, but some of them. There are almost always some very short intervals and repetitive sequences of rapid intervals, and there is, and on a dedicated bipolar lead, that is those with the ring electrode where the ring is dedicated to the sensing channel, you don't see them on the abnormal signals on the shock channel. Now, I was very proud when I made this little list a few years ago, and then I actually did an experiment recently where, which I'm not going to go through in a lot of detail, and this won't be on the boards, but for those of you who are interested, where we actually found a way to identify the first abnormal signals you get as leads are breaking, and it turns out there is one every time the lead bends, that's the make-break connection between two little filers, and they don't look anything like what are in textbooks, and I contributed to that misinformation, and so why should you care? We should care because sometimes, occasionally, you see signals that look like this, and I didn't recognize them as lead fractures in this case, which was a number of years ago before I learned this stuff, and three days later, this is what the signals look like in the same patient, so you see that sort of stuff, whether or not it's on boards, it's a good thing to pay attention to. All right. Moving on, we're going to forget about this and this too much. How about impedance trends? You could get some impedance trends on the exam. Which combination of over-sensing and impedance trend, and by that means there's an impedance trend that you see, and I put a little red marker, which ones have over-sensing associated with them and which ones don't, which one is consistent with a patient's conductor fracture, and it turns out more than one of these is consistent, and this is very bad, so I'm going to give this a few more seconds because I thought these would be up and you could refer to them, but you'll have to think about it, and when you have them in your head, then we'll go on to ARS. This is even more of a silly memory test. All right. Yeah, okay, connecting to live content, there you go. I'll remember not to make a question like this for next time. Okay, well look, I mean, this isn't really fair to have you memorize all that stuff, but let's just go through, so one and four and two and four, so I think everybody thinks number four is, but there's some disagreement, right, whether it's, okay, so this is good. Number four you identified because conductor fractures are associated, can be associated with high impedance measurements. It turns out impedance always goes up in conductor fractures, but the finding is often too subtle until the conductor, until very late in the condition, so you can have plenty of over-sensing in conductor fractures and an entirely normal looking impedance trend. The single most important thing to know about this clinically is that majority of pay sense lead fractures in ICD leads present with over-sensing and the patient can get inappropriate shocks while the impedance trend is entirely normal. A intermittent abrupt falls in impedance is highly suggestive of a insulation breach, right, this is the metal upon metal smacking to each other. There are very rare, very few other causes of low impedance. They include things like EMI. You do an impedance measurement during an RF ablation and depending on how the RF current is being, you know, conducted and how the voltages are applied to the leads, yes, you can get that, but you have to be, you know, it's a hole-in-one kind of thing. This pattern, to the best of my knowledge, is never a conductor fracture. This pattern of gradual increase in pacing impedance is an intact lead that has mineralization with hydroxyapatite calcium forming on one of the pay sense electrodes and the lead does not need to be replaced unless the pacing or sensing characteristics of it are a problem. Okay, it doesn't affect, you know, if it's, and if this effect only occurs on the pay sense channel, it won't affect your shock efficacy. All right. Do you think that process occurs in sub-Q leads or no? I don't know, sorry. Great question and I don't know the answer. We have four minutes. Okay, well in that case, I think we all know that we also see arrhythmias in devices and let's try this one. How, what's the tachycardia diagnosis and how would the ICD diagnose the tachycardia? And then I'll stop. And I'm sorry, what I'm showing you here is a atrial electrogram, the sensing electrogram from the defibrillator, dual chamber marker channels, and then the morphology match score right is a SVT-VT discriminator that makes the determination in which if the shape of the far-field shock electrogram is very close to that of a sinus template stored in the solid line as a sinus template stored, then it will call it SVT. If the shape is very different, is different enough, it will call it VT. And each company has a different rule, but the concept is the same for every company. Okay, let's vote. Oh, I'm sorry, that's me. No, oh, isn't there a vote? Is there no ARS thing with this one? The next slide is my answer slide. Oh, did you put it after my answer slide? No, no, there's none, okay. All right, so we're out of, we're running out of time. At least, at least some of you, at least you had a chance to think it over and I hope you're going to tell me that you will, that your diagnosis is VT and the device's diagnosis is VT. But just to go through this, in a dual-chamber ICD, the discrimination of VT from SVT is first based on how the device compares, and I'm used to use this euphemistically because not every company does this explicitly, but compares the atrial rate to the ventricular rate. And in every device, if there's a tachycardia where the atrial rate is slower than the ventricular rate, it will diagnose VT. In this case, now, how do we know what the device diagnoses? We know that by looking at the marker channel. Those are the sensed events that the device has to analyze, and it's very clear that your eye can tell, right, that there are fewer atrial sensed events than ventricular ones, so the device is going to call this VT. And you're asked a question like that, what does the device think? You look at the marker channel. If you ask, what is the diagnosis? You look at the actual cardiac electrograms, because that's what we do for a living. Now, the potentially confounding, one potentially confounding part of that, this tracing that I like, is there are all these other signals on the atrial channel, but the device is not confused, or mostly not. Very few of them are over-sensed, right, on the atrium, and these signals are far-field R-waves. We know this because they time with the time with the ventricular electrograms, whether or not we're in VT or in sinus rhythm, right? So, although there are far-field manifestations of the ventricular signal on the atrial channel, the device is not consistently sensing them. If this were a single-chamber ICD, the device would have declared the rhythm as SVT. However, in all dual-chamber devices, the comparison of atrial versus ventricular rate is the first step, and if the ventricular rate is faster than the atrial rate, no other analysis is performed, and the device diagnoses VT. So don't, you know, don't be confused by a question like this, and think the morphology match has something to do with it. I'm out of time. Thank you very much. Okay, thank you, Dr. Sweatlow. We don't have time for questions, but there was one question that came up here that I will quickly answer, which is, what resources do you recommend as a starting point for studying for the board? We are actually happy to let us know that under the leadership of Dr. John Miller, the HRS board review has been updated, and so the 2025 HRS board review and self-assessment prep is available now. Thank you to all our speakers. Thank you to everyone in the audience for attending this session. This concludes the second session of the board review. In about 10 minutes, we'll be starting the third session of the board review, which will focus on pharmacology. Thank you.

ventricular arrhythmias

PVC localization

ECG

anatomical mapping

RVOT

LVOT

outflow tract PVCs

VT localization

entrainment

paced QRS mapping

ICD electrograms

oversensing

arrhythmia management