It's Greg Michaud again. We're going to talk about SVT diagnosis part two. This is coming from Nashville Vanderbilt University Medical Center. Thanks for sticking with me through the first part. I know it was long. This is going to be a little shorter and sweeter. I don't have any disclosures relevant to the content. Our objective is to understand how ventricular and atrial pacing are used to differentiate mechanisms of supraventricular tachycardia. Again taking a step back, orthodromic AVRT is usually not difficult to recognize because of eccentric atrial activation. However, remember that AVNRT may have eccentric atrial activation in the proximal to mid-CS and mimic ORT. Usually typical AVNRT is easy to recognize because of a short septal VA time, the features that make it AV nodal, concentric atrial activation sequence, and the fact that atrial tachycardia usually doesn't have that relationship. And orthodromic AVRT using a septal accessory pathway is usually pretty easy to tell if it's not decremental. But when they're decremental, that's when it really gets more difficult to sort out. So let's talk about the post-pacing interval minus the tachycardia cycle length and the stem AVA used to determine the distance from a circuit. And we'll talk about using QRS or intracardiac fusion to recognize presence and perhaps participation of an accessory pathway. So the first part measuring these intervals has to do with when you come off of pacing. The QRS fusion part has to do with when you start pacing. So this part is pacing's finished, you entrained it, you didn't terminate it, and tachycardia continues. You accelerated the As to the Vs, and you've proven that you actually overdrove the tachycardia. Then you look at the response following entrainment. You can exclude atrial tachycardia if you see a VAV response. And then you look at these intervals. So you can measure the stem AVA, meaning the stimulus to atrial activation time during pacing versus the VA time in tachycardia. You measure the VA time from the surface V to that same A that you measured the stem A to. Now, theoretically, you take the earliest one. Sometimes it's not so clear, you might use a different atrial electrogram to be able to be sure you're measuring to the same fiducial point in both cases. When you do so, septal ORTs have a short stem AVA time. Atypical AVNRTs have a long stem AVA time. What's the exception? Septal ORT with decremental properties can fall into this category. If you have a decremental pathway indicated by a long VA time, so VA time more than 40%, these can fall into this bin. That's important to recognize when you have 40% or more VA time, then you need to do some other maneuvers to sort that out. Can't rely completely on the stem AVA or the post-pacing interval. Post-pacing interval gets more press, I guess, because the separation between the forms of tachycardia is greater. As you can see, there's not many that come close to the line, which was 115 milliseconds. This is, others have reported closer and some overlap than what we saw in our original study, partly because they pace faster relative to the tachycardia than we did. We tried to pace just faster, just enough to tell that we had entrained it, but not fast enough to cause a lot of decrement in the AV node. You can correct for the decrement in the AV node, and this number is very similar, 110 milliseconds becomes the number. I'm somewhat gratified that our original work has stood up over time. This number for stem AVA and post-pacing interval, others have reproduced it and come very close, if not exactly the same, but within five milliseconds in most cases. The corrected AH is 110. But if you pace close to the tachycardia cycle length, you don't really have to correct much for the AH. So why does this even work? Well, when we pace during a circuit and there's an accessory pathway, we're pacing into the excitable gap, right? So you get collision with the orthodromic and antidromic wavefronts, orthodromic being through the AV node, antidromic being from the pacing, but also that antidromic wavefront gets to the accessory pathway earlier. So you're able to spin the tachycardia at the accelerated pacing rate over and over again. When we come off pacing, we can see that we go out through the pathway, through the AV node, through the right bundle to the ventricle and back to your pacing catheter. So since the ventricle is a part of the circuit, and particularly if the catheter is on the same side as an accessory pathway, the STIM-AVA and the post-pacing interval will be short, sometimes even close to zero. If you push this out near the right bundle for a right-sided pathway, you will get STIM-AVA and post-pacing intervals that approach zero. Here's an example of a pathway with overdrive pacing. There's a couple of things here. We're looking at the STIM-AVA, for instance. We look at STIM-A being 195, VA being 190, post-pacing interval being 440, tachycardia being 400. So we've way less than 85 and 115. We probably don't have to correct much, but even if we correct it for this, we might bring the post-pacing interval to zero actually, because there's a little delay maybe in that AH. But 40 is good enough. If it's short, you know it's a pathway. If it's long and the VA time is long, then you might have more work to do to sort out that it's not a decremental accessory pathway. But whenever you see a short post-pacing interval or a short STIM-AVA, it's a pathway. And again, I've not seen an exception to that one. Why is it long with AVNRT? Well, because you have to go back up through the ventricle Hispokingy system, get into the AVNRT circuit, spin it, and you can do that over and over again with pacing faster than the tachycardia. But when you come off, it's got to go a long way to get to the AV node, spin it around, and then come all the way back to your catheter. So it's going to be more than 85 and more than 115, pretty much without exception. That part is true. Now what I've said, and it's rare, but it's something you need to look out for, is decremental pathways can give you these same numbers. So accessory pathways that are decremental will always have a VA time that's long, so a VA time more than 40% of the tachycardia cycling, and may mimic atypical AVNRT. Here's an example of atypical AVNRT, overdrive pacing. This V is going to that A, so this is a VAV. You've eliminated atrial tachycardia as an option. His post-pacing interval is forever, and the VASTMA is forever. Now could there be enough decrement to produce this long a post-pacing interval and a VASTMA? It's possible, I guess. So you still would need to sort out, in this case, we looked at his refractory behavior of pacing and showed that it did not affect this tachycardia, so therefore it was AVNRT. That's how you sort that part out. You look at his refractory PVCs or pacing during fusion to see what happens to a tachycardia like this, to be absolutely sure this is not a decrementally conducting accessory pathway. Now some nihilists would say, well, who cares? Just map the earliest day in a blade. I can't argue. You could do that as well. But if you want to know what it is, you do additional maneuvers. This is the reference for the correction factor for post-pacing interval. There's some other things you can look at that make the post-pacing interval minus tachycardia cycloneath even more valuable. So if you have a left free wall pathway and your post-pacing intervals would expect it to be long from the RV, but if you went to the LV base, nearest the earliest atrial activation sequence, it will be short. So when you pace near a pathway in the ventricle, it's going to be short if it's not decremental. So just go near the earliest atrial activation and do your post-pacing, and it will be short if there's a pathway present. You can do differential base versus apex entrainment, similar to differential RV pacing, it works in the same direction. With an accessory pathway, it will be shorter at the base than at the apex. And again, the caveat, and I'll say it again just so you remember, VA time greater than 40% of the tachycardia cycloneath, concentric atrial activation, you need to consider a decremental accessory pathway. The same cutoff values for pacing, overdrive pacing, apply to induction of tachycardia when pacing near the tachycardia cycloneath. You can also look at VA, AV, VAVs, post-pacing intervals, STIM, AVA, differences with PVCs. It's a single bead of resetting, so it works exactly the same as overdrive pacing, so you can also look at all that. You can pace near the, but if I'm going to do that, I might as well overdrive, that's, at least that's my, that's my take on it. You can, again, pace near the earliest A, or pace base and apex and look at the difference. So, to summarize that then, the short post-pacing interval, the short post-pacing interval, the short post-pacing interval when pacing in the RV or LV implies the ventricle as part of the circuit, and it, there's really, I've not seen exceptions to this. So, if you have a short post-pacing interval and you're trying to sort out AV and RT from ORT, if it's short, it's ORT, there's a pathway present. Another thing that implies the ventricle as part of the circuit is if you get surface QRS fusion during entrainment. We actually already saw an example of that with the septal accessory pathway. You can also find intracardiac evidence of QRS fusion, and that would be driving a HIS orthodromically. So, if pacing the V doesn't cause retrograde HIS bundle activation, but you drive it antegrade, then that has to be going over an accessory pathway and not through the AV node, because to get there through the AV node, you have to go retrograde through the HIS. So, if you see a retrograde HIS during entrainment, it could be either, potentially, but if you see an orthodromic HIS activation during entrainment, that is evidence of entrainment with fusion. It may not be obvious on the surface, but if you see the intracardiac evidence of that, you've got your diagnosis. You can even see that in ventricular electrograms. It's less easy to tell, but HIS activation is easier to tell. So, here's orthodromic HIS activation. I think you could probably tell on the surface this is fused, but it might be somewhat confusing. You don't know for sure whether that's true, but what you can see is that the HIS is activated orthodromically. So, here we're pacing. There's a stimulus, and what comes right after the stimulus, a HIS. A HIS, a HIS, exactly at the same timing, and then another HIS. So, how do we know that this HIS is driven orthodromically? Well, first of all, this stem to HIS is probably too short to be a retrograde HIS, and second, when you do the measurements, you can see that the tachycardia cycle length is this HH time. This HH time is PASTE cycle length. So, the last PASTE beat that produces this HIS is this one. This PASTE beat produces that HIS orthodromically through the circuit. It's got to go through the node, I mean, through the pathway, through the atrium, back through the node to get there. It's in an orthodromic direction. The fusion zone of RV pacing is quite useful to look at. It's a concept similar to PVCs scanned during SVT, where you can time it so that they become progressively earlier and earlier, but you can also look at the transition zone because that includes progressively earlier and earlier PASTE beats relative to the tachycardia that produce this zone of fusion, and then you can look at when the fusion appears to become stable or when fusion's lost completely. If atrial activation is perturbed in that zone where you first start to see fusion and fusion appears to disappear or become fixed, then if anything happens in that zone, that's indicative of an accessory pathway. The nice thing about this is that you don't have to depend on entrainment. If something happens to the tachycardia during that zone of fusion or well after and then tachycardia terminates, fine. You still have either excluded an accessory pathway or you've diagnosed one, even if you can't look at the entrainment because it terminates. So the fusion theory is that you begin pacing, you have a tachycardia, so your wavefront of tachycardia is being impinged upon by this wavefront from pacing, so over the AV node produces all of this activation, but now your pacing starts to take over a little bit more and a little bit more and a little bit more ventricle, so this QRS starts to get wider and wider with each paced beat because it's just relative to the tachycardia, it's coming a little bit earlier and a little bit earlier until it actually takes over tachycardia and entrains it. So on the surface, this is what you see. You see periods where the QRS starts to get wider and wider and changing slightly. On the surface here, it's not totally clear. This QRS doesn't look like that one. So I know all of these are fused. I think this one looks a little different. It probably doesn't get fixed until about here, but you have 12 leads to look at, so you can look at all of them to be sure. Eventually, with the right free wall accessory pathway, you get constant fusion. We saw an example of constant fusion where there's a constant collision between a wavefront wavefront coming through the AV node and one coming from your pacing catheter. And you get part of the ventricles to polarize by way front of pacing and part, and it becomes a fixed relationship. That's demonstrated here where you entrain with fusion. It never becomes fully paced because you're able to entrain it with fusion. Now, if you have a left-free-wall pathway and you're entraining from the RV, you might see little to no fusion apparent with entrainment. You're so far away from that circuit that you may have to even go retrograde through the His bundle before you get to the left-free-wall pathway. So it tends to become, when you get to that first fully paced beat, that's when you'll definitely see the left-free-wall affected, but it may not come until you get to that first fully paced beat. Whereas other pathways that are closer to your, now, if you put the catheter in the LV, then it would clearly entrain with fusion. So if you're on a pathway or right next to it, it's gonna entrain with fusion. If you're far away from it, it might have to get all the way out to the first fully paced beat before you see anything happen. With AVNRT, you're never gonna see fusion with entrainment because you have to get through the His bundle completely before you get to the AVNRT circuit. So you'll have to take over activation of the ventricle completely with pacing because you have to get through retrograde through the His bundle. And so no activation, if activation, even a little bit has occurred in the ventricle, then you're not gonna be able to get there with ventricular pacing. So you'll never see AVNRT affected during entrainment with fusion, except in the very rare circumstance where you have a bystander accessory pathway in AVNRT. Possible, but really unusual. Here's an example where atrial activation advances with fusion. We have tachycardia cooking along at 340 milliseconds. A couple of seconds, we then start to pace and we see this beat is clearly fused. It's getting wider and wider here, right? I don't know exactly where this becomes a morphology that's unchanging, but it's definitely not that one. It's definitely not that one. And we see that the AA time gets pulled in by this pace beat. So this is fused. This fusion, this paced beat, which is clearly fused, pulls in your A, and then your stim A becomes fixed. The combination tells you you're driving the tachycardia and you started driving it during a period of fusion. So if you can drive or start to drive a tachycardia or affect the tachycardia during a period of fusion, that indicates a pathway is present, probably participating as well. That part you don't know for sure. The advantage of this, it's sort of like putting in PVCs, his refractory, but you're doing it all in one shot. So you've got tachycardia, instead of putting this one in here, waiting a bit, putting this one in that comes a little earlier, waiting a bit, putting this one in that comes a little earlier, waiting a bit, just do it all in one shot. What you lose a little bit is if you put a PVC and reset, you lose that part of it. But you also can look at the end of the drive and interpret that as well. Here's a train where we started to pace and we terminated tachycardia. You might say, oh shoot, need to repeat this entrainment. We didn't entrain at all, we just terminated it. But if you look closely, it terminated because there was a history factory PVC that came just right around the hiss. So the very first beat that was fused terminated the tachycardia. So this would be, if you'd ignore this, we were trying to pace and entrain, doesn't matter. The very first PVC that came in terminated it. This is where you earn your money in EP. So here's a VA time that's long. So the VA time's more than 40% of the tachycardia cycle that we're doing. You have to start to wonder, okay, well, I'm trying to sort out, is this atypical AVNRT or potentially a decremental accessory pathway? I already said that in these cases, it may be not useful to look at the post-pacing interval or the VA STEMI time, because they can be long when you have decremental pathways. But what should happen is you should be able to affect this tachycardia during a period of fusion, and you do. So in this case, you see a stable interval here, AA, AA, AA. You come on pacing, and the very first beat that's barely fused on the surface causes a delay in the next day. There's no way that happens unless the pathway is part of the circuit. You delayed the next atrial activation because conduction to that accessory pathway was decremental. Now, it could have advanced, it could have delayed, or it could have terminated. Any of those things would indicate an accessory pathway is present. But delaying it or terminating it tells you it's participating in the tachycardia. So just advancing it tells you a pathway is present, probably participates, but not for sure. Delay and termination tell you it's participating for sure. Here's an example of atypical AVNRT, where you've got a longer VA time than usual for typical, and then we get, finally, we affect the tachycardia, but well after two, three beats after we've become fully paced on the surface. Where you become fully paced is not always easy if you don't use all 12 leads. So in this case, I'm looking, okay, here's paced one, paced two, paced three. Is it paced four or paced five where it becomes fixed? I think it's gonna be paced five because I think there's a slight change from here to here, but it's pretty slight, and you can make the argument that you're seeing things. But when I look at all 12 leads, then it becomes clear paced five is correct because look at this. Lead three pretty much tells you this is fixed. Starting here, this is all different. Same thing with probably this lead, slightly different. But it can take sometimes looking at all the leads before you can be sure. So in this case, this is your first, your zone of fusion is from here to here. Anything that happens in this zone, pathway. There are other useful maneuvers. Entrainment with fusion we mentioned. We talked about all these things. Pre-excitation index, it's worth going back and reading that paper at some point. This is analogous to Hiss refractory PVCs, Bill Miles' paper from way back when. Then there's another thing looking at the delta HA during SVT compared with V pacing during sinus rhythm, John Miller and the delta AH, Ching Man. I'm not going to go over them because again, I think they're adjunctive, but not necessarily things that often come up given that we've come up with easier ways to do it. These are useful numbers to know for those particular indices and those particular maneuvers. You can pause on this and look at these at your leisure. One more word about junctional tachycardia. This is an unusual form of de novo tachycardia in most adults. However, it's not unusual following ablation of the cell pathway and you give isoprol. It sort of wakes up that junction by ablating it and you get junctional tachycardia frequently and you're trying to sort out, did I leave behind a damaged AVNRT circuit or is this junctional? Some clues to junctional tachycardia is it's often induced with V pacing, not A, and there's periods of VA block during it. HO pacing can help differentiate it from AVNRT. Here's a paper that's worth looking at, but the concept is that with junctional tachycardia, to overdrive it, you have to overdrive the junction directly A to H, A to H, A to H, and so you produce an AH and then there's a period after you come off. The first thing to fire is the junction again so that you get an HA. So you get an AH, HA response when you overdrive pace junctional tachycardia. AVNRT is different since you're conducting, when you pace, you conduct down the slow pathway and tachycardia resumes. If you don't terminate it, then A, H, A response is seen because this A affects the far H here because it's going down a slow pathway. I'll show examples. This is pacing during AVNRT where we have overdrive pacing of tachycardia that's 430 milliseconds or so. You pace at 400 and we can see that the HH, the HH is at the pace cycle length when we come off. So this A produces that HISS because the HH is at the pace cycle length. So you would interpret this as an A, HA response. This A is not producing that H. It's pretty short. That's a clue. But when you measure the HHs, you see this HH is at the pace cycle length. So this A is producing that H, not that H. You can do the same thing with atrial extra stimulus instead of overdrive and interpret it exactly the same way. Here, you've put in an atrial extra stimulus. We pull this H forward. So we'd interpret this as an A, HA. This A did not affect this H. It's too short a time eyeballing it, but also when we measure it, we pulled this H in, not that one. So that's AVNRT, AHA response. Here is atrial extra stimulus during junctional tachycardia. Now, which H got pulled in? Well, we measure the HH intervals, 480, 480. This HISS got pulled in by this A. It wasn't this one. So it's an A, H, HA response. Eyeballing it too, there's enough of an interval here that it's plausible. So we have A, H, HA response to a junctional tachycardia with an atrial extra stimulus. Here is an atrial extra stimulus that terminates AVNRT. So this A did not affect this H, comes on time, 470, but tachycardia terminates. So we had to block in the slow pathway. So this would be another, although we didn't get an AHA response, we got just as good from an interpretation standpoint. We got an A that blocks in the slow pathway and causes termination. We know it's not junctional because we didn't pull this HISS in. So how do we approach SVT diagnosis with a one-to-one AV relationship? First thing I'm always eyeballing is the septal VA time. So if it's greater than or less than 70 milliseconds, AVNRT less than 70. Rare instances where a septal accessory pathway could have less than 70, not by much. In children and young adults. Atrial activation is the other thing immediately look at. Concentric or eccentric. In order for this to work, you obviously need multiple catheters. If you only have a HISS catheter in, you're not gonna be able to tell because you're not gonna see where the high RA or the CS activates relative to the HISS A. HISS refractory PVCs. Do they advance, delay, or terminate SVT is what you're looking for. I honestly, to be truthful, I don't often give HISS refractory PVCs anymore because overdrive pacing in my mind gives you all the information, all the same information without having to time your HISS refractory PVCs in this way. So I don't really have to do that. You have your HISS refractory PVCs and it's one run and you're done for the most part. So for overdrive ventricular pacing, first of all, don't be fooled into interpreting something that never wasn't trained. So if you never caught up to the tachycardia or you didn't capture a number of other pitfalls, then don't interpret it. You're looking for the AV or AAV response. The AV response excludes atrial tachycardia. You're looking for the post pacing interval corrected to 110 milliseconds for the AH following pacing versus the AH during tachycardia. Stim AVA, it's less than 85 milliseconds. It's a pathway. If it's more, it's atypical AVNRT, possibly a decremental accessory pathway if it's along VA tachycardia. You want to, if you entrain the HISS orthodromically, it's a pathway. Or entrain with fusion, it's a pathway. The caveat is you won't see this very often, but you don't want to be fooled. The VA time more than 40%. Caution interpreting the post pacing versus tachycardia or stim AVA. Go to entrainment with fusion and look to see whether you affected that tachycardia. Usually delay it, but it might advance slightly or you might terminate it during that zone of fusion. And that's where the money is to figure out the decremental pathways. So in summary, I think RV pacing will lead to a diagnosis in most cases, but beware of the pitfalls. You may never get a diagnostic finding. And I gave many examples of where alone, there is not one thing you could point to, but when you combine it with something else, becomes pretty diagnostic. Example would be AVNRT terminating with AV block. And you have a short VA time and it terminates with VA block. That'd be an example of combining two observations to give you a diagnostic finding. Use a systematic approach. Don't assume anything, do measurements. If you eyeballing something and you think you understand it, take calipers out, do the measurements. You won't get fooled by a pseudo VA AV, for instance, if you actually measure out the AA intervals. Look at the surface QRS, look at the surface P wave. If you have an upright P wave inferiorly, and the question is, is this AVNRT? It's not because it doesn't produce an upright P wave in the inferior leads. So look at the surface. If you're taking the boards, do a lot of practice tracings. And practice tracings are good, even if you're not taking the boards, honestly, they're fun because they're puzzles. You like to see if you can get them right. And they're very useful when you actually have a case. If you can practice some of the tools in practice tracings, and in real life, doing the maneuver for the first time, and you've never seen it before, see how it's expected to react, then you may get confused. So practice is good, whether you're taking the boards or not. Well, I'd like to thank you for your attention. I know it was a lot of material, and I hope it was helpful. Best of luck.

ventricular pacing

atrial pacing

supraventricular tachycardia

AVRT

AVNRT

post-pacing intervals

accessory pathway