Hi, this is Greg Michaud from Vanderbilt University. This is a lecture I've given over the years many times. I try to spruce it up a little bit each year, but SVT diagnosis hasn't changed all that much in the last 10 years. So the testable concepts for the boards and also in the tools I'll give you in real life haven't changed all that much. I have no relationships relevant to this topic. So our objective today is to understand the observations and maneuvers that will correctly identify the mechanism of paroxysmal supraventricular tachycardia. And then when we're talking about that, we're not really including atrial flutter, which we see more and more commonly after afib ablations and atrial fibrillation. Those are supraventricular to be sure, but we're really talking about garden variety PSVT like the 12-lead ECG pictured here, where we get a rapid tachycardia. P waves are not easy to see in this case, but they peak out at the end of the QRS here, giving you this pseudo R prime. And then in the inferior leads, they tend to give you these little pseudo S waves. Now, this type of EKG is actually very common to see with AV node re-entry. So AV node re-entry is the most common form of supraventricular tachycardia. Of the three major forms, AVNRT and orthodromic AVRT are the most common, and they're both AV nodal dependent. So they use the AV node as part of the circuit, and that can be really helpful when you're trying to sort out mechanisms of tachycardia. Atrial tachycardia is usually focal, again, unless we're talking about scar-related atrial flutters after a fibroblation or related to surgery or some de novo atrial scar. They don't involve the AV node, so you can also use that fact to help sort things out by maneuvers and by observations. The most common type of accessory pathway is A to V. However, there are other variants. They are frequently tested on the boards, but not very frequently seen in real life. So those of you who are looking at this for board review, it's useful to be familiar with these, familiar with these, but you don't have to spend a lot of time. Atrial hyssian are really rare. I've seen one or two in my day, but they are really uncommon. Notoventricular and notofascicular have interesting cardiac electrophysiology that really helpful to know how to sort those out if you need to. Atrial fascicular is something you'll see probably a couple of times in a career, unless you're a referral center for these. And fasciculoventricular is useful to know because it looks like a very slightly pre-excited anteroceptal pathway. It's a little leak of a fiber off of the hysperkinesis system, usually the right bundle. And that gives you that pre-excitation pattern, but they've never been implicated in SVT mechanism. So they don't participate in tachycardia. They're purely cosmetic. You don't ablate them. It's useful to have a systematic approach to diagnosing SVT. And I usually start with sinus rhythm, and I look at anterograde conduction with and without atrial pacing. Obviously, you're looking for pre-excitation, a jump in sinus rhythm, retrograde conduction during ventricular pacing. These are all in sinus rhythm. You haven't yet gotten to the PSVT part. And then once you're in SVT, there are some observations that are really useful, particularly when you look at transitions like the initiation, the termination, or any perturbation of the tachycardia like development of bundle branch block, for instance. These are all things you want to be on the lookout for. Pacing maneuvers are also quite useful and often necessary for you to feel confident about the diagnosis. Brad Knight, when I was at Michigan, put this observational study together looking at what baseline observations and tachycardia features you see during SVT with the prevalence, sensitivity, specificity. I'm not going to go through this table, but suffice it to say that some of the more diagnostic things like development of bundle branch block don't occur all that frequently, so the sensitivity is pretty low. Specificity is very high for a finding like that because it's considered diagnostic, but it's not all that common. So the bottom line from this paper is to understand that diagnostic features may not always occur during tachycardia, even with pacing, and that you need to sometimes accumulate evidence that leads you to one diagnosis over another. So let's start with clues to the mechanism during sinus rhythm and pacing in sinus rhythm, and that would be first to look for dual pathways because in the presence of dual pathways, then AVNRT becomes quite likely, although not definite. Dual pathways are defined as an AH discontinuity, or jump, as we use the vernacular, of 10 milliseconds for a decrement in A1, A2, producing a 50-millisecond increase in A2, H2. This also determines the fast pathway effective refractory period. Pre-excitation, obviously, is something to look for, and then you want to look at the initiation of SVT, whether it's spontaneous or whether you produce it with pacing. Is the initiation dependent on a critical AH, dependent on bundle branch block to initiate, or loss of accessory pathway conduction? We look for evidence of AV nodal dependence, and remember that when VA conduction is absent with ventricular pacing and sinus rhythm, it can be difficult to sort out stranger forms of AVNRT from atrial tachycardia, and you may be reliant upon a critical AH to determine whether it's AV nodal dependent or not when there's no retrograde conduction. This is an example of a discontinuous A2-H2 curve. So here we see the ERP of the fast pathway. So as we deliver progressively shorter and shorter coupling intervals between A1 and A2, we then see a jump in conduction of A2-H2 of 50 milliseconds or more. In this case, it's quite a bit more than 50 milliseconds, but 50 milliseconds is all you need to make the diagnosis. And that being said, you can see fast and slow pathways without a clear jump. So is 40 milliseconds jump mean it's not jumping from fast to slow? No, you can sometimes see that, and it can be difficult to sort out. So there's not always going to be clear-cut, slow pathway jumps with AVNRT. Refractory period definitions are confusing. I always try to think of concepts. When I try to put it in words, I often fumble or you throw the wrong word in, honestly. But if we're gonna look at the definition, it's longest coupling interval between impulses that fails to propagate. So in other words, it's measuring the input. It's an AA interval for the AV nodal output. So, but we're measuring the input, the AA interval. The functional refractory period is the shortest interval between consecutively propagated impulses produced by any coupling interval. So for instance, if we're looking at the output of the AV node, the shortest AH would be the functional refractory period. And the relative refractory period is the longest coupling interval between impulses where conduction of premature impulse is delayed compared to the basic drive. So this, for atrial or ventricular tissue is a reasonable thing to look at. You see this all the time when you're doing ventricular stimulation to try to produce ventricular tachycardia, and you suddenly see the delay between the stimulus and the output of the ventricular impulse. So that starts to get wider and wider. So you've reached the relative refractory period when there starts to be a delay in the stimulus to V, and you see that a lot. And you get, so you're not really functionally getting a tighter V1, V2, because every time you bring the stimulus in, there's more delay in producing the V. And so your V1, V2 is actually maybe even getting longer despite the stimulus getting shorter. So the relative refractory period of the atrium can be demonstrated here, where you see this relative delay in stimulus to the output of the action potential. This is with monophasic action potentials. You can see as we go from 210 to 205, we get another 10 millisecond delay in the production of the action potential. So although we brought the stimulus in by five, the produced V is 29 milliseconds later. So we actually, the V1 to V2 gets later despite the stimulus being brought in. That's the concept of a relative refractory period. Now, fast pathway conduction is demonstrated here, where we bring in A1, A2, we get conduction to the ventricle. We can see it here, we can see it here. There's a short AH interval produced by that, likely over a fast pathway. When we bring in A2 at 10 milliseconds shorter, we suddenly see the AH increase by more than 50 milliseconds. Now the AH is 160 milliseconds. This should probably say two, or the delta AH is 160 milliseconds. So we've reached the ERP of the fast pathway. This is the longest coupling interval that fails to conduct over the fast pathway. If you want to put it into words. There's other evidence for dual pathways, and this is the PR greater than RR, or crossover phenomenon. You can see often with patients with AVNRT, it actually becomes a good endpoint for ablation. Once you eliminate this, likely you've done the job and you frequently don't need to do any more ablating. You obviously do other testing, but if you've eliminated this crossover, you've usually successfully ablated the slow pathway, because it's not usually present in the absence of a slow pathway. Now, as you pace a little faster, you start to see the stimulus cross over the previous QRS. So this, you don't really know in looking at this, is this stimulus and A going to this V? Although this looks like a pretty short, the A and the H are right on top of each other, so it's unlikely, but you don't really know until you come off. And when you come off, you can see that this A would produce this HISS. And so you've actually crossed over because the stimulus here is not on this side of the QRS, it's crossed over to the other side of the QRS. So this is a really useful thing to look at when you're doing burst pacing, decremental burst pacing. Retrograde conduction, if it's absent, makes an accessory pathway unlikely, but not impossible. Definitely seen this, where you have a isopryl-sensitive accessory pathway or a decremental accessory pathway, and it's not present when you begin pacing sinus rhythm. And once you give isopryl, it suddenly appears. If retrograde conduction, this is a really important point, and you'll see lectures from John Miller explaining this as well, but if it's tied to HISS bundle or right bundle conduction, then it is over the AV node. You can demonstrate this with ventricular extra stimuli or parahysian pacing as well. They also show you that conduction is tied to the HISS-Purkinje system if it's going over the AV node. What if you have a concentric retrograde atrial activation sequence? Well, AV nodal conduction is the most likely thing, statistically, but certainly a septal accessory pathway is possible, and that's where differentiation of tachycardia mechanisms with retrograde concentric conduction is, that's where the money is, because those are the hardest ones to sort out. Seeing concentric retrograde atrial activation sequence does not exclude the presence of a left lateral pathway, because conduction may be quicker getting to the AV node than to that left lateral, and you may not see evidence of it unless you do some more maneuvers, or if you have a slowly conducting accessory pathway, AV nodal conduction could beat it, potentially. What if there's an eccentric retrograde atrial activation sequence? I guess the answer would be how eccentric. So if there's really eccentric, like free walls, right free wall, left free wall, then accessory pathway is highly likely as the, if it's not atrial tachycardia, it's very likely, but we're talking about retrograde conduction, not atrial tachycardia. The proximal CS activation can be leftward with AV nodal conduction for a left inferior extension, or possibly just leftward activation of a right inferior extension, that if you look in the coronary sinus, it may be a centimeter or two into the AV node. So here's an example of right free wall accessory pathway, where you have a catheter in the high RA, one in the his, coronary sinus electrograms, and you're pacing from the right ventricular apex here, and you see that activation looks funny. In the high lateral right atrium, you see early activation relative to the his bundle and the coronary sinus. That is not the usual. So for concentric activation, you'd see his early RA usually significantly later. Now, obviously you'd have to make sure this is where we say it is. It's in the lateral right atrium or right atrial appendage. It's not sitting on the septum near the his bundle, but you have to trust me on that. So this is an activation sequence that's really pretty much incompatible with AV node reentry. In fact, the other thing you could look at is the P wave on the surface, and it appears to be an inferiorly directed P wave. It's not inverted inferiorly. This is a clue. Look at all your clues. So if it's not an inverted P wave, it's not likely to be going over the AV node unless there's something really funny going on. Here's an example where the retrograde activation is tied to the his bundle or right bundle. So in this case, we can see pacing the ventricle. We get this sharp component here. We see a V, and then we see an atrial activation sequence. Here we see another pace beat, same thing, same activation sequence in the sharp guy here. When we bring in an extra stimulus, V2, we see the sharp potential kind of disappears, jumps out here. So it jumps retrograde, and tied to that, the atrial activation sequence jumps out with it. Now, the atrial activation sequence really looks the same. So we know we're going over the same route of conduction, the AV node, but it now, instead of getting directly to the AV node through the right bundle, when you're pacing from the right ventricle, you now have to cross the septum, come up the left bundle, takes much longer to get to the his, and then you get this jump. Now, it's not a jump in the AV node. How do we know that? Because we see the H jump out. If the H had been fixed and the HA jumped out, then you may be diagnosing retrograde, fast and slow pathways. But in this case, we know this is AV nodal conduction, retrograde, because it's tied to the His-Purkinje system. This is a really useful thing to sort out mechanisms. This is the opposite. Here we got an activation sequence that looks kind of like mid-coronary sinuses early, and we see a V1, V2 that jumps out in terms of the his, but nothing happens to the A. So this route of conduction to the A has to be independent of the His-Purkinje AV nodal axis, because when we get retrograde right bundle branch block, nothing happens to atrial activation, nothing happens to atrial timing. So this is clearly evidence, very strong evidence of an accessory pathway presence. This was a useful observation during a case we did a long time ago. You can tell by the lousy resolution of these electrograms, but we're pacing here, giving V1, V2s. We're wondering because this patient had extensive ablation in the septum, and we had an accessory pathway present, and we were wondering, is it gone? Because we have this funny activation sequence produced by ventricular pacing, and we're wondering, well, is this just funny AV nodal conduction with relative block in the CS, or is this still an accessory pathway? We gave V1, V2, and we could see, here's a retrograde His, pretty big His. It jumps out from here to here with the extra stimulus, and the atrial activation goes with it. And the atrial activation doesn't really change. So we've got no change in atrial activation. It jumps out with the His. This is AV nodal conduction. So this was a quite useful thing to know. Yes, we probably did eliminate the retrograde slope, slowly conducting accessory pathway. But it's also important to not look at activation sequences and decide that it's a pathway. I've seen this mistake multiple times, where you look at the activation sequence, and you make a decision based on that alone, that this is gonna be a pathway because it's later, it's earliest in the mid-coronary sinus electrodes, a few centimeters over. But when you deliver parahysian pacing here, you've got no hiss capture, wide QRS on the surface, narrow QRS on the surface when you do capture the hiss, and you pull in the activation sequence and it doesn't change. So this is another way to demonstrate. We demonstrated that with retrograde right bundle branch block, the hiss A moves out because it's going over the AV node. Now we pull it in when we capture the hiss because it's a shorter route of conduction. So in this case, again, we've demonstrated conduction is tied to the hiss bundle. And so, and there's no change in atrial activation sequence. This is the AV node. Now, when we do parahysian pacing, there's three possible QRS morphologies you might see. We'd see pure hiss bundle capture where there's an isoelectric interval and an equivalent usually to an HV time. We'd see a mixed response where we're capturing both the hiss bundle and local ventricular activation, which gives you a fused QRS and kind of a delta wave appearance. When we lose his bundle capture and we capture only the local RV, we get typical RV septal pacing morphology where it's wide. And you can look at these on the surface and sort out whether you've got pure hiss capture, fusion, or RV capture. So here's an example of that where on the surface, we get a little bit of a delta wave. We've captured both the hiss and the local RV myocardium. We lose his capture and the RV QRS gets much wider and then it narrows back up again. And often the way to do this, I find, is just to take the catheter and move it back and forth a little bit or just leave it there. Often it'll do it on its own. And you can also, another way to do this is to take the output of pacing and take it very high and then drop it very low. And often then you'll see loss of his capture and continued RV capture as you get to lower outputs. I'd like to just take the catheter, slide it back, slide it forward a little bit until I lose his capture. In this case, obviously, the activation is tied to the AV node, just like the previous one where you can see we pull in the atrial activation with capture of the hiss. So this is a schematic demonstrating what I'm talking about. So when we're capturing the area near the insulated hiss bundle, we can capture just the RV alone, even though we're right next to the hiss. This is insulated and it's hard to capture. So it usually takes higher outputs or you have to be directly on it. Or in the case of his bundle capture with pacing, you have to actually screw it in there to get past the fibrous part. So in this case, we capture RV alone. We're not capturing the hiss bundle. To get to the AV node, we can't go directly because this is insulated. That wave front will not go past that insulated portion of the hiss bundle. So it's got to turn around and head up the right bundle retrograde to get to the AV node. So it's a relatively long VA time when you capture the RV alone and there's conduction through the AV node. And what happens when we capture the hiss? So now we've perhaps turned up the output. Perhaps we just slid the catheter back and forth a little bit. Now we've produced this QRS on the surface that looks fused. So now we know we've captured the hiss in addition to the local RV. And there's now a shortcut. We don't have to go all the way down, retrograde up the right bundle. We've captured the hiss directly and we have this shortcut through the AV node. So you'll pull in the A with hiss capture when you're conducting retrograde over the AV node. If you get pure hiss capture, what would you predict? Well, the pure hiss capture, it doesn't matter that you haven't captured the RV because that's not the shortest route. Shortest route is over the hiss. So when you lose RV capture and you capture the hiss alone, that stimulus to A time won't change because you've captured the hiss in both cases. So you don't see any change in the stim A time retrograde when you capture pure hiss or with fusion in the presence of AV nodal conduction. Here's an extra nodal response. And this is always useful because sometimes it can be difficult to look at the surface and know for sure that you've captured hiss in this case and not hiss in this case. Although I think it's fairly clear in this instance, QRS wide, QRS narrow, but here's a hiss bundle recording. And you can see when you lose his capture, the hiss bundle pops away from the stimulus. It's buried in the stimulus artifact here. So you don't see it, but when you lose capture of the hiss, it jumps out. That's very useful to see. But when we see activation in the atrium, it doesn't change. So when the hiss pops out, we don't see any change in the atrial activation timing or sequence. So we know we have a route of conduction that's outside of the hiss-Purkinje AV nodal axis. So these schematics will demonstrate parahysian pacing with an accessory pathway. So in this case, we've captured the RV alone, the wide QRS on the surface. The short route here is from the pacing site through the accessory pathway and retrograde conduction through the right bundle and AV node is blocked. So there's no conduction through the AV node. So this is a pure response through a pathway. Now, again, AV node conduction is still blocked. So when you capture the hiss, there's no conduction through the AV node, but conduction when it's fused is still shortest by capturing the RV locally. So whether you capture the hiss or not doesn't matter. The STEM-A time will not change. And we just saw an example of that. No change in the STEM-A despite capturing the hiss. Now, where it gets confusing, and I'll show you an example of this, that you can get a mixed response. So when you capture the AV node or you capture the hiss and it goes through the AV node as a shortcut, you can also see fusion with that and conduction over a pathway. So you can get conduction over two separate pathways with one paced beat. And this is a really confusing thing, but here's an example. So here we have pacing where we capture the hiss and the local right ventricular myocardium. So it's got a delta wave appearance. It's narrower than when we lose his capture. We see when we measure the V or STEM-A time in the hiss, it's 89 milliseconds. We measure it to the proximal CS, it's 115 milliseconds. We lose his capture, the hiss pops out and the STEM-A time increases to 117. So that would indicate that this hiss A was produced by AV nodal conduction because it delayed when we lost his capture. So there's a longer route to get through the AV node so it delays. But the proximal CS has a fixed conduction time. So we saw a change in activation sequence. So this is conduction when you have both AV nodal and pathway conduction at the same time. When we lose his bundle capture, we can see there's a change in atrial activation sequence. His A moves out, but the STEM to A in this proximal CS is fixed. That's probably over the accessory pathway. Doesn't change when you lose his bundle capture. Whereas the septal A changes because that's over, at least here was over the AV node. Don't know, this still could be fused or it could be purely over the accessory pathway. Don't know. So here's the pure hiss capture with an accessory pathway. I really don't see this. I honestly not even sure I can remember seeing one like this where you capture the hiss alone and it echoes up. It looks exactly like an echo beat in SVT with an accessory pathway. I don't think I've ever seen that blocks in the AV node, echoes up, but it's possible. Again, an extra nodal response may be mixed. So it's useful to look at these two papers and I'm not gonna spend a lot of time because we discussed this already, but it's useful to read these papers if you wanna get a deeper understanding. They're both from Sonny Jackman's group published in Cirque in 1996, looking at Parisian pacing. And then here's another paper in 2006, looking at when you have pure hiss capture and how that influences retrograde conduction. So this is useful to go through these two papers if you want a little deeper dive. Now, there are some pitfalls to capture when you're trying to capture the RV and the hiss and jump back and forth between the two to determine retrograde conduction because guess what else is right on the annulus, the A. So sometimes you capture the A directly and what's the clue for that? So here's an example of it clearly, right? Here you've got no change in atrial activation sequence and you don't capture the V or the hiss or anything other than the A and the atrial activation sequence didn't change. So the A activation sequence is purely produced by capturing it directly. Clues to that are the stimulus to A in the proximal coronary sinus is really short. So when it's less than 60 milliseconds or stim to the high RA is less than 70, in this particular study, it was only seen in the presence of direct atrial capture. When they saw a stim to proximal coronary sinus greater than 90 or in the proximal CS and high RA greater than 100, that was only observed when there was retrograde conduction and not direct atrial capture. In between, it could possibly be either, but it's usually pretty clear cut when you're pacing and trying to capture and you get this shorter conduction time in the proximal coronary sinus, you've captured the A directly. The other caveat to throw in, and this is where it can be surprising to people, but it definitely happens, that when you have a left free wall accessory pathway, your extra notable response may not be perfectly what you expect. And here's an example. So here we're capturing his and RV locally. There's a conduction time of 132 milliseconds to the distal coronary sinus, which is the earliest atrial activation. We lose his capture here because we can see the his bundle pop out and the QRS gets wide on the surface. The stimulus to the earliest A in the left free wall now jumps from 132 to 150. And then we pull it back in and it doesn't go to 132, but back to 142. So what's happening here? Well, it turns out that capturing the his bundle when you have a left free wall pathway and you're pacing from the RV is actually a shorter route than capturing the RV alone. So you don't get a fixed stem to A time because it's actually a shortcut to go over the his Purkinje system when you're pacing the RV and you're trying to get way over to a left free wall. Now it doesn't jump out the timing you'd expect with the AV node. So the AV node is gonna jump out 40 milliseconds or so, 35 milliseconds or so. This only jumps out 18 milliseconds. So you have to be a little suspicious when it only jumps out 18 milliseconds. It's not likely that doesn't really fit with AV nodal conduction. Say you didn't have a CS catheter and you're wondering is this pathway behavior or is this AV node? You might be tempted to think this is over the AV node because it jumps out a little bit when you lose his capture. But if you think about it, the timing doesn't really make sense. It didn't jump out enough. There are other means to sort out retrograde conduction without recording or capturing the his bundle. Here's an example where it looks like there's just conduction over the AV node when you're pacing the V. Looks like concentric earliest here at the CS proximal. His A is slightly earlier than that probably and the high rate atrium is late. So this looks like more or less typical conduction potentially over AV node if you just look at it quickly, at least. You then give a V1, V2 and then you see there's clearly a jump out in atrial activation at the septum in the high rate atrium. But there's earliest activation now clearly at the distal CS. And you can kind of actually, if you look at it, there's sort of a Chevron pattern in the CS. So that may be somewhat fusion over that left free wall pathway. But here this is probably over left free wall pathway alone. Differential RV pacing is another method other than what we've already seen with parahysian pacing to sort it out. This takes advantage of the fact that pathways insert at the base and it's a shorter cut to get to the AV node from the apex. So shorter from the base for accessory pathways, shorter to the AV node from the apex. And that difference is reflected in these kinds of different timings you see with and without a post-receptal accessory pathway. Now, this doesn't work again very well when you're talking about left free wall pathways because the time it takes to get from the pacing site in the RV to the left free wall may not sort out in your favor depending on where you're pacing and whether you capture a little bit of hysperkinesia. So this may not be a good way to sort out free wall pathways, but it's a very good way to sort out post-receptal accessory pathways. And here you can see how the data broke out, clear cut cutoff, it's plus 10. But again, if you remember that pacing from the apex it's shorter to get to the A, that's AV node. If pacing the base is shorter, that is an accessory pathway. So I like to remember concepts, not numbers. And I think that if you understand that concept you can clearly get that correct. This, another important thing is that mixed responses were not a part of this study. So mixed responses can occur just like they occurred with parahysian pacing. You could get a mixed response with pacing at the apex where you now conduct over the AV node and a pathway and it could look confusing. So keep that in mind. Here's a schematic to demonstrate what I'm talking about. When we have AV nodal conduction and we pace from the base up near the his bundle but capture only the RV, it's got to come down just like we saw before, retrograde up the right bundle and through the AV node. However, if we push our catheter down towards the apex closer to the insertion of the right bundle we can get into the right bundle directly and it's a shorter conduction time now because we don't have this piece that we have to worry about we right next to the right bundle and we go up the AV node. So it gets shorter when you pace from the apex when the AV node conduction is present. When accessory pathway conduction is present capturing the RV base is a relatively shorter route than pacing from the apex. You're just closer to an accessory pathway in the septum when you're at the base than at the apex. Now again, if the pathway were over here this difference may not be discernible because you're too far away from your pacing site. This works because when you're pacing at the base you're close to the site of activation. Now this would work if you wanted to do base and apex pacing from the LV to prove that a left free wall. It would work, but we don't usually do that because we're starting usually with just catheters in the RV. You can give adenosine for diagnosis and in sinus rhythm if you see VA block with adenosine during ventricular pacing that suggests there's no accessory pathway present that's reasonable. However, keep in mind that even with 12 milligrams of adenosine in this particular study, 38% of patients with typical AVNRT did not see block in the fast pathway. It behaves a little bit more like an accessory pathway in that regard, so don't get fooled. Here's an example of doing that where you're pacing the V and seeing retrograde block. There's antegrade block proving that probably there's no accessory pathway conduction. All right, we haven't even talked about SVT yet. All we talked about was sinus rhythm and we're 40 minutes in. So you can see that there's a lot of important work to be done in sinus rhythm, but the money comes in SVT because that's the thing you were trying to diagnose. So you're trying to, you could come up and diagnose that there's accessory pathway present in sinus rhythm and it turns out it's AVNRT or atrial tachycardia. So the money is always in the SVT. What are the important observations that you can initiate or terminate tachycardia depending on AV conduction? We can look at the activation sequence just like we did in sinus rhythm with retrograde conduction. An important thing to look at is the VA time. So if it's less than 70 milliseconds in septum in adults, that pretty much excludes orthodromic AVRT. So VA time at the HISS less than 70, but in children and some smaller, younger adults, you may see values as low as 50 milliseconds for accessory pathway conduction. So this number isn't completely firm, but it's served me pretty well over the years. AV or VA block is important to recognize because it excludes orthodromic AVRT if tachycardia continues. And obviously if tachycardia is coincident with AV block, that's also important because that tells you it's AV nodal dependent. Tachycardia wobble is useful to scan because if you can show that the VA time is fixed and the HH intervals drive those AA intervals, then that excludes atrial tachycardia. Bundle branch block is also potentially a diagnostic observation because when a bundle branch block is ipsilateral to a free wall accessory pathway, it will usually increase the VA time by more than 35 milliseconds. And that is a diagnostic finding. Now, why do we even bring up whether something's dependent on AV node conduction for termination or induction of the tachycardia? Well, occasionally you'll get a tachycardia with VA dissociation, and that's not always atrial tachycardia. There are cases where AVNRT can be present in the presence of V pacing and VA dissociation. So then it can be really important to try to sort out whether it seems to be AV nodal dependent or not. And I've even seen AV node reentry in the absence, sorry, in the presence of complete AV block. So there was infrahissian block and the patient was having AVNRT and it looked like atrial tachycardia until we proved that conduction was critical to get a jump first in the AV node. And then tachycardia would begin every time, had to be a jump. So then we ablated the slow pathway and it went away. It was not atrial tachycardia. AVNRT is more likely when induction is dependent on a critically long AH, particularly when you get a jump. And when it terminates, associated with the short conducted AH interval, indicating the pathway has blocked in the slow pathway and now conducts over the fast. Now, the accessory pathway is also dependent on a critical AH, but not usually a jump. Sometimes it is. So there are pathways where it needs a jump in the AH to induce. But if you also see delay in the hisperkinesis system, coincident with induction, that also indicates an accessory pathway. It's really important. It's similar to saying that when you develop bundle branch block, you get a VA time prolongation. Well, sometimes bundle branch block is necessary to get the tachycardia going because there's not enough delay in the AV node to produce that. But you get delay in the AV node plus bundle branch block. Now you've got the delay necessary to produce a circuit. So here's a clear cut example where you get a very long stimulus to AH time that's coincident with induction of tachycardia. And if you did this over and over again and you always needed this kind of AH interval to produce tachycardia, that would be very good evidence that this is AV nodal dependent. Here's another example where you start to pace. And when we see termination of this tachycardia with a long AH time, it's coincident with a short AH time because we've blocked in the slow, we're now going down the fast and we no longer see tachycardia. For most accessory pathway conditions, you're gonna see block in this accessory pathway integrate before you see tachycardia because ORT is the most common form, which goes over the AV node and back up the accessory pathway. And if you've gone down the AV node integrate, you're not gonna go back up at retrograde. So you have to see integrate block first. Here is something that you could very easily ignore. And this is what I'm saying about being somewhat fastidious about looking at what's happening during SVT and looking for changes. Now there's clearly a change, this terminated. But there's another observation, did it just terminate? It terminates with an A, H and a V. And you'd say, well, atrial tachycardia can terminate like this. Maybe AVNRT could terminate like this. Maybe ORT could terminate like this. But there's a really important finding here. And that's the beat associated with termination is narrow. You lose right bundle branch block. So when you lose right bundle branch block, it terminates. That's not a coincidence. Particularly if you see this over again. Now it could be a coincidence obviously, but it wasn't. This was a right free wall accessory pathway. P wave is upright inferiorly. High RA is early. So you're already suspicious. Well, maybe this is atrial tachycardia. If it terminates with a narrow QRS, not likely. Because what's happening is for a right free wall accessory pathway, the circuit's bigger when there's right bundle branch block. Because it has to go down the left bundle, come across the septum before it comes back to reach the right free wall accessory pathway. So that circuit is effectively bigger when you have right bundle branch block. You lose right bundle branch block. Now it's got to take a shortcut. It's going to come down the right bundle and reach the accessory pathway earlier than it would have with right bundle branch block. And because it reaches it earlier, it's refractory and it terminates retrograding this. So this was no coincidence. And recognizing this would be a really important diagnostic finding. Now, two-to-one block absolutely excludes typical types of ORT. The typical type of pathway inserts at the base, A to V, and is not decremental in most cases, but it's never associated with two-to-one AV block. Because the atrium, the pathway, the ventricle, the hysperkinesia system, the AV node are all part of the circuit for ORT. But not so for AVNRT, the ventricle is not part of the circuit. So it's not uncommon to see periods of two-to-one AV block. The other way around for AVNRT is really uncommon. But for typical types of AVNRT, often in the lab, you'll see this where you get a P wave dead in the center of two QRSs. For those of you reviewing for the boards, this would be an EKG you might see and have to recognize. In this case, there's a hys bundle recording here, and you can see a hys bundle recording here and an A. So this is clearly in for hysine block during AVNRT because we can see in for hys block, hys but no V. However, a lot of times when we see AVNRT two-to-one, you don't see evidence. Again, P wave dead in the middle of two QRSs, narrow inverted. You don't see any evidence of the hys. So clear hys when there's conduction, not a clear hys at all when there's blocked. And the tendency is to say, this is lower common pathway block during AVNRT. But Fred Marotti's group did a study where they looked at converting two-to-one block to one-to-one block during hys refractory PVC. So you time it to where the hys would be refractory based on where you'd expect it to be in the next feed. And when you brought in a hys refractory PVC, regardless of whether there was a hys present there, it restored one-to-one conduction. So obviously if there were in for hys block, you wouldn't be able to do that. It wouldn't restore. I mean, if there were, I'm sorry, if there were just lower common pathway block and not in for hys block, you wouldn't be able to restore one-to-one conduction because you wouldn't be able to reach the AV node, the lower common pathway to restore one-to-one conduction because the block is below that. So this was a really good indication that most block is probably in for hys even though we're not recording a hys. Something about the way the catheter jumps or moves doesn't allow us to record a hys in every case with two-to-one block during AVNRT. This is a pretty diagnostic finding during SVT. It combines two observations. One is that the VA time is very short. So if you look from the surface QRS down the proximal CS, you don't see the hys A very well, because it's buried in here somewhere, but proximal CS is almost exactly on time to the QRS. This is a very short VA time, zero or maybe even slightly negative. And the termination is coincident with AV block. So that combination is AVNRT. So when you see a short VA time and termination coincident with VA block, you pretty much have your diagnosis, that combination of those two things. Here's an example where looking at tachycardia wobble can be useful. So here we have an example where AA intervals are lengthening. So 412, 435, 465, 510. And if you look at the age, they're predicted and preceded by the AA interval. So the AA interval goes to 412, the HH goes to 412, the AA goes to 435, the HH goes, and it happens all the way until this is terminated. The other thing you notice is the VA time is not fixed. So this is an example of atrial tachycardia termination, where the A's are driving the V's, the VA's are not fixed. Could this be, you know, there's never 100% here, because, you know, is it possible that you have a retrograde decremental pathway of some sort, either over the AV node or a pathway, and it's terminating by decremental conduction in the pathway? Yeah, but that's pretty unlikely. And so this is what you typically would see with AT, A's driving V's, and not a fixed VA interval. So this is an example of where H's, HH changes, are preceding AA changes, and there's a fixed VA relationship. So the VA time, just eyeballing it all the way across here, that's very consistent. What's not consistent is the cycle length. Cycle length is wobbling a lot, and here are the numbers. So here we're clearly getting that AA changes are preceded by the VV changes. So when you see a lot of wobble with an absolutely fixed VA time, just eyeballing that, you can pretty much say it's AV nodal dependent. And this can happen with both accessory pathway conduction and AV and RT. In this case, we know it's not an accessory pathway because the VA time is too short. So this is another one where you can be pretty confident, combination of observations, tachycardia wobble with a fixed VA time, VA too short for ORT, this is AV nodal dependent, and it's gonna be AV and RT. Here's another example from that same patient I showed before, who has a right free wall accessory pathway and we see, instead of, if you remember, when the right bundle disappeared, it terminated. In this case, tachycardia continues. What we see is you lose right bundle and your VA time shortens from 148 to 108. Like we said, there's a shorter route of conduction when you can go over the right bundle in tachycardia than when you can't. So, cause this has a long, you've created this longer route, transeptal. Here you've lost the, you don't have to go transeptal to get, so you shorten the VA time. Now look what happens to the AH here too. So, you get a compensatory or perhaps even a jump into a slow pathway for one beat and then it goes back to its normal pattern. So, we went up through this pathway, which in this case, it wasn't refractory when the right bundle branch block was lost, but we see ipsilateral shortening of VA time because of loss of right bundle. This is another example with left bundle and a left free wall pathway. The activation here is sort of mid coronary sinus and we see left bundle branch block. The VA time is 167. When we lose the left bundle branch block, we see shortening of the VA because again, we have a shorter route. Now it can come down the left bundle and get to that left free wall pathway quicker. So, the VA time shortens. Notice that you don't measure the local VA interval cause it gives the opposite impression. The local VA looks shorter with left bundle branch block and longer when you lose left bundle branch block because with left bundle branch block, the ventricular activation on the left side's delayed so they actually get closer together than when you lose left bundle. So, don't measure the local VA interval for this phenomenon. You measure surface V to A, surface V to A. I'm going to show you a schematic that we're going to use for several points. And that is, in this case, a schematic of ORT using left free wall accessory pathways. We have here all the elements of a ORT circuit, atrium up here, AV node, Hispokinji system, ventricle accessory pathway itself. With left bundle branch block, the VA time will always increase. So, if we measure the surface V to A, you'll always see VA increase during ORT or when you gain left bundle branch block. So, it goes from narrow to wide, the VA time's going to get longer. Obviously the opposite if you lose left bundle branch block like on the previous example. It's just the mirror image for the right-sided accessory pathway and right bundle branch block. Now, the tachycardia cycle length may not change. That's less predictable in these instances because let's say this is your circuit. You get left bundle branch blocks and now it's got to come here. The VA could get longer, but the AH could get shorter in a compensatory fashion. So, the tachycardia cycle length may not even change at all in this scenario, but the VA will. So, that's predictable. The tachycardia cycle length is less so. These papers give sort of ranges for what you'd expect to see for VA interval changes with bundle branch block and ORT. So, if you have orthodromic AVRT using a free wall accessory pathway and ipsilateral bundle, you usually see a 35 millisecond or more increase in the VA interval. Patients with septal pathways have VA changes less than or equal to 25 with either right or bundle, right or left bundle. In patients with antreceptal pathways, the VA interval will prolong with right, but not left, important point. And in patients with post-receptal pathways, the VA interval frequently will prolong with left, but not right bundle. So, post-receptals are essentially more leftward pathways. Antreceptals are more rightward pathways as indicated by the pattern you see with bundle branch block. For mid-septal pathways, you usually won't see a change with either right or left bundle branch block. For left anterior fascicular block, you may increase the interval for left free wall pathway in that 15 to 35 millisecond range. That's analogous to what I showed you earlier when you capture the His bundle from the right side, you get a shortcut to the left free wall pathway. So again, left anterior fascicle is the shortest route possible to a left free wall pathway. So if you block it, you're gonna see a little bit of an increase, but not so much as if you block in the left bundle completely, where then you'd expect it to be more than 35 milliseconds. This is another paper you might wanna take a look at. It looks at results of complete or incomplete bundle branch block and the pattern and the times you'd see with free wall and septal pathways. All right, so now we've gotten by observations. We're now looking at pacing maneuvers. Finally, I'm sure you said, why didn't you just start with that? We don't need anything else. Well, sometimes pacing maneuvers don't always work out. And so all the other things we've talked about are building blocks for this. The key concepts for understanding pacing maneuvers are that we're trying to reset or entrain narrow complex tachycardias from the V, particularly when the HISS is refractory. That's when we're gonna get our most information. We may try to dissociate the HISS-Purkinje system from the tachycardia or observe that. And then we can reset or entrain from the A when we're trying to sort out AVNRT versus junctional tachycardia. Now, as a de novo rhythm, unless you're a pediatrician, junctional tachycardia is not that common. We see it rarely, but it's very common after you've ablated AVNRT and you're trying to sort out, do I have a damaged AVNRT circuit or am I looking at junctional tachycardia after I've given isoprop? That can be difficult to sort out, but this maneuver will tell you. Ventricular pacing, there's a couple of ways you can do it. One is you can scan PVCs throughout diastole. So some will be HISS refractory and as they get earlier and earlier, they no longer will be HISS refractory. And if a HISS refractory PVC advances, delays the atrial activation, or it terminates SVT with block to the atrium, that's ORT. If an early PVC terminates, if an early PVC terminates SVT with block to the atrium, you can't be sure whether it's ORT or AVNRT because if you get pre-HISS, you can affect AVNRT, but it does exclude AT because you've proved that you blocked retrograde, you didn't affect the atrium with that conducted beat, can't be AT. We'll see examples. With ventricular overdrive pacing, we're attempting to accelerate the atrial rate of the tachycardia to the pacing rate. And you wanna pick a rate that's just slightly faster than SVT and how fast does that need to be? Fast enough that you can discern differences. So is one millisecond fast enough? No, you're never gonna be able to sort that out. 10 milliseconds might be, and I often will start 10 milliseconds. 20 milliseconds usually will do the trick. And again, the more wobble there is in a circuit, the more difficult it is to sort out. Wobbly circuits, overdrive pacing can be difficult. PVCs can be difficult to interpret. However, one thing I, one trick that I do use is so I take the shortest interval in the wobble, and pace just 10 or 20 under that. So I can be sure that my pacing is affecting the tachycardia, not the natural wobble that's occurring. So I know that when I bring it in 10 or 20 milliseconds earlier than the shortest wobble interval that my pacing is really what I can interpret. So that's a little trick that tends to work. During overdrive pacing, if we've accelerated the A, then we then look for an AAV or an AV response to tachycardia. We can look at the stim A, VA difference or the post-pacing interval tachycardia cycle length difference. We can look during the zone of fusion for a fixed stim A or whether we advanced, terminated or delayed the A with fusion. We can look whether we trained the tachycardia coincident with QRS fusion. You can only do that if you have both orthodromic hiss activation and a pathway present and part of the tachycardia. Atrial pacing, again, we'll go over. All of these things you're looking for with atrial pacing to entrain it, APCs, and then termination dependent on AV nodal conduction when you pace below the Wenckebach cycle length during SVT to try to get it to terminate. So here is a schematic of ORT now using the right free wall accessory pathway. We see a PVC here that is HISS refractory. Now, how do we know it's HISS refractory? There's a couple of ways. One is we can look at the HISS-HISS timing and you can see there's an anagrade HISS here that's on time with the other histopolarizations and it looks the same, it's anagrade. There's a pacing spike almost coincident with that HISS. It's not early enough to have produced that HISS. That timing is too short. To get from the V to the HISS, you need some time. And that is usually something like 35, 40 milliseconds. This is just 10 milliseconds. So this is HISS refractory. The other way you can tell is look on the surface. So if you knew what this pace beat looks like in sinus rhythm, you would know for sure this is fused. It's fused between activation over the AV node and the pacing wave front. And that's what gives you the surface fusion because some of the ventricles already been depolarized through the HISS-Purkinje system. And you can see that because the CSV is on time and it doesn't change. But the activation wave front collides with the paced wave front. So if you know it's fused on the surface, then it's HISS refractory. We take advantage of that fact when we do overdrive pacing. So here's a schematic of how that works. So here's the circuit and we have pacing from a catheter in the right ventricle. We then get a wave front that emerges from that catheter paced wave front in the V. It then collides with the one that comes through the right bundle. So we get fusion between these two wave fronts, but we also get to that accessory pathway sooner. Because it gets to the accessory pathway sooner than it would have through the circuit, the paced wave front gets there first. Then it finds the pathway refractory and it terminates. So that's what we just saw on the surface on that electrogram. This is the schematic indicating how that works. Now here, the other thing you can look at, even though it didn't terminate the tachycardia, a HISS refractory PVC in this instance advances and then resets the tachycardia. So how do we know that this is reset? Well, we put our calipers and do the measurement. So if we were to take this 280 time and then double it and take this caliper, which would be double the tachycardia cycling. So we had one caliper that's double and we slid it over one. If it falls on the right caliper, then that was not reset, but we pulled it in by 20 milliseconds. So that right caliper would have been out here and it would have been 20 milliseconds later. Here's an example, a schematic of how this works. So here we're going along a tachycardia at a rock solid cycling. Here we have the same tachycardia. Now we put in an extra stimulus. That red bar indicates the pacing stimulus. We actually pull the tachycardia forward. So it didn't come at the expected time. It comes earlier, presumably, usually by the same amount that this stimulus is early, and it resets, meaning that the next beat comes earlier than expected if we were to march out this tachycardia and we hadn't done anything to it. So we pull it forward, that one beat, and it stays forward by the tachycardia cycling. So you've reset the clock completely. You pull it forward, it stays forward of the expected timing. What happens if we didn't reset it? Well, we could still bring in an extra stimulus. That timing comes on time, so we didn't affect the tachycardia at all. And it just moves as if we hadn't done anything. So the timing stays the same as if we hadn't done anything. You could also potentially pull something forward, and then it, again, resumes exactly. So we could pull it forward, but not reset it. And that would be a fourth condition where we pull it forward like this, but then this one comes on time. So that's a little more difficult to interpret. And I gave examples here of what you'd expect to see. This was the one that was reset. And I did some fancy cutting and pasting to show that if it weren't reset, this would have been the expected interval here. So this is that example where we paste the RV and the wavefront collides with the previous one because it's HISS refractory, so we get a fusion on the surface. We advance the tachycardia because your paste wavefront gets to the accessory pathway early. It gets over and you reset the tachycardia, basically by the degree of prematurity that this ventricular beat comes in. The other thing that's really important to recognize, and this is to try to sort out these relationships, is that when you're doing this, you have to make sure that you're doing it right. You have to make sure that you're doing it right. So when the VA time is more than 40% of the tachycardia cycle length, some of these pacing maneuvers of looking at short post-pacing intervals, short stim AVA, all of these things, you have to make sure that you're doing it right. You have to make sure that you're doing it right. So when the VA time is more than 40% of the tachycardia cycle length, some of these pacing maneuvers of looking at short post-pacing intervals, short stim AVA, all of the things that we've learned is not really true all the time because decremental pathways with pacing will decrement. That's the nature of them. So what we see is that when you have a long VA time, So what we see in this case is we bring in a history factory PVC, but we delay the next day. So the timing here is 360, but this AA interval is 420. How do we know this is history factory? You could look at the surface. If we knew what this looked like during sinus rhythm, we could recognize this as fused, but we can also look at the HISS bundle recording here. It comes on time. It looks antegrade, and it's too short of an interval here for this H to have been produced by this V. So we know this is history factory, and we know it delays the next day. There's only one thing this can be. It has to be accessory pathway. It's ORT, and it's decremental. That's why it delays. So this is a really important finding when you're trying to sort out decremental accessory pathways from AVNRT. Here, the fused beat that you produce here, the HISS bundle's already been depolarized. You get wave fronts colliding between hisperkinegy activation of the ventricle and paste wave front of the ventricle. It reaches the pathway early. So when it does reach the pathway, it slows through the pathway because of decremental properties of that pathway, and that delays the next A that you produce with paste. So that's the explanation. Overdrive pacing is what I prefer because single ventricular extra stimuli just take more work. They're useful. Sometimes we do it if we can't sort out the overdrive pacing, but that almost doesn't happen because you can get pretty much all the same information with overdrive pacing that you can get with single ventricular extra stimuli. In fact, in some ways more, because with single ventricular extra stimuli, as you come more and more early with that single extra, you start to develop relative refractory period of that pacing stimulus to V, whereas with overdrive pacing, it's just getting slightly earlier, slightly earlier, slightly earlier. You don't get that same relative refractory period problem. A VAV response indicates an AV nodal dependent mechanism, and a VAAV response indicates a focal mechanism, or namely AT. So here's an AAV response or an AAHV response, more correctly. We're pacing the V. We produce an A retrograde, and then an A comes back at the tachycardia. Now there's two things to notice. One is the atrial activation sequence changes because you're conducting through the AV node and producing an A that is compatible with retrograde AV nodal conduction. It overdrive suppresses the atrial tachycardia. So you get a change in atrial activation sequence. You get a beat of AV block in between, and then tachycardia resumes with AV conduction. VAAV, the last A driven at the pacing, the cycle length is this one. So you measure A to A, A to A, that's at the pace cycle length. This is longer. So this AA is not at the pace cycle length. This is the last one driven by pacing, AAV response. Now this is another example of an AAV response where the atrial activation sequence is more clear because we have more catheters in. So here we're pacing. We get retrograde conduction over the AV node. We produce an A that looks exactly like retrograde conduction over the AV node because this is a focal tachycardia and you don't get fusion with focal tachycardias. You just overdrive suppress them. So you overdrive suppress the atrial tachycardia, VA, VA, VA. This part of the tracing looks exactly like what would happen if you were doing this in sinus rhythm. It doesn't look any different. You've suppressed the atrial tachycardia completely by pacing and conducting through the AV node. Then it resumes its tachycardia on the right. So VA, this interval is the last paced interval. So this is your last A driven by pacing and then tachycardia resumes, VA, AV. Now, another one where you get clear example of it's actually a VA, AA, it's a VH, AA, HV. If you really want to get complicated because there's a retrograde to get through the AV node, you have to come and produce a HISS retrograde. So you come through the AV node by producing a retrograde HISS, the A, and then when it comes back, it goes AHV. So that's really what's happening. You just often don't record the retrograde HISS or it's not as easy to see. This is a schematic or a ladder diagram illustrating how this works in the presence of atrial tachycardia. Since you've come through the AV node to produce that A, it's not going to be able to come back down the AV node until the next day comes because the AV node's refractory from the retrograde conduction, but on the next day, it's no longer refractory. And an AAV, VAAV response, correct? Well, this is one that you'll see frequently with long VA tachycardias. It looks like a VAAV response. It doesn't look that different than the ones we just looked at, honestly, but what you have to do are the measurements. So when you do the measurements, you see that this interval is the paced interval, not the tachycardia interval. So this V is producing that A because this interval is the paced interval. So this is not a VAAV response because the last paced beat produces that A. So this is a VAV response. This is the so-called pseudo VAAV response. You can see with atypical forms of AVNRT, usually. Now, in patients who have long HVs, you can also be fooled by the, and get something that looks like a VAAV response. I mean, if you just look at this, there's a V, an A, an A, and a V that comes before it, but the truth is there's a hiss coming before that A because there's a very long HV time. So this A could not have produced that hiss, right? I mean, the A has to conduct to the hiss. It doesn't come after. So this is another example of a VAAV response that is sort of a trick, visual trick more than it is real. So in this case, you had to recognize this is a VAAV response, but has a long HV time. So this is somebody who has probably got AVNRT and a long A and infrahissian disease. The VAAV response is seen with AV nodal dependent mechanisms and I've never seen that principle violated. So when it does, it's gotta be very rare. It basically excludes atrial tachycardia with very high specificity. So the VAAV response here, there's a few things you can see here that if you're paying attention, we haven't gone over them yet, but we will see soon enough. This is an accessory pathway. I can tell that by looking at the VA stim A times, by looking at the post pacing interval, by seeing that I'm entraining it with fusion on the surface. All of those things are important observations. So linking is something that may be useful. Honestly, usually other things sorted out for you, but linking is something you can look at when trying to see whether the return VA time is fixed or not, if you entrain it, in which case a fixed VA interval indicates something that's AV nodal dependent, not atrial tachycardia. Seen with accessory pathways, may not occur with decremental accessory pathways or atypical forms of AVNRT. Linking may be lost because when the retrograde limb is decremental, you may not see linking. Here's an example of VA linking after overdrive pacing with junctional tachycardia. We paste A to overdrive. We get, first of all, an AHA response, which is what you see with junctional tachycardia. We'll go over that again. But the other thing we see is that the VA time is linked. So during tachycardia, you get the same VA interval as the one that comes back. That's usually an AV nodal dependent. Now it doesn't tell you what AV nodal dependent mechanism, but it tells you it's probably AV nodal dependent. Atrial tachycardia versus the AV nodal dependent mechanisms is usually easy to sort out, mainly by the VAV response. So when you see a VAV response, you've essentially eliminated atrial tachycardia. HH driving AA changes, very strong evidence with the fixed VA time that you've got AV nodal dependence and not atrial tachycardia. If there's a one-to-one AV relationship and it reliably terminates with AV block, again, strongly favors AV nodal dependence. And if you can terminate by pacing the V, but don't affect the A, again, strong evidence that it's not an atrial tachycardia. Same thing with termination. But there's a caveat. So there are some forms of atrial tachycardia that terminate reliably with the pacing, but it's not usually one beat. It's not on the first beat of the set. You have to pace for a while and then it'll terminate, probably due to autonomic tone. What favors AT? Well, eccentric atrial activation with AV block. If you see that combination of observations, very likely to be AT. If you have a variable RP relationship and the AAs are driving the HHs, likely to be AT. Again, decremental pathways can mimic atrial tachycardia sometimes. An AAV pattern following RV pacing, pretty good way to differentiate, but the problem, unlike the AV nodal forms, where VAV is really easy to get in most cases, you can usually, with isopril, under different conditions, you can produce a VAV response eventually. In atrial tachycardia, sometimes there's VA dissociation and you will not get any conduction retrograde. So you'll get VA dissociation with pacing. That's actually more common than seeing the AAV response with atrial tach. Probably because atrial tach is often in older people, they often don't have robust retrograde conduction. Again, the absence of VA linking with atrial or ventricular pacing is another. Maruyama, you could look at this paper here if you're more interested in that. I find the linking part not all that useful in general because there's so many other things to look at and maneuvers you can interpret. We'll take a break here and move on to the second part of our SVT discrimination talk in just a minute. ♪♪

diagnosis

supraventricular tachycardia

AV nodal re-entry

AVNRT

AVRT

atrial tachycardia

accessory pathways

fascicular tachycardia

observations

specific maneuvers

sinus rhythm

pacing maneuvers