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Session I: Basic Science and Fundamentals of Elect ...
Retrograde Conduction
Retrograde Conduction
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This is John Miller from Indiana University where I'm a professor of medicine and director of electrophysiology training. I'm going to speak now about retrograde conduction. These are my disclosures for your viewing pleasure. Retrograde conduction is a topic not often visited, but it's an important one in electrophysiology. We practice it every day. We're going to try to look today in the next few minutes as for several learning objectives. First to be able to determine if retrograde conduction is present or absent, and when it's absent, be able to recognize rather quickly at what site the block is occurring, what level of the conduction system. It's important to know different patterns of retrograde conduction that has implications for what rhythm disturbance is being dealt with. It's important to be able to appreciate the difference between the term eccentric retrograde conduction versus eccentric atrial activation and atrial tachycardia. The importance of this will become clear. We also want to understand distinctions between retrograde AV node hiss conduction and accessory AV pathway conduction and the importance of being able to tell whether conduction is hiss dependent or hiss independent in the case of an accessory pathway. As an overview, assessment of retrograde conduction is something that we, know it or not, make every day. It's glossed over by most people. It's poorly understood by many. And it's usually not very hard to correctly determine if you know a few things to look for. There are several tools for this assessment. One is the surface ECG. It has a lot of information that can help us. Hiss bundle recordings, of course, the presence of a hiss bundle potential can be pivotal, but you don't have to have that. You can infer a lot of what's going on by the effect of premature ventricular complexes or ventricular pacing on the subsequent PR or AH intervals, as the case may be. Obviously, we usually have other atrial recordings to look at an atrial activation sequence. So what's the big deal here? When talking about retrograde conduction, we're usually referring to what happens with atrial activation coming from the ventricles. Is there atrial activation or not? If they're there, how did they get there? Did they go over the AV node hiss-purkinje system? Did they go over an accessory pathway? Did they go over some combination of these? Almost as useful to know about whether there is or is not AV conduction is when it fails, where in the conduction system does it fail? Does it fail in the AV node? Is the block in the hiss-purkinje system an accessory pathway or, again, some combination of these here? Retrograde conduction may be present, and if it's present, I like to think of it on two axes. Each aspect of these should be considered. One is the horizontal axis or what goes along with the timing of atrial activation. Is it close to the previous ventricular complex? Is it a medium distance, or is it a long distance away? So that's the horizontal timing of it. And then the vertical, the activation sequence, is a hybrid atrium earliest, is the AVJ earliest, so on and so forth? What's the atrial activation sequence? Then we need to talk about conduction ratios. How many V's are there per A? There shouldn't be more A's than V's if it's retrogradely conducted. There should be more V's than A's or the same number. You could have a one-to-one VA ratio. You could have type I or type II second-degree block. So you could have a Winkiebach retrogradely. You can have two-to-one block retrogradely. Or you can have no retrograde conduction. But when you have no retrograde conduction, the block is always occurring somewhere in the conduction system. When pacing at a fixed rate or very slowly incrementing the pacing rate, decremental cycle length, the AV node is far more commonly the site of block when conduction fails than is the hisperkinesis system. So even at a very, very slow rate, or if you gradually pace a little bit faster, when you first see block under those circumstances, the AV node is generally where the block is occurring. Hisperkinesis system can do this, but the hisperkinesis system tends to improve its conduction parameters with faster rates as long as you gradually sneak up on it. If you surprise it, it's not very happy. So premature stimulation results in block in the hisperkinesis system as opposed to block in the AV node. When block is present, it may not be permanent. Catecholamines may invigorate conduction in any portion of the conduction system or in accessory pathway. They are much more active at invigorating the AV node than they are invigorating an accessory pathway, but both are susceptible. Now if you talk about the continuum of block to one-to-one conduction and everything in between, and whether you're considering the sudden onset of pacing or continuous pacing and gradually increasing the pacing rate, we see some differences in these different conduction structures. So AV node is pretty good at soaking up a sudden change in rate. It just delays a little bit more, but it eventually gets there. So one-to-one conduction is the rule at slower rates if it's present at all, but then it fails when you pace at more rapid rates. The AV node fatigues, if you will. Hisperkinesis system is just the opposite for this. If you have a sudden onset of pacing, it's very likely to show block somewhere, and sometimes complete block retrogradedly in the hisperkinesis system, but if you gradually increase the pacing rate, it goes slowly and gradually increase the pacing rate, it's your friend. It will stay there for quite a long time. Accessory pathways behave very similarly to the hisperkinesis system, but they get to a certain point and then they just suddenly fail and go to two-to-one block. Hisperkinesis system will do this also in many cases. Here's an example of a single individual who was blessed with having three different forms of AV nodal reentry, one with a short VA or RP interval from QRS to atrial activation. This is a medium RP interval. It's almost in the middle of the RR interval here, and then we have this long RP interval where the interval from the QRS onset to the atrial activation is quite long, and you could also call this a short PR tachycardia. We call it a long RP tachycardia. Now, when there is no visible R wave, no R, one, three, two, one, when there is no discernible RP interval, that is the atrial activation is contained within the QRS complex, this is practically always AV nodal reentry. It could be an atrial tachycardia with conduction down an AV nodal slow pathway. That's possible. It could be a circumstance where the AH interval is basically the same as the atrial tachycardia cycle. One can have a short RP interval, that is the P wave is roughly in the first third of the RR interval. This is most typically orthodromic atrial ventricular reentry with a close second being AV nodal reentry, most usually the slow-slow variety or anterograde slow, retrograde fast in older individuals where the fast pathway takes a little bit more time, like a lot of things with older individuals, takes a little bit longer time to get back to the atrium. Atrial tachycardias can also do this. It's just happenstance what the AH or the PR interval is versus a tachycardia cycling. An intermediate RP interval, that is the P wave situated roughly in the middle third of the RR interval, is usually seen with atrial tachycardias more so than AV nodal reentry, the slow-slow variety, or orthodromic AV reentry with a relatively slowly conducting accessory pathway. These are a little bit unusual. The long RP interval tachycardias are a very interesting lot. They can be atrial tachycardia, even sinus tachycardia is technically a long RP tachycardia. They can be AV nodal reentry, anterograde slow, retrograde fast, so-called. They can be orthodromic AV reentry with a slowly conducting or even decrementally conducting accessory pathway. Any of these is possible. A lot of electrophysiologists don't like to use the term RP interval in talking about tachycardias because of a variety of problems. It can be hard to tell where the P wave is in SVT, so being able to judge what the RP interval is problematic in those situations. With intracardiac recordings, it can be extremely difficult to know whether the tachycardia has a short, medium, or long. Which of these three is this? It could be any of them. I'll show you an example of why this is a difficult topic. And anyway, the differential diagnosis is always the same. One particular possibility may rise a little bit higher depending on whether it's a long, short, or medium RP, but you're always considering the same culprits here. Here is the RP interval in a table form. As I had discussed previously, there's really not much new information here, but the highest probability is, as shown here, the lowest probability. But again, each of the major possibilities, orthodromic re-entry, AV node re-entry of some variety, and atrial tachycardia are represented. It's just a question of which rises to the top under what circumstance. Here's what part of the problem is. Is this a short, a medium, or a long RP interval tachycardia? Well, it's obviously a short RP interval tachycardia. There it is right there. But it could be a medium RP interval tachycardia. If you look at the AV nodal or AVJ atrial activation, or it could be a long RP tachycardia. So here's what some people don't like about... One of the things that some people don't like about the RP interval during tachycardia, the differential diagnosis is always the same, and who can tell what the RP is anyway? Are you talking about intracardiac recordings or the surface P wave? Makes it difficult. Now, I want to talk about different patterns of atrial activation. We've talked about the X-axis, horizontal axis, now we're going to talk about the vertical axis, atrial activation sequence during retrograde conduction. Here is a CT digest of four chambers of the heart. I've peeled off the ventricles here, so now we're dealing with only the aorta, left atrium and kind of orange, and right atrium and periwinkle, light purple. Now with concentric activation, we're coming up the center and activating both atria nearly simultaneously. This has important implications, as we'll talk about. This is an eccentric pattern coming up the left. You see it going from left atrium all the way over to the right atrium. This has important implications as well, and if there's a left eccentric, there's got to be a right eccentric. So it comes up this way, activates the atrium. In this case, from bottom of the right atrium over to the left atrium, but it could occur at the top of the right atrium or the top of the left atrium of the mitral angelus, and conducting downwards to the rest of the atrium. Here's an example of concentric activation, where we have the right atrium, lateral right atrium represented, the lateral left atrium and its conjuncture at the coronary sinus represented, and we have the AVJ atrial activation here. We see this during ventricular pacing. We have one-to-one VA conduction with a constant VA interval here. We have retrograde hisc potentials here, quite visible in the distal hisc recording, the H prime there. And we see these activations in the atrium kind of fanning out from the center of this concentric activation going to right atrium about the same time as it's going to the left atrium. This is an example of eccentric activation. A lot of eccentric things in electrophysiology, as it turns out, but this is eccentric activation. And coming from the left side, we have, again, a retrograde hisc potential, nicely seen here, this sharp deflection right here, before the local ventricular activation. We'll remember that a little bit later. And we have our activation proceeding from the left side towards the midline, and then finally towards the right atrium here, eccentric left-sided activation. Here's an example of eccentric right lateral activation with activation kind of looking like sinus rhythm. It starts in the right atrium, goes past the AVJ, and it goes proximal to distally within the coronary sinus. And again, we have a nice retrograde hisc potential here. Now don't confuse the terms eccentric activation as always being retrograde conduction, because after all, atrial tachycardia is coming from the lateral portions of each atrium can have eccentric activation patterns. Here's an activation of left atrial tachycardia, and the lateral left atrium is first. This looks exactly as it would with retrograde conduction over a slowly conducting pathway, for instance, on the left side. Contrary-wise, we have right atrial tachycardia looking exactly like retrograde activation over a right lateral accessory pathway would look if it had a long conduction time here. So there's that, and there's that. Concentric activation has the AVJ earliest with going up the AV node, typically the fast pathway, or it could be a perceptal accessory pathway. Concentric doesn't mean AV node. Concentric means stuff in the septum is earliest. If the coronary sinus osteo activation is the earliest, it could be coming up the AV node over a slow pathway, or again, a septal accessory pathway. But in either case, simply a concentric activation, depending on which of these sites is most early activated, can either be AV node or septal accessory pathway. And atrial tachycardia, of course, from the right atrium, parahysian, coronary sinus osteos, tricuspid annular, or even the left atrium coming to the right superior pulmonary vein, septal aspect, aortometric continuity, non-coronary sinus or valsalva, can all have a pretty concentric-looking activation pattern. If the earliest activation is on the left, that is from the mid to distal coronary sinus lateral aspect of the cardiac shadow, if those electrodes are the first in the lateral right atrium or high right atrial electrodes are the last recorded, then this is typically a free wall accessory pathway or a left atrial tachycardia with a minor representation of AV nodal fast or slow pathway with one of these far left lateral inputs. Concentric activation on the right side with the right atrium first, coronary sinus going from proximal to distal last, assuming it's in a standard location for recording. This is a right free wall accessory pathway or right atrial tachycardia, not much else we'll do for that. Now, here's a situation in which we're coming along with ventricular pacing, my narrow business, and we have a nice retrograde hyst, we have this activation pattern over here with the AVJ earliest. It's a little bit funny because although the CS electrodes representing left atrium and the high right atrial electrograms follow the AVJ, they don't follow it by the same amount. It's a little bit earlier getting to the AVJ than the high right atrium, and the activation pattern in the CS recording is a little funny here. It's not really fanning out from proximal to distal the way it should. And as we keep pacing, we see something happen here. All of a sudden, the AVJ recording shoots out, and in fact, it's been getting later and later and later. And finally, it goes all out late. And with it goes the lateral right atrium. And we see this very different activation pattern now that CS recordings are fundamentally unchanged from what they were over here. So we've been conducting up a left lateral pathway in both circumstances, both here and here. We were just conducting up an AV nodal pathway here, and it finally fails as we get to this point here. Now, in this case, this is just reiterating what I just said here. With faster pacing or decremental cycling, incremental rate pacing, the AV node typically loses its conduction first and leaves whatever is left behind and accessory pathways to conduct, and that's the usual case. The more recordings you have available to analyze, the easier it is to see changes along the way here. So if we only had coronary sinus recordings, we wouldn't perceive any change because that's the only game in town here. If we only had higher rate atrial recordings, we might say, well, we're just retrograde the winky balking here because the electrogram looks the same, it's timing this later along the way. There are actually blocks, but it has a gradual prolongation of the conduction. And if you only had the AVJ, you'd finally see a change somewhere along the way. This is another change in retrograde activation. This is a young woman who's been blessed with two accessory pathways, one right lateral and one left lateral here. So she's conducting up both pathways here. Finally, the right-sided pathway fails, and now she's conducting up only the left-sided accessory pathway over on the far right there. Both of those were ablated. Now, I want to get to a topic that can be extremely useful in the EP lab, and that is looking for whether retrograde conduction depends on the presence of an antecedent and believable his potential, or whether it seems to be independent of his activation. Here's a case in which we're coming along with a retrograde conduction during retrograde abasing at a premature extra stimulus here, and the VA gets longer. Great, it can do that with any type of conduction. That doesn't help us too terribly much. We have a nice retrograde his here in front of the local V, another retrograde his between the stimulus artifact and the ventricular activation again, and now we don't see that over here because in this situation, it's a premature complex. His Purkinje system says, I don't like that. So it blocks retrogradely, and the right bundle goes across the septum and up to the his bundle this way. Meanwhile, the atrial activation is patiently waiting for the his to be activated so it can go up to the AV node. So this HA interval and this HA interval here are very similar. It might be a little bit longer in this case over here. This is his dependence of atrial activation during retrograde conduction. Contrast that with this case here in which we have, again, retrograde hisses, and again, the his goes so-called out the back after blocking the right bundle transverse transseptal conduction up the left bundle, and finally, the his out the back over here. But this HA interval here is impossibly short. In fact, it's almost actually after some of the CS, about the same time or even after some of the CS recordings have been inscribed. And so how are the atria dependent on the his? They're not. It's a different way to get back to the atrium than the his. His is there. That's great. And the AVJ is after it. But there is some atrial activation that precedes the his or is at an impossibly short HA interval. And so this is evidence of an accessory pathway. Here is another his independent case. It's very clear what's going on here. We have this extraordinarily short HA interval during the drive, and the cats out of the bag here because here are the A's on the extra stimulus, and the poor his is almost after everything has already been inscribed here. The atrial activation has already occurred, and now here comes the his. So this is his independent atrial activation. This is a case of a concealed septal accessory pathway in which we found it extremely helpful to be able to determine whether atrial activation was his dependent or independent. The way to do this is to give a burst of ventricular pacing. Only a few beats is necessary here. Once you start pacing a little bit more consistently for the several beats in a row, 8, 10 beats, this Purkinje system will catch up, and it'll be one-to-one. What we want to do here is get it to come out the back a little bit here and see if atrial activation is dependent on it or not. In this case, it looks like there's an H and an A, But here is an H and an A. And another HISS over here, maybe, hard to know. Here is no HISS. Here's a retrograde A. Here's an H. And we know that these are andrograde HISSes because we have fused QRS complexes here, these two black arrows here. And again, here's a retrograde HISS. And the following A, we don't learn much from that. Here is a HISS out the back because of the prematurity there. And so the HISS-Purkinje system says, I'm going to do what I can do. The atria say, we're doing what we're doing. We're on a different track than the HISS-Purkinje system. And maybe you know it is. So this shows the presence of an accessory pathway. If we've already done some ablation of this pathway, we have more work to do. If we haven't, we have more work to do. Now, so there's our A's there. And the retrograde activation, retrograde conduction is independent of HISS activation. Here is after successful ablation. And now we see the A's here. But every time you see an A, you see a HISS before it at a predictable interval here. It doesn't get paradoxically shorter or longer. So here we have retrograde conduction exclusively up the AV node. The pathway is gone. And we get heave a sigh of relief that at least we didn't get heart block because this is still conducting over here. All right, so second degree VA block, where we, first degree, you just have a long VA interval. That's nothing too special. But second degree is where we don't have one-to-one conduction during incremental rate or decremental cycle in particular pacing. A gradual increase in the VA interval with more rapid pacing followed by VA winky block can occur that occurs much more commonly in the AV node than an accessory pathway. There may be no or minimal increase in the VA interval with increased rate of pacing. And then all of a sudden, it goes to two-to-one block. This is much more characteristic of an accessory pathway than AV nodal conduction. The fast AV nodal pathway can do this on many occasions. But typically, the node will decrement first. Retrograde conduction in response to extra stimuli is slightly different. There will be a gradual increase in the VA or HA interval after extra stimuli when you're dealing mainly with the AV nodal activation as opposed to accessory pathway activation. If you see no or minimal increase in the VA interval or a shorter apparent HA, think accessory pathway. And that's really not an HA interval. Yes, there's an H. Yes, there's an A after it. But they're not intrinsically linked. They're not causally linked. The A is on its own schedule. The HISS is on its own schedule. It's very helpful to have a good HISS recording to determine whether atrial activation is dependent on or independent of the HISS activation. Inference is not very easy in this situation. You have to really work for a good HISS potential. And that's something that simply looks like one but acts like one. Here is a retrograde AV nodal Winkiebach. We know this is in the AV node, that this block is in the AV node because we have retrograde HISSes that are seen all along the way here. They only get better with retrograde conduction and continued pacing. But the AV node says, I'm just about out of here. So we see a HISS. And it gets to the AV node, but not through it to the rest of the atrium. And the cycle restarts via Winkiebach. And there are A's. And there's a block from HISS to A. Here is retrograde 2 to 1 block. And there really isn't any significant change in the VA interval on the normally conducted versus the blocked beats here. Here's an example of retrograde 2 to 1 block without any significant incremental VA interval change. You can see the local VAs are about the same, whether there's 2 to 1 conduction or 1 to 1 conduction. The stem to A is about 153 milliseconds with 1 to 1 VA. And it's about 149, not much different with when we go to 2 to 1 along the way there. This is a patient with orthodromic reentry related to a left posterior accessory pathway. AV nodes can do this. It's more typical of accessory pathways. Here's 2 to 1 block with VA interval increase. And so the stem to A, when 1 to 1 conduction is present, is a little bit long. And it's 193 milliseconds. And when it fails, the stem to A is 159 milliseconds. And either the AV node or the accessory pathway can behave this way. This is AV nodal fast pathway in a patient with AV nodal reentry. Where is the site of block? This can be determined a couple of different ways, a direct way and an inferential way. Here we have several stimuli, three of which definitely capture ventricle. One has no chance. And one might or might not over here. And what we see here is that there is, number one, no VA conduction. The A's along here are perfectly regular. All of these are A's. And they're not only regular, but they have the same activation sequence. We know that this is sinus rhythm over here. It looks like a sinus rhythm as is this over here. So the rest of these in which the activation sequence looks the same are therefore going to be sinus complexes. So these are regular A's for the sinus activation that are slower than the ventricular activation. So we have retrograde block. Where is the block? Well, we look for a couple of things. One is that we see a hiss every single complex. It's pretty gained up. Another one here, another one here, and then there's another one somewhere over here. Oh, I'm going to start over there. 3, 2, 1. This is 3, 2, 1. This is an example of retrograde block. And where is the cytoblock? This can be directly assessed or indirectly assessed, inferentially. So one way to do it is to make sure we have retrograde block. And that is by identifying what we know to be a P wave over here, the sinus P wave. This atrial activation sequence is the same as this, is the same as this, is the same as this, is the same as this sinus complex over here. So all these are sinus complexes. They are same rate. They have same atrial activation complex. Activation sequence are all sinus. So there's no communication between the faster ventricular activation and the slower atrial activation. Second, we look for a hiss potential. Here's an anterograde hiss potential. There's another anterograde hiss potential. Here's another anterograde hiss potential. Here's a retrograde one, and a retrograde one, and another retrograde one here. So if we're correct in assessing that those are retrograde hiss potentials, but we don't have conduction to the atrium, then block must be in the aveno. That's the only thing that is interposed between the hiss-purkinje system and the atrium. You can do better than that. Because what if you don't have a visible hiss? Or you don't even have any atrium recording. So all you have is P waves to look at. If you look at the effect of conduction of partial penetration of the aveno, but not getting through the aveno, that's concealed conduction. So here we have a retrograde hiss that got into the aveno, but not through it. This is not retrogradely conducted. But the AH interval that follows it is longer than our baseline here. So you might get a question like this somewhere along the way from one of your attendings or a colleague. Where's the level of a block? And all you have to do is look at the baseline AH interval. And if you have an AH that's somewhat a P wave that is shown as a longer PR following it, and it was preceded by a ventricular phase complex, that's going to indicate concealed conduction in the aveno. If you look really smart, you say, oh, it's avenodal block. No big deal. So there are retrograde hisses. And there's that long AH interval versus the shorter normal conductive AH interval. Rarely does one see block in the hysperkinesis system. I look for this. I've looked for this for close to 40 years. And I have about a dozen examples of this. I look for this in practically all cases. So it is rare. And if you say the retrograde conduction blocks in the AV node, you're going to be right 99-plus percent of the time, probably 99.9% of the time. But here's an example where that's not correct, where we have retrograde block in the hysperkinesis system. And the clue here is that the AH intervals are always constant. There is no VA conduction. We've got sinus complexes here. But the AH interval is invariant regardless of whether there's a local ventricular activation or not. So in this case, we have regular A's with a sinus activation sequence. And they're slower than the B's. Therefore, we have no retrograde conduction. The cytoblock is indicated by the fact that the hys is seen with every atrial recording. And the AH is constant. There's nothing penetrating the AV node from below to render it partially refractory and conceal into it such that the next AH interval should be prolonged. And in fact, here is the guy's native sinus complex, wide, left on the ranch block. All these people have hysperkinesis disease and easily identified from their sinus rhythm ECG. Long AHV interval. And he has block below his going retrograde. All right. Dual AV nodal pathways. These are very common. They're generally irrelevant. These are retrograde dual pathways. They can cause confusion in trying to assess VA conduction as well as they can cause SVT. But far more often, they cause confusion. Recognition of the presence of retrograde dual pathways relies on being able to discern that there are two different and relatively discrete VA intervals with typically two different atrial activation sequences. And quite commonly, when they switch from going up the fast pathway to going up the slow pathway, it turns around in the AV nodal and comes down the fast pathway. We'll see examples of this. During pacing, the fast pathway is preferentially traversed with a short VA interval with earliest activation in the AVJ recordings. When the fast pathway fails, it jumps to the slower conducting AV nodal slow pathway. And this has a longer VA interval with earliest activation in the proximal coronary sinus. Echoes occur after this shift with block the pathway conduction up the slow and back down the fast pathway with the same QRS as baseline or if it occurs at the same time as a paced complex, it's a fusion event. So here we are coming along with ventricular pacing. We seem to have one-to-one conduction except over here. We're pacing just a little bit faster here. There's our nice retrograde just all the way along here. And so there's that. And all of a sudden we go from a fast pathway to a slow pathway without any change in perceptible change in heart rate. And now the atrial activation sequence is no longer earliest at the AVJ, it's earliest at the proximal coronary sinus, the osteo region. And we go turn around and go down the fast pathway and end up with a fused complex between, fused between ventricular paced and conducted here. Here's an example of a bidirectional right bundle branch block. And we see that there's a right bundle branch block inside of this rhythm, but right bundle branch block retrogradely during ventricular pacing. Here's our so-called out the back. It can't get up the right conduction system here very well, so it traverses a septum that comes out on the other side as they retrograde his potential so-called out the back. The physiology of this is pretty simple and straightforward. Here we've got a situation over here where we're conducting up the right bundle with ventricular, right ventricular pacing. It goes quickly, inscribes that his potential. And finally, the local ventricular activation is observed when we're conducting one to one slowly up the septum. In this case over here, the person has right bundle branch block in both directions and retrograde and retrograde. So when you stimulate from the right ventricle, it goes very slowly up the septum. It goes slowly to this portion of the transeptally up the left bundle, goes up the left bundle, and then the his comes out the back. I'll show that again. So we're rocketing up, making ventricular activation. And finally, we make electrical activation of his Purkinje system coming up the left bundle system here. There is our his out the back. There's our his out the front there. Now, adenosine can also be used to make this discrimination. I'll leave this to most everyone's reading here. It's a lot of adenosine here, 12 and then 24 milligrams. And basically it distinguishes reasonably well between normal avianodal conduction and conduction up an accessory pathway. Here's another application of it. This is the work from the cardiologist, electrophysiologist at Cornell. And their workflow is to give adenosine during ventricular pacing and see where the activation pattern is. Sometimes give some additional adenosine along the way and looking for patterns of eccentric conduction versus concentric conduction and VA intervals as well. Little odds and ends here about retrograde conduction. It may be present when AV conduction is absent. So you might have somebody in whom you put in a pacemaker for complete AV block and yet they have retrograde conduction. A little bit unusual as does occur. Retrograde avianodal or even accessory pathway conduction may be absent in the baseline state, rarely, but present and pretty good after administration of exogenous catecholamines. Retrograde avianodal conduction pattern is typically midline but can be eccentric going up the AV node still, remember the slow pathway can do a lot of different things with early acedral activation in the proximal or even mid coronary sinus in some cases. Demonstration of a concealed left lateral pathway, the presence of good AV conduction may require stimulation on the LV, but it may not. Here is a situation in which we have retrograde conduction with right ventricular pacing and left ventricular pacing in the same patient. And you see, we have this early atrial activation here. It's probably actually the HISS. And then we conduct both concentrically to the atrium. In this case here, we have a HISS right here and we have atrial electrograms that are really messed up and have a non-concentric activation pattern here. And we didn't even see that these guys were early when we were pacing the RV because avianodal conduction got there earliest. When we paced the left ventricle, now we have an advantage with it. And this funny pattern here where the CS is, doesn't really know what it wants to do. It looks just as proximal, but also some proximal just here. So there's that pathway stuff. And it is concentric at this portion, but it's eccentric coming from over here. Perhaps that's what the problem is. So in summary, retrograde conduction is important to understand. It can be present or it can be absent. There are different patterns of atrial activation that imply different things about conduction. Don't forget to look at the surface ECG for P-wave morphology. It can help you a lot. Don't equate retrograde P-waves with inverted P-waves in the inferior leads as they may most likely be conducted. Retrograde conduction block has consistent features. At fixed rate pacing, the AV node is more likely than the Hispokingy system to fail at those cyclings. And with that modality, with premature extra stimuli, the Hispokingy system is more prone to failure than is the AV node, which just kind of slops it up. Pay close attention to differences between drive complexes and extra stimuli when trying to assess retrograde conduction pathways, especially with IVRs. And keep an eye on the Hisp. I'm going to do a redo on this last statement here. Pay close attention to differences between the drive complexes and extra stimuli to assess for the presence or absence of accessory pathways. You may block in one, be able to conduct up the other. And keep an eye on the Hisp as VA conduction dependent on the presence of an antecedent Hisp or not. And beware the retrograde dual AV node pathways. They can show up in all kinds of settings. I have a couple of questions here. This 34-year-old man undergoing a peace study for evaluation of palpitations in the figure shows one of these choices. You can stop your own recording and mull this over. I'm going to continue. This shows that there is no retrograde conduction. And the block is in the AV node as opposed to his Purkinje system. We have concealed conduction. The AH is longer than our basic baseline AH over here. That was not too hard. It's just AV nodal conduction. Now, the sinus activation sequence is quite regular. And OK, 3, 2, 1. The sinus activation sequence is quite consistent. And the atrial rate is quite regular and independent of the ventriculars. And it says that there is no VA conduction. Then we turn to the second part of the question, where it's a block. And the evidence of concealed conduction tells you the side of the block. Here's the second question. Which of these statements concerning retrograde conduction in the above figure is true? It is over the AV node in all four complexes. It's over the AV node in the first two and left lateral accessory pathway in the last two complexes. It's over the AV node in all four complexes plus a left lateral accessory pathway in the last two complexes. Or it's over a left lateral pathway in all four plus the AV node in the first two complexes. And again, you can pause your session, pour over this, and come back when you're ready with your answer. I'm ready with my answer. And it is that it's over a left lateral accessory pathway in all four of these complexes plus the AV node in the first two. Why is this? Well, if you look at these activation sequences, there they are. The first two are the same. And the last two are the same as each other. But what's constant here is the atrial activation sequence in the distal coronary sinus there. They're all the same. And sorry about that. They're all the same, but you see that the AVJ has moved out. So we certainly have an accessory pathway that is just the same in all of these cases here as the AVJ that's moved out in these cases. All right, third question, which of these statements concerning retrograde conduction in the above figure is true? It is exclusively over the AV node in all three complexes, the two and the extrastimulus. It's over the AV node in the first two complexes, left lateral pathway in the last complex. It's over the AV node in all three complexes plus a left lateral accessory pathway in the last complex. Or it's over the AV node in all three complexes plus a right lateral accessory pathway in the first two. OK, you can make your choices. I've made mine. And the correct answer is it is over the AV node in all three complexes plus a right lateral pathway in the first two complexes. Why is this? Well, there's our hiss there. That doesn't help us a ton here, though, because the atrial activation in the hybrid atrium actually precedes these. And it's going top to bottom, right to left. So this is a right lateral accessory pathway in the first two complexes. That finally fails. And we then go up to Hespergenia system with this familiar now red and white pattern here. Thank you very much.
Video Summary
In this video, Dr. John Miller discusses retrograde conduction in electrophysiology. Retrograde conduction refers to the backward propagation of electrical signals from the ventricles to the atria. Dr. Miller explains that retrograde conduction can be present or absent and has important implications for rhythm disturbances. He discusses several learning objectives, including how to determine if retrograde conduction is present or absent and recognizing where the block is occurring in the conduction system. Dr. Miller emphasizes the importance of understanding different patterns of retrograde conduction, such as concentric and eccentric activation, and distinguishing between retrograde AV node conduction and accessory pathway conduction. He also discusses the distinction between hiss-dependent and hiss-independent conduction. Dr. Miller explains that assessing retrograde conduction can be done using tools such as ECG, his bundle recordings, and atrial recordings. He also highlights the importance of knowing where in the conduction system the block occurs and how different conduction structures behave under different conditions. Overall, understanding retrograde conduction is important in electrophysiology practice but is often poorly understood.
Keywords
retrograde conduction
electrophysiology
rhythm disturbances
conduction system
AV node conduction
accessory pathway conduction
ECG
block occurrence
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