This is Sam Asurbadham, electrophysiologist at Mayo Clinic, discussing some cases, variety in electrophysiology. No relevant conflicts with this discussion. So I'm going to show you an ECG. It's a patient who's had some PVCs, runs of VT. And what I'd like you to think about is the most likely, not necessarily the site, but the most likely site of origin of the arrhythmia based on these choices. So here's the ECG. And here are the choices. Is it free wall of the RVOT, tricuspid annulus, posterior LV apex, anterior interventricular vein, or right sinus oval server? So when we think what's most likely here, let's just try to look at some of the features of this arrhythmia. The first thing is you probably notice lead one is negative, completely negative, suggesting left side of the body origin. So left side of the body origin, small R wave and B1. So not entirely right on top of the heart, right below B1, but either slightly leftward or slightly posterior on both. Otherwise it's an outflow morphology, 2,3-AVF positive, AVR, AVL, both are negative. So if we think about the choices that were presented, the one you should immediately exclude is posterior LV apex. That'll be a complete right bundle and it will have a superior axis, nothing like this at all. When we think about all the others, we have free wall of the RVOT, tricuspid annulus and right sinus of the alcella. They're all on the right side of the body. So right side of the body should give you a positive deflection in lead one. So of the possibilities given here, the one that you would map before finally ablating is the region in or near the anterior intraventricular vein. So this is an LAO view showing this complexity of what's right, what's left. So if we think about line right down the middle, so left side of the body, lead one is here. So origin on the mitral annulus laterally, the anterior intraventricular vein region, the very distal right ventricular outflow tract. The LVOT region, but to the left of the body, all could have origin there. But the free wall of the RVOT, the tricuspid annulus, this bundle region will all have a vector towards lead one. V1 being slightly positive is a reflection of either origin that's a little deep in the heart or origin that's towards the left. So this is where we would place V1. So anterior intraventricular vein here, left sinus of valsalva here, mitral annulus here, all of those would give you a vector towards V1. When you're way back here, posterior annulus, LV inflow, you'll have a huge vector towards lead V1 giving a pretty much like a right bundle branch block morphology. Now it's going to be a figure from intracardiac traces. And this time have to think what you can exclude. So several of these are possibilities, but one that you really can be confident in saying that's not what we're dealing with here. So here's the tracing. ECG leads, RV, RA, this bundle region, ablation catheter with large ventricular signal, coronary sinus electrodes. So which of these can you think about excluding? AV node re-entry, junctional tachycardia, spinal tachycardia, or left pre-wall accessory pathway related tachycardia. So this is not going to be a left pre-wall accessory pathway related tachycardia. So main finding here is you have more ventricular electrograms than atrial electrograms. So V and A, V, no A. Now, if we had just this beat to look at, looks pretty much like AV node re-entry. And some patients with AV node re-entry can have blocked to the atrium. Junctional tachycardia will produce a similar pattern and can block to the atrium. So also can origin in the his bundle itself, a his bundle tachycardia. But pre-wall accessory pathways, they're going to, first of all, have a discernible VA interval, 110, 120 milliseconds or more. The early A on those beats will be in the distal coronary sinus, would not be concurrent when you have both V and A. And it's very, very unusual, especially in normal hearts to ever get some dissociation or change in the number of A's or V's in a pathway related tachycardia. So variety of reasons that we can pretty much forget about that and the rest of the case would hinge on do you take this as a AV node re-entry that just happens to have more V than A should we think about junctional tachycardia should we think about a his bundle tachycardia. So sometimes we'll see something like this where the key is look at the beats where there is a V and A, looks an awful lot like AV node re-entry. But sometimes like in this patient, you have an A but no V. This can also happen in AV node re-entry. So his bundle signal, there's an A, but there's no V without a change in the otherwise in the pattern of tachycardia. So AV node re-entry, although usually A and V are present and A and V are very close together in most forms of AV node re-entry, there is no necessity for the ventricle to be the same number of the A tree. In other words, if you took a patient with AV node re-entry and we were to just dissect out the ventricle, you could still get tachycardia because the circuit involves a small portion of A, parts of the AV node, and it's able to sustain that tachycardia. So you can block in some parts of the AV node that's not necessary. You can block in parts of the A that's not necessary. And you can certainly block in the his and the V and still continue tachycardia. So a little change in location here. We're going to think about a figure where I'm marking a yellow arrow. And we're thinking about the least likely association, mitral valve prolapse, ventricular arrhythmia, difficulty with left atrial flutter, especially mitral isthmus-dependent flutter, Epstein anomaly, or abnormalities on cardiac MRI. So here's what we see here, echocardiogram, left atrium, left ventricle arrow. And here are the choices again, least likely association. So this is definitely not Epstein anomaly. So most of you would have recognized the classic picture of mitral annular disjunction. Mitral annulus valve leaflet should be right at that transition point between ventricle and atrium, but it's disjunction. It's getting pasted on back in the atrium. So as a result of this, some patients can get ventricular arrhythmia. Almost by definition, there's mitral valve prolapse and there's actual association with mitral valve prolapse. Cardiac MRI can show fibrosis in the papillary muscles, submitral apparatus, sometimes at faraway sites as well. And if you were trying to draw a line, say from the pulmonary vein to the mitral annulus, if you just reach the valve here and don't ablate in this disjunction area, there may be atrial myocardium still there and you haven't anchored this lesion. Now, Epstein anomaly is an issue with the tricuspid valve. We're looking at the mitral valve here. And the tricuspid valve is displaced towards the ventricles, almost like a mirror image. You can get a left-sided Epstein anomaly like an association with corrective transposition. However, it would still be malposition of the leaflet plus lot of leaflet abnormalities that would be towards the ventricular side. So not going to be Epstein anomaly. Watch out for ventricular arrhythmia in some of these patients. Be prepared for challenges with left atrial flutter ablation and cardiac MRI has become part of the workup for the stratification of these patients. So I'm going to show you an electrocardiogram before and after giving adenosine. Otherwise healthy patient, sudden onset, sudden offset tachypalpitation. So healthy patient, structurally normal heart. This is the presentation ECG. And this is after giving adenosine. Now an additional maneuver is done where ventricular extra stimuli are placed. And this observation is made. No change in the atrial activation sequence and putting in the extra stimulus. So we have tachycardia, white complex tachycardia, termination with adenosine, ventricular extra stimulation testing. And what I'd like, what I'll also tell you is at EP study, once this was observed pretty reliably that you put in an extra stim and you got this observation, which is most likely? Retrograde conduction. Is AV node dependent or is it pathway dependent? Is it fused? No retrograde conduction. Or is it, we really need parathysian pacing. That's the way to tell whether retrograde conduction is AV node or pathway. Key observation. Many of you would have recognized that retrograde conduction is through an accessory pathway. The way that you would recognize that is you see that this bundle electrogram is now clearly visible, not so visible with the drive train, but with the extra stim. And you know this phenomenon, retrograde right bundle branch block. So conduction goes across the septum, left bundle and to the his, giving this sudden jump out of the his signal. But even though the his signal jumps out, the atrial signals with the same activation sequence stay linked with the V. What that tells you is the way you're getting from V to A is not through the AV node. As if it was, it would come after the his. So it's an accessory pathway. Activation sequence is exactly the same. That means there's no fusion. It's only accessory pathway retrograde. So remember extra stimulation testing, we so often see retrograde right bundle branch block. And the simple interpretation may give you information very similar to what we get with parathysian pacing. Just to contrast with parathysian, we're always pacing near the his at high output where we capture his and ventricle, narrow complex, or just ventricular myocardium at lower output. When you capture just the ventricle, you'll often see a retrograde his, especially if you're using a dedicated catheter. But the telltale observation is your stim to A and activation sequence stayed the same whether you captured the his or not. So it's a way of saying, doesn't care about the his. It only cares about ventricular myocardium to get back up to the atrium. That's an accessory pathway. Only cares about the V, does not care about the his. Capture the his, don't capture the his, doesn't make any difference. Similarly, when we look at this maneuver, his pulled in, pulled out, retrograde right bundle pushing it out. A is the same, doesn't care about the his. It's all accessory pathway. So remember parathysian pacing, very useful maneuver to define the mechanism of retrograde conduction. You have to observe whether the activation sequence changes. If it does, there's fusion. There's both a V node and a pathway or more than one pathway. If it doesn't change at all, but the V-A, so the activation sequence doesn't change, but in addition, the V-A interval is also unchanged. That's an accessory pathway. The key things in this that we have to keep in mind is when there is a change in sequence, that's when we should suspect there is fusion. And why is that important? Is because if there's fusion, you don't want to map at that particular drive train pacing rate because you won't be sure whether you're mapping the atrial activation as a result of the pathway or going up through the AV node. So you may need to change your pacing rate or map during tachycardia, orthodontic reciprocating tachycardia. On the same patient, tachycardia was induced and each time tachycardia was induced, each time, a hispinal electrogram could not be seen or would be dissociated from tachycardia. PACs were placed from the distal CS. And I'm going to show you those tracings. And we want to know when you combine the previous phenomenon that you now recognized as induction of retrograde right frontal branch block, what is the most likely diagnosis? So putting it all together. So here's tachycardia in the lab and here's putting in a PAC from the distal CS. So distal CS, PAC, distal CS, PAC, even before it reaches the septum, is bringing in the next B without a change in the QRS morphology. So PAC from distal CS pre-excites and resets the tachycardia without changing the QRS and without affecting the septal atrial activation. So we have one phenomenon here. Couple it with what you learned from the previous tracing and question. And what is your diagnosis? Pathway to pathway tachycardia. Antigrade pathway giving the white QRS, retrograde pathway completing the circuit. AV node re-entry with a bystander pathway. Antidromic tachycardia, antigrade accessory pathway participating in the tachycardia but the retrograde limb is AV node. VT, or none of these. Two phenomena, one we've discussed. The second, PAC, distal CS, brings in the V, no change in QRS, resets the tachycardia. The PAC is delivered at a time where the septal A is not advanced. I think most of you would have got this when you think it through. This is a pathway to pathway tachycardia. So how do we know this? We know it first because we already demonstrated with retrograde right from the bench block. Retrograde is a pattern. And the same sequence we're seeing in tachycardia. Plus antigrade, a PAC advanced the V without changing the QRS, no fusion. So it's only one way to go from A to B during this tachycardia. And then you're able to reset the tachycardia. So antigrade is a pathway, retrograde is a pathway. PAC is able to reset the tachycardia without any fusion. Another key point is something that I mentioned while reading this out, is that the PAC was delivered at a time where it doesn't pull in the septal A. So it doesn't even reach the AV node. So if it cannot reach the AV node and still brings in the V, has to be a pathway. So all components are important. The QRS morphology, is it pulled in? Is it pulled in without pulling in the septal A? Does it reset? Does it change the next or subsequent beats of tachycardia? Sometimes if you put in the PAC early enough, you will terminate the tachycardia. The same thing, you terminate the tachycardia without reaching the septal A. So you never got to the AV node and yet it terminated. Why would you affect a tachycardia without reaching the AV node? Because you're blocking in the pathway. You're blocking the pathway, another way of saying pathway is necessary for this tachycardia. So one way to think about a wide complex tachycardia SVTs, here I'm using the example. Of AV node, pathway is on the right free wall and illustrates the concept of placing PACs. Place the PACs where you suspect the pathway may be. So if it's the right free wall pathway, place the PACs in the right atrium free wall. If you suspect the left free wall pathway, right bundle morphology, distal CS is early V. Then place the PAC from the left atrium free wall or the distal coronary sinus. When you place the PAC, watch for a few things. Does that PAC bring in the next V? Does it do it even without bringing the septal atrial electrogram? Does not reach the septum, but still gets to the ventricle? That has to be pathway. And does it reset the tachycardia? Then you have proven there is a pathway and the pathway participates in the tachycardia. How do we know there isn't another pathway or simultaneously another arrhythmia? Two main things, is there fusion? If no fusion, there's only one way you're going from A to B, the QRS looks the same. How do we know it's not a bystander? Because you not only pre-excite the V without getting to the AV node, but you are able to reset the tachycardia, perturb the subsequent beats, make it later, earlier, every time that you put in this PAC.

Dr. Sam Asirbadham

electrophysiologist

Mayo Clinic

arrhythmia

adenosine

diagnosing