This is Sam Asravatham, one of the electrophysiologists at Mayo Clinic, going to talk through some cases, AFib, SVT, and some common scenarios. No relevant disclosures for these slides. I'm going to show you an intracardiac tracing. The patient has normal heart, sudden onset, sudden offset palpitation. Based on the tracing, I'd like you to think what's least likely. Is it typically renal re-entry, a right pre-wall accessory pathway, left atrial tachycardia or junctional tachycardia? Coronary sinus is well-seated with the distal CS electrodes on the mitral annulus, so distal CS, proximal CS, his bundle recording catheter, right atrial catheter, right ventricular catheter. So based on this, what's unlikely? Typically VNRT, right pre-wall, left atrial tachycardia, junctional tachycardia. So pretty much the one you're not going to think about in this case is a right pre-wall accessory pathway. So why is this something we have to think? So whenever we see a V and an A together, we have very few conditions to think about. Mainly it's going to be AV node re-entry. Circuit is very close to the compact AV node and nearby atrium, so you're able to simultaneously or near simultaneously get to the A and B. But we have a differential diagnosis, could be junctional tachycardia, although less common, but it's possible with a very similar pattern. And we have to have a knowledge of some maneuvers to make that distinction. Atrial tachycardia is a possibility when A and B are together, but what it is is one A is taking a long time and it so happens the PR interval, the AV interval approximates the rate of the tachycardia, the cycle length of A to A. So it looks like the A and B are together, but it's really this A that goes to the B. But why this is a somewhat mystery case is the distal CS is earlier than the proxen CS. Certainly could be a left atrial tachycardia, but this could also be AV node re-entry or a junctional tachycardia. What it won't be is a right pre-wall early tachycardia, like the right pre-wall accessory pathway ORT, because the right atrial signals are clearly late or significantly later. So how does this happen when you have AV node re-entry and get CS activation that may be unusual mid-CS or distal CS early? For that, we have to think about the atrial part of the circuit of AV node re-entry. We know we go towards the AV node, back out from the AV node, and then you have to complete the circuit. At the very least, that circuit has to jump over this Eustachian ridge and tendon of toddaro. If there is block in these structures, Eustachian ridge, crista terminalis, then those are the patients who need left atrial myocardium to participate in the circuit to complete it. And when you have to get to the left atrium, then from the left atrium, you cannot go anywhere you like into the CS. You may drape down the septum and the proximal CS will be early. But if you go further into the atrium and then use one of the distal CS to LA connections to get into the CS, this will produce an eccentric or eccentric sequence where distal CS is earlier than proximal CS. Note, however, the fast pathway region just behind the tendon of toddaro will still be earlier than the distal CS. It's only when you look at the CS in isolation, it's confusing. It looks like, why is distal CS early? But what you'll notice, if you put a catheter right at the fast pathway region, that will be even earlier than the distal CS. So let's switch chambers here. So I'm going to show you an endocardial RV unipolar voltage map. Patient has syncope, palpitation, who's getting risk stratification, and also possible ablation. I'm going to show you an area of low voltage, and I'd like you to think what's least likely. So voltage here, this purplish is pretty normal voltage, endocardial unipolar map, red is very small voltage, RV endocardial unipolar map. What's least likely, ARVC, sarcoid, epicardial fat, poor tissue contact. Any of these may be possible, but what's least likely? Sarcoidosis is unlikely. So right ventricular cardiomyopathy, we have this fibro fatty kind of change from myocardium, and that's often free wall. You can be out in the outflow tract free wall, can be near the tricuspid annulus. So this pattern of low voltage on the epicardial surface, as suggested by unipolar endocardial map is consistent with, and probably the most important diagnosis to consider, right ventricular cardiomyopathy. But we also know the annulus has fat, and sometimes that fat can be quite prominent when you get towards the outflow tract. And as a result of this fat, you may see a normal, slightly less, usually not this dramatic a difference of the amount of voltage in this area. This is more important consideration when you do an epicardial map, and you may not see small ventricular signals because the fat is separating your catheter from the myocardium. Poor tissue contact is a very important cause, even with unipolar mapping, for free wall having low voltage. Instinctively, we want to avoid perforation of the RV free wall. So often contact is leased on the RV free wall. So all those are important things to consider. But first you would think ARVC, you're going to think, well, could it just be fat? And do I have good contact? Sufficient doubt that you will now do an epicardial map. Sarcoidosis tends to be a disease of the septum. It can be anywhere, including the free wall, but it's prominently in the septum conduction system area, just below the membranous septum, is a common site for sarcoidosis. In the outflow tract, it's also septum, which is the posterior part of the RVOT. Whenever free wall is prominent problems, we think less of sarcoidosis. So this is a question to try and understand localization of catheter position in the sinuses of that cell. So I'll show a figure, patient has tachypalpitation, first based on the signals alone, I want you to try and tell me, ablation catheter position, unlikely to be with right sinus, non-coronary sinus, tricuspid annulus, tricuspid annulus of mid-septal or left mid-septal location, least likely. So ECG leads during tachycardia, misbundled recording catheter, ASV, CS, right atrial, right ventricular, ablation catheter. You can see the relative timing of the ablation catheter to other signals. You can also notice the type of signals, VA, near-field, far-field, spend another few seconds looking at this, and which is least likely, saying, no, that's not it. This is very unlikely to be the right sinus of Valsalva. And the reason is, the right sinus of Valsalva is right underneath the RPOT in the fundopilum. So you'll get a large, near-field-looking ventricular electrogram. And very rare to see any atrial electrogram. And if you do, it will be far-field and it will not be shown. So right sinus, the electrogram itself cannot look like this. And you can exclude that location just based on the electrogram. The left sinus can have B and A. The non-coronary sinus usually has A that's prominent. But when you're deep in the non-coronary sinus, you can pick up the neighboring LV myocardium as a far-field signal as well. So if you see B and A, it could be left sinus or non-coronary sinus. If you see only B, it's usually right sinus. If you see only A, it's usually non-coronary sinus. Now also take a look at fluoroscopy. LAO view, leftward orientation of the catheter. RAO view, posterior, posterior, behind the annulus. Leftward is either left sinus or non-coronary sinus. Posterior is non-coronary sinus. Or it's junction with the left coronary sinus. So right sinus, you'll see it here in the LAO, and it will be way up here, anterior, just underneath the RVOT. And that's why in the right sinus, you will record only ventricular electrograms. This kind of illustrates this figuratively. It's a cartoon description. Notice right sinus under the RVOT. Left sinus also a little under the RVOT, but next to mitral annulus, which means left atrium. Non-coronary sinus, like a finger poking in to the interatrial septum, mostly atrial signals, but when you go deeper in, you can pick up some far-field ventricular signals. Sometimes in heart disease, you'll get this kind of distortion, some preferential chamber enlargements, but still, these relationships are pretty fixed. Non-coronary sinus, finger into the interatrial septum, right sinus underneath the right ventricular output. So we'll switch arrhythmias here, patient with suspected pre-excitation. There's a delta wave, which I'll show you in the surface ECG, and we're going to do differential pacing, pacing from different sites in the atrium, CS, and then right atrium. So ECG leads slurred upstroke. Look at the QRS. Pacing from left atrium, distal CS, right atrium. So this is classic maneuver for fasciculoventricular pathways. So if you have an accessory pathway, A to B connection, it's generally going to be right-sided or left-sided. If you pace close to the right side, right-sided pathways will have more pre-excitation. If you place close to the left side, like the CS, left-sided pathways will have more pre-excitation when compared to right-sided pacing. Septal pathways are either favoring right or left, and while the changes can be less dramatic, you will see some change. In addition to this maneuver for fasciculoventricular pathways, you will do some other things. You pace the A faster and faster till you get AV block, and you see no increase in pre-excitation. Standard pathways, the more you block in the AV node, the more pre-excitation you'll see. This doesn't happen with fasciculoventricular pathways. If you see AV winky block with pacing or administration of adenosine, you will see no difference in the pattern of pre-excitation, even just before or after AV block. Why does this happen? Fasciculoventricular tracts are not really atrioventricular bypass tracts. You still go through the AV node, so whether you pace here or here, you block or you decrement, you reach this tract only after you go through the AV node. It's kind of like a breach in the normal insulation of the proximal bundle branches that you get to the V a little quicker than you normally would by going down here. Because you get there quicker, VR is shorter because you're reaching ventricle earlier than you get to the Purkinje network. You get the slurring of the upstroke because once you reach the hiss, it's not too long before you get to the V, the HV will be short. All things that suggest a pathway that these patients do not get tachycardia, you would put them on a treadmill. If you look at a holter, sleep, daytime, atrial pacing, differential pacing, no difference in the pattern of pre-excitation. Atrial fibrillation situation question. So patient has had wide area circumferential ablation. History of persistent AFib. The circumferential mapping catheter is placed in the right upper pulmonary vein. And the question you often have to ask yourself in a case like pulmonary vein isolation, do we have exit block? Do we have entrance block? Do we have both? Or do I need to do something to get more information? So here's the tracing. ECG, circumferential mapping catheter in the right upper pulmonary vein. Ablation catheter in the left atrium. Coronary sinus catheter. CS1 and 2 are distal, or pacing from the distal CS. So can you tell from this tracing? Exit block, entrance block, both need information. So we need more information. Specifically, we should consider a maneuver with a pacing close to the vein. So here's the reason for the difficulty. If we see an ectopic beat and it doesn't get out to the atrium, we say it's exit block. The problem here that's a little confusing is, well, if there's exit block, there should be entrance block. An entrance block, when you pace the CS, you shouldn't see signals in the pulmonary vein, but you do. Could it be that this would have conducted out, except it would have taken a long time and it just paced and came into the vein too quick, so not sure. Now, there is a way without doing any maneuvers to start reasoning this out. One of them is you notice the signals on the circumferential mapping character in the pulmonary vein are only partial. They're in one sector. And whenever you see in one sector and there's been no ablation inside the pulmonary vein, then look what that sector of electrodes is next to. And it could be signals from that neighboring site. Well, could it be that this patient had had ablation in the pulmonary vein? Very unlikely, because when you got the ectopic, you see living tissue, electrograms throughout the entire circumference of the pulmonary vein myocardium. So this should lead you to the suspicion that maybe these signals are from some neighboring structure. What is this pacing maneuvers principle? So we pace, we see whether we're getting inside the vein, but that same pacing wave front also gets to the right atrium. So if this mapping catheter is close to the SVC or neighboring right atrium, that may be what's picking up those signals. What you can do is pace the right atrium or the SVC and wherever you pace, those signals will come earlier. So now when you pace, instead of seeing these signals of timing like this, if you see those signals pulled in, the ones that you're confused about, these signals, if you saw those pull in when you pace the right atrium or SVC, then you know they are right atrial or SVC origin. So here you can see the mapping catheter, circumferential mapping catheter, RSVV. Catheter and the SVC are in junction just inside the SVC. They're very close together, just anterior. That's why this sector of electrodes might pick up SVC activation. So critical moment, the space from that catheter and you see those signals disappear. They're pulled in and fused with the saturation artifact of the spacing site spike. So the origin of those signals is where you're pacing from. You should try to pace at low output and pace facing in the SVC away from where your lasso catheter is. So you don't get just far field capture of that site. So very important questions that come up in patients where we have pulmonary vein isolation, end points, when we lose all the signals and we see ectopics that clearly have exit blocks spontaneously, it's easy, but when it's confusing, remember the principle. See where those electrodes are facing and consider pacing from that neighboring structure to see if those signals are pulled in. I'll stop there. Thank you very much for your attention.

cardiac arrhythmias

intracardiac tracings

diagnosis

atrial tachycardia

junctional tachycardia

AV node re-entry