All right, so this is a topic that I've been giving it to our fellows and to fellows in other places on several occasions. Usually it's very interactive and attracts interest because during our fellowship teaching we don't give a lot of time to electrogram interpretation in the devices. I think there is a little bit of a gap in the education. I am very fond of the topic and happy to answer any questions as we go along. So, okay now, all right, so I tried to subdivide it into several groups of questions that you can answer when we're interpreting electrograms. So one of the key things is the differentiation between SVT and VT. And we have investigated this in the past. Let me minimize that. We actually did a study on how well fellows do interpreting, differentiating between SVT and VT. This paper was published a couple years ago in a hard-written journal. So this is from this paper. What criteria do we use to differentiate? So if you have a single chamber electrogram, so VEGM, if you only have VEGM, so you can see my mouse, right? Correct, we can see. So if we have single chamber electrograms, we can use local VEGM morphology. We can look at the VV stability at the onset, if it's sudden or not, the response to ATP or shock. And sometimes you can see, this is less well-known, you can see atrial far-field signal on the ventricular channel. And that will tell you something about A and V relationship. If we have dual EGMs, dual chamber electrograms, then you have the same thing, plus you can judge the mechanism of onset. You can see if it was a PAC or PVC. And you can judge the AV dissociation or association. So this table shows this AEGM exposed. How did we do the study? We took 100 device electrograms that were complex. And we, so there were 50 SVT and 50 VT electrograms. And we hid, we covered the atrial channel initially. And we gave it to EP specialists, seasoned attendings. We gave it to fellows. And we gave it to EP nurses. And then we had them interpret and say what it was, and what criteria they used. And after that, we uncovered the atrial channel and gave them same electrograms in a different order and had them reinterpret. And then we, so the results were, so this is an example. So this is a dual chamber device. We have the atrial channel covered. And you just have ventricular, ventricular electrograms, far-field. Actually, this is bipolar. So this is local AGM. And then we have markers. And so let's see if we can sort of interpret that. So does the morphology change? Morphology looks similar. Is the onset sudden? It is sudden. Is it very fast? No. Is the V to V stable? No, it's actually unstable, right? It's a variable V to V. So do we see atrial signal on the V channel? I don't think so. So any suggestions what this may be? Is it SVT or VT? It will probably take some time to unmute people, right? So, well, anyways, let me make it simple because this is a teaching case. So this was actually VT, even though that this is an example that the electrogram morphology can be very, very similar. If you look at the atrial channel on top, you see that there is a AV dissociation. All right. So it's illustrating that atrial electrogram is actually very helpful. Well, here's another example. This is more complex. Again, atrial channel is covered on top. And then at the bottom, I already uncovered that you see that morphology changes, but despite the fact that the morphology changes and the device thinks that this is VF, see this VF? And I'll enlarge it a little bit and we'll go over why the device thinks this is VF. So morphology change, device is thinking this is VF, but when you look at the atrial channel, there is one-to-one AV association. So this was actually SVT illustrating that. And it starts with a PAC, not with a PVC. Let me enlarge it so it's a little easier to see. So this is the same electrogram, just larger. So we can see that when it starts, it starts with a PAC. And the reason for this double counting is actually also interesting. This is something that we'll go over a little bit later. Why is the device double counting here? It's T-wave over-sensing. See, it's seeing the T-waves. Always look, if there is one thing that you will bring back from this lecture is always look at the markers, always look at what the device is thinking. So looking at the markers, this marker corresponds to the T-wave, this marker corresponds to the QRS. The device is double counting. All right, so device thought this was VF, but this is actually SVT as I have demonstrated to you by using those additional criteria from dual chamber electrograms. And this is the end of this episode, how it actually device shocked it. There is a high voltage shock, it terminated it, of course, it would terminate SVT as well. But this is the end of this episode. This is from the same study, we looked how much presence of HL electrograms actually helped. And you can see that as far as diagnostic accuracy for VT, AP attendings did the best with single chamber electrograms. They did significantly better than fellows and EP nurses, so gray hair does matter. And all groups improved when we gave them the information on dual chamber electrograms. This is as far as VT diagnosis. With SVT, all groups were similar, and they improved, they all improved when they were given additional dual HL channel information. So here's another example. This is not from the study, this is something else. And maybe this can be interactive. Nishant, if we can. So this is, oh, I already gave the answer. This is a single chamber actually, sorry, here's my marker. So you have HL channel on top, ventricular sense, so this is bipolar next to it, and then there are markers, A sense, V sense, and then there are numbers at the bottom that help you to differentiate. So on the first glance, it looks like one-to-one tachycardia. Anybody ventures to tell me what it might be? Looking at some other numbers that are given on the screen, any thoughts? Look at the irregularity, look at what is driving what. Who is driving whom? Atrium is driving the ventricle, or ventricle is driving the atrium? You all are able to unmute and talk. You're not unable, all right. So, well, let's see. Michael, they are able to. Oh, they're able to, okay. All right, so. The ventricle is driving the atrium. Ventricle is driving the atrium, exactly. So here is one example, right, longer V to V, and then longer A to A. Here, another one, longer V to V, longer A to A. Here, another one, longer V to V. So you suspect that this is VT, correct? All right, let's see if I. Okay, so this is the same patient's continuation of the same episode. Look here, very clearly, and at the bottom, you have V-A dissociation. So it was VT. So one-to-one AV relationship does not necessarily mean SVT. Always look at who is driving whom, right? And then, so that's continuation of this episode. It took actually several rounds of ATP. So ATP number one, ATP number two, and then finally it breaks it. All right, another VT-SVT case, actually cases, several cases. So this is an episode. Device thinks it's VT-VF. I actually don't remember what it was. Let's see. So again, looking from the top, on the top, there is atrial channel, and you can immediately tell that this is atrial fibrillation, right? Very fast, a lot of atrial activity. At the bottom, you have a regular ventricular signal corresponding to atrial fibrillation. This is ventricular bipolar signal. And then you have markers. There is intermittent undersensing of atrial fibrillation, as expected. And then there are predominantly V-sensed signal at the bottom. This is a St. Jude recording. So you have this morphology markers. The asterisk means that this is 100% morphology match. T, it's a tachycardia. So it's very important to know, at least have some idea about most common markers and designations on those. So they change all the time. So I'm trying to keep myself up to date as far as those markers and designations. Very important. All right, let's see what happens next. So this is a little small, but you can see that all of a sudden, ventricular rate accelerates. It's very, very fast. Cycle length, about 250. Is it actually compatible with rapid atrial fibrillation or is it incompatible with life, so fast it is? And then it goes even faster and then organizes itself very regular, slightly different electrogram. And then eventually it actually breaks, right? It breaks, but then the device delivers a shock. So any idea what that was? Any takers on this one? So let's go over this together. So atrial, we know patient is in atrial fibrillation. Then it's all of a sudden it accelerates to a faster rate. The rate is so fast. I cannot be, this is again, this electrograms come from a lot of places. You don't always know the clinical scenario, but this is so fast that most likely this is ventricular fibrillation. And then it organizes a little bit here. Electrogram looks different. So probably ventricular flutter. And then it breaks. It breaks and here it's interrupted, right? Why does the device shock here? You have three beats that are faster. The device was already reconfirming, getting ready for a shock. You got three more beats, boom, it shocks. And actually not for a good reason. It was during the reconfirmation that it delivered a shock. So, but the teaching point here, interesting point here is that atrial fibrillation can sometimes set a nidus for ventricular fibrillation. We've seen it in some old device trials that patients who were in atrial fibrillation would more frequently go into VF. So here goes into VF and then device shocks and shock actually restores sinus rhythm. AFib was terminated, even though the shock was delivered after VF or flutter stopped. All right. So here's another one. It also calls it for VTVF episode. Let's see if that's true. So you have atrial channel on the top, ventricular bipolar again next to it, and then markers. What is the device thinking? What is the device doing? So first of all, the rhythm is sinus here, right? And then at the bottom you have sinus with PVCs, a couple of beats, and then very fast rhythm starts and then probably slows down a little bit and then continues. And then you have a shock. And what happens with the atrial rhythm? Atrial rhythm actually accelerates here. So this is a shock for ventricular arrhythmia, ventricular fibrillation, or very fast ventricular tachycardia, ventricular tachyarrhythmia. Let's see what happens next. So then it actually restarts again. And here's another shock. It terminates it. What happens next? Another PVC, it restarts. And then continues, continues, continues, another shock, and finally sinus rhythm is restored. So this is an example of kind of relentless VT requiring multiple shocks. VTVF, I would say. All right. Another VTSVT case. So the device calls it high ventricular rate episode. And we can look at the designation of the device. This is actually a pacemaker. So this will not be an ICD. This is a pacemaker. Let's look at the electrograms. This is position one HLSEN signal. Second is leadless ECG. So this is the far field signal that you would like to see. It helps you to differentiate better between VT and SVT. It gives you some semblance to one of the surface leads. And there is the local bipolar signal. And then the markers. Let's go over the markers a little bit because this is important. So asense pace is obvious. What is SIR? SIR is sensor indicated rate. What does it mean? It means that the patient is probably exercising. And the sensor is telling the device what to do, what rate to pace. And that's why here asense, asense, and then the HL pace appears. So the device thinks the patient is exercising and needs more heart rate. Sensor indicated rate. What is VIP? Ventricular intrinsic preference. So this is the feature that promotes intrinsic conduction. So it was working here. But then when APACE takes over, it continues to do that. So VIP is present and SIR is present. Let's go back for a second. So here you have a PVC, a bunch of PVCs. And then this is continuation of the same episode. And then something interesting happens here. You have continuation of HL pacing. Then there is a ventricular paced event. After the ventricular event, probably the intrinsic, the sinus A falls in the refractory. That's why it's blacked out. It's called AR, atrium in the refractory. That A in the refractory is actually ignored for timing purposes. And we'll go over this in more detail a little bit later. And that's why the device paces in the atrium. So this is an example of competitive HL pacing. And it does it again after the second paced beat. And then something interesting happens. So after this HL paced event, you have another V paced event, probably sinus, and then an arrhythmia starts, right? And how does it start? Starts with a PVC or with a PAC? So there is this, this is HL pacing, right? So this is A paced. And then there is another V paced event and another A. So is it possible that this HL paced event, HL pacing stimulus caused this HL arrhythmia, HL tachycardia, rapid HL beat, rapid HL rhythm? And then as a consequence of that, rapid ventricular response. So this is one-to-one tachycardia where we need to decide whether it's ventricular tachycardia or SVT. Morphology, if we compare it to sinus rhythm, morphology looks kind of similar, maybe a little different. It's definitely different from ventricular pacing, right? So ventricular pacing is drastically different. Arrhythmia probably starts with this. So this is HL event that is superimposed on ventricular paced event. So it is likely that this HL pacing stimulus triggered HL tachycardia going fast, conducting one-to-one and resulting in this rapid, rapid rhythm. So my interpretation of this is that this is actually HL tachycardia, supraventricular tachycardia, conducting one-to-one. It's very regular, so it's very hard to tell what is driving what. But the sequence is such that this HL, it starts with a PAC, basically, and not with a PVC. Any questions, any comments about this electrogram? Let's move on. Another SVT-VT case. I think you're already getting tired from this. Maybe we'll skip that. I want to skip that. All right, let's go to this. This is a multiple choice question. So this is to conclude this section on SVT versus VT. So this is a single chamber pacemaker programmed VVI at 70 beats per minute with hysteresis on. So the question starts CPR, defibrillate, place an ICD, program hysteresis off, all of the above. And already, unfortunately, the answer is below. So... Well, you're right. I mean, the answer is already revealed below. So it's all of the above. Well, what happened here? So you have a single chamber device. Hysteresis is on. Hysteresis is a function that allows the device to actually not pace to come in when the rate slows down. So there is, because of that, there is a pause. There is a pause between the sinus or it's probably a child's fibrillation between intrinsic beat and the next V-paced event. And then that causes a PVC and triggers ventricular fibrillation. So do we need to start CPR? Probably. Defibrillate? Probably. Place an ICD? Probably. But most importantly, program hysteresis to off. So that's this question. All right. Let's see. Can I get this? Okay. So the next section, I wanted to spend some time on looking at different forms of HL, the Hicardian HL fibrillation. And just to illustrate this, when you look at multiple device electrograms, you can see that HL fibrillation can look like this. This is very coarse, very rugged, very irregular, very chaotic, multifocal kind of rugged HL fibrillation. It can also look like this, be more organized. And maybe we can look at another feature here. Again, we'll talk about this a little bit later. What is happening here? Why is this, again, in the black, AR, AP, HL in the refractory and then HL-paced event? What is that? What does it mean? Why is it pacing? Why is the device pacing the HL when there was an intrinsic HL event? Because the intrinsic HL event was in PVARP? Yes, it was in the PVARP. So why is it pacing? Why is it pacing? Because it's ignored for timing purposes, right? So what is this? This is an example of what kind of pacing. It's a competition, right? It's competitive HL pacing. So it's competing, and we'll talk about this later. So this is an example of when this was ignored and then AP-paced, and what happened possibly? What could have happened because of this AP-paced event? You went into AFib or HL-tachycardia? Possibly, yes, exactly. So it could have been a trigger for that. So, but this is, I'm primarily showing it here because of the more organized nature of this ATAF. It can also look like this. So this is another example. So this is very organized. Here, you may want to say this is probably HL flutter or more organized HL fibrillation. All right. All right, so let's see. Here is something that frequently happens during HL fibrillation. And you can see that the electrograms are pretty crisp here, and the device is recognizing pretty much all of them. But what is happening at the top? Did arrhythmia start here and finish here, or was AFib going all along and then continued here? You kind of get a sense that AFib is still going on here, even though the device is APacing. So this is an example of just undersensing during HL fibrillation, and that's why the device doesn't see it, doesn't recognize it, and APaces. And this is very common because the amplitude is low and the lead may be in such a location that during HL fibrillation, it records very low amplitude signals and will undersense. However, when you see something like this, oops, let me go back. It's also important to think about noise, right? And that's why the next question is, is it noise or a real thing? Let's look at some examples of that. Very important to look at the device markers, as I already mentioned earlier. So this is a different manufacturer. This is Biotronic, not a very high quality electrogram. I apologize. It was sent to me from somewhere, but let's look at the markers. So markers, there is more markers. This is single channel. So this is, it's a far field. So this is basically your leadless ECG, and this is ventricular local signal. And these look like QRSs, right? But then between QRSs, there is something, and there is more markers indicating that the device is actually seeing that. So, and down at the bottom, you have even more. Is this real thing or is it noise? What do you think? Oh. Well, this is an example of noise, and let's see what happens next. So here, noise actually gets more frequent. There is some kind of a, so this is QRS and this is QRS, and then between them, there are those signals, and the device is seeing them. And then something happens here, and then very, very fast and different arrhythmia appears. Let me enlarge it for you. So this is this event that actually triggered that. And you can see that the device declared ventricular fibrillation there. And then even though I don't know what happened, this was sent to me from somewhere, I see the 73 ohms, so it must have delivered a shock. So the device was seeing noise. Noise eventually triggered a shock, and shock by RNT phenomenon triggered ventricular fibrillation. So this is an example of false detection of VF because of noise triggering real VF. And then this is after the shock. So the shock was actually after multiple shocks. You see a lot of noise. So what happened here? Why is it so much noise after the shock? It is possible that multiple shocks have actually fried the lead. So the lead disintegrated even further. The conductor is not as good, even worse than it was in the beginning. And then you see a lot of electrical noise. And when we look at the counters, you see the device thought that it had seven unsuccessful shocks. So the device was delivering shock after shock because it was seeing more and more noise. And then I looked at the pacing parameters. Amazingly, pacing impedance is pretty normal. High voltage impedance is also pretty normal. R-wave is okay. So that brings another subject. How do the leads actually fail? You see a lot of examples. So there are possibly three different ways. You see patients with high impedance or low impedance. You see patients with noise on the leads, or you can see a combination of those. And in some observations, it looks like the noise may be actually preceding the development of impedance changes. And in this particular case, you see that. So impedance is normal, but patient had noise. So that's indicating that the lead is disintegrating. All right, so here is another example of noise. And here, maybe somebody from the audience can help me with that a little bit. So this is atrial channel up on top, then ventricular sense channel, and then markers. So what kind of noise are we seeing here? And is it noise, first of all? No volunteers? EMI? What's that? EMI? Yes, that's probably. And why do we think about that? Because you see it on both channels, right? So if you saw it in one lead, you're more likely to have something wrong with the lead. If it's on both leads, then the chances that both leads failed simultaneously is probably less. So that's correct. Okay. Here is another example of sort of noise or false detection. And let's see if we can figure it out together. So this is dual chamber electrogram. Again, ATM on top, ventricular next to it, markers, and then whatever the device is thinking. So the device is thinking here, the device is thinking here, ventricular sense. And then there is another marker down below. And the morphology, there is no, X means no morphology match, and definitely no morphology match here. Then here there's a morphology match, and then another marker. And that marker corresponds to the T wave, right? So what is that an example of? This is T wave over sensing. So that's another thing that can be. Can result in inappropriate therapies from the device. And this is the same thing enlarged. So you can see it more clear. All right. All right, so let's, this is a multiple choice question again. So what are we seeing on this 12 lead electrocardiogram? Ventricular capture, pseudo-pseudo fusion, safety pacing, all of the above. Well, you saw my answer unfortunately there, I think. But, all right, we're gonna wait for the poll. Well, the true answer is all of the above, and let's see if we can find them. So ventricular capture, example of ventricular capture. I'll just close that. So example of ventricular capture is this. So ventricular capture is present. What is pseudo-pseudo fusion? This is more esoteric. Anybody remembers? Well, pseudo-pseudo fusion is when HL pacing actually falls on the QRS. And looks like a pseudo fusion, but it's not ventricular signal, which we typically call pseudo fusion. It's HL pacing. So this is an example, right there, one, two, three, four, five, six beat. First spike is not the ventricular spike, it's actually the HL spike, right? Because it's followed by the other little spike. So this is an example of pseudo-pseudo fusion, when HL pacing spike falls on the beginning of the QRS, looks like pseudo fusion, but it's not because it's in the HL. Safety pacing, that's pretty simple here. That's this short timing between two spikes. This is safety pacing. Example of HL undersensing. Well, this is an example of HL undersensing, because there is a P wave, and it still paced the HM, right? And HL failure to capture, right there. So that's an example. All right. All of the above. This is an interesting topic that I already alluded to, and then you don't get a lot of teaching on this during your AP fellowship. It kind of looks esoteric, but it turns out by the analysis of large volumes of electrogram data that this is very, very common. And I will tell you a little later how common it may be. So what is competitive HL pacing, and particularly, a very specific form of it called repetitive non-reentrant ventricular HL synchrony? You can probably look at that, because the slides will be saved later on. So I'm not gonna go in a lot of detail. So you can just go why this occurs. But basically, it's a sequence when after ventricular pacing, a retrograde conduction falls in the refractory. It's not used for timing purposes. Therefore, the device will pace the HM if it's told to do so by, for example, by the sensor, if there is a sensor-indicated rate. Because the HM was already excited retrogradely, so HM is refractory, HL pace will not capture. HL pace event will trigger AV interval. This will be followed by ventricular pace event, and again, will result in retrograde conduction. And the same sequence will continue, and this will cause something very similar to endless loop tachycardia, but it's somewhat different from PMT. And on the, this is an example of how it may look on the 12 lead. And this is, this may be proarrhythmic, as we've already seen, and so this may induce HL fibrillation. So this is an example of that clinical example. And in this particular case, this old algorithm was present, this was since debunked, it's not used anymore, it's AFX, it's HL overdrive pacing, that was believed to suppress HL fibrillation. In reality, it was actually triggering HL fibrillation by promoting competitive HL pacing. So here we have V pace, V pace, and then after V pace to vent, there is retrograde conduction in the refractory, and then HL pacing because of that, and then it triggers HL fibrillation. Actually, I'm sorry, this is not triggering HL fibrillation. This is just triggering the sequence of HL in the refractory and the pacing, and the device thinks that it triggered, that HL fibrillation is present, because the device will count this, all these events, and will think that there are too many HL events in HL. So this is just ongoing AFX with retrograde conduction and with HL pacing. So this is an example of this repetitive non-reentrant ventricular HL synchrony. And as I said, this will cause an appropriate mode switch, because the device will count all these events in the HM, and will think that there are two HL events for one ventricular event, and that will result in mode switch. As you see here, AMS stands for mode switch, and so the device mode switched for, actually, not for a real thing, because this was not AFib. It was just competitive HL pacing. And here's an example of why RNR-VAS and PMT are two sides of the same problem. What happens here, the rate changes a little bit, and the refractory periods change. And when the refractory period gets a little shorter, it gets 254 from 269, retrograde conduction comes out from underneath of the PVARP, and then it is sensed, and then it triggers PMT. So a slight change, and this all happens because of the sensor-indicated rate, slightly faster, patient is probably exercising, so conduction changes, refractory periods change a little bit. And when it becomes a little faster, then PVARP actually shortened because of the exercise, and then the HL-sensed event comes out from underneath the refractory, and then RNR-VAS becomes actually pacemaker-mediated tachycardia. So these two things may occur almost simultaneously and represent two sides of the same problem. Just in one instance, HL retrograde conduction occurs within the PVARP, and with PMT, it's outside of the PVARP. Therefore, if you think about it, curing PMT by lengthening the PVARP may not necessarily solve the problem because you may convert PMT into RNR-VAS in future instances. All right, RNR-VAS consequences. I've already mentioned that it could be prorythmic, and you've seen examples of that. So here's an example of competitive HL pacing, and the type of this pacing is RNR-VAS. You see the typical sequence, V-pace, A-sense in the refractory, A-pace. And this is, again, sensor-indicated rate, so a patient is exercising. And then when the timing is right, the appropriately or inappropriately delivered HL pacing stimulus in the refractory, probably similar to RNT phenomenon, triggers HL fibrillation. Let's see what happens next. So this is the same event enlarged. You can actually see that there's a slight prolongation in this timing. And so slight lengthening of the period between the retrograde conduction and delivered A-paced event, and that became prorythmic enough to trigger this HL fibrillation. Let's see what happens next. So rhythm accelerates, becomes faster. Device is thinking that this is ventricular tachycardia. So you see here tachy-sense, and then it delivers ATP. Doesn't do anything, delivers another ATP. And slowly, so it slows down, and then device thinks that it's done. So this is an example of inappropriate triggering of HL fibrillation by embedded HL pacing, and then subsequent mistaken recognition of ventricular tachycardia, or fibrillation and tachycardia pacing. So this is not a benign phenomenon. It could be very prorythmic and could result in dangerous consequences. All right, so this is a sort of summary of how to prevent or fix competitive HL pacing. Again, I'll leave it, you can look at that later, but not to go into all the detail. But so PVC algorithms can be used, and basically the thing is to try to avoid faster, so pacing at faster rates. So, and whatever intervals are there to adapt them to faster rates. So if there is a rate-adaptive AV delay, turn it on. If there is a rate-adaptive PVAR, turn that on, and use those other algorithms. There are no specific algorithms for RNRVS termination, and there are algorithms for PMT termination. So that also you have to keep in mind. So PMT is probably easier to deal with than RNRVS. Okay, so here are some examples of combination of things. So you can have over-sensing and competitive pacing. So this is an example of both. And again, let's look at the markers. Initially this starts, so first of all, the device thinks that this is ATF detection. This is, if we can turn, I would like to hear what the audience thinks about this one. This is sort of interesting. So it starts as a sinus, then again, sinus sensor-indicated rate. And then you have this interesting combination of markers. So you have V-pace, V-pace, but in between them there are three markers. There is one ASense, another ASense, and then APace. Why are there three markers? What is the device thinking? What is it seeing? So this one is obvious, right? This is retrograde conduction. So there is a big HL spike. What is this marker corresponding to? It corresponds to this little blip there. What is that? Any takers? It's a very rounded signal. So it's just almost at the same time that ventricular pacing occurs. So this is probably a far-field signal there. So this is far-field over-sensing followed by retrograde conduction and then followed by competitive HL pacing. So this can be seen as well. So obviously the device will mode switch for this because it's seeing three events in the HL. All right. All right. Here's another example of some over-sensing. So it starts as HL sensing and by V pacing. And then again, because of the sensor indicated rates of probably patient is exercising, APacing starts. APacing and then this little signal again. What is that? Nobody wants to answer. Yeah. So it's a far-field. It's a far-field signal again. All right. Let's see. Can I ask something here? Sure. Why isn't the far-field detected in the first part of the? Well, it's a good question. The timing changed. See, the timing slightly changed because APacing starts. So, and just literally probably a millisecond of something of conduction changed and then it just, it's detected. The timing changed. So, and then APacing and here is the same thing, right? So it's a far. So with APacing, you have, it is also possible that the amplitude has changed a little bit, right? So, because APacing versus ASense. So, and this is an example of an appropriate detection. Again, device mode switches for that in the appropriate mode switching because of the far-field signal. And HL pacing for the same reason, right? Okay. So here is an example. This is another multiple choice. This is fairly straightforward. So this is a dual chamber device. And so, the device is doing something. On the HL channel, you see the markers, then ventricular markers, and then here are the electrograms. So what do we do? We reprogram upper rate limit. We replace the ventricular lead, replace HL lead, lengthen PVARP, or lengthen AV delay. All right, and everybody got it right. So reprogram upper late limit because this represents, obviously, the upper rate behavior. So that's a Benkei-Bach at the upper rate. Good. Excellent, 100%. All right. Get rid of that. All right, so that's, with the knowledge of this, we can probably get this couple continue their relationship. I don't remember if I have any more slides after this. Yes, so that was it. So that was the conclusion of this talk.

electrogram interpretation

SVT

VT

local electrogram morphology

VV stability

ATP

shock

atrial far-field signal