Transcript for:
Understanding Pacemaker Timing Cycles

Okay, so I'll just introduce myself. I don't need that fancy introduction. My name is AJ Hale. I am a certified cardiac device specialist.

And today we'll be talking about pacemaker timing cycles. You know, obviously, we're going to be going over actual EGM and real life examples. And if you have any questions as we go, feel free to raise your hand.

We'll be monitoring the chat. Reach out, use a Q&A, however you'd like to. We can also give you permission to talk.

We'd love to hear from you. This doesn't have to be, you know, a one-sided thing. And we'd rather we can communicate and figure out a way to grow and move forward.

So to start off with here, I'm going to go ahead and do a pop quiz for the folks in attendance here. So pop quiz. Question one, what is happening in this EGM? So what are you observing here in this EGM?

That'll be question one. Question two has the same. exact questions as well. So I'll show you that once you've had time to review this slide. What do you think is occurring here?

Jared, are you seeing the pop quiz on your side? Yeah, I'm seeing the pop quiz now. I've got the EGM with the questions on the left, answers on the left, sorry. Perfect.

And then something pops up where you can actually vote on it, correct? Yeah, it did pop up, but it's disappeared for me. So I'm not sure if the other colleagues have got that.

Huh. Okay. Let me restart that one more time. Okay. Well, tell you what, it's not going to work.

So let's go ahead and take a look at this first EGM here. We're still a work in progress with our pop quizzes. Jared, do you want to take a shot at what's occurring here? or anyone in the chat want to chime in okay well plain and simple we just have uh is just pacemaker wikibox so um looking at this you're wondering why we're having these random dropped events why you know you're not having the steady ventricular rate why you have the steady atrial rate but you're not tracking it this is just normal device activity based upon the programming that it has What is occurring is the device has the max track rate or the fastest rate with which the device will track what's happening in the atrium.

The atrial rate is exceeding that max track rate. And what the device will do is it will continue to pace at the max track at this nice steady rhythm. And the behavior that manifests is an extended AV delay every single time until eventually the atrial event falls into the atrial refractory period, the PVARP right here. This causes the device to not actually track the atrial event, but it does count it towards mode switches, which is why you see this little tick mark. And then obviously there's no corresponding ventricular tracked event.

The next atrial event falls outside of the atrial refractory. So the device tracks it with a normal AV delay. And this process continues on again. Once the atrial rate actually drops below the max track rate, you will see one-to-one atrial synchrony. But when you start having these upper rate behaviors, as they're called, you'll end up having something called pacemaker WinkyBock.

This acts exactly like you'd see the avinodal WinkyBock or at least a surrogate of that. Any thoughts on that, Jared, at all? No, no, that's perfect, mate. That's really good. Yeah.

So I thought this is a good example and kind of leads into what we're seeing next. How about this next one here? What are we seeing that's occurring? Anybody want to take a crack at it?

We do have a chat. You can post your answers in the chat. All right.

So if we're simply going to diagnose what's occurring, if you look here, this is your ventricular channel. Channel three is your V sense amp. Typically, I would have a far field and not a leadless ECG.

If you've ever worked with me in the field, I absolutely despise leadless ECG. I think that it confuses and convolutes things. And I like to use a unipolar tip vector instead for my EGM. However, you can see here the ventricular activity, a nice steady ventricular rhythm.

You see bivy pacing occurring with no evoked response on the Sensam channel. This indicates to me that this is loss of. a ventricular capture.

So not ideal. And I would recommend probably increasing your outputs considering this is a bivy and neither seem to be programming. Before we do any immediate troubleshooting, it would be increasing the outputs and seeing what kind of thresholds we have. You may need a chest x-ray. There may be a number of different factors to look into this, but for whatever reason, you're not able to capture it all in the ventricle.

Do you have any thoughts on that, Jared? No, I totally agree. And I think there's also clearly an issue going on with the atrial lead as well.

We've got loss of atrial capture as well. Yep, dead on. Yep.

So, and again, as what AJ was saying about the leadless ECG, I agree. The first thing I do is turn it off. It can be misleading.

And even just as simple as if you were to have an ECG, have it at the top and then maybe your atrial and ventricular EGMs next to each other. So it's a little bit easier to track one-to-one. So you can kind of walk through and see, is there a... a v to every a and just try and get a pattern here but um but yeah you can see that on the atrial channel you get those big spikes that's just probably the sinus rate coming through and then uh and then you try to see the pacemaker trying to pace but it's not capturing most likely because the atrium's in refractory from the previous sinus piece um so yeah that's so we've got both loss of atrial and ventricular capture there yeah I completely agree with you.

And I would say, you know, Atrium's probably had a refractory for a few of these and it's not capturing at all. So there's definitely something going on. So, yeah, as Jared said, I would get rid of this. And then what I like to do is I actually like to move my marker channel here in between and then my ventricular channel here.

So then the tick mark in the A points to the A, the tick mark in the V points to the V. And then I'll have a unipolar EGM here. that shows me the evoked response across the myocardium. Remember that your sense amps, these right here, are going to be a near field, like an unfiltered bipolar, and it's great to see what the device is seeing with the sense amp, but for actual diagnosis of what's going on it's not ideal.

You really can't tell the difference between a PVC and an intrinsic event using a sense amp channel, not well at least. So yeah, all right, so we'll go ahead and jump right into it then. So we're going to be talking about timing cycles.

So just to go over the basic timing cycles, we're going to see here you have refractory periods, which is where the device can see the signals, but it does not respond to them. This would be your PVARP. This would be your VREF. You have blanking periods. This is where the device completely has its eyes shut.

It's not paying attention to what's happening at all. This would be your PVAB, postventricular atrial blanking. And... the ventricular blanking or V blanking period. And then finally alert period and that is the time when the device has its eyes completely open to respond to any kind of intrinsic activity or any kind of activity that can occur not just intrinsic unfortunately.

So we'll jump straight into atrial timing cycles. The first one, the one you're going to see a lot is paced AV delay, sensed AV delay, so it's your AV delays. I just went ahead and visualized it here on an Abbott programmer and a Medtronic programmer. but this is the most common one you're going to be programming.

So AB delay is in a patient who requires V pacing. So AB delay, basically it occurs, the AB delay, it occurs after an atrial event, either paced or sensed, and it allows time for diastolic filling and then also allows time for intrinsic conduction to occur. As we've talked about in the past, We're trying our best to avoid pacing-induced cardiomyopathy, so ventricular pacing. So in these instances, proper AV delay programming is ideal. So here we'll just see we have a sensed atrial event.

It kicks off what's called your sensed AV delay, which generally is a little bit shorter than your paced AV delay. The reason being that by the time you start to sense an atrial event, you probably have some degree. of the atrial vent already having occurred because you don't sense it right when it initiates depending where in the atrium the lead is placed.

So you have a slight delay. So you tend to have your sensed AV delay just a little bit shorter than your paced AV delay. So if we're looking here at an EKG, this is not an EGM. You see a P wave. It initiates the sensed AV delay clock.

This clock times out your ventricular pace. Same thing occurs here, occurs here, occurs here. We're just tracking what's happening in the atrium. Finally, it waits.

for the intrinsic atrial event to occur nothing occurs so then it initiates a atrial pace this initiates the paced AV delay which like I said is just a little bit longer it's waiting for the intrinsic ventricular event to occur it does not so it ventricular paces it waits again nothing occurs atrial paces sets the paced AV delay nothing occurs if ventricular paces remember that your pacemaker is just a bunch of different clocks that all start and stop at different times. But so whenever you say atrial apace, you're starting the clock waiting to see when the next atrial event occurs. You're also starting the clock waiting to see when the ventricular event occurs.

So just keep in mind that we're just taking into account one more clock. Okay, so patients who have intrinsic conduction. it allows for those R waves to come across.

So we're here looking at this surface EKG. You have your atrial paced event, your paced AV delay, nothing occurs, ventricular pace. You have your sensed atrial events, starts the sensed AV delay, nothing occurs, so ventricular paces.

Here we have a sensed atrial event. There is an occurrence of an intrinsic ventricular event, and you can tell. by the morphology you can tell because there's no pacer spike. This will go ahead and withhold the ventricular pace that might have occurred right around here and it allows for intrinsic ventricular activity to occur.

The timer continues, no atrial event occurs, so you have an atrial pace, ventricular pace. Common sense, but I think it's good to go through it with a little bit of imaging here. Do you have anything to add on that? No, the only thing I was going to say is that you do see it a lot is they're the tricky ones, those ones there where you've got a patient that is pacing in the ventricle quite often, but also has good intrinsic rhythm conduction and trying to program the AV delay because we obviously, we always want to minimize ventricular pacing where possible.

So there's a big habit that a lot of people extend the AV delays out to like 300 milliseconds, which in theory is very long first degree heart block. but then when they do get into half-lock, they're now pacing at a very long AV delay. And that can cause things like cannon waves, et cetera. So we've just got to be careful about programming AV delays.

There are fancy kind of programming methods around that with things like AAI and DDD. So if you can use those kind of features in the device and do so, it means that you can always program kind of, I say, normal AV delays, something like paste 180, sense 150, something like that. without having to extend those AV delays out to 300 to minimize ventricular paces.

That's dead on. And as you were saying, AI, those would be your VIP and your MVP algorithms. So MVP is Medtronic, VIP is Abbott. And what these are meant to do is they're a dynamic algorithm that will extend the AV delay when the patient is conducting.

And then when the patient is not conducting, it shortens the AV delay up to be more hemodynamic. So you still get your atrial kick, you still get the benefit of your atrial activity, but then when they do conduct, it does extend it out to allow the intrinsic conduction. And I've never gotten a straight answer from a physician on which is better.

If it's better to have a 450 millisecond AV delay with conduction or better to have a tighter paced event. I've heard both answers, but a lot of people say that. obviously you want to avoid the v pacing because pacemaker induced cardiomyopathy is no fun okay so that brings us on to pvar so um we've talked about this before but we're going to go over the actual pvar or postventricular atrial refractory um uh programming here so the postventricular atrial refractory period essentially is a time where the device it will not respond to a retrograde atrial activity.

So you might have heard of pacemaker-mediated tachycardia, PMT. PMT occurs when you have a ventricular apace. The atrium is out of refractory period. The ventricular event runs retrograde to the atrium, and then that is sensed by the device, causing it to then V-pace. So you see here on this EKG, we have an apace-V-pace, apace-V-pace.

We have a PVC that occurs, and then we have a, looks like a P wave right here buried in that PVC. The device sees this P wave. thinks that it's a true atrial event when in reality it just ran retrograde up the AV node.

The device then tracks that atrial event, ventricular paces, you have your retrograde event, the device sees it again, ventricular paces. And this is basically creating an endless loop tachycardia, but it's device mediated. And the only way to really break this up is certain algorithms or proper programming of PVARF.

So I would see this a lot of times when I worked in rural settings where patients were not properly programmed and their PVARP was too short, especially the rate responsive PVARP. And patients would have a retrograde conduction of, say, 375 milliseconds and PVARP is set to 325 milliseconds. Well, it's not going to do you any good then.

The device still has its eyes open. And as a result, it tracks those events. So we're looking at... Actually, I don't know if I have an EGM of PVARP.

We'll go over that a little bit more in detail, though, later in the presentation. Do you have anything to add on that for me, Jerry? No, I was just going to say with PVARP and PMT, more importantly, PMT, to have a PMT, you need to have usually two things, and one of them is a retrograde conduction.

So if your patients don't have retrograde conduction, then you're not going to have a PMT because you need that retrograde beat. to go back up to the atrium to initiate it. So if they don't have retrograde conduction and you see these tachycardias, then the chances are it's actually an atrial tachycardia, maybe a slow atrial tachycardia conducting at the upper tracking rate. And usually you see PMTs in patients with complete heart block who don't have good AV conduction because usually it's a paste-mediated tachycardia.

It's not an A sense, V sense. Usually they're the two things that you see. You need to have retrograde conduction and you need to have either usually half block or some kind of sluggish AV conduction.

And then another thing to mention here is that a lot of times when you read the manuals, they'll say that PMT occurs at the max track rate. That can be true, but PMT is actually a function of your sensed AV delay timing. and your retrograde conduction timing added together. So if you have very long retrograde conduction and you have a very long sensed AV delay, you can have PMT below the max track rate. And that may actually come up in the IBHRE for those who take that test.

So don't just assume because we're seeing what looks like PMT, but it's only occurring at say 100 beats a minute instead of 120, which is the program max track rate, that it's not PMT. It very well could be if they have long retrograde and you've programmed long sense day V delays. Yeah, that's a really good point.

Okay, so we have PVAB. So that brings us on to the next. This is your postventricular atrial blanking. Remember, blanking means the device has its eyes completely closed.

So PVAB is meant to avoid what's called far field R waves. And this is actually the device sensing the ventricular event. on the atrial channel.

This isn't a retrograde. This is actually like an antenna picking up interference from what's occurring down below in the ventricle. So what can happen here is the device will double count these atrial events, and this can lead to a lot of mode switches for no reason at all. It's not really necessarily as detrimental as other forms of oversensing.

But it's definitely something to be aware of. And it's why you want to program your PVAB out longer. And we'll go through an actual example of where it could be complicated later.

But just remember that the far-field R waves that are occurring, they're over-sensed ventricular events. It's not actually a true event that's happening in the atrium. And you can see here on this example, you have your atrial sensed event. You have your ventricular pace. It obviously depolarizes the ventricle.

And then you see this little atrial spike here occurring in line with the ventricular depolarization. This is your far R occurring. Okay, so this is actually a little confusing because PVAB and PVARP technically start at the same time. So this is just a way to kind of visualize when it's going. But PVAB is usually shorter than PVARP.

PVAB is shorter than PVARP. So your PVAB will occur as soon as you have your ventricular pace. Same thing as PVARP.

Those clocks are started at the same time. Your PVAB extends out and then. will terminate, I don't know what, 80 milliseconds or so after, depending on how it's programmed, 80 to 150, something like that.

And then your PVARP extends out to try to avoid double counting any kind of retrograde events that occur. So these are just these two visualized right next to each other. Just remember that PVAB means the device is completely blind to anything occurring in the atrium at this time.

And then PVARP... Its eyes are open, but it's not going to track in DDD mode. And this just keeps it from entering into a pacemaker-mediated tachycardia. Any thoughts on that? No, mate, that's good.

I actually, my implant yesterday, I did an implant yesterday, as I mentioned, that we actually had far-filled R waves on the atrial channel. And just with the right programming, and if you've got, by changing the sensitivity, we can program around it. It's just very, for those implanters out there, just be careful when you are implanting your RA lead that you're not putting those bipole electrodes too close to that mitral tricuspid valve because that's when you can pick up those far-field R waves. So it's just, you know, if you can keep that RA lead a little bit higher where possible, then you can usually limit the amount of these over-sensing on that atrial channel. I appreciate that.

Yeah, so placement is definitely key. And it's also something to be aware of people who are programming. If you see where the lead is being placed, take into account that it may cause trouble when you hook up to the programmer.

So be ready to see that. All right. So scenario one, things to consider while we're looking at this EGM. What rhythm is the patient in?

What is the device? Why did the device mode switch? What issue is occurring?

Why are there AR events on the marker channel? And then what programming solutions can address this issue? So I'll show you this EGM here and give you a little bit of time to reflect on it. I think this is your first time seeing it, Jared, so I won't quiz you too hard on it.

No, that's cool. I like it. So here is slide one. Here is slide two. All right.

So let's go ahead and jump into it here. So what rhythm is the patient in? Sinus bradycardia with ventricular pacing. What is the device? It's a pacemaker.

And then why did the device mode switch? So it's far field oversensing of the ventricular paced events on the atrial channel. And then the patient's intrinsic atrial activity.

So if we take a look here at these EGMs again. You can see here that we have a V-pace. Corresponding with this V-pace, you have this little atrial event here, and it looks like this is a steady atrial rhythm. But when you actually march things out, these are occurring just in line with the ventricular event.

And then you have this totally different morphology here, much higher amplitude events here that are occurring very steadily right here. So what you're seeing here, these AR events, are the true atrial intrinsic activity. These right here, this is your far R. Why this is obviously an issue is because this device here is thinking that this is the intrinsic atrial activity and it's trying to follow along with what's going on here. In these cases, this is when you need to extend your PVAB out.

And we'll go back to the answer question or the answer piece. I just want to show you this some more. Once again, AR, this is your true atrial activity. This is your far R.

occurring in line with every ventricular pace. You see here, this is not, these true intrinsic are not affected by the, um, these false atrial events here. It's just this nice, steady sinus bradycardia.

Then eventually when the device has enough of these competing events, these, um, far are, and then the true atrial activity, obviously the AR, A in refractory means it's counting towards mode switch because it's still within P-VARP. it will go into auto mode switch. When it auto mode switches, it breaks the cycle where it's trying to track its actual own activity in the ventricle and then you end up with this v-paste here.

So once again we're no longer tracking, we're in a non-tracking mode. You have your intrinsic activity. You can clearly see here now the far r rhythm has completely slowed to match the ventricular.

That's a dead indicator that this is far R. Obviously, this is an EGM. It's much easier to see live because then you can modulate the rate. And if you see these atrial events continue to occur based on your ventricular rate one-to-one, this indicates that it is far R.

So what can you do to address this issue? You can lengthen PVAB to cover the far R. You can also... uh decrease the sensitivity of the atrial channel but things to be aware of when you decrease that sensitivity um you know you're raising that little threshold here if you raise it too high you may block out the intrinsic atrial events and then you are effectively no longer seeing what's happening in the atrium the device is no longer able to track any anything to add on that one jared no man that's really nice really nice example you may look at that EGM and think that the patient has programmed very long from that ascents to the next V pace it looks very long it's 340 milliseconds so you could be mistaken that perhaps this patient has programmed long AV delays but what we're seeing here is a bit like before with that winky back phenomenon is that we see the pacemaker the ventricular rate is just pacing at the upper tracking rate of Probably 120 beats per minute. It's about just under 500 milliseconds there.

So, yeah, that's why we're seeing these long AV delays because the ventricle will not track the atrium only up until a rate of 120. So it's probably got very normal AV delays, but it may come across like they're very long, but it's just the device at the upper tracking rate. If that atrial rate seemed to go... Sorry, Matt. I was just going to say if that atrial rate got quicker, you would then see that winky back situation that we saw before.

Dead on. Yeah, exactly. But because it's actually modulated by the ventricular pace, it's never going to exceed that that rate there because it's going to go as fast as a ventricular rate. And then one thing I think that was really nice you pointed out is at the max track rate, it is 120 at the max track rate of 120 here that, you know, you may immediately cue in your head. Oh, is this PMT?

Well, the reason you know it's not PMT is because of these other true atrial events coming through. So if this was PMT, you would not see these at all. And if there was any kind of intrinsic atrial activity like PACs and stuff, they would be affected by the retrograde.

Remember that we're looking, you know, with retrograde conduction, we have the human heart here. And with retrograde, it's running from the ventricular pace up into the atrium. Right.

So it would affect the. atrial rate if these were PACs. But because these are nice and stable here in rhythm, this indicates that this is just intrinsic activity.

And these events here are not actually occurring in the atrium at all. They're just a ventricular event that's being over sensed by the atrial lead. It's seeing what's going on and just interpreting it as a true atrial activity. All right. So things to consider for this next one.

What rhythm is a patient in? What device type is used? What's occurring in the strip?

Why did the device mode switch? And how do we address this issue? All right, let's take a look at this one. So right off the bat, we see ventricular pacing. We see atrial sensing.

This tick mark right here on an Abbott device means that it's an atrial refractory in Abbott high voltage devices. So if you ever see just a tick mark with no AR, that means that it's a high voltage device. If this was a pacemaker, it would say AR. So just to clarify that right here.

So we have a V pace, we have an atrial sensed event, and we have another atrial sensed event that falls within the refractory period. Your EGM channels, your discriminator channel is going to be a far field channel. So this is going to be similar to like a unipolar tip, but this is actually a coil to can vector. And then Your other channels are an atrial sense amp and a ventricular sense amp.

Really quick, I guess, Jared, you want to take a shot at what's occurring? I won't put you on the spot if not. No, no, it's cool. Have a go.

So we've got ventricular pacing and, again, a bit like a similar scenario. We probably have some form of either VA conduction or some far-field R-wave over sensing on the atrial channel. And that's allowing the device to see that AS coming in. So we obviously have some very short PBAPs going on here.

And then the marker after the AS on the atrial channel is then the bigger of the spikes on that atrial channel is probably just the sinus rate coming through. But that is falling probably in a kind of atrial refractory period and it's not being conducted. So I think and I think that's a fair judgment.

So this one I'm cheating because I actually know the answer to this. This is actually your retrograde because it's an EGM. It's hard to tell.

um because you really can't modulate the rate if you're in person you could say okay increase the rate to 90 beats a minute and if these both stay pretty similar uh then that indicates that it is ventricular driven if you start seeing a disassociation between the a's and v's this would indicate that this is a true sinus but because this is being driven by um by the ventricular events these are actually going to be your far R, and this is going to be your retrograde. So going through it, what's the dual chamber ICD? We know that because the unlabeled tick mark indicates that it's an ICD.

I knew it was a dual chamber because we have a V-pace. If it was a CRT, you would say BP. Could it be a CRT programmed RV only?

Sure. But for now, it's functioning as a dual chamber ICD. What's occurring there is far R wave oversensing.

and retrograde conduction. So we got both of them here. Why did a mode switch? So it's counting both of them towards the mode switch.

When you're double counting two atrial events, eventually it's probably going to lead to a mode switch depending what your mode switch rate is programmed to. What's the issue? Your PVAB is too short and that's causing the device to double count the atrial events. So PVAB will need to be extended to blank out the oversensed events or... you could technically make the atrial sensing less sensitive and try to miss this PVAB or miss this this far-R.

So once again here we're seeing an RV pace, we're seeing the ventricular event on the atrial channel with your far-R, and then we're actually seeing the retrograde event run backwards through the AV node into the atrium, depolarizing the atrium here. Yeah, that's a good point. And with that one as well, if we were to just only deal with the first little spike by, say, increasing the ventricular blanking or the sensitivity, then the device would then pick up the bigger atrial signal as an AS. So then because we still haven't really dealt with the retrograde conduction part, so we'd probably also have to extend the PVARP to blank out that second component. I suspect that would happen.

So if we dealt with the first component, then the second component. our age or signal will become an issue. And that's when we could end up with maybe PMT.

So we'd have to also extend that PVARP to deal with the second component. That's dead on. So yeah, right now we're in mode switch, so we're safe here. But as he's saying, when we leave mode switch, even if we address this, this is what, like about 320 milliseconds.

If your PVARP terminates at 300 milliseconds, you're going to track this and then you're going to have the PMT issue. So without... addressing both. This is why PVARP and PVAB are both really important.

All right, moving along to ventricular timing cycles. If there's any questions, by the way, once again, feel free to raise your hand in the chat. We can give you permission to talk.

We'd love to hear anything that you might have for us. So please reach out. Okay.

Ventricular timing cycles, maybe. Okay. There we go.

Okay. So just as you had blanking and refractory in the atrium, You have blanking refractory in the ventricle. So your V blanking is to avoid crosstalk, which I'll kind of explain here later. It only is initiated after an atrial pace occurs.

It's typically programmed anywhere from 12 to 52 milliseconds or an auto. I'm not as familiar with what Medtronic uses, but what it essentially does is after an atrial pace, it closes the device's eyes and will go into. why that's important.

So V-blanking exists to cover up crosstalk. Crosstalk occurs when a ventricular channel senses an atrial pacing output and inhibits the ventricular pace. Obviously, if a patient is dependent, this can be deadly. So you see here on this EKG, their patient has an atrial pacing spike here.

The device immediately senses a ventricular event right after that. and withholds pace. But if you look at the EKG, there's nothing that is occurring here. There's no ventricular depolarization.

So it's basically over-sensing its own pacing spike, withholding its ventricular pace, thinking this is a true ventricular sense. As a result, the patient could very well have atrial pacing in perpetuity with no ventricular backup, which can be deadly. Here's another example of it. So you'll hear crosstalk is technically, by definition, oversensing of an event on one channel by the other channel.

Uh, typically though, when we talk about crosstalk, we talk about ventricular crosstalk. So that's the one that you're going to see in your IBHRE. This is the one that's going to manifest itself in very dangerous ways with your patient.

Um, so it's just things to be aware of. And as a result, anytime we atrial place, the device just closes its eyes to avoid, um, to avoid that. Anything to add on there? No, just, um, yeah. Crosstalk, as you said, is a good, back in the day, it was a very unwelcoming thing, especially.

patients with a complete heart block but most modern devices now within that kind of cross-talk window they've introduced this thing called ventricular safety pacing so if there is any signal detected on the ventricular lead within that very very small window then the pacemaker will immediately admit a ventricular paced event at a very short av delay so that you're not pacing on the t-wave or anything like that um so yeah so if you do see an egm with some very short av delays and uh it usually comes up on the market like vpp or something like that or vsp um it may just be ventricular safety pacing so just to recap that yeah if the if the device sees a signal within that uh that's vulnerable period um it will have a backup pacing uh in some devices dead on And we'll actually see an example of that later. So I appreciate you bringing that up. That's actually well-timed. All right.

So we have ventricular refractory period. So this is going to be your VREF. This is going to be the ventricular equivalent of PVARB. It's a relative refractory period, which means the device can still see, but it's just not responding to anything. And the point of this is to avoid double counting T waves.

So it's just a certain period of time after a ventricular event where the device is not responding and won't double count those. Devices also have auto sensing algorithms that can actually change your sensing threshold to try to avoid, which we'll kind of cover in a question from the quiz later. But these are just ways to avoid these tall T waves that can occur that could be double counted by the device. All right.

So. Scenario three, things to keep in mind when you're looking at CKG. What is the rhythm of the patient? What device type is used?

What does VSP stand for on the marker channel? What does VS2 indicate? Why does the device not mark the ventricular event VS2 on the 14-second mark? And then what programming changes should be considered to prevent the non-sustained RV over-sensing alerts in the future?

Okay, so here's slide one. We'll go ahead and give you a second to look at that. Once again, this is the thing that Jared had brought up, VSP.

If you were actually to change the sweep speed on these Abbott programmers, it would actually read VSVP because they're occurring so close to one another. This S just kind of overwrites this ventricle. So even though VSP makes sense for ventricular safety pace. In reality, it's actually a marker channel issue. But you're seeing the device atrial pacing.

It's fearing that it may have crosstalk. So it's ventricular safety pacing here. And then you have these other vents. I'll give you time to kind of interpret it before we get into what's actually occurring.

And here's slide two. Here's this 14 second mark. It's asking why is there no VS2 right here like there is there.

So, Jared, I don't want to put you on the spot. Do you have any thoughts on maybe what is happening here with the VSP? Yeah, I think there's a we can go back to the original slide.

Yeah, absolutely. Cool. So if we look at the top channel, that's our atrial channel.

And if we look at that very first atrial event, which is marked as an AR in black bold, I suspect that Sorry to just interrupt you really quick because I just want you to know because you don't know this. A-PACE on PVC is programmed on for this patient. So the A-PACE on PVC algorithm, when it sees a PVC, it extends PVAR.

um ignores the atrial refractory and then 330 milliseconds later atrially paces okay gotcha so yeah so i suspected that first marker is probably the true atrial uh sinus beat that is then uh probably conducting down to the ventricle at the same time you're getting an atrial paste event which is probably then falling in that vulnerable window we spoke about in that ventricular kind of blanking window, cross-talk window. So it's V safety pasting. And then the VS, that could be a ventricular ectopic maybe. Yep, PVC. Yeah, looks like a PVC.

And then again, as AJ said, we then, and then the second, the third, then we go back up to the atrial again. We've got, it looks like another sinus beat, which is falling in probably some refractory period from that PVC. Yep, that one.

Which, because it's falling in a practical period, it is now just timed out from the previous A-paced event. So we have another A-paced event, probably at the base rate. uh 330 milliseconds this is the algorithm that's the one is uh that's the algorithm there right left-handed i'm using my right hand here so this is a very complex one but yeah that and then that ar is the sinus p which is then conducting down to the ventricle at the same time we get natural pacing but it's then obviously mr red has been uh v safety pace in there again and then we get a probably another ventricular topic unless yeah so that's an a yeah that's a pacing and then i assume we got another perhaps ventricular topic uh yep that's exactly what's occurring yeah and then we're kind of in a vicious circle after that yep but then eventually it stops and then we get ascent by the pacing so we get a bit of normalization there for a little bit and then we get right back into it here so yeah uh dead on so first nso everyone if you wonder what that is that is the trigger for the egm non-sustained rv over sensing which means that it's seeing rv event here um as a possible either ventricular event but it thinks it may be t wave over sensing which is what's queuing that nsr vo event or NSO is the marker channel.

Excuse me. VSP is going to be your ventricular safety pace. Remember that it's VSVP that gets compressed on each other.

As you said, Jared, dead on, you have your intrinsic atrial event here that occurs, but unfortunately you can't see what occurred, but it's this repeating pattern here. The device saw PVC. It then... puts on a pace on PVC where it waits for the intrinsic atrial event to occur.

It then waits 330 milliseconds and atrially paces. You might ask, why does this happen? This is to avoid PMT. It's an algorithm that whenever it sees a PVC, it ignores what's happening in the atrium, paces the atrium to gain control of what's occurring in the atrium, and then tries to just break that cycle that could be PMT. In this case, though, This is a true atrial event, not a retrograde.

We atrially pace. This conducts down to the ventricle. But because the ventricular event is occurring right around the same time, it's very idiosyncratic, but it occurs around the same time as the atrial pace. The device thinks, oh, this could be crosstalk.

I don't want to withhold a pace because crosstalk can be deadly. So I safety pace, which... It may or may not be in the vulnerable period right here. I don't know.

It's up for debate. So it safety paces here, which does nothing. It doesn't evoke any kind of response because luckily the tissue is in refractory. So nothing occurs.

You have a PVC occur here. The PVC occurs. The device says, oh man, I better apace on PVC.

So it waits till the atrial event occurs. It then atrially paces and the cycle goes on and on and on. This is a really complicated example. And we'll... post this on YouTube so you can kind of go over it again and I'll show you the answer to it.

But yeah, you can see this occur. Sometimes you see these little idiosyncrasies where timing cycles just align to create this perfect storm. So once again, VSP stands for ventricular safety pace.

You asked, or it asked why on the 14 second mark, we didn't see a VS2. right here. This VS2 on Abbott devices is just when it's confirming what's happening on the near field as what's happening on the far field to say, is this noise or is this truly occurring in the heart? So it looks at the near field channel.

It looks at the far field channel. If it sees it on both, it says, oh, this probably isn't noise. This is probably legitimate. This one here, there is neither a mark on the ventricular channel here, and there's not a mark. on the VS2.

That is because this falls into complete refractory and is not sensed at all. So it fell completely into the ventricular blanking period here. It ignored the entire thing and nothing occurred as far as the device is concerned because this is in your V blanking. Interesting case. But here, let me show you this again.

And like I said, this will be on YouTube, so you can pause it and watch or read the description of what's occurring. So what programming changes can we do? We can turn off a pace on PVC. I typically don't use this algorithm a lot anyway, because it causes stuttering quite a bit where every time if they have a lot of PVCs, you'll end up with this big pause and then a pace again. And then inevitably, at least in the US, somebody will call me, would call me in from the telemetry to ask why the pacemaker isn't functioning correctly and that I have to explain to them that it's an algorithm.

that's doing it. So I tend to just leave it off if we can avoid it. However, in patients with extremely long retrograde conduction, say their retrograde is 400, 450 milliseconds, you may have a lot of trouble programming your AV delays around it, or sorry, your PVARP around it. And in those cases, you may just need to turn on these special algorithms like APACE.

Lost my mouth, so I'm just going to use this. Any questions for me? Or any comments on that, Jared?

No, man, that's a doozy. That's a good one. Yeah, it's an interesting one.

And if you have specific questions to the rest of the group on this event, I'm happy to sit down on a one-on-one or as a group and we can talk through it again. And I can also look up more examples if you want to see them. Unfortunately, all my examples are Avid devices, but it does occur in all devices.

So keep an eye out. If you ever see interesting cases, feel free to forward them along to any of us to review. because it could be something that we can share to the group and how we can all learn together. So here's the quiz. For those of you who answered, I really appreciate you participating.

We're going to go over the answers to the quiz. So first one, a DF4 lead will fit into an IS4 port. That answer is true. However, an IS4 lead will not fit into a DF4 port. And the reason being is that if you, the DF4 port.

actually gets more narrow. So where this pin actually plugs is more narrow here. And you can see that reflected on the DF4 lead as well.

It narrows here at the tip. This will avoid you getting confused and sticking an IS4 low voltage lead into a high voltage port. However, it can be advantageous if you're trying to downgrade. You can actually put a... Sorry, sorry.

Yeah, DF4 lead will fit into an IS4 port. Yeah, yeah. Okay. So yeah, if you're trying to downgrade, you can, however, put a DF4 lead into an IS4 port because the IS4 lead maintains this thickness. This lead will plug into it.

It's just a way of avoiding confusion here. And then you don't run the risk of having put a low voltage lead, thinking that the lead is where it's supposed to be. The device tries to defibrillate and it has the small electrode surface area.

It can't. possibly deliver enough charge and the patient will not be defibrillated. Plus, it might cause some damage to the circuitry because it's trying to unload a lot of electricity through a very small electrode.

So if you're trying to stick a DF4 lead into a port and it's really not fitting, maybe take another look at it and see, is this the correct or IS4 lead? Any questions on that? No.

I learned something. Yeah. We try to do. Okay. Things to keep in mind about unipolar pacing, sensing configuration.

Big one here. It will not capture outside of the body. So if for some reason, you know, the pacemaker is not capturing and you realize that you're set to unipolar, you want to either stick it inside the tissue, stick it to a metal instrument that's touching the body.

And I've seen like a wet rag placed on top of the chest also work. as well. So just remember that if a device is programmed unipolar pacing and you're doing, say, for example, a gen change, as soon as the physician pulls the device out of the pocket.

the device is no longer capturing. And if this patient is dependent, you're going to have a really bad time. So just be ready with whatever you're going to be doing here. Some devices too will go into a unipolar mode. If, for example, you cartery over the device itself, you tend not to see that anymore.

It happened more with older devices, but just keep that in mind before you do any kind of gen change, always check the polarity. That's one of the most important things you can do. And it can also stimulate the muscle tissue. Just remember that your anode is a device itself, and the electrical pathway is running up to the anode.

So you can kind of depolarize any tissue across here, and you may see pectoral stimulation. And then also, if you're sensing at this vector, because your antenna is this big, wide antenna, you're not only going to pick up the intrinsic activity of the heart, but you could also pick up the muscle activity, any kind of muscle activity between the tip and the device itself. So you could pick up pectoral movements as well.

So I try to avoid any kind of unipolar sensing if I can at all help it, especially in an independent patient, because you're going to get over sensing most likely, and you're most likely going to inhibit pacing when you need to actually pace. So properly implanted, you'd expect unipolar impedance to be lower than bipolar impedance. Remember that impedance is the ... is the amount of resistance on a circuit. When you're going to a tiny electrode, you have more resistance because it's just pinned.

It's just like little electrode, a little electrode versus when you're running all the way up to this large anode, you're going to have less resistance because you have a lot of surface area for this to run through. Also, you're running through a lot of tissue and then can disperse a little bit as well. So things to keep in mind if you have a higher impedance.

on a unipolar vector, you could be outside of the cardiac tissue. And that's a nice little test when you're PSA testing and you think, oh, we may or may not have perfed. If they switch the polarity and they go from unipolar or from bipolar, which I'll show you the pins again, if I can, my mouse is gone.

If they switch the polarity and instead of going from, for example, on this lead from the tip. to the ring electrode. Instead, they go tip and then to skin and the impedance increases that could indicate that you're actually outside of the heart with the tip of the lead.

So it's just a little indicator. It doesn't always capture it, but if you do see it, it's a red flag to consider as possible perf. Any thoughts on that, Jared? No, totally agree, mate. Sweet.

Okay, this is just a little... For Abbott devices, you do have LV sensing as an option for an Abbott pacemaker, but not for Abbott ICDs. So if for some reason, you know, you're having trouble with your RV lead, you can still use your LV vector. Just remember that stability is not generally not as good in LV leads, especially newly implanted LV leads.

So if you just put it in, if you just added an LV lead and then you change that to your sensing vector for a dependent patient, If that drops into the atrium, then you're going to have trouble here. It's going to incense atrial activity and withhold pacing when you may actually need it. So I tend not to use it. And when I do, it's when I'm very sure that the LV lead is stable. Okay, so where's the anode and bipolar pacing?

Well, it's on the ring. Everyone who answered that question got it 100% correct. So yeah, your anode is on the ring.

with bipolar and then with unipolar your anode is the can itself. Pacing output is expressed as I think pretty much everyone got this answer correct too. It's amplitude and pulse widths. Your amplitude is your voltage. Your pulse width is your time.

And I thought this was actually kind of cool. A lot of times it's expressed as a simple square here but it's actually you have this dictation. this decay of energy. So when you first administer voltage, it's not like you're not administering five volts all the way across the board.

It's five volts with the initial leading edge. And then with the tail edge, it may be half of that. It doesn't really matter as much with stimulation on pacing.

But when you start talking about defibrillation, you see this same kind of curve. And it's even more so because defibrillators are delivering a ton of energy and you just can't deliver as much over time. So that's when it really starts affecting is in defibrillation. But just remember that it's amplitude or voltage and pulse width or time. You can kind of see that too with the strength and duration curve as well.

Pulse width is your time, voltage here, and you're trying to find the ideal output playing with that. There. All right.

Raising the threshold makes the device less sensitive. A good way of thinking about this is your threshold is like a fence. If your fence is high, you're not able to see as much intrinsic activity that's occurring. You can lower it to allow sensing of this case, this is actually a QRS, intrinsic activity. But if you lower it too much, you may end up over sensing T waves.

So certain companies have created algorithms that are not just this flat line sensitivity. This one is called Sensibility by Abbott. I'm sure other manufacturers have something along those lines. I just don't have it offhand. But what this does is it actually starts off with a high fence, which is going to be about half of your measured R-wave at six millivolts or less.

And then depending what programming setting you have, and then it will decrement over time until it hits the max sensitivity floor. The idea being, why do you have this slow decrement? If you have a T wave, you're hoping to miss this T wave, but then get more sensitive to allow it to pick up intrinsic activity.

This becomes more important for obviously dependent patients. And then also when you're trying to sense like. for intrinsic ventricular activity for tacky devices.

So when you're worried about fine ventricular, like VF and things like that, you don't want to have your sensitivity fixed at 3.5 millivolts because it could be very low. You could have torsades as well, which can be problematic for any of these algorithms. But things to keep in mind. Jared, you got anything for me on that one? No, it's very, just be careful when programming sensitivity, especially in an ICD, as you say.

You don't want to not sense anything, but you don't want to over-sense other things as well. And then this can obviously be changed depending on where the T-wave is at. If it's a tall T-wave, you can raise this higher and then decrement at the same speed.

If the T-wave occurs later, you can extend this decay delay longer and then decrement later, but maintaining the sensitivity. So these are ways you can kind of customize it. If you ever need to talk through it, reach out to one of us, or you can actually call the tech services of any of these companies and they can talk you through it as well.

And then finally, which is typically true in regards to lead impedance, these were all false. So conductor failure is associated with the drop in impedance. It's actually the opposite. You'll see a rise in impedance.

Lead mineralization is a sudden jump. It's actually a slow increase, typically, is the way it manifests. And then... insulation breach associated with a slow rise, it's actually going to be a drop in impedance here. So if you think about, once again, we use that hose metaphor here, normal resistance to the system here, it just flows normally.

If you have a hole or a insulation breach that allows water or electricity in this case to escape through those holes, which means there's less resistance. which means the resistance will drop. If you have a knot or a lead conductor fracture, the electricity can't flow as well across the system, which means you have a rise in impedance.

So you typically, you know, I kind of gave you these. Also, I would recommend reading this or any number of studies here, papers here about impedance and how you can use that to detect lead malfunction. So. I kind of gave you these examples here.

Here's your steady decline. This is because there is probably a insulation breach. Here you have a sudden jump here above 3000 ohms and then drop back.

This indicates a conductor failure. And the fact that it drops back to normal indicates that you're having what's like a make break where occasionally, you know, the patient may stretch and you have a separation of that conductor. And then it...

goes back together so it functions normally except when the uh the conductor wires are separated and then you end up with this jump in impedance uh and then finally you have this slow steady increase doesn't always mean um that there is lead mineralization but it could be an indicator so this slow steady rise indicates possible mineralization on the lead which is not really much you can do about it. A lot of times, actually, the lead may function fine. So you just want to, you know, monitor these leads. And if it's starting to fail, you may need to add a lead and or extract if that's capable. All right.

And that is it. Any questions from the group? Anyone?

Any comments, Jared? Anything like that? No, I just want to say a big thank you to me.

That was really, really informative. It can be quite daunting looking at that and thinking about all these timing cycles. But, you know, if you just focus on the basic timing cycles and, you know, just go through everything in a methodical way.

Look at the atrium, look at the ventricle. and just think about what the device is seeing. You know, as clever as these devices are, they're quite simple as well.

They don't think like a human, so you've got to kind of think for them. So they simply will think, well, if there's something there, I'm not going to pace. If there's nothing there, I'm going to pace.

And if you just think of it in a simple way like that, then you really have to become the brains of it. So they just go through everything methodically. Is there an A to every V? And if things are...

are blanked out then think about why they're blanked out thinking about your pvaps and your refractory periods and things like that but um timing cycles can be very daunting to get your head around but um with some time and we're here to support you all so please reach out and obviously review this um fantastic talk by aj and um i think it'd be a good uh good tool to having your belts moving forward as you learn pacing awesome yeah i i appreciate it and i i think that's dead on i had a teacher my the teacher initially taught me devices. He would always say like, these are very intelligent, dumb devices. They know what they know. So if you don't like the output the device is doing, if it's acting strangely, generally that doesn't mean there's something wrong with the device. It means there's something wrong with the input.

So you have to, it's your responsibility to program around it. I mean, lead failure and things like that can be a factor, but the computer chip itself is very reliable in these devices. So if the output is wrong, if it's acting weird, then you need to do. take a look at the inputs and adjust that accordingly. Perfect, Jared.

I really appreciate you, man. That was fantastic having your insight and keeping me on topic throughout this whole thing. I appreciate everyone else for joining us this week. We'll be back to our regular scheduled physician-led training here next week.

So I appreciate you all sticking with me. I'll get this posted on YouTube. And if you have any questions, like I said, reach out to me directly and we can talk through it.

But it's been a great Sunday. You enjoy the rest of your day. Thanks, AJ. Thanks, everyone, for joining.

Thank you. Take care.