Okay, good morning everyone. We're gonna get started to try to keep ourselves on time. Thank you for joining us for our keeping pace session. We are very honored to have Dr. Ekoro here with us today. I'm going to do some brief introductions and then we'll go ahead and get started. As a reminder, again, if you have questions make sure that within your Quality Summit app you're opening this session and then you hit the Q&A at the bottom. Some of you probably have been in the EP sessions earlier yesterday. I just quickly want to again introduce our new product manager if maybe this is your first session you're attending for EP. So Sarah Lash, I'd like to welcome her in her new role for product manager of EP device and plant registry, AFib ablation registry, and the new CVASC outpatient registry. So first time at Quality Summit for her. Again, a big applause for all of you because I want to thank you for all the work you do, all the hard work day in and day out to help improve our patient care. And Dr. Ekoro is another one here who has a great passion for helping patients with their quality of life, very dedicated to her practice as an electrophysiologist and passion for AFib ablation and arrhythmia management and improving patients quality of life. She's in the Texas state of Texas, so she's from Houston and she has just started a new role as a medical director at the Arrhythmia Care Center. So she also does a lot of international work. She was just telling me in Nigeria opening centers there to help patients with their arrhythmia disorders and problems. So I'd like to welcome her and we're so honored to have her here sharing her expertise with us. So thank you. So thank you everyone. I'm really excited to be here. This is my third year here and I always love presenting at this conference because it brings together what I love to talk about, which is electrophysiology and also the things that make us do what we do. Improving quality is basically why we're here and so I just kind of love talking about it. So we'll be talking about keeping pace and I will be kind of introducing what happens on the clinician side when we're talking about how we decide what kind of pacemaker we're going to put in, whether or not we put in a pacemaker and the decisions that go for that. So I wanted to kind of go through all of this, basically identifying what we think about when we see a patient, how do we decide if this patient needs a device, a pacemaker in general, and then basically discuss the different types of pacing that we have available. We'll be talking about the conduction system, exploring different levels of heart block, and management of bradycardia, so all the things. If you have any questions please put it in the app and I will try to get to all your questions at the end and you can stop me in the middle if I'm doing something a little bit too high level. If I need to get a little bit more granular, please let me know. All right, so typically this is representative of our typical patient. So let us say we have this woman and she comes in and she has a history of sudden falls. There's this saying that they say, to a hammer everything is a nail, right? So to an ortho guy they'll say, oh it's a motor issue. To a neuro they'll be like, oh it's a stroke. And to the EP person they'll be like, huh maybe it's an arrhythmia, particularly with somebody who is 45 years old. And so there are a couple of things that can happen, but the EKG is usually where we start off. And so I'm sure if you look at this EKG you can tell that there's something not quite right, right? So typically we usually have a P wave, you have a QRS, and you have a T wave. And here it doesn't quite follow that way, right? So you can see the P waves, but they don't seem to be following with the QRSs. And the P waves are kind of marching out, so they're doing what they need to do. And the QRSs are there, they're also marching out, but they're doing it at a different tempo. So that means the top chamber, whatever is happening in the sinus node, is not really communicating with whatever is happening in the ventricular system, right? So that could be one option. Another option, which is a little bit more terrifying, is this EKG, where you know you'd see, okay, there's some P waves, but where are the QRSs? So you see one there, you see one cry for help over here, and you see nothing else. So this can be a problem, right? And how about this one, right? So you saw this person, they're going really fast, and all of a sudden you see nothing. No P waves, no QRSs. And then the ventricle seems to wake up, finally, and then the P waves start to kick in. So these are typically, you know, the different areas that you can find problems where you have conduction system abnormalities. So how would you evaluate the patient? How would you treat the patient? Those are the two things that we're going to start off with today. So let's start at the beginning. We'll start at the introduction to what is the conduction system. So when you look at the heart, right, we know about the muscles, we know about the blood flow. Where I get excited is where we're talking about the electrical part of the heart. So it starts all off with the sinoatrial node. So the sinoatrial node is the pacemaker of the heart. It starts off when you are four to six weeks old in your mother's tummy, and it doesn't stop until it's time for you to say bye-bye from this earth, right? And it keeps on going. There was a time when, you know, once it stops, then that was it. And typically, if it's not quite your time yet, the body is able to have lower levels of pacing. And so you have the sinus node that typically beats at about 60 to 100 beats a minute. If that gives off, or if that stops for whatever reason earlier than it's supposed to, then sometimes in the atrioventricular node, or the junction, you can actually have this pacemaker that kicks in. And it will do it at a slower rate, between 40 and 60 beats a minute. How do we know that the junction is taking over? Well, you don't see a P wave, right? So it's happening in the junction, it's not happening in the atrium. So you don't see that atrial contraction that's typically seen when you have sinus node activation. A little bit lower than that, even the ventricular cells are able to pick up where, you know, if the junction isn't picking up, or if the sinus node isn't picking up. But if the ventricles are the ones that are, you know, running the charge, then eventually they're going to give up. And so that's typically when we say, okay, there's something wrong, we need to do something about it. And, you know, luckily for us, about 80 years ago or so, somebody came up with a pacemaker. So important things, when we look at the EKG, we look at, you know, your P waves, your QRS, your T waves, you also look at certain intervals. And all of these things on the EKG tell us different things about the health of the conduction system in the heart. So the P wave is the sign that the sinus node is working. The P wave is actually just telling us about atrial depolarization. So why is that important? Well, if you don't see a P wave, or depending on where the P wave is coming from, it can tell us, is this coming from the sinus node, which is basically the natural pacemaker of the heart? Or is this coming from someplace else? And sometimes it can be something pathologic. Let's say somebody has an atrial tachycardia, those P waves look a little bit different, but they're a little bit faster. If it's slower, then it becomes a little bit of a problem, and we start to wonder if the sinus node is doing what it needs to do. QRS, it basically tells us, hey, we've gotten the message from wherever, either from the junction or from the sinus node, and we're depolarizing the ventricle, right? So, and that's the one that's responsible for all the beats in the heart. So if you do not have a QRS, even though you might have a P wave, your sinus node is working, if you do not have a QRS, then you don't have an effective heartbeat. That means that your heart is not beating out any, or squeezing out any blood flow, your cardiac output will drop, and so those two parts have to work together. Those two parts have to be seen, all right? So there are two things that we have to look at. The first thing that we look at when we see a patient who has a conduction system abnormality is, you know, first of all, we look at the levels of block. So you can have different types of block. You have the first degree, second degree, third degree, right? First degree means that there's some prolonged conduction, there's some delay between wherever is generating the impulse and where it's supposed to act. So in the level of the sinus node, the sinus node is an epicardial structure. Between the sinus node and the atrium, it has to go through these transitional cells. If there's a delay from the sinus node generating your impulse to the atrium getting that signal, then you would have a first degree block, right? A first degree sinoatrial block. The second degree means that there is intermittent conduction. So sometimes it beats, sometimes it goes through, sometimes it doesn't. And then third degree means basically there is no connection between these two levels. So wherever the impulse is generated and where it's supposed to be polarized or its effect, there is no communication between that. So another thing that I want to mention is that typically if you have a first degree or a third degree, you usually will have a regular rhythm. And if you have a second degree, that's when you have this irregular or regularly irregular rhythm where you have group beating. So if you look at an EKG and it just kind of looks as if, okay, things are not quite going the way that they should, then you should be thinking about a second degree AV block or a second degree block rather. And we'll discuss this a little bit later. The second thing we have to look at is the locations of block. So typically I'm sure that you know about atrioventricular block. That's the easiest one to look at on an EKG. You see a P wave, you see QRSs, they're not quite doing what they're supposed to do. That's the easiest one to diagnose. However, there is such a thing called a sinoatrial block. Like I mentioned, the sinus node is epicardial, you know, the atrium is endocardial or basically where the atrial conduction happens is endocardial. And then you have these transitional cells that go between the sinus node and the rest of the atrium. If there is any block between those, then that can cause a sinoatrial block and that can, you know, show up in the EKG in very surprising and funny ways. But both of these, if you have an issue with no matter what the location of block is, if you have an issue with your conduction, then you have to decide does this patient need a pacemaker or not and then decide what kind of pacemaker this patient needs to have. So you could have a dual chamber pacemaker, which is typically what we see. You can have a single chamber pacemaker, which we typically will put in those patients who either they're very young, so the babies that are, you know, have congenital heart block, you want to control exactly how much, you know, you have to change the leads. And so typically you would put one lead in. Or if somebody has atrial fibrillation and has heart block, you would put only one lead there. Sometimes we put in what's called biventricular pacing. So kind of similar to a b-e-i-c-d, except that it doesn't have the defibrillator part. And we'll discuss this a little bit later. Of course, we now have, you know, the new kid on the block, which is, you know, conduction system pacing. So either you can have it in the HISS area. That has kind of fallen out of favor just because of problems that we've seen with increases in thresholds and increases in function of the pacemaker. And so we don't really do that anymore. But we do do left bundle area pacing, which kind of still looks the same. You can tell basically on the PA view of your chest x-ray, it looks exactly the same as a normal dual chamber pacer, except that the RV lead seems to be a little bit higher. And then you can tell when you do your lateral view, this is kind of pointing into the septum. And then, of course, you have your leadless pacemakers. And now we have the dual leadless pacemakers. So, you know, all of those are the different types of devices that we can put in. So let's kind of just go back and explore exactly the different disorders. As I've mentioned, you know, the sinus node is an epicardial structure. It sits right outside the crista terminalis on the lateral part of the right atrium. And basically what you see is that between the tissue, which sits right here, and the sinus node, which is right here, you have these transitional cells that if you have a lot of fiber, if you have a lot of fibrosis, it can actually impact your transmission from the sinus node, which surrounds the sinus nodal artery, to the rest of the atrium. So what kind of sinus node dysfunction can you have? You can have sinus node arrest, or you can have exit blocks. Basically what this means is that, you know, you are not having the sinus node generate an impulse if you have a sinus node arrest. So a sinus node arrest and a sinoatrial block, depending on what kind of sinoatrial block, they can kind of look the same. And we'll go through, you know, what the first degree, second degree, and third degree would look like when we talk about sinoatrial nodal disease. So sinoatrial block of first degree is not really seen on an EKG. Let me give you an example. If you have, like, normal sinoatrial conduction, where this S denotes where you are actually creating that impulse from the sinus node, right? So you'd have some, you know, maybe minimal delay, right? And then you have the P wave, which represents the depolarization of the atrium. So this is a normal conduction right here. Here, this is your first degree, where you have a little bit of a delay. But you won't know you have a delay unless you actually put something in the epicardial space, because the actual activation that comes from the sinus node is so small, you're not going to see it on EKG. So the reason why we know this exists is because back, back, back in the day, before, you know, my time, there were some people who actually did this. They put catheters on the sinus node, and they were able to define what the sinus node was doing and how the body would react. And that's how we know that this is something. However, does that mean anything for us? Not necessarily. You still see your P wave, you still see your QRS, not really anything of a problem. All right, so how about a second degree? Well, what you see in a second degree sinoatrial block is the same thing that I talked about earlier. When you see a second degree block, you have group beating. And so sometimes you'll see folks, you know, they'll have this on an EKG. Some people would say, well, maybe it's a, you know, rhythmic breathing. Maybe it's just a normal sinus node dysrhythmia. It's not really anything to think about. And as long as the patient is asymptomatic, we don't really pay much attention. And this is really just more so that they can give me grief during my exams. But if you have, this is more like a second degree type 2 sinoatrial block. When you have a third degree sinoatrial block, it really comes out like it's a sinus arrest. So you have your sinus node kind of firing. It's not going into the atrium. And so you don't have that atrial depolarization. And so you won't see any P waves. So what do you see on an EKG? You'll see a pause and then you'll see a QRS where the junction kind of kicks in. And this is what we kind of really feel strongly about when we, if we see a pause that's greater than three seconds, then this is something that we would worry about and we would want to put in a pacemaker. Now this is an example of what could be considered to be a sinoatrial block. As you can see here, you see your P wave QRS, P wave QRS, and then all of a sudden you don't see a P wave. This is a little bit too long for you to say, hey, this is as a result of, you know, either the patient was, had vagal breathing and it seems to also be one of those things that we call a regularly irregular rhythm, right? So you have this group over here, you have this group over here, pause there, pause there. And if you were to actually measure this out, this measures out to exactly two times what this PP interval is. So from this P wave to this P wave, if you were to measure it, you would think to see that there would be a P wave over here. And so this would be a sinoatrial block, definitely a second degree. If this patient is symptomatic, then they should get a pacemaker. So if somebody has a sinoatrial disease and let's say they're having symptoms, so they're having pauses or they're having, you know, dizziness or fainting, then what kind of pacemaker would you put in? Well, you would put in a pacemaker that would respond to just the sinus node. If you decided that you were just going to put in what we call an AAI pacemaker, which is one lead in the atrium, or now that we have leadless pacemakers, you just put in a leadless in the atrium, then actually that would be fine as long as you could guarantee that this patient will not develop nodal disease as a result later on. Typically, even though this is a sinus node dysfunction, it's mainly sinus node dysfunction, which can happen either because of age or, you know, after surgery. Some patients who have bypass surgery, sometimes they have to put the bypass through the crista, but they destroy the sinus node as a result, so you have to put in a pacemaker. Sometimes for patients with heart transplant, for instance, they don't have those neural inputs, and so they have to go a little bit faster, and so that's mainly sinus node dysfunction. Typically, if we're going to do that, we would still put in, especially for adults, we would still put in a dual chamber pacemaker. Why do we do that? Because we don't want a situation where, you know, two, three years from now, this patient comes into the hospital after a syncopal event because they've developed a venodal disease, and so that's the reason why we would typically put in the ventricular lead just more as a fail-safe, but a lot of times when we are checking the patient, checking the device, we want to make sure that they're not pacing in the ventricle as much as they possibly can, and we'll discuss the reasons why for that a little bit later. Now, the atrioventricular node is, you know, the node that kind of controls, basically it allows the slowing of conduction through the atrium, allows the atria to get all the conduction from the sinus node squeezed in conjunction before setting things down into the ventricle, and so it's located at the apex of Koch's triangle. Basically, it is bounded by the CS os, so if this is the CS, then it's bounded inferiorly by the CS os. You have the septal leaflet of the tricuspid valve, and then you also have the inferior, the tendon of terdoro, where it binds it posteriorly, and right there you would see your compact AV node. In between your compact AV node and your hiss, those are the two important parts of the conduction system that really allow for conduction to go from the atrium to the ventricle. Between the atria and the ventricle, apart from this area of conduction, everything else is electrically inert. What does that mean? That means that if there's any damage to the compact AV node, then you will not have conduction from the atrium into the ventricle. So the way that we test this out is usually by using, doing an EP study. We don't do these anymore because these have been kind of, they have been studied so much in the past that we're able to predict exactly what's going on just based off of the EKG, but what we see on the EKG is really defined by what we had seen on EP studies of time past. So what we are looking at here is, you know, when somebody says they're going to do an EP study, what we're looking at here is putting in a catheter in the atrium, a catheter in the ventricle, putting one in the hiss and one in the CS. What does that show us? It shows us, okay, what's happening in the atrium closest to the sinus node. Remember that the sinus node is actually epicardial, so what we're going to see is the effect in the atrium from the epicardial activation. And then we want to see how it translates into the rest of the ventricle. Typically what should happen is that your sinus node activation should start from the high right atrium, go down into the septum, and then into the left atrium before you have ventricular activation that goes down the conduction system, so it hits the RV apex first, and then it goes back up into the rest of the walls of the heart. So on the EKG, we look at, if we're looking at atrioventricular conduction, we're looking at the PR interval. What do we expect to see? We expect to see a PR interval that's less than 200 milliseconds. If it's too short, so less than 120 milliseconds, then we suspect that there is, you know, another conduction or some other bypass tract that's something for another day. But if it's longer than that, then we expect that there is some disease in the atrioventricular node, either in the area of the AV node, which can be physiologic. So for instance, if somebody exercises a lot, they have a high vagal tone, sometimes you can kind of see that PR interval become a little bit prolonged, so it's not really that much of a problem. Usually when the patient does any activity, so if they start to run or if they start to exercise, you actually see that PR interval get shorter, so that's physiologic, right? Sometimes you don't see it get shorter, and actually we see this in older patients, for instance, where their PR interval is really prolonged, but most of the time that still doesn't give us a lot of symptoms. When we start to see symptoms is when it's so prolonged that the ventricle actually, or the AV valves, actually close before the atria is actually able to squeeze. When that happens, you see somebody coming in saying that they're a little bit short of breath, they can't really keep up with activity, and typically when we see that, then that might be an indication for us putting in a pacemaker. So with regards to numbers, what are we looking at? We're looking at a PR interval that's usually between 120 to 200 milliseconds. If it's up to even 300 milliseconds, we're not really worried. Above 300 milliseconds, we start to take a look at it, but it still doesn't mean that we've put in a pacemaker. For the intracardiacs, what are we looking at? You have your AH interval, which basically talks about what's happening in the compact AV node, and then we also have the HV interval, which talks about what's happening in the His-Pikinji system. That is actually a little bit more important, because if you have any disease that's below the level of the compact AV node, then that's a little bit more problematic. That shows us somebody who might not recover if you have sudden loss of conduction below that area. So we've already talked about the locations of block. I'm going to kind of concentrate on the AV node here. When we look at the AV node, we have what we call superhissian block, which is basically where we're talking about the above the level of the His, which is basically in the compact AV node. Typically, superhissian block is usually physiologic. It's usually something where we say, OK, well, if the patient doesn't have symptoms, this is typically something that we don't need to worry about, because the heart, well, it's a normal physiologic function. Intrahissian and infrahissian block, however, that's below the level of the His. That is something that is an all or none event. So what does that mean? If you have any block that's there, then it could become a little bit more of a problem, and those are the patients who show up with syncope, with sudden falls, because all of a sudden, they're kind of going along their merry way, and then all of a sudden, they lose conduction below the level of the His. That typically does not come back as quickly as you would like, and so once they start having symptoms, there's something that we need to do about it, or that is something that we need to do something for. So I have two examples of second-degree AV block where you're looking at your P waves, and then all of a sudden, you don't see a QRS, and you can see here where the PR interval is prolonging and prolonging, and then it drops. So this is a second-degree type 1. Similarly, we have a second-degree type 2. Here, you have your PR intervals that are pretty much marching out. However, then you have this P wave. There's no QRS, and then it starts off again, and then you can also have what we call a 2-to-1 AV block. The reason why we call this 2-to-1 is because you have your PR interval, and then you have one that conducts, one that does not. You cannot really tell based off of the fact that you have one that's conducting and one that does not. You cannot really tell whether it's increasing, right? So if it's like a sudden drop or if it's something that is continuing and then it drops. However, from the EKG, you can kind of get a little bit of some hints as to whether this is happening at the level of the compact AV node, which is what is important, versus at the level of below the AV node or in the level of the HISS. So the main things that we look at, we look at the QRS width. If it's wide, then we worry that this is a ventricular escape rhythm, which means that there is something happening below the level of the HISS. That's something that we would worry about. If the PR interval of the conducted P wave is less than 300 milliseconds, then we would, or sorry, greater than 300 milliseconds, then we worry that, okay, this is something happening in the level of the AV node, in which case it might be something that's physiologic. It might be as a result of just increased vagal tone. A lot of times we'll see patients come in, they have a Holter monitor, and then all of a sudden you see these two-to-one AV blocks that happen in the middle of the night. We won't do anything for that because that's happening as a result of maybe sleep apnea or basically just them being in sleep. However, if it's otherwise normal, and then all of a sudden it drops, then we worry that that might be in the HISS Purkinje system, and that would be something that we would want to put in a pacemaker for. Atropine or exercise and what that does to the two-to-one AV block. So if it, you know, improves conduction, so that means that if you have more nervous output into the sino, into the atrioventricular node, and the patient starts to run, and then all of a sudden you see conduction come back, then that means it's happening in the AV node. It's responding to your sympathetic tone. If it does not respond below the level of the HISS, because below the level of the HISS, it's not going to respond to anything. Interestingly, if you have what we call, if you do what's called a carotid massage, and it actually improves, that actually tells you that this is below the level of the HISS. It's something that you need to worry about. If it improves with a beta blocker, then, you know, that's something that we need to be worried about, and we should put in a pacemaker for that. Retrograde conduction, that's something that's a little bit more, you know, we don't typically look at that, but if you see it, then that shows you that it might be in the HISS bundle. Now, this was an example that I showed you earlier. This is what we call like high-grade AV block. It's not quite a complete heart block, but it's not also quite a second-degree AV block. So, you see this term being pushed around when you have a lot of P waves and no QRSs. Usually, if you see a QRS, it's a junctional escape rhythm. It doesn't really show that there's a conduction between what's happening in the atrium and what's happening in the ventricle. That might be something that you would otherwise worry about. So, this is an example of a patient who has that high-degree AV block. As you can see here, you know, what's happening in the QRSs and what's happening in the P waves, something that's totally different. Here, we also talked about it earlier where we saw the P waves and the QRSs not quite paying attention to each other. In both of these, you actually see that the QRSs are actually marching out. So, if you kind of take a backwards view, you can kind of see here that the QRSs are pretty regular, right? And so, if you see a regular QRS, even though you don't see any relationship between the P waves and the QRSs, then you can kind of say that, hey, this looks like it could be complete heart block and this is something that we should pay attention to. So, we've talked about what's happening in the AV node. We've talked about what happens in the sinus node. How do we decide who needs a pacemaker and who does not? Well, a lot of people who are much smarter than me have come up with guidelines that basically say, hey, these are the patients that we should either kind of try to figure things out. And typically, we don't have to, if somebody comes in and they have symptoms, so if they're fainting, if they're passing out, if they have some dizziness, a lot of times, depending on the severity of the symptoms, that will determine how quickly we go to getting a pacemaker versus not, right? So, if we have somebody who comes in with something that's kind of like, oh, you know, I had some dizziness, oh, I had some falls, I have an EKG here, that doesn't quite show, you know, something that's really suggestive of sinus node dysfunction or atrial ventricular dysfunction, then what could I do? Well, you could do an EP study. So, in a patient who is symptomatic but you can't really tell what's going on, you'll hear us say, okay, well, let's do an EP study. Let's take a look and see what is the sinus node doing on a regular basis and maybe we should put in a pacemaker for that or not. How do you determine if the sinus node is not working the way that it should? Typically, what, you know, there's a particular behavior that the sinus node does. So, what we would typically do is take the patient to the EP lab and then we start to pace in the atrium. What typically happens after you pace for about a minute, if you let things go, then the sinus node should recover within a particular time, usually within half a second, right? If it doesn't recover, if you don't see the sinus node kicking back in within half a second of when you stop pacing, then that means that you have some sinus node dysfunction. That means that this patient, depending on their symptoms, might need to get a pacemaker. Usually, we don't typically do an EP study for either sinus node dysfunction or atrial ventricular node dysfunction. It's kind of come back into, you know, what we do with the TAVR procedure. So, like a lot of you know, with our TAVRs, sometimes you can have this sudden AV block and you don't really know if it's something that's permanent, you don't know if it's something that could progress later on, and sometimes there are some signs on the EP study that can tell us, hey, this atrial ventricular disease is a little bit more prolonged or more significant than we would think. And so, what we would typically do is measure our different, you know, intervals. We'll look at our AH interval, look at the HV interval. If the HV interval, which typically should be between 30 and 55 milliseconds, and we're talking about really small numbers here. So, if it's between 30 to 55 milliseconds, then we know that it's normal. If it's greater than 70 milliseconds, then that is actually an indication for us to put in a pacemaker. And so, for those patients who have either surgery in the level of the AV node, let's say you have somebody who has mitral valve disease and it's not really, or it came back, but it came back a little bit later, these are patients that you might want to do an EP study for. Right now, in 2018, they actually came out with new guidelines that are pretty much similar to the old guidelines that we had, except for a few things. New focal points included that for patients with either third-degree AV block or second-degree Mobitz II, you know, those show that you have infrahissian disease. Those patients should get a permanent pacemaker regardless of symptoms. So, if somebody comes in, has complete heart block, looks to otherwise be fine, or has a junctional rhythm, looks to otherwise be fine, doesn't really complain about symptoms, you should still put in a pacemaker. And the reason why is because we don't know when that escape rhythm is just going to stop, right? For patients who have an ejection fraction that's between 36 and 50 percent, we get a little bit more concerned when we're talking about pacing, particularly if they're going to be pacing in the ventricle. Because we have found that if you have pacing that's greater than 40 percent, and actually in block HF, which was a study that was done in 2013, actually greater than 20 percent, we found that if you have consistent RV pacing, that can decrease your ejection fraction. And so, for those patients, we've actually talked about putting what we call more physiologic pacing or conduction system pacing. So, putting your RV lead either in the his bundle area or the left bundle area, or actually just going ahead and putting in CRT, which is cardiac resynchronization therapy, basically putting in an LV lead to make sure that your conduction is as physiologic as it can be. And then, of course, I mentioned after TAVRs, we have some recommendations as a result of that. But going back to the regular guidelines, the other guidelines pretty much stay the same. And so, how do we look at it when we see a patient? If the patient comes in, they have symptoms, they have an EKG abnormality, those patients get a pacemaker regardless. And so, what are we looking at in symptoms? We're looking at fainting, we're looking at significant dizziness or presyncope. If the patient says, oh, you know, I felt dizzy, or you noticed that they were hypotensive, and at the same time, the patient was on telemetry, and you just noticed that, oh, they had a pause, or, oh, they have like complete heart block or second degree AV block during that time, then it becomes an easy thing for you to say, hey, you need a pacemaker, we need to put in a pacemaker for your help. For those patients who do not have symptoms, but have other worrisome findings, so for instance, if somebody who has sinus node dysfunction, if they have a heart rate that's less than 40, then it's somebody that you might consider putting in a pacemaker. I have patients today who have heart rates of 36, and they don't want to have a pacemaker placed, which is fine, as long as it's sinus node dysfunction. What does that mean? That means that you see a P-wave, you see a QRS, every time you see a P-wave, you see a QRS, maybe sometimes it's actually the sinus node, so their P-waves are slower. If that's the case, and I put them on a treadmill, they walk, and their heart rate goes up, then most of the time, I'm OK waiting. But there's some patients who, you know, I have a patient, actually. She was 26 years old, and her heart rate was 26. But she was an athlete. And you know, for somebody like that who says, look, I have never had any symptoms, I come into, you know, I came in to get my physical, and everybody's been sending me for all of these tests, and that's why they show up in your office, then in that patient, I wouldn't want to put in a pacemaker in that patient. She's 26 years old. What is that going to do? And then if I put her on a treadmill, and she goes up to 100, what is a pacemaker going to do that's even better than that? So those are the things that we consider. Definitely, you do not want to put in a pacemaker if you have sinus node dysfunction, and even if you have AV nodal dysfunction. Asymptomatic patients, or if they have something, let's say they say, oh, I felt some queasiness, and then you don't notice any EKG abnormalities, you don't notice anything, then putting in a pacemaker as a result is really not the thing to do. AV nodal dysfunction, third degree AV block, second degree AV block type 2, those patients should get a pacemaker regardless for a class 2A. Those patients who have no LV dysfunction, but persistent third degree AV block, or if they have asymptomatic third degree or second degree AV block. But either way, class 2A, class 1, those patients should be getting a pacemaker. You have patients who have neuromuscular diseases or genetic diseases that we know are going to progress. So if you have sarcoid, if you have limb girdle muscular dystrophy, we know that that's going to progress. And if we see anything, then we should put in a pacemaker because we don't want you to show up in sudden death as a result of having significant bradycardia. And then, of course, for those patients who have first degree AV block, those patients don't really need to get a pacemaker unless they are symptomatic. So like I mentioned, first degree AV block, typically if you look at your PR interval, you're looking at what is happening in the top chamber versus what's happening in the bottom chamber if things are happening for too long. So for instance, the top chamber squeezes, you have that equalization of pressures between the atrium and the ventricle. And that's typically what will make the AV valve, so your mitral valve and tricuspid valve, close. So if you have blood flow going through between the atrium and the ventricle, that pressure in the ventricle increases so much that those AV valves close. And then you have that PUA. That's when you have that atrial contraction. Those patients can become very symptomatic. They get very short of breath. They get sometimes this head rush, this head bobbing, and they get really uncomfortable. For those patients where you have that, what we call pacemaker syndrome or that AV dyssynchrony, then they would need a pacemaker because that delay is a little bit too long. Other than that, for first degree AV block, you don't need to put in a pacemaker. Another paper that I want to bring to your attention is the 2023 Guidelines on Cardiac Physiologic Pacing. Basically, like I mentioned, when you have a patient who has a high degree of ventricular pacing, they can have a situation where their RV actually starts to get weak. What is that number? Between 20% and 40%. And this has been seen in many studies, most recently, like I mentioned, in the BLOCK-HF trial, where you looked at patients who had RV pacing that was greater than 20%, and you saw that their ejection fraction started to go down. So for those patients, what we have decided is these patients should be getting either CRT, the cardiac resynchronization therapy, if their ejection fraction is less than 50%. Or if you anticipate that they're going to be pacing a lot of the time, then maybe we should do conduction system pacing. Now, there are a few things to consider. First thing is, for research with regards to conduction system pacing versus CRT, there is definitely much more evidence with regards to CRT than conduction system pacing, which is the reason why, if you have an ejection fraction that's less than 50% with a high degree of pacing, it is still considered you should still be putting in CRT above conduction system pacing. However, if you do not have a good branch for you to do CRT, so typically, when we're putting in that LV lead, we're looking for a branch that is away from the phrenic nerve, because you do not want to have phrenic nerve discomfort or diaphragmatic stimulation as a result of conduction to the phrenic nerve. Or you don't have a branch that's lateral enough. Sorry about that. You don't have a branch that's lateral enough. Then you might not be able to put in a good, or you might not be able to get good CRT, good cardiac resynchronization. In which case, putting in what we call conduction system pacing, or CSP, might be the next best thing. And so if we have patients who have the same thing, significant RV pacing, ejection fractions than less than 50%, you don't have a good target for your CRT, you can definitely put in conduction system pacing. If you have an ejection fraction that's greater than 50%, you really don't have an indication for CRT, then just go ahead and put in conduction system pacing if you can. And if you can't, then hopefully, you hope that those are not part of the patients who are going to end up needing the conduction system pacing at the end of the day. So this was a good kind of summary statement from that paper that basically looked at patients with indications for pacemaker therapy. If they have cardiac surgery, then they just do epicardial replacement, though most surgeons are actually just saying, hey, you guys do it so much better, so why don't you guys just put in the pacemaker. For those patients with indications for pacemaker therapy that are not going to cardiac surgery, if you think that they're going to have significant ventricular pacing, then basically, you look at the ejection fraction. If they have an ejection fraction between 36% and 50%, then you do CRT. This is a 2A. Otherwise, if you cannot get CRT, then his bundle or left bundle area pacing would be a good alternative. If you think that this patient has an ejection fraction that's greater than 50%, you can do CRT, but most likely, people will just do a dual chamber pacer and then CRT only if needed. This is typically not what we would do. For a patient who you think is going to become ventricularly dependent, there are some times that in addition to putting the left bundle area lead or the HYST lead, you will put in a backup lead. That's a 2B indication. But most of the time, with left bundle area pacing, which has less of the issues as of HYST area pacing, we typically don't end up having to put in a backup lead. And as I mentioned, if you don't have significant ventricular pacing, if the ejection fraction is greater than 35%, just putting in an RV lead and programming your device so that you have minimization of ventricular pacing should be sufficient. Otherwise, you definitely want to go with your conduction system pacing. So in summary, when you're looking at your indications for a pacemaker, anybody who has sustained or documented bradyarrhythmias, if they have symptoms as a result of paroxysmal bradyarrhythmias, sometimes you can have bradyarrhythmia-induced tachycardia, but that is more rare. Or those who are asymptomatic but have EP findings or EKG findings that put them at high risk for heart block and bradycardia, those are the patients that you'd want to put in a pacemaker for. The type of pacemaker really depends on your level of heart block, and then also the degree of pacing so that they don't go into heart failure later. And this is basically a summary slide talking about the different kinds of AV block or the different kind of inferhiscian or AV nodal block and when you would put it in a pacemaker. And with that, that is the end of my presentation if you have any questions. Thank you so much. We did get a number of questions throughout the session. The first, this being an NCDR conference, is about documentation. So what's your best practice around indicating the reason for pacing? And how would you encourage clear documentation of that in the medical record for purposes of the registry? Well, so I am typically, whenever I write my notes, I typically will do a separation, like an assessment and a plan. And for us, I mean, they're either in the consult note or in the progress note just preceding the procedure. You should have a place where it says bradycardia, secondary two, whatever. The good news also is that in my hospital and in a couple of different, I work in a couple of different hospital systems, they will actually have an area in the order set where you actually have to fill out a form that says, this is the reason why we're putting it in. So either it's going to be a class one indication, class two indication. It's because of atrioventricular block that's irreversible. And they have a whole sheet of paper that looks at the different reasons. So between those two things, typically the folks who are able to, who are filling out our forms, are the registry, they're able to kind of get the diagnosis from there. Thank you. For RV pacing greater than 40% as an indication for pacing, what are the specific ICD devices inserted and does the type of ICD correlate to the pace setting? So if you have a ejection fraction that's less than 40%, typically, so typically the number we use is 35. We hate 35, 36 to 40% because that's terrible. But if it's less than 35, then it's easy. Then it's like, okay, either we're putting in a dual chamber ICD or putting in a bivy ICD. The reasons why you would put in a bivy ICD are if you have left bundle or like in the left bundle or some sort of intraventricular conduction delay that's either greater than 120 if it's a left bundle, greater than 150 if it's a non left bundle. Or if you see the patient has complete heart block, then you know that this patient is going to have a high degree of pacing. So those patients will get CRT. If not, they'll just get a dual chamber and you'll program it like a dual chamber pacemaker with an ICD. Now, if it's greater than 35%, so 36%, 35.5 even, and that's just because I'm a purist, then I will put in a pacemaker and see how it goes. And it's really the same rules that apply. So if you notice that the patient is going to have a high degree of pacing, then you want to put in CRT. If the patient's ejection fraction is greater than 50%, then you should put in a dual chamber, but put it in the conduction area. So put in conduction system pacing, either putting it in the HISS bundle area, but like I mentioned, even though they say don't diss the HISS, everybody's dissing the HISS these days. And so we typically don't put it in the HISS area anymore, just because there has been high levels of fibrosis as a result. Typically, you'll see an increase in the thresholds where your pacemaker isn't lasting as long because the thresholds for the RV lead are going up. And it happens over a period of time. So you're looking at it now and everything is great. And then a year later, the patient comes back and it's like, oh, I'm fainting again. And you notice that your RV lead has thresholds in the fives and you can't program around it. So typically, those are the things that we look at. So the first thing is you look at the patient, look at the EKG, see what the indication for pacing is. The second thing that I look at is look at the ejection fraction, and then I decide what device the patient is going to get from there. We capture syncope on the registry, but see documented symptomatic bradycardia and near syncope often. What is the difference? So syncope means that the patient actually passed out. If the patient said, oh, I felt a little bit dizzy and then sat down, but didn't actually lose consciousness, then that would be the presyncope, dizziness, et cetera. So if you actually passed out and that's basically the patient says, hey, I woke up on the floor and I didn't know what was going on. Or the patient says, no, I feel great. But then half of their face is blacked out because they have black and blue because they fell straight into something. And that means that they passed out. So that would be considered to be syncope. Great. How does your hospital use registry data for quality initiatives? How well is the data received and what's been the level of engagement from fellow EPs? Well, my hospital is an interesting one. So the main hospital that I work at, they've just started to kind of take a look at this data. Everybody says that they're okay with it, but everybody's so sensitive, you know? So it really depends on the physician. And I think that there is that kind of tension, I guess, because we have you guys who are like, okay, these are quality initiatives, this is what needs to happen. And then you have the physician who has kind of been going at it by themselves for so long that sometimes there is that tension. But really, I feel that once you have the discussion where you're like, okay, look, this is the reason why we're doing it, these are what we're looking at, and you are open to the fact that it's not anything personal and it's just to improve patient care outcomes, then I think it helps. We have a quality meeting every month now, but that was a long time coming. And so I think that just kind of slowly and steadily just trying to kind of break that tension, I think that that's really the only thing that you can do. Unfortunately, us physicians are a very sensitive bunch, so please be gentle. That's good advice. What's your view on if adding a follow-up data module to the ePDI registry would be valuable to look at outcomes post-implant, and what sort of outcomes would you be interested in? So it's interesting, right? Because I feel like, I mean, all data is great. I love looking at data. Having said that, collecting that data can be a little bit more challenging, particularly since, depending on your practice. So for instance, I have half my patients who I put in a pacemaker, they come by to see me, and I'd be able to collect their data. But then there's some of them who, either because of access or because they have a long relationship with their cardiologist, that cardiologist is the one that follows them up, in which case, then you're now coordinating care between multiple people. And so I think that it would be very, there would have to be a more uniform way of follow-up, and I don't know that that can happen. There's some places where it can because everybody's in a system, and some places where it just can't because different people are working in different areas. And so it might be a little bit more challenging. I think that for right now, just concentrating on getting the information that you have, I think that would be the best thing. And then seeing what can happen later, that would be something for the future. Okay, last question, it's a long one. So patients that have chronic RV pacing with dual chamber device that actually have intact conduction underlying with prolonged PR without RV pacing prevention turned on, should the patient be trialed with the algorithm turned on, or should the patient be upgraded to CRT device if the EF is trending down? So your answer to that really depends on why did you put in the pacemaker in the first place? So if you put in the pacemaker because this patient was having symptoms, then yes, you should upgrade the patient to a Bi-V because the patient is going to have to pace. You put in the pacemaker for the patient to be pacing all the time. So that actually is pretty simple. Now, if you had a nebulous reason for putting it in, let's say, and there's sometimes that that happens to me too, right? Somebody comes in from outside, we check their underlying and their underlying is a PR interval of 340. But the patient is like, I'm fine. I feel great. In which case, sometimes I do perform like a trial off of pacing where I say, okay, well, let's see how you do. We'll wait for about three minutes, three months, see how you're looking outside of that, see if your ejection fraction improves. And then if you still continue to do well, you come back and you say, you know what? I never had any symptoms. I'm able to run, walk, do all of these things. Then it's unfortunate, but I'll just kind of turn the pacer off and see how things go. So it really depends. Most of the time when I'm putting in a dual chamber pacer for somebody who has a prolonged PR interval, there is a clear indication why. And so if there's a clear indication why, if the patient is symptomatic because of that prolonged PR interval, then you do want to upgrade the patient if the ejection fraction is going down. Okay. Thank you everybody for the questions and thank you Dr. Aker. All right, thank you. Thank you.

electrophysiology

pacemaker

EKG analysis

heart blocks

pacing technologies

patient management

cardiac pacing

quality initiatives

treatment protocols