This is our final installment for the electrophysiology series for the cardiovascular advanced practice provider, and we're going to end with device management. So device management is fairly complex, and if you're going to be interrogating devices and reprogramming them, it's something that you'll, I think, feel really good about when you get some hands-on practice and training. And I'll try to provide you with some of the basics that'll get you started. Here are some readings that you can check out to help you. There's an up-to-date article there that is very straightforward, and I think gives you some nice basics of that cardiac pacing, which sometimes people struggle with when they're starting. So we're going to cover pacemakers and defibrillators. So pacemakers, there are clear indications that we have discussed in our bradycardia lecture. They are meant to relieve or prevent symptomatic bradycardia that is not due to a reversible cause, allow for treatment of tachycardia without worsening or inducing bradycardia, and prevent future symptomatic bradycardia if the risk of progression is high. So that might be something like someone with advanced hisperkinesia disease and they don't have an adequate escape rhythm. This slide has a lot of things on it, but I wanted to point this out. This is from the ACC guidelines for bradycardia. Just a little bit of a review here. There are clear indications based on a class one recommendation for who gets a pacemaker. So just to summarize, this is symptomatic AV block that does not resolve despite treating the underlying cause, or patients with second-degree type 2 AV block, high-grade AV block, third-degree AV block, if that is an indication for a pacemaker. And you can read through the rest of those, but symptoms that are directly attributable to sinus node dysfunction, pacemakers indicated as well. There are varying levels of evidence, and I put a little key there for you to review that as you look at this chart. So always follow the recommendations. There's clear guidelines for who should get a pacemaker and who shouldn't. Different pacing techniques and methods for chronic therapy in patients with AV block. You also have to decide, once you decide a patient needs a pacemaker, what kind of pacemaker do they need? A single chamber in the atrium, a single chamber in the ventricle. How do we make that decision? So patients with sinus node dysfunction, if they've got intact AV conduction, you can put a single chamber device in just an atrial lead. If they've got atrial fibrillation that's persistent or chronic, and you're not going to try to get them back out of rhythm, then they can have a single chamber device just with a lead in the ventricle, for example. For patients who require atrial pacing, as well as they need some backup for AV block, then they need a dual chamber pacemaker. So there are also clear guidelines for who gets what type of pacemaker, but you need to consider why they need that and what type of benefit you're looking to achieve. We also have indications for a biventricular device, which we'll talk more about in a minute. Here's some pictures just showing you what that looks like. We have our pacemaker generator and the first picture here. We have our device generator and we have just a single lead going into the right ventricle. A dual chamber device has a lead in the right ventricle and the right atrium. And then a biventricular device, we have leads in the A and the RV, and then we thread a little wire over into the left ventricle as well. And what we're doing there is we're trying to resynchronize the ventricle so that they beat together. There are two types of pacemaker leads. There's active fixation leads and there's passive leads. So active fixation leads are fixed to the inside surface of a heart using a small corkscrew like device to hold it into place. A passive lead means that it's attached to the heart muscle without that little mechanism. And it's held against that heart muscle mostly by pressure exerted by the leads. So two different types of leads there. These leads can have bipolar pacing or unipolar pacing, which basically tells us about how they transmit energy through a circuit. So a unipolar lead is going to transmit energy through a larger circuit from the tip of the lead back to the pacemaker. And as a result, it will cause a larger pacemaker spike on your surface EKG. So it's always very obvious when you're looking at this, if someone has unipolar pacing programmed. The downside of this is there's a greater chance for pectoral muscle stimulation because that electricity is having to travel over a larger area. Bipolar leads will transmit energy through a much smaller circuit and both those poles are located at the tip of the lead. As a result of this, it has a very small pacemaker spike that oftentimes you really have a hard time even picking out at all. There's also leadless devices now. These are small self-contained devices that you can insert right into the right ventricular chamber of the heart. So there's single chamber. Chest x-ray, I just want to show you what this looks like when you're looking at a chest x-ray. So you can see in this image here, here's your device right here, generator. And then we see the leads going. We've got one lead in the right atrium here, and then another lead in the right ventricle right there. This is what a leadless device looks like on chest x-ray. So chest x-rays can be helpful if you are concerned about device malfunction. Like maybe there's a problem with the connection at the header. Sometimes you can see that on an x-ray as well. Or if a lead has pulled loose, like maybe there are new leads that were just put in and a patient moved their arm around a lot and now it looks like their device isn't functioning properly. Or misplacement of that lead on a chest x-ray. Single chamber versus dual chamber versus biventricular device. So you've made the decision that someone needs a pacemaker. Now you have to figure out what type they should get. I mentioned a few indications already. Single chamber, we think about permanent atrial fibrillation because you don't need an atrial lead. They're just an AFib. There's nothing really to effectively capture there. Sinus node dysfunction, we can put a lead just in the atrium and then it can, we have intrinsic conduction down through the AV node. A dual chamber device is put in when we want AV synchrony. So we need a little help in the sinus node and a little help in the AV node. That's when we get a dual chamber device. And then a biventricular device is put in for patients with advanced heart failure symptoms. A significant interventricular conduction delay, because that tells me that the ventricles are beating out of sync already. Significant LV dysfunction. And our goal here is to resynchronize those chambers. So if I already have a patient whose EF is not great, and they already have heart failure symptoms related to their decreased EF, and then you're going to force paste the right ventricle ahead of the left ventricle, you're going to cause some dyssynchrony there. And a lot of times those patients won't do well in the longterm. So when we put an extra wire in and we cause resynchronization of those two ventricles, a lot of the time, those patients are going to not only just feel better over time, but you can actually see an improvement in their LV function. And we always want to consider if our patient qualifies for biventricular pacing. So I've got a few flow charts throughout this lecture to show you how you might work through these things. And there's a lot to take into consideration here. And as you can see, there are many things you must consider and documentation becomes very important. What is their New York Heart Association heart failure classification? What is their LVEF and how wide is their QRS? So a take-home point from looking at all of these things is that if their EF is 35% or less, if their QRS duration is 130 milliseconds or more, if the patient's going to require ventricular pacing, consider cardiac resynchronization therapy. In someone with more advanced heart failure, particularly if they have atrial fibrillation and you anticipate they're going to pace from the right ventricle, then that CRT cardiac resynchronization therapy is going to help take some of that workload off the ventricle. So you can see here there is some variability in the class of recommendation from one to two B depending on what the underlying patient is. But the wider the QRS, particularly if they have a left bundle, you can see there in those patients with heart failure, those patients are going to do pretty well with this therapy. Sensing and pacing components. So let's talk more about how this pacemaker works. Sensing is what the device sees. So there's depolarization wavefronts that pass that tip electrode and the device will compare that to what we set as a threshold voltage. And if it exceeds that, the pacemaker says, I see that intrinsic beat and a pacing is withheld. If there's no depolarization noted, then pacing is delivered. So in its most basic terms, that's how sensing and pacing works. So if there are a few other mechanisms or programmable features that are pretty neat that we can use. So there's something called rate adaptive pacing. So that device, what we don't want is the device just pace at a set beat. So just 60 beats per minute, whether you're on the couch or running a marathon, that's not helpful. So we have rate adaptive pacing. So your patient's sitting on the couch watching TV and they run upstairs to grab a drink from the fridge and we want their heart rate to increase. So in response to metabolic demands based on body motion, respiration, and cardiac motion, the device will sense that and allow for an increase in that ventricular rate. So that patient doesn't develop shortness of breath or fatigue, kind of like that chronotropic incompetence that we talked about in our bradycardia lecture. So rate adaptive pacing allows for a better quality of life for patients. There's also mode switching and atrial arrhythmias. So the ventricle can track the atria. If you've got a dual chamber device, it can track the atria up to a certain rate because that's what's going to allow for that physiologic response to exercise. However, what you don't want is someone goes into atrial fibrillation and now the ventricle is trying to track the atria up to really high rates. That would also be bad. So we can set mode switching capabilities where we'll say ventricle will track the atria up to maybe 110 beats per minute, and then it switches to a non-tracking mode. We'll talk about that here next. AV synchrony is also something we can program with a PR interval. So we want intrinsic conduction to the ventricle as much as possible, because if we start force pacing the right ventricle before the left ventricle, what happens is you create dyssynchrony. That's just the way it looks. So if you look at someone with a pacemaker, ventricular pacing spikes on EKG, you'll notice they're wide. Their QRS is wide. That's because we're forcing a little bit of dyssynchrony between those ventricles. So you can program the PR interval to draw out so that you can allow for that intrinsic conduction to come through. So we want to give the ventricle a chance to beat on its own. So prolonging a PR interval, basically causing a first degree AV block, which we know is usually asymptomatic, that can allow for a reduction in RV pacing. So that's kind of another nice function that we have. Pacemaker modes and timing cycles, I want to give you just a basic intro into this. And so you'll get really good at this if you do it a lot, and you can figure out what is the best programmable features that I can use for this patient. So we describe pacemaker modes with four positions. So position one is the chamber being paced. So it's the V, the A, or both, depending on what they have. Position two is the chamber being sensed, same concepts, the V, the A, or both. Position three refers to how the pacemaker responds to a sensed beat. So I indicates that a sensed event will inhibit the output pulse and causes the pacemaker to recycle. The T is triggered, and that indicates that the output pulse is triggered in response to a sensed beat. And then dual means that there are dual modes of responses. So this is only used, of course, if there's a dual-chambered device. And so an event that's sensed in the atrium inhibits that output, but it will trigger a ventricular output. And there's a programmable delay that we use there. So if the ventricular lead senses a ventricular signal during that delay, it will inhibit the ventricular output. So position three just tells us a bit more about how the pacemaker is going to respond when it senses something. And then position four is that rate response that we already discussed. We either turn it on or we turn it off if they don't need it. So to maybe illustrate that point a bit better, let's just discuss a few common pacing modes. So VVI is a single-chamber device. There's no atrial sensing. There's no AV synchrony. So this would be our patient with atrial fibrillation. We've got a single-chamber device. There's a lead in the right ventricle. And we have kind of minimal functionality there as a result of it being a single-chamber device. AAI is a single-chamber device with intact AV conduction. So this would be someone with sinus node dysfunction. And so same concept as the VVI, except we're only functioning in the atria because we have intact conduction. DDD, this is when you want to preserve AV synchrony. So DDD or you can have DDDR if you want that rate response turned on. So the atrial rate cannot go below programmed. A ventricular pace beat will be delivered if needed. And the ventricle will track the atrium. So this is going to be a lot of your patients will be programmed to DDDR or DDD if they have a dual-chamber pacemaker. Pacemaker modes and timing cycles useful in atrial arrhythmia. So the device will allow the ventricle to track the atrial rate up to the upper rate limit and the device will detect an atrial high rate suggestive of an atrial arrhythmia. Then it switches modes. So it switches from a DDDR to a VVIR, which essentially just turns off that tracking. So it doesn't go really, really high. So rate responsive pacemakers can be programmed further to allow for this mode switching. In paroxysmal atrial fibrillation, the ventricle will only track the atrial rate as fast as the upper rate limit is set. And you can program that to whatever you want, but usually we'll set it to something like 110 beats per minute. The device will switch to VVIR, no longer sees what the atrium is doing and stops tracking it. So that's mode switching. So automatic mode switching, optimizing dual-chamber pacing, we're going to initiate a temporary mode change to a non-tracking mode in response to an atrial sense rate that is above a specified value. As the atrial rate slows, the mode will switch back to a tracking mode. So here's a flow chart from some bradycardia guidelines from the ACC that just shows you about what is the best way to program this device. So we consider, do you need AB sequential pacing? Do you need rate response, depending on the underlying patient? What type of sinus node conduction do you have? So those are all things that you would consider when deciding single-chamber versus dual-chamber, and then what is the best way to program this device? And the nice thing is, even if things change for that patient, you can always go back in. Now you can't just easily go back in and add a lead or take out a lead, but you can certainly change some of these programmable features, it's very easy to do that. And that's part of why we see these patients often in the clinic is because what works for one person may not work for somebody else. And we always want to program these devices so that we enhance that patient's quality of life. All right, pacemaker troubleshooting. So what if this is something you'll get consulted on, maybe in the hospital, we say the telemetry doesn't look right, come and check out this pacemaker, what's going on? So there are a couple of things we think about, failure to capture and failure to pace are two things we see. So with failure to capture, this can also be referred to as output failure, or it could be a lead dislodgement or a lead fracture. So you see a pacing spike, but nothing's capturing. So either you don't have that output programmed high enough, that's one possibility, or maybe the lead is fractured or broken, or it became dislodged and it's not functioning the way it should. Failure to pace can be due to over sensing. So it's sensing something that's not there, and so it's not pacing. So you can see in this strip, here's an atrial channel and here's a ventricular channel. And right here, you see there's nothing there. So it should be delivering a paced beat because there's no intrinsic rhythm coming through, but it's not. So a couple options that I have mentioned there. Maybe there's a connection problem between the header and the lead. The lead could be fractured, or it could be programmed such that it's sensing things that aren't there. And so we can test that with our basic programming. All right, let's move into implantable cardioverter defibrillators. So one thing I'll just mention here is that defibrillators, these defibrillator leads, the defibrillator lead also will function as a pacing lead. If you just have a pacemaker, it's not the same. Not all pacemakers are defibrillators, but all these defibrillator leads will also function as pacemakers. So the same things we've talked about here, we can apply already to the defibrillation part of this lecture. So indications for an ICD would be prevention of sudden cardiac death because we need a little device there that is gonna deliver a defibrillation to bring that person out of that abnormal rhythm that they're at risk for. We have primary and secondary, which we mentioned already in our previous lecture. So primary have not had VTVF, but are sufficiently high risk. And then secondary people have been resuscitated from VTVF or remain at high risk of VTVF, and they have a sufficient life expectancy and a quality of life to justify the implantation. The vast majority of ICDs are implanted for primary prevention based on these two randomized controlled trials. So we have patients who have 30% EF or less. There's a significant survival benefit through eight years of follow-up from the MADE-IT-2 trial. And then sudden cardiac death, half to LVEF, 35% or less. There is a reduction in total mortality in non-ischemic and ischemic cardiomyopathy. So what's interesting about this is that these things were done, really before we had the same type of guideline-directed medical therapy that we have now, but really great data there to show that these patients who get defibrillators, they do better in the long run. So no ICD in a low EF patients within 40 days of MI or 90 days of revascularization. So we wanna make sure we give them a chance to recover their ejection fraction with goal-directed medical therapy after these events. So the ICD generator is larger. It's larger than a pacemaker because it has to be able to deliver these defibrillation therapies. So here in this picture, you can see this is the ICD, we call it the CAN or the generator. And then we have a defibrillation wire going down into the right ventricle. And then when you interrogate these devices, you can see all kinds of different things on there. So it's really amazing all the information you can get from these devices, but you can see, you can get electrical, atrial electrograms, ventricular electrograms. You can see what the shock coil is seeing. So what this allows you to do is kind of take the vantage point of whatever component of that lead you're looking at. What does that lead see in the intrinsic conduction? And so that's what that looks like when you interrogate that. So single chamber versus dual chamber, we make a lot of these decisions same way that we make the pacing decisions. Do you need an atrial pacing lead in addition to your RV defibrillation lead that also functions as a pacemaker? So dual chamber devices are put in for several reasons. The most obvious is that someone needs dual chamber bradycardia pacing. They need that AV synchrony. A couple added benefits of this would be atrial egrams or electrograms will enhance diagnostics for atrial fibrillation. We have dual chamber algorithms that can discriminate SVT from VT because sometimes what can happen is maybe a patient has tachybrady syndrome and they have runs of atrial fibrillation that are very rapid. Well, you may not know, is that person getting appropriate therapies for VT or are they getting shocked for a rapid atrial fibrillation? So when someone has a dual chamber device, it's quite a bit easier for us to discriminate between those things. Atrial egrams will enhance diagnostics for AFib. We have better diagnostic algorithms where the device can compare things and can say, yes, I think this is ventricular or no, this is atrial, I'm gonna withhold therapy. So let's look at a couple of ways it can do that here in a minute. But first I wanna talk about the therapies that these devices can deliver. So there are two types of therapies. We have anti-tachycardia pacing or ATP and then there's high voltage cardioversion or defibrillation, depending on what the scenario is. So therapy is typically tiered. So ATP is a really neat thing these devices can do. So let's point out a few things here. So here's your atrial channel. This is what the atrium is doing. And here's your ventricular channel. And then down here, you can see kind of a summed approach to what's called a marker channel where we can see everything that's going on. So the device senses that this patient is in a ventricular arrhythmia, VT, because look how much faster the ventricular rate is. And you can actually see here how it starts with a ventricular beat. And they're often running here with VT much faster than the atrial channel is going. So you can program ATP, which is typically done at slower VT rates, but you can program it however you want. And so what this device will do is it will deliver a pacing train or stimulus at a rate that's just faster than the VT cycle length. So let's say you've got VT at a rate of 160 beats per minute. Well, maybe it'll deliver a pulse at 170 or 180, whatever you program it to be. And oftentimes that will break that reentrant circuit, because remember, fastest pacemaker always wins, even if it's not supposed to be there. So that might break that reentrant circuit. That's what you want. Now the patient converts out of that VT and they don't have to get a shock. So that's ATP pacing stimuli that terminates a reentrant tachycardia. Now concerns about this is there's always the potential that you can actually accelerate their VT. You can turn VT into rapid VT or turn it into VF. So that's one of the concerns there that would be bad. But in general, VT that is a slower rate, like 160, generally we look at certainly less than 180, but a little bit slower VT has an excellent chance of terminating with ATP. So oftentimes that is the way we will program patients. So therapy zones, you can set multiple therapy zones. There's a monitor only zone that allows you just to see what's going on. I don't want to deliver therapy, but I want to see what happens in between what I think would be a normal sinus tach rate and where I think they're going to be in VT. Maybe they're having little runs of this or slower VT. So that's a monitor only zone. Then you set a slow VT zone, which you might deliver a couple sequences of ATP for. Faster VT, you're going to deliver maybe just one or two sequences of ATP. And then with ventricular fibrillation, while the device is charging to deliver a shock because it senses VF, it's going to shock. So it's going to charge before it can shock. And while it does that, it might deliver a round of ATP because why not? What's the worst that could happen? So they're already in VF. So if ATP is unsuccessful, then that device will just deliver a shock. So your therapy zones are typically set based on defibrillation threshold testing, which is performed during implant because you don't want to just put a device in and say, well, I hope I got those settings right. So usually you'll do some defibrillation threshold testing. And that's particularly important just a little clinical pearl at the patients on antiarrhythmic therapy, because that might change their defibrillation thresholds. ICD shocks are the most reliable therapy to terminate VT and VF. And most will terminate with the first two shocks. We always want to minimize shocks because as you'll see, when you start working with patients that get shocks, it is uncomfortable and it creates a lot of anxiety for patients. So there's psychosocial aspects to consider here with minimizing shocks. And when patients do get shocks from their device, they need to go get checked out usually. So it uses healthcare resources as well. So I showed you what ATP looks like. Let's look at what an ICD shock looks like. So here's our atrial channel. And then this one in particular is showing you the shock channel for that shock coil. And then here's our marker channel where you can see everything all together. So atrial lead, you can see those atrial pulses are certainly slower than the ventricular channel. And then so the device senses this is VT and it's going to just actually sense this VF here. And it's going to sense that there's, just needs to deliver a shock. So here's what's delivered right there. And then it looks like this. And you can see that now the patient goes back into rhythm like that. So when someone gets a shock and you're looking at their egram, this is what you're going to look for and say, yes, that was a shock. And it's clearly marked there for you as well. What about some things that can go wrong with defibrillators? We talked about some of the pacemaker malfunction. So ICD sensing is incredibly important because high sensitivity can cause over-sensing and unnecessary shocks. So ICDs will look at our wave intrinsic, our wave amplitudes, and it will adjust sensing thresholds, which is incredible all the things that these devices can do. So let's look at this picture over here. If we just have a fixed threshold that's set, and then what happens a lot of times, particularly with like polymorphic stuff, it's going to change. So the amplitude of those R waves will change. And so if it changes like this, then you're not going to have detection occurring for a long enough period of time because of that fixed threshold. And then that patient can just tack away there or the device will sense maybe three or four beats and then it won't sense it appropriately. And then it comes back up and it senses three or four beats. But really that patient's been in BT that whole time, but you just don't know because of the sensitivity issues. So to fix that, you can have dynamically adjusted thresholds with the sensing. So we have a changing threshold that's going to constantly reevaluate that T wave, that I'm sorry, the R wave, to tell you what's happening there with their rhythm. So it reduces T wave over-sensing as well. So that's what this is showing down here. So in this example, if someone has, some people have large T waves. And so if it, the device can sometimes sense that as an R wave and it will essentially double count their ventricular rate. And so that's another thing that can lead to unnecessary shocks. So there are also additional algorithms to withhold therapy in the setting of lead failure, because something else that can happen is like a lead fracture can happen. And then that can cause problems with sensing as well. And so if there's a sudden change in things like impedance and there's other values we can look at, that can cause the device to maybe withhold therapy and send a message to us and device on the device clinic and say, there's something wrong with this device. So ICD sensing, it is imperative for that to be reliable. Here's another flow chart showing you how you might, or kind of how the device goes about sensing and responding to what's happening. So there's basic sensing. It has to meet criteria for a certain period of time for the device to say, yes, this is an arrhythmia. Then it goes through enhanced detection to say, this is ventricular, not super ventricular in origin. More on that next. And then there's enhanced sensing to say, this is not over sensing. I'm not seeing something that's not really there. So it's not over sensing. And then the device will select a therapy based on a number of things, like how fast the ventricular rate is, for instance, and we can select ATP or a shock. And then it will, as the device is charging, it will confirm that's what's going on and finally deliver a therapy. So lots, and this all happens obviously very quickly within the device. SVT discrimination, just a quick note about this. So ventricular rate and duration. So it's tricky when patients have SVT and VT. So if we only went off of the ventricular rate, then you can imagine if someone had rapid atrial fibrillation or flutter, and that's conducting down to the ventricle, very easy to have ventricular rates, 180, 210, something like that, which would be easy for the device to say, that's too fast, I need to shock it, that might be VT. So the device doesn't do that though. It has SVT discrimination, and another really neat feature of these devices. So the device will look at the morphology to help determine the underlying rhythm. And so the device will store what intrinsic R waves look like essentially. And so it will match that up and it'll say, this looks different because think about it with VT, remember we have different axis. So oftentimes the axis is totally different. And so the QRSs are gonna look totally different. So the device can sense that it knows what to look for to say, yes, this matches or no, this doesn't, I think this is SVT. And therapy can be inhibited or delivered based on that. And there's additional features we can look at. For instance, there's cycle length from R to R, R to R wave, is it regular or is it irregular? So the device can sense this is very irregular. This is less likely to be VT. A sudden change in ventricular rate. So if they're 60 beats per minute, and then all of a sudden they're 180 beats per minute, that might be more likely to be VT. And then we talked about the morphology. So lots of things the device can do to discriminate. And here's another picture just showing you that T-wave over-sensing that we talked about before with potential problems. So in this picture we can see, here's an R-wave and a T-wave that it's double counting essentially. ICD troubleshooting, we consider the possibility of ventricular over-sensing. So the T-waves, as the slide I just showed you, there's T-wave over-sensing that can cause a problem. There can be electrical interference. So maybe a patient is doing things like welding, or if they're chainsawing, the device can sense an abnormal rhythm from that as well. ICD lead failure. So we always wanna track impedance trends and the devices now will usually send us a message that we have these remote monitoring systems. And if there's an abrupt change in impedance trends that tell us there's a problem with this lead, it's at risk for fracture, we'd wanna know that as well because the device can deliver inappropriate therapies as a result of that. Imaging, we can look for dislodgement. I showed you the chest X-ray because if those leads aren't where they're supposed to be, that can result in abnormal functioning of the device. So when you consider a problem with the defibrillator, these are all things that you should rule out initially. Managing ICD shocks. First things first, you wanna analyze that e-gram. So look at it really closely. We've discussed some different ways that you can look for things like over-sensing or a possibility of a lack of discrimination between an SVT versus a VT. So analyze those EGMs, look at all the channels that you have. It's a lot easier when you have a dual chamber device to do those things, but we discussed some ways that you can do that as well with a single chamber device. If a shock was delivered, was the rhythm VT or was it SVT? And that comes back to examining those e-grams. Could a shock have been avoided by strategic programming or enhanced pharmacologic therapy? So this can maybe make you think, you know what, maybe I need to up this person's medication or maybe you might consider them for an antiarrhythmic drug and maybe they've maxed out their beta blocker, for example. You can program the device such that you can allow maybe longer periods of the VT if it's shorter, or maybe you can change the rate detection of when that happens. Other considerations you should always think about, things like reversible causes. What is their potassium level? Are they ischemic? Patients with decompensated heart failure are more likely to have these ventricular arrhythmias. And then lifestyle triggers, somewhat goes back to heart failure, but maybe this is someone who had some dietary indiscretions and now they're having sodium and fluid overload that can predispose to ventricular arrhythmias. For a single shock, you should evaluate in-person or remotely within 24 to 48 hours. So if they've got a remote monitor at home, which a lot of these patients do, they can send a transmission or sometimes it'll send automatically and you can evaluate that. Oftentimes the patient may feel more comfortable being evaluated in the office if they have some concerns or if you have some concerns about a reversible feature. Repetitive shocks, this is more emergent because people can develop VT storm, in which case they can get recurrent ICD shocks. And there's a lot of bad things that can happen from that. You wear out your battery as a result of that. It's certainly very anxiety producing for patients if they have repetitive shocks and it's possible with VT storm that they can exhaust therapy and not break that arrhythmia. So repetitive shocks, we wanna tell those patients to go be evaluated emergently. And that concludes our lecture on device management. Thank you very much.

device management

pacemakers

defibrillators

indications

pacing techniques

patient selection

sudden cardiac death prevention