Thank you. I appreciate the chance to give this talk and I hope everybody's doing well. So devices, you know, comprise four talks or five talks really. I'm going to focus on device malfunction and pseudo malfunction. And I think as my former mentor put it, most of device malfunction, most of the consults you'll get in practice will be comprised of a lack of understanding on the physician's part. And that is due to automated and programmable device features in pacemakers and defibrillators that have really exploded. While this pie chart represents the consults for device malfunction, while most of them will be this, this represents a nuisance and a consumption of your time, but the real issue that affects patients and will really matter is the true troubleshooting issues and true malfunction. And if you blow up true device malfunction, I think a small minority, and these are just my interpretation and not database, but a small minority of device malfunction will really be related to impulse generator in the microprocessors. These have to do with bleed malfunction. And so what I'm going to do for this next 45 minutes, 50 minutes is talk about problems in a case-based fashion that have come from former trainees early in practice that represent real practical things that you all might face. This is the recent blueprint of our EP board exam. It's important to remember that devices can burn you on the boards because everybody's focused on catching them a high and making sure they know the response to the hysterefactory PVCs and this sort of thing. But devices comprise a large amount of question content and it's something you cannot forget during your board preparation. This talk assumes you understand basic undersensing, oversensing, basic lead anatomy and timing cycles in the NBG code. If there is a desire to go over those in another talk, I'm sure that can be arranged. And it also assumes that you're willing to participate. Devices, let's face it, are usually not the reason most of us go into electrophysiology. It's not the sexy part of our business, but it's realistically half of our world. And in these recent times, I think it has shown itself to be a very important life-affecting issue that we have to deal with and we have to know well. So I want to focus most on lead noise. Lead noise represents the most common text, cell phone snapshot I'll get from colleagues or former fellows wondering what to do. And it's important because identifying lead noise correctly, it's a decision of leaving the patient alone versus reprogramming versus taking the patient for a high-risk extraction. Lead noise is best split between non-physiologic and physiologic. Non-physiologic can be set screw problems, air bubbles in the header, or of course, lead fractures. It can be from electromagnetic interference. Lead noise can be from skeletal muscle or diaphragmatic muscle potentials, myo-potentials, or it can be from intrinsic cardiac events, either from T-waves, the QRS itself, or far-field chamber over-sensing in an opposing lead. So let's pretend we're assigned to be the person on call for our busy device clinic and it's 8 a.m. and you get this transmission. This is an 80-year-old with a Medtronic Clarius CRTD, end-stage colon cancer, dies at home on August 15th, which is the date of this transmission, and it was witnessed by the wife at home hospice. And we had a problem with this hospice because, as most of us know, we should always turn off the defibrillation aspect of devices if someone's on hospice, or most people think that's the most appropriate thing. So his family noticed his device to be making alerts after the patient died and the following transmission was received. Here you can see the current AEGM at 1.30 showing atrial pretty much nothing, ventricular low-frequency sensing with undersensing and AV pacing intermittently. Here's an event showing a chaotic smattering of pretty much atrial far-field sensing and bizarre QRS morphologies and a shock and then undersensing and a shock and undersensing. So my question to the people watching are what do you do on your phone call with this wife? Do you ask the time of death, give condolences, reassure? Do you ask if he convulsed at the time of death? Do you ask the time of death and then call risk management because he had undersensed VF? Or do you ask the time of death and ask about preceding symptoms? And I don't expect too many folks to participate. We'll give them 30 seconds. Does that sound reasonable, Nishant? Yeah, I think that's good. And that's great. And so the majority of you got the appropriate answer, and that is ask the time of death and that's it. This is an example of a non-cardiac death ICD transmission. Death EGMs are important because you will get them in people who have died non-cardiac deaths, hopefully not on hospice because they know to not look, but some people look and it becomes an important medical legal aspect as you have these bizarre waveforms after someone has died, after the blood is congealed, gas bubbles cause unusual things. You'll have a systole in pacing with no apparent capture. And you'll get alerts like this showing really just thousands of alerts, sometimes VF. And a good clue is when the patient dies and it's witnessed and there's been therapy delivered but no noticeable tetany or skeletal muscle capture from therapy, that patient is dead and that was defibrillating essentially a corpse. That's a clue that the patient died and then the therapy was delivered because of these death EGM patterns. This is important. You will get them and the clinical context in which they died is key to figuring these out and to diagnosing this as a pseudo malfunction rather than a true malfunction of the device. They're usually found, most of our tracings have been from defibrillators due to auto gain amping up very small amplitude signals. They'll often have a bizarre V sense with absent A EGMs. If you have the fortune of having an atrial lead, usually the atrial lead will be just complete flat line or far field, which is a tip off that the patient has expired. And interrogation of these devices after a clearly non-cardiac death and a non-cardiac context is usually not helpful and in some cases, especially in the medical legal world is harmful. This is an example of a sub-Q and someone that suffered a non-cardiac death showing apparent under sensing of VF, which is really nothing. This is absent A systole. So you've got through that one. This is our next one after a couple of patients. Your PACER nurse comes to you and this is the 34 year old. She's a congenital patient with LTGA. She's fainted while swimming in a swimming pool. Her device is a Medtronic that should say CRTD. She has a tender lead in the A, a Sprint Quattro and a 4698 in the LV. She is PACER dependent and below is her transmission. The two questions we need to address is why did she faint and what is the noise from? So why did she faint is one and what is the noise? That's actually good there. So as time went on, as time went on, the success rate of the correct answers diminished, which is good. The correct answer is the patient fainted from asystole, and the noise is not myopotentials, but EMI from the pool. So let's go over this. We have noise on two leads. So this is the A and V. Here are the channel markers. The patient inappropriately detects the noise on the ventricular channel, inhibiting pacing, which causes a long run of asystole. This is the cause of faint. So the cause of the faint is asystole, not true VF, right? This is not true VF. Most people can appreciate the noise that's seen on both channels, and whenever you see noise on both channels, yes, you can have lead-lead interaction, but this pattern of noise is specific. And if you don't recognize this already, you need to burn this into your brain. Here's a good example of what we call aliasing. Aliasing is a result of a consistent regular input from an extrinsic source, such as AC 60 Hertz, and that being different from the sampling rate of your sense amplifier, which is why you get that sine wave sort of appearance. This is classic aliasing from EMI from an AC mains power source. In the US, in Europe, it'd be 50, but it still would alias and give you this sine wave appearance. This needs to be recognized. It's on a couple of leads. Whenever you see this sine wave, you should take some sort of AC leakage current. The noise, where's the noise from? Most people guessed EMI from pool, and that is correct, because we know it's leakage current. Here's the tip. This is a sacrificial anode for most pools. We wrote about this earlier, I think last year, or maybe the year before. Most pools these days are saline chlorination units. Saline chlorination units generate chlorine by injecting current directly in a salt pool to create electrolysis and generate chlorine, or chloride ions. So there are some many fault protections, but there's no regulation about how much leakage current you can have in a pool and this sort of thing. And they, in fact, make viable sacrificial anodes to protect your metal components from electrolysis. So it is a real deal. Luckily, I'm surprised more people with devices don't get EMI from this, but luckily, most people, the leakage current is not enough to result in noise sensed on the device, and my suspicion is that people that do have this problem already have a subclinical impedance breach in one or more leads, rendering them more susceptible to leakage current. But this is something that we need to familiarize ourselves with. All right, everybody should recognize this. This is an interval plot showing VV intervals oscillating in a short and long cycle length in a variable fashion. This should automatically trigger you to think, okay, this is tram tracking and double counting. So our third case of noise today is one where your pacer nurse comes and says, hey, doc, I wanna decrease the sensitivity on these T wave oversensing. This case, I stole from Chuck Swerdlow in an article that's been published. This is one of the cell phone shots of, hey, what do you think this is, from one of my former colleagues, Mike Hoskins. So this, we see cyclical noise. So we see QRS noise, QRS noise, QRS noise that roughly corresponds with the T wave. The problem is that it's intermittent in high frequency. Here we see A pace, B sense, with some weird high frequency noise right after each B sense event. So for these cases, what do you tell your pacer nurse? Do you say, okay, increase sensitivity plan for NIPS for the ICD and the above case, decrease sensitivity plan for NIPS, do you decrease the sensitivity and just recheck later, or do you plan for extraction? And thank you all for participating. That's the only way you can stay awake in a device talk. Excellent, so this is a case of cyclical noise and most of the time, cyclical noise has to do with over-sensing of intrinsic cardiac events, such as T waves or QRS. But it's very important to remember that if you have a conductor fracture or some through and through electrical contact that should not be there due to insulation breach, that's in the heart, in a beating heart. Frequently that will result in a cyclical noise pattern. So that ventricular systole generates that contact, re-contact noise. And so just because it's cyclical does not mean it's not a conductor fracture. Both of these represent lead malfunctions. This is not over-sensing. This is not T wave over-sensing because it's multi-component high frequency immediately after the QRS. This looks like noise. This is not QRS double counting or T wave over-sensing. This turned out to be from a high voltage denuded conductor cable banging on the ring of the PACE sense in a device, which was proven and this was also proven. So my message here, the take home here, is that cyclical noise does not always equal T wave or QRS double counting. So don't be dissuaded from worrying about these sorts of features. And look at the waveform of the noise. If it's not consistent or if it looks high frequency, multi-component like this, worry. And the correct answer was plan for extraction. Good. All right. I think two more noise cases and then we'll be done with that. This is the COTS. This is your next clinic patient referred for extraction. This is a 60 year old from a rural area in your state with a Boston Scientific CRTD that had this incidentally detected no symptoms on his system and it was referred for device extraction for lead fracture, lead conductor fracture. And the question that I pose is what's the most important question to ask him before scheduling an extraction? You ask the date time of the CEA surgery that he just had. You ask if he's on NOACs. You ask if he has advanced directive or you ask if he'd like to have a lead addition, a PACE sense addition instead of extraction. Perfect. So the majority of you got this correct. You asked the date of his CEA surgery, of his carotid endarterectomy. This noise, sorry. This noise is classic Bovee artifact, electrosurgical artifact. And the tip off should be, as in the other EMI noise, non-physiologic noise, extrinsic, is that it's on both leads. Sometimes it's hard if it's a single lead because electrosurgical artifact is very junky, high amplitude, and for all the world, resembles conductor fracture noise. And so understanding and remembering to ask about any surgeries or recent surgeries is important, but when you have the advantage of numerous leads, it's usually fairly apparent. It's amazing to me how many people forget that they've had surgeries and how many surgeries occur in the absence of the knowledge of an implantable device. So you will see this. And if you forget to suspend detections when you're doing some lead revision or something like that and you see the same impulse generator, you will see it on the device memory as well. It's curious to me that Bovee noise looks like fracture noise because Bovee input, this is the Bovee duty cycles of either cut or coag or blended, is very regular. And so you ask, well, why is this not, why does this not look like that classic artificial EMI? Why does this not look like aliasing? And the answer is that the noise is really not from the duty cycle. It's not that you're continuously seeing the noise. You're just seeing intermittent arcing contact. And so it doesn't look like, does not look like Bovee waveforms. That's a typo. Say it would not look like Bovee waveforms. All right. One more and then we'll stop beating this. This is an incidence of cough shocks. Here we have a dual chamber, Boston Scientific ICD in a 26 year old with hypertrophic cardiomyopathy. And my question to you with this tracing is what is the most common cause of this noise? And then separately, perhaps, hand to hand, what would you do if this were reproduced with pectoral contraction? If people, this is not, this is an afterthought. I don't know the experience of the audience. Let me show you as a reminder, integrated dedicated bipoles. I don't know if that's backwards or not. Remember that dedicated bipolar uses the ring as the pace sense, the pace sense sensing circuit. And a dedicated bipolar uses a separate ring. The point here is that Boston Scientific devices use the dedicated, sorry, integrated bipolar. This is a broader sensing circuit, broader sensing circuit, as opposed to the dedicated bipolar, which is a narrower antenna and a narrower sensing circuit. And of course, some manufacturers now, you can alternate between integrated and dedicated. All right, so what is the most common cause of this noise? And then what if the noise were reproduced with pectoral contraction? So Mike, we had a question that was sent to me through the chat on that exact topic. It's from one of our fellows, Jeremy. So I'm just, I'm gonna let him ask his question here. Sure, sure. Okay, Jeremy. Thanks. If you notice noise on a patient's pace sense conductor, is there ever a role for reprogramming them from dedicated to integrated bipolar? Or do we have to consider that the risk of, conductor fracture for the high voltage kit lead is wire is also too high and you wouldn't expose the patient to that? What kind of noise are you referring to? Let's say it's a chatter that looks like a fracture, conductor fracture. So you're asking if you notice noise on the pace sense circuit only and everything else is fine, high voltage impedance is fine, are you asking, can you replace the pace sense lead or do you have to just, you have to worry that the whole thing is crummy and replace everything? Or could you reprogram them, let's say the site of the fracture is located in such a way that if you reprogram them to, let's say from dedicated to integrated bipolar and the noise goes away, can you leave them programmed that way? You can. So if the noise, but that's a specific situation, you would have to have a ring electrode fracture, a ring electrode fracture that's isolated. And if you had the luxury of being able to exclude that pace sense ring and change it over to a integrated bipolar, that's a theoretical fix, you could program around that. I would say, I would worry, especially in defibrillator leads in any conductor fracture that you're gonna run into future problems. So if I were to do that, let's say in a frail patient, I would probably do DFT checking to make sure that VF is not under sense and make sure that you stress those high voltage cables with a high voltage gradient that we'll talk about in a minute to make sure there's no impending failure. Does that answer your question roughly? Yeah, I think that got to what he was basically asking. Okay. And then I put up the poll results here for you. So, good. These are good questions because we're across the board and that's what I want. And this question is probably not framed correctly because it's two separate questions, but the most common cause of this noise, and this is an integrated bipole where you have a broad sensing, the most common cause is diaphragmatic myopotentials. This noise, let me show you, this is classic myopotential noise, very high frequency, sometimes waxing and waning, no aliasing, no sine wave appearances anywhere. And it's on the pace sense, as you'd expect, and the RV coil, because in an integrated bipole, the RV coil is part of the sensing circuit. The most common cause is diaphragmatic myopotentials. However, if this were reproduced by pectoral contraction, that represents a major problem. A defibrillator lead should never oversense myopotentials by pectoral contraction. So, we need to talk about that for just a minute. This is a little flow chart for myopotentials and on an ICD lead. If it's reproducible by valsalva or cough, then we're thinking diaphragmatic myopotentials. You could switch to, that should say dedicated bipoles, so you could switch from the broad antenna of the dedicated bipole to integrated bipole to the dedicated bipole to narrow it and that may overcome it. You should radiograph the lead for position if it's a dedicated bipole, because that's very unusual to see phrenic myopotentials, diaphragmatic myopotentials in a small antenna. You'd think about perforation or they might have slipped it down the middle cardiac vein. So, get a radiograph. And this can be overcome by simply adding a PACE sense lead because it's all about the sensing. The defibrillations should work. However, if you have myopotentials on an ICD lead that are reproduced by pectoral contraction, or you're worried about skeletal muscle, non-diaphragmatic skeletal muscle myopotentials, you have to ask yourself the following questions. First, is it a DF1 or DF4? Remember, you all will still be doing generator exchanges and occasionally use DF1 devices which involve different pins for the superior vena cava if you were crazy enough to use a dual coil device or this is just clipped. The RV coil is a separate high voltage pin and then the PACE sense lead, they plug into different ports. This is what we're implanting nowadays, which just you insert it in one port in the epoxy header so you can't switch the two. But this is the first question you have to ask yourself. And that is because if it is DF1, it's possible that the operator flip-flops the superior vena cava and the RV, or they plug the RV, sorry, they flip-flop superior vena cava and the RV. And if you do that, and it's a integrated bipole system, you now have your sensing circuit in the RV tip, the little helical fixation, and the RV quote ring, which is the coil, is if you flip it, is in the superior vena cava position. So now you have an incredibly broad antenna and would theoretically be able to sense myo-potentials by muscle contraction. God help us if that happens. I've seen it. If it does happen, that's a problem. You operate on the patient. Hopefully you don't go to court. If this is not an issue, if it's a DF or if it's a DF4, if you have myo-potentials on an ICD lead, you need to replace the whole lead. This is a high voltage impedance breach of some sort and needs to be fixed. Why does it need to be fixed? Well, let's remember here, this is shock vectors again. Remember that the CAN and the RV ring always need to oppose themselves in polarity, and the SVC is always the same. Now, the polarity can be flipped amongst these pairs, but you cannot change B to X. If you do that, as in this example, and let's say this is a congenital case where we put a subcutaneous coil, and you accidentally plug in this subcutaneous coil to the RV port, and this is a SVC coil out of the coronary sinus. We're trying to spare the tricuspid valve by not crossing. If you switch these, you're gonna have a zero shock impedance because this is gonna just short when it touches the CAN with this naked coil. You replace the whole lead in an impedance breach between RV high voltage coil because of this issue. This is an arcing artifact. Here's an example of what I'm talking about. This is a woman that had a cardiac arrest brought in from an outside facility to RCCU at 2016, who had a functional ICD, a functional ICD. There was a good battery life. There was no noise. The HV impedance is 35 ohms. The sensing was fine. She arrested for VF, was shocked in the field, and this is the interrogation result. If you ever see this naked page, you're in trouble. This is a VVI power on reset, power on reset, and this means that something blew in the circuitry. So what happened here? If you have an impedance breach between your high voltage and your CAN, and it's usually in the pocket, right? Because it's gotta be near the CAN. And you deliver low voltage at HV impedance. If you have just a little micron of insulator, that low voltage may be okay. These electrons remain fixed in the insulator. Insulators, remember, their electrons don't move. And so your HV impedance in a low voltage test may be okay. 35 ohms instead of two ohms or zero ohms. Because of that micron of insulator in between an abraded RV high voltage and CAN. But that's not good enough. That's not good enough. Because when you deliver 800 volts, and you have a huge electromotor force, what can happen is that huge voltage gradient will then rip that micron thin insulator barriers. It'll rip their electrodes off. It'll destroy the molecular integrity of what was left of the insulation. And create a through and through plasma arc and blow the circuit. Now, luckily, most defibrillators have a way of detecting that and diverting all the amperage. But this is basically a two ohm or less bridge so that you're delivering all that energy right to the CAN and you'll blow the circuits up, which is what happened in that case. Alternatively, you can have a through and through fracture, but just enough insulation capability of fibrin and it be just far enough that low voltage doesn't create the plasma arc. But then when you create that high voltage, you get what Chuck Swerdlow and Mark Kroll call plasma streamers, where it blows the hole and creates that arc, that low impedance arcing, which basically shunts all the current through your breach and none of the current to the heart. So the point here, and it's an important one, is that my potentials on RVs are always bad. And through a nice set of experiments, you should never use normal impedance to reassure yourself that the lead is okay. Especially when it comes to high energy versus low energy. This is a thing from Ellen Bogan showing how impedance predicts lead failures. You know, so impedance predicted lead failures a minority of the time in four of the total of 65 in this paper. More recently, Swerdlow and Kroll and coworkers did a nice set of experiments showing how you can be falsely reassured of a low voltage, high voltage impedance check like you would do just when you're checking through the diagnostics compared to a high voltage shock. And what they did is they spaced a through and through high voltage impedance breach next to the can, zero, 350, 500, and 1,000 micrometers apart. They did a low voltage check and at 500 micrometers, for instance, even if they have a through and through breach, you still get normal shock impedance. But when you deliver that 800 volt shock or a defibrillation type of shock, that plasma stream is able to form and you blow a hole. So when you're doing your generator exchanges or whenever you're worried about a high voltage lead, it's incumbent upon us to always check higher voltage. And these are the people that I would do either a synchronized, you know, a QRS shock, or if you want to induce, you need to stress the high voltage components and carefully inspect the area around the high voltage in the can to make sure there's no denudation. Enough of that. So let's look for time. I'm gonna, I'm gonna talk briefly, I'm gonna skip over this. I'm gonna talk briefly about pseudo malfunction for the next five to 10 minutes. This is more, if you want to do control print screen, that, you know, it's more for reference and we're not gonna go over too much. Pseudo malfunction represents the majority of consults you'll get for device malfunction. And I think it's most appropriate to group them in categories of unexpected pacing or pseudo undersensing, unexpected inhibition, pseudo oversensing, or failure to output, and then automated reprogramming or special filters. So these are the three categories. This mind numbingly busy slide is just to show you how hard it is to keep in your brain all the types of automated features that we are responsible for knowing. And this is why you have to rely somewhat on your good representatives in the field, or more importantly, your good pacemaker nurses, because this is their job is to know these. I don't expect our trainees to come out knowing every detail, I certainly don't, but it's important to know that they're out here. Let me show you an example of how painful this can be. Now here's a patient earlier this, let's see, Christmas 2019, that had AFib and a dual chamber Boston scientific device. And it's showing AFib and occasional V pacing and a bizarre A pacing here, AV pacing, AV pacing. So most of us detect, see this and we say, okay, this is easy. This is the most common cause of atrial undersensing that exists and that's undersensing of AFib. That's all this is. So what do you do? Well, for now to get rid of this, we'll program it VVI 40. Okay, fine, so done, you're done, VVI 40 and we should be good. So we turn it VVI 40 and we get this strip. So here we see V pacing at rates much higher than 40 in between intrinsic conducted AFib and here's a fusion beat. Here's a pseudo fusion beat if that isn't a cure about pace artifact. Okay, what now? Aha, I'm smart. I know this must be an automated feature. This must be rate smoothing. Rate smoothing is a feature that basically looks at preceding our intervals and then adjust the lower pacing rate or the sensor indicated pacing rate to sort of reduce the irregularity. Here's the EGM of what we saw and so we look for rate smoothing and oops, it's off. So it's not rate smoothing either. Okay, now I'm really looking dumb in front of the fellow. What the heck is it? It's not rate smoothing, it's not any kind of, it's not a programming thing, it's VVI 40 and so we scan all these special bells and whistles and then we see that the ventricular rate regulation is on and ventricular rate regulation is a form of rate smoothing but it's not rate smoothing. It's specifically with a FIB in these devices and it's in the guts and that was on and that was the reason for this unexpected pacing. So the point is not to know why Boston has ventricular rate regulation but to know that if you have unexpected behavior, you can dig in the guts and find some idiosyncratic bell and whistle that usually accounts for the pseudo malfunction. This is a table of unexpected pacing causes per the four major manufacturers. We've excluded ELA but ELA and Soarin has similar features. I'm not gonna go through these but they're just for reference so control, print, screen it if you like or this is recorded. Let's talk about unexpected inhibition. Before we end, this is a case of a 72-year-old pacemaker-dependent patient with a St. Jude CRTD experiences a shock. She's on guideline-directed medical therapy. Which of the following is most appropriate? So here is apace, bivy, apace. Here's the V channel, V sets. And this long short then triggers VF. So last ARS question. Good. So 23% scheduled for lead revision. And I think that's fair. I think that's fair because this could be noise in the PaceSense component channel of the CRTD. And to take this patient to extraction is a big deal, right? And the point that I wanna make here is that especially when it comes to St. Jude, their sense amplifiers are different. And they have this feature called low frequency attenuation, this filter. And the low frequency attenuation filter is meant to reduce T-wave over-sensing. It attenuates low frequency signals, so it's meant to reduce T-wave over-sensing. However, there are numerous cases of the low frequency attenuation filter to augment high frequency signals. And so you can see phrenic myopotentials or other high frequency nothings that don't represent lead malfunction, but are solely attributable to the filter itself. And in this case, it resulted in a systole long short and true VF that luckily was sensed and treated. You would have taken this patient to lead extraction because this does look like bloody high frequency noise, either from phrenic or something else. You would seriously consider taking this person to lead extraction or lead revision had you not known about these bells and whistles. And that's why it's important, painful, but it's important to know about these things. So the LFA filter nominally at our institution is turned off because we've seen this too many times. We believe these are from phrenic myopotentials, but we can't prove it. But nominally it's turned off at our facility, but you have to know about it in St. Jude PACE amplifiers, PACE sensor amplifiers. So the correct answer is turn LFA filter off. So here's some other unexpected inhibition algorithms. I'm not gonna go through them, but feel free to copy them. This is actually in a review that we've done actually this year for device automated features. And there are many others. The bests are from doctors Ellen Bogan and Swerdlow. And I think, because I don't wanna talk about this case, it's too depressing. I think we're going to end there. My take home messages for this device troubleshooting talk is to be aware of non-arrhythmic death EGMs and be aware that they will pick up noise and send noise to your device clinics. So be familiar with those. Remember that cyclical noise is not always over-sensing of cardiac signals, but can represent conductor fractures in a beating heart. That lead impedance is the worst way of monitoring for lead failure. And also, the absence of lead noise is not terribly sensitive for a failing lead as well. You have to at least know the list of automated features. You don't need to know how they operate, but you need to know that they exist. And the more you realize that, the more you think you know about these things, the more you realize that you don't know. They're very complicated algorithms and you can really get into the weed, but just know they're out there and have a cursory knowledge of them. And then a reasonable familiarity of these features will address most clinical questions that you're going to see, especially those first couple of years in practice regarding malfunction to help you make that critical decision of extracting the lead, taking a patient to the lab and ripping something out versus, oh, this is nothing to worry about. This is a reprogramming issue. So I'll stop there and take questions. Keep it brief.

device malfunction

pseudo malfunction

pacemakers

defibrillators

common causes

lead noise

physician understanding

device troubleshooting