The title of this lecture is Device Evaluation, Management and Troubleshooting. My disclosure of relationships is shown in the following slide. It's really impossible to cover every aspect about device management in one lecture. So what I'm trying to do by this lecture is cover what I think are the important and evolving areas that you should be knowledgeable about. And of course, also areas that could potentially end up on any sort of examination you might have to take in the field of electrophysiology. So let's start off with really the nuts and bolts of device implantation. And that is summarized in this slide. This slide is up to date, includes the 2021 ESC guidelines for device implantation. And I recommend that you become familiar with these guidelines. These are the latest European guidelines. There are some differences between the 2018 ACC, AHA, HRS guidelines, and you should be aware of areas where the ESC guidelines differ from the ACC, AHA. There's also guidelines for the management of patients with ventricular arrhythmias that touch upon the indications for ICDs, both transvenous and subcutaneous. And then there are several subsidiary guidelines, or actually they are expert consensus statement on the use of ICD therapy in patients who were not included or well represented in clinical trials and also appropriate use criteria for ICD and cardiac resynchronization therapy. Don't forget that indications are going to be different in special groups of patients, such as patients with hypertrophic cardiomyopathy, sarcoidosis, long QT, arrhythmogenic right ventricular cardiomyopathy, and the neuromuscular disorders. The last major update to the CRT guidelines for the AHA-ACC was in 2012. I draw your attention to several very important areas, such as limitation of class one indication to patients with cure aspiration greater than 150 milliseconds, limitation of a class one indication to patients with left frontal branch block, expansion of a class one indication to neocardial association class two, and with left frontal branch block and cure aspiration greater than 150 milliseconds, and class 2B recommendations for patients with left frontal YQS class one symptoms. Just remember, again, I emphasize, for example, the device selection for a sarcoid patient with right frontal branch block and YQB conduction, that is, the patient has conduction system disease and cardiac sarcoidosis, would be a defibrillator, not a pacemaker. So those are the sorts of differences you need to be aware of. This is the CRT guidelines, where red is shown here are class three indications. This brownish tan is class 2B, yellow is class 2A, and green is class one indications. I think it's very important that you're familiar with the two, all the different classifications, including the 2B, the 2A, and of course, the class one indications, which we're all very familiar with. Now, this is a flow chart from the Heart Rhythm Society guidelines for management of cardiac sarcoidosis, and this just takes you through the field in terms of management of patients with unexplained Mobitz type two or third degree AV block in adults under 60 years of age, where unexplained third degree AV block, it's recommended because of the incidents of cardiac sarcoidosis, patients have a CT of their chest or advanced cardiac imaging, such as a CMR of their heart or a PET scan. And this talks a little bit about the management of those patients, specifically when you would put an ICD in, obviously, if they have sustained VT or low EF, that's a no brainer, that's a class one indication. But as in the example I just showed you, if somebody has heart block and they have cardiac sarcoidosis, there are certain situations, such as unexplained syncope felt to be a rhythmic or inducible VT where an ICD can be useful. If their EF is moderately reduced, then an ICD might be considered, so class 2A, class 2B. And then if the MRI shows some late gadolinium enhancement, how you would manage those patients in EP study could be considered as well, and if positive, an ICD might be implanted. Again, another very important patient subgroup is patients that have hypertrophic cardiomyopathy. And these guidelines summarize the indications for ICD implantation, class one indications, class 2A, again, in the yellow, class 2B in the brownish tan color, and class three where it's harmful. And this basically goes over that if a patient has none of these, no non-sustained VT on a monitor, but has extensive LGE on CMR, then it would be a class 2B indication for an ICD implantation. So again, this goes over all the circumstances of class one, class 2A indications. It's important you become familiar with this because, again, these patients are handled differently. They have normal EFs as opposed to low EFs for primary prevention. And this goes over the specific criteria for recommending what type of ICD you're going to recommend, whether it's a single chamber transvenous ICD or subcutaneous ICD. Strongly recommend single coil devices, dual chamber ICDs if they have atrial pacing or they have conduction abnormalities. And then this slide, which just was recently published in Heart Rhythm, describes how you would manage patients with conduction system disease who have these types of neuromuscular dysfunction, decreased LVEF. What do you do with these patients? When do they get defibrillators if they have a left bundle, a wide left bundle, and or expected to have a fair amount of RV pacing, then what type of device would these patients get and when would they get devices? This talks about myotonic dystrophy, again, how to monitor these patients. Again, these are patients who you want to be screening by their surface EKG if their PR is longer than 240, their QRS is longer than 120 milliseconds, so they have second or third degree AV block. Then you might consider an EP study if the EP study shows an HD greater than 70 milliseconds, then they're going to end up with a device or if they have inducible DTVF. And this shows how to manage limb girdle muscular dystrophy and emory dry fist muscular dystrophy. Again, if these people have conduction system disease, you're going to want to evaluate them and ICD is a class one indication of these patients if they have a long PR, second or third degree AV block, or an HV interval greater than 70 milliseconds. These includes the mitochondrial myopathies, including phragocataxia, again, how do you manage these patients? Now, as I said, different groups of patients have different management strategies. These are management strategies for patients who have Brugada syndrome. And it's important to remember a positive family history of Brugada syndrome or sudden cardiac arrest. Even a family history of sudden cardiac arrest is not a significant predictor of adverse events in Brugada syndrome. It is not a factor in recommending an ICD for these patients, although it is in patients that have long QT. And again, a flow diagram for how you manage patients with Brugada syndrome with a specific emphasis on whether these patients end up with a device therapy. This is long QT syndrome. And again, whether these patients end up with device therapy, whether they're candidates for ICD therapy. And this goes into that in detail. Now, this comes from more of the, not so much from guidelines, but what do you do with patients who don't meet the classical, or were not included in the studies that were done to see if patients need defibrillators? So what do you do with patients who weren't part of the clinical trials? And this talks about how to manage those patients. And there are a lot of important flow diagrams there. For example, if a patient has an EF of 40%, but then 35 to 40%, they undergo a CABG, and a week, four or five days after CABG, a week later, they have heart block. And then you have to figure out what type of device they need. Well, if they have a low EF and they have heart block, even though they're right after revascularization, it would be very reasonable to put a defibrillator in. This goes, what do you do with somebody who has sustained or hemodynamically significant VT more than 48 hours after an MI? Well, you have to, could VT be due to myocardial ischemia or injury? If you believe it's due to myocardial ischemia, then an ICD is not recommended. If you consider a patient a candidate for ablation, no, then an ICD would be recommended. If yes, then he might be a class 2A indication. And then you go through all the different diagrams. If a patient requires pacing and they have a low EF, then ICD is recommended as a class 1 recommendation. And this just shows for secondary prevention, a patient with CABG has VF or hemodynamically unstable VT associated with an acute MI. But look, they have VF or polymorphic VT within the 48 hours of an acute MI, but they're not amenable to revascularization. So then it would be acceptable to put an ICD in those patients. And it may be appropriate, again, if there is above 35%, but you can't revascularize them and you believe they may have ischemia-induced VF. It's important to know the indications for sub-q ICD. This comes from the VT VF guidelines, and it is a class 1 indication when patients have inadequate vascular access or at high risk for infection, in whom pacing for bradycardia or VT termination is not needed, not, or not anticipated. And of course, a class 2 indication in patients who meet indication for an ICD, just like above, implantation of sub-q ICD is reasonable if pacing for bradycardia or VT termination is neither needed nor anticipated. Class 1 when they don't have vascular access or a high risk for infection or reinfection. This is a survey from European Heart Rhythm Association, and it shows what type of patients get sub-q ICDs. You can see younger age, patients have prior lead complications or device infection, vascular access issues, or sometimes just patient preference. And on the other hand, patients who get transvenous defibrillators, well, often they need CRT devices, or they have an indication for pacing, or they have had ATP, or in some places cost issue or occasionally patient preference. So what you should know about subcutaneous ICDs is the risk of inappropriate shocks is about 2% per year. The main cause, of course, is over-sensing, and the main cause of over-sensing is T-wave over-sensing, which counts for about 90% of cases, then EMI, or rarely SVT. There are very few ways to get around it. That's the beauty of the subcutaneous ICD and the limitations. It's simple, but there are limited programming options. You can program on a conditional shock zone. You can reprogram to a different sensing vector with a larger R to T-wave ratio. For example, they get shocks during exercise where the R to T-wave ratio may go down, or you can change the sensory sensing vector. And occasionally one even has to abandon the sub-QICD and go to transvenous ICD. In the A panel, A panel is shown a patient who gets inappropriate therapy. You see they get an inappropriate shock, and this is due to sensing over-sensing. In this example, a patient has over-sensing secondary to T-wave double counting. This is the patient's screen before they had catheter ablation, and they were okay in this vector. But after they had extensive catheter ablation of VT, they ended up with an R to T-wave ratio that resulted in a loss of detection capabilities of this particular vector. So a good explanation for why the patient got an inappropriate shock. Here's a tracing from a patient who is programmed to the secondary sensing vector. They have VT at a rate of about 140 beats a minute with double counting of the QRS complexes as noted by the T here. The lightning bolt here is when the shock is delivered. You can see the double counting here, and VT, although slow, is terminated with the shock, but the patient only received shock therapy because of the double counting. As you can see here, they get a double counting, so the rate is not 140, but 280, and gets treated. So subcutaneous ICD still can have over-sensing, over-sensing is primarily the T-wave, or a smaller R-wave would result in a diminished R to T-wave ratio. These are the important consensus documents you should be aware of on cardiovascular implantable electronic device leak management and extraction and infections. They're all, both of these are well worth reading. It is important to know risk factors for infection include age, chronic kidney disease, hemodialysis, diabetes, heart failure, COPD, malignancy, skin disorders, immunosuppression, prior device infection, anticoagulation, a big, big one, and pocket re-interventions resulting in pocket hematomas and long procedure durations. Now the risk factors for lead extraction complications include female sex, low BMI, advanced heart failure, chronic kidney disease, diabetes, coagulopathy, number of leads extracted, dual coil ICD leads, and the risk is actually decreased with prior open heart surgery. The approach to patients can be summarized in three charts in the following slides, pocket site infection with bacteremia, local infection signs and positive blood cultures, pocket site infection with lead or valve endocarditis, again, local pocket signs and positive blood cultures, plus lead or valve medications, endocarditis without pocket infections, recurrent positive blood cultures and lead or valve medications, occult bacteremia with probable device infection, absence of an alternative source, resolves after CIV extraction, and situations in which device infection is not certain, impending exteriorization of a lead or pulse generator, isolated left heart valvular endocarditis in a patient with an implanted device. Now, take home messages, class one indications, a patient with bacteremia with definite pocket infections and or lead-related endocarditis and bacteremia with valvular endocarditis is an absolute class one indication for device removal, definite removal. And studies strongly support complete removal of the system. And further studies support removal should not be delayed. To not do so results in significantly higher mortality. Risk of relapse without complete removal is very high, 50 to 100%. Lead extraction on the other hand, major surgical risk is only about 1%. So this is the flow diagram for suspected device infection, whether it's pocket infection or systemic infection involves blood cultures and ID consultation. Negative blood cultures leads to TEE, positive blood cultures leads to TEE. And then from TEE, the definitive diagnosis is made either valve vegetation or lead vegetations, program, a prolonged antibiotic treatment or consider CIED removal alone and with a negative TEE. And I mean, CIED removal plus leads and then re-implant at some point later. This is bacteremia without evidence of CIED infection. And again, take out all easily removable other sources of infection, such as IV lines. If there's no identical source of infection or continued clinical concern or evidence of infection. If yes, and it's Staph aureus or Staph epi and these bacteria, it's a class one recommendation to remove it. If it's alpha hemolytic strap or beta hemolytic strap or enterococcus, you can remove it or you can observe without lead removal. CIED removal if recurrent or continued bacteremia despite appropriate therapy or get gram negative bacteria, pneumococcal, pneumococci and then basically you can follow these guidelines. CIED removal if recurrent or continued bacteremia despite appropriate antibiotic therapy. This is recommended for diagnosis of infections and or infective endocarditis. This is from the international CIED infection criteria. What criteria do you need? You need microbiological criteria. You need imaging criteria and you need some clinical criteria. And I highly recommend you become familiar with all these criteria. And the definite CIE, a definite system, definite infection of pulse generator and the leads systemic infection is the presence of either two major criteria or one major plus three minor. And then the recommendation is clear, complete removal of the whole system by extraction. Possible is when you have one major, one minor or three minor criteria. So one major plus one minor or three minor criteria are possible. And then the recommendation is observe, repeat blood cultures and imaging. And rejected is patients who do not meet the above criteria look for an alternate source. I think it's important to be aware of the recent study in New England Journal of Medicine using the Tyrex pouch. The Tyrex pouch is a combination of minicycline plus rifampin, which is eluted over several weeks. Also know the following, infections are consistently higher with CRT devices than ICDs, which are higher than pacemakers. Upgrades, replacements have higher infection rates than initial implants. And additional antibiotic strategies beyond pre-procedural IV antibiotics or antibiotic pocket flush do not decrease infection rates except for the antibiotic pouch. As in rapid, here's a pouch or envelope versus control. You can see the risk of infection with the envelope is down about 50% from the control. Okay, we have to talk about conduction system pacing because that's an important new area. And I would be remiss if I didn't mention that. Pacing induced cardiomyopathies in major clinical trials accounts for anywhere from 10 to 40% of patients develop it over a number of years, up to five years, up to 25 to 40% of patients develop a pacing induced cardiomyopathy, so it's common. Here are the guidelines. These are the AHA, ACC, HRS guidelines. In patients with AV block who have an indication for permanent pacing, EF moderately reduced and are expected to require ventricular pacing more than 40% of the time, is reasonable to go with CRT or HIS bundle pacing over RV pacing alone. And class 2B, if they have AV block at the level of the AV node and have an indication for permanent pacing, HIS bundle pacing may be considered to maintain physiologic activation. Here, there are two types of conduction system pacing. There's HIS bundle pacing and left bundle branch area pacing. HIS bundle pacing is technically challenging. It is a narrow target zone and the HIS bundle is encased in electrically inert fibrous tissue. There's a low success rate in patients who have AV block, particularly if the site is distal and some of these patients will have high pacing thresholds. The left bundle branch area pacing is technically less challenging. There's a wide target zone and it is encased in muscle and relatively little fibrous tissue. There's a very high success rate for pacing in patients that have AV block and low pacing threshold, almost invariably. Here's the physiology of HIS bundle pacing. You see to the left, non-selective HIS bundle pacing. As you can see, there's a slurred upstroke in many leads, not in these B leads, but you can see in particularly in the septal leads, you can see a slurred upstroke or downstroke, almost looks like parahysium pacing because you're capturing both the conduction system and the septal myocardium followed by selective HIS bundle pacing where there's an isoelectric interval between the stimulus artifact and the onset of QRS. That isoelectric interval is approximately equal to the HV interval. So it'd be about 40 to 60 milliseconds or one to two boxes in detail. Left bundle branch block pacing, need to pay attention to detail. This just shows you a left bundle branch block pacing. This is site one and you're deep in the septum. Site two, when you're closer to the left bundle, again, an incomplete left bundle. As you screw the lead into the interventricular septum, you get a complete left bundle branch block. You activate the left bundle branch block and your stimulus to LV activation time goes from 90 milliseconds to the peak of LV activation time and V5, V6 going down to 70 milliseconds. And because you capture conduction system, the stem to LV activation time is the same regardless of whether you're pacing at a high output or low output. In this example, where you have incomplete left bundle branch block pacing because you're not really quite as close to left bundle, if you pace at a very low output, you'll just pace ventricular myocardium. But if you pace at a higher output, as seen here, you get septal pacing as well. And so the stem to LV activation time, of course, will be different here. We'll go from 90 milliseconds where you get both to now here you're only capturing the septal myocardium. Here you're capturing both the septal myocardium plus the conduction system because you're pacing at a higher output. You're not right on top of the conduction system, but at a higher output, you can now capture the conduction system. And so the LV activation time is shorter. This diagram shows you how to confirm direct left bundle branch capture by using retrograde HISS potential and or an integrated left conduction system pacing. I strongly recommend you look through this to get a better idea of how to confirm conduction system capture in patients with a left bundle. This is just a table, which is in press that summarizes how you can tell you're pacing the left bundle, how you're doing conduction system pacing with a left bundle. These are EKG based markers of left bundle pacing shown here. And these are electrogram based markers of left bundle pacing. This is just an example of various different depths of screwing the lead in. You can go from LV septal pacing to non-selective left bundle branch block pacing. As you screw the lead in further, you can actually get into the LV subendocardium. Typically your electrogram will have a QS configuration these are intercavitary. And then you see the LV activation times, you only have a selective left bundle pacing and non-selective left bundle pacing. But the peak in the V leads is about the same, at least in V6 about the same which measures LV activation as close as possible. Whereas if you're not as deep in, you'll have LV septal activation. You'll have LV septal pacing and non-selective left bundle branch block pacing. With non-selective left bundle branch block pacing, the stem to LV peak activation time in V6 is shorter than it is with LV septal pacing. And again, you can see that here, you have to increase the output to capture not just the LV septum, but to get the conduction system. A couple of words about imaging. You should know some information about imaging, particularly the main teaching point. Should be able to recognize lead position on X-ray. Should be able to recognize an abnormality of the rheotid lead. That is this abnormality shown here where you can see the insulation is outside the lead body itself. You should know how to follow patients with lead problems such as that, remote follow-up and programming. Patients who have a high risk lead failure with inside-out failure. Management will depend upon patient age, indication for ICD implantation, prior arrhythmias, need for pacing. You should be able to recognize the lead position on an X-ray. You should know where the lead's in the LV through a patent frame and ovality, and the LV lead's in the AIV. These are the important aspects of LV lead location, whether the LV lead is dislodged into the CS or located from the LV branch, where the location of the pacing lead is in the CS. Is it too apical or not too apical? Is it in the AIV or is it in an appropriate poster or posterolateral or lateral branch? What about, is the lead perfing? And where is the lead? Should be able to recognize where leads are in persistent left superior vena cava. You should be able to recognize and manage dissection of the coronary sinus. And when there are leads in the vein of Marshall, well, how would you manage it? Here's an example of a lead that's actually pulled back very, very close to, this lead obviously has pulled back and you can see where this lead is. This was a CS lead. So it fell out of the CS and somehow this lead is where? It's over here. It's in the outflow tract. So it's not in the CS at all. Here's an RV lead. Here's an ICV lead. Here was a CS lead and now you can see on X-ray in this patient as a tab R that the lead is in the pulmonic outflow tract. And here you can see the patient's EKG. You can see a QS pattern in ABR or ABL, negative in lead one. And you can see a delayed transition of R wave throughout the precordium. Miscellaneous. Just a couple of miscellaneous points I'd like to make. And that is as follows. Managed ventricular pacing can create ICD proarrhythmia. In other words, by allowing for pauses, such as shown here, you have a send speed and then it comes in with a pace speed here, pace speed after a long pause. And that sets up a rapid ventricular tachycardia with changing of the QRS morphology in the near field. So polymorphic ventricular tachycardia, where this is the pacing facilitated short, long, short sequence results in induction of sustained DT. This is an elderly male with high-grade AV block and LV dysfunction. There's a CRT pacemaker. This is a tracing from a remote transmission because of an alert. Here's a triggered event. This is a mode switch event, DDIR, where the patient went DDIR. And you can see that there is noise on the atrial lead. So the mode switch was not for atrial fibrillation, but noise on the atrial lead. Think about inappropriate automatic mode switching, such as can be caused by myo potentials, by EMI, by far-field to R-wave oversensing, or a variety of lead-related problems can cause an appropriate mode switch. So it's important to be able to differentiate pacemaker-mediated tachycardia from atrial tracking of an atrial tachycardia. How do you know whether a patient has an atrial tachycardia? Well, you'll know the patient has an atrial tachycardia from a VAA V-pace response. The atrial rate's unchanged. There should be no change in atrial electrogram or surface P-wave morphology. And so your atrial tracking of an atrial tachycardia or even sinus tachycardia, and this is a termination of pacemaker-facilitated tachycardia with P-Morph extension with a VAAV response and getting termination. That could be atrial tracking of atrial or sinus tachycardia. With a VAAV-sense response, a VAAV-sense response, this is a VAAV V-pace response, but a VAAV-sense response means the patient has a pacemaker-mediated tachycardia. You should know something about implant testing for defibrillator efficacy. We have two randomized clinical trials. It is reasonable to omit testing in patients undergoing initial left-sided pectoral transvenous ICD implants that have appropriate sensing, pacing, and impedance values obtained with fluoroscopically well-positioned RV leads. Testing is still recommended in patients undergoing sub-Q ICD implantation, and you should be familiar with that. For right pectoral ICD implants, it would be a class IIa indication, and patients undergoing generator changes, a class IIa indication. These are a smattering of excellent review articles on device troubleshooting. Most of these have to do with ICDs, and most troubleshooting will be related to ICD lead. This is just an example of what you look at when you look at troubleshooting, whether it be for a pacemaker or a defibrillator patient. You have a leadless electrocardiogram, as shown here, leadless ECG. With defibrillators, you have a Thard field or a morphology electrogram, shock electrogram. It can be the ICD CAN versus the RV coil is typically what we look at for Thard field. Near-field sensing is the ring to tip in a dedicated bipolar lead. In an integrated bipolar lead, it will be the tip to distal coil, and the marker channel just tells you what the device sees. Here's a nice example of how useful a shock electrogram can be. It's much like a surface EKG. It gives you a global picture, Thard field, atrial activity, VA patterns, and morphology. The shock electrogram is a Thard field P wave, as you can see here, QRS. So we're looking at sinus rhythm, pacing begins, and you can see now once pacing is initiated, you can see ventricular pacing, you can see that far field atrial electrogram, and you see the patient has VA conduction very beautifully illustrated here. In the next 15 or 20 minutes, I'm gonna go over a variety of teaching examples that review important points that are useful to the practicing clinician, but also are valuable to remember if you're taking an examination in this field, regardless of what the exam is. These are important basic principles and some advanced principles of device troubleshooting. So here's an example of the device treating an SVT, and here you see the patient is in a tachycardia, and there is template matching. That is the template, the morphology template, morphology template is not shown here, matches the template during sinus rhythm. However, the SVT is associated with a one-to-one VA relationship. However, the atrial activity is in the P bar. So this atrial electrogram is not seen. The patient is felt to be in ventricular tachycardia, they get ATP, and then eventually they get a shock. They eventually get a shock because tachycardia persists and they don't see the atrial electrogram. So because they don't see the atrial electrogram, it causes a VT because there are more Vs than As. This is an example of an appropriate detection of VT and the importance of looking at the electrogram source in morphology analysis. This is high voltage A to high voltage B. So using the electrodes, the high voltage coils, and what you can see here is, here's the patient's sinus rhythm with a morphology of a big R wave and a smaller S wave. And you can see the morphology changes dramatically, and the morphology changes dramatically. It causes VT and it pace terminates and we're back in sinus rhythm. This is another example of more challenging electrograms, near field on top, far field on bottom, marker channel shown here. What's the important take-home message? Well, this tachycardia begins with the PAC. The morphology looks really good. And in fact, the morphology match as shown in the bottom, the match is 82%. The match looks very, very good. So you know you have an SVT here. Here, your eyes tell you, here's RV coil to CAN plus the SVC coil. The patient has a distal and proximal coil. This is the rate sense. This is a morphology. And you can see, boy, this electrogram during sinus rhythm, to me, it looks spot on, spot on. So why did the device call this VT? Because it clipped the electrogram during this tachycardia. So when the electrogram is clipped, the match is terrible and it treats this as ventricular tachycardia. So be aware of template changes over time. Aberrancy can cause a change in electrogram morphology. You can have alignment errors. You can have distortion post-shock. You can have similar morphologies during VT and SVT just in that particular analyzed lead. Another example of a patient who begins the tachycardia with the PAC. The morphology electrogram fails here. You can see this sinus rhythm electrogram is different from this tachycardia electrogram, but it begins with an A, so it's probably an SVT. However, you get aberration. You can see the morphology looks really good. Then all of a sudden it changes, okay? All of a sudden it changes here. So change morphology with aberration. You don't get a match, it thinks it's VT. I think it's important in clinical practice. And again, when you think about clinical problems to try to classify the arrhythmias in your own brain and try to understand what the device is doing. The device may misclassify arrhythmias. And these are some of the examples of difficult arrhythmias for the devices to detect. But I want you to think about it as an electrophysiologist. So use the atrial and ventricular electrograms. Look at the onset of arrhythmia, the relationship of A to V, response to pacing maneuvers, response to shock. Look at wobble. Wobble is when there are changes in atrial or ventricular cycling, what drives what? Do the A's drive the V's or V's drive the A's? Examine the termination of the arrhythmia. Examine response to interventions. Look carefully at far field and morphology electrogram, but know the limitations of those electrograms. Examine the morphology, compare them to sinus rhythm. Watch out for double tachycardias present at the beginning or ATP or shock can induce a new arrhythmia. And as I said, look at the effect of RV pacing on the tachycardia. VT with one-to-one retrograde VA conduction is difficult. The differential diagnosis is sinus tachycardia and SVT. Atrial fibrillation and VT. Patients can be in AFib. Patients who have AFib are more likely to have VT, but you have to differentiate AFib plus VT from AFib with a rapid ventricular response. AT with one-to-one conduction versus VT with one-to-one retrograde conduction. And be careful about oversensing of far field R waves and T waves and P waves. You can have VT occurring after sinus tachycardia at a very similar rate. That makes it very complicated management problems. For example, here's a great example. You can see here from the interval plot that the patient's heart rate picked up. And what happened? They actually went into a ventricular tachycardia because you can see in this sinus rhythm, they have a Q wave on their morphology electrogram. And then when they go into tachycardia, they sort of lose that Q wave. So that's important to look at. Remember what I said, look at what's driving what. So look at how the arrhythmia begins. This is an example of initiation. And this is initiation of an arrhythmia with PACs. If you initiate an arrhythmia with PACs, they trigger it, it's probably an SVT. See, here's another arrhythmia with sudden onset. But this arrhythmia is actually initiated by Vs. And then the Vs drive the As. You can see the Vs are faster, the As are faster. The Vs are slower, the As are slower. So Vs drive the As, then you have ATP in termination. Here's an example of a patient where they have some sort of atrial tachycardia. It's ongoing. Then we assume this is atrial tachycardia with a rapid ventricular response. There's a pause. And after the pause, their morphology of the electrogram changes. Now, this is tachycardia at a cycle length of 340. And this is tachycardia at a cycle length of 340. So what are the chances you went from atrial tachycardia at 340 milliseconds to continuing atrial tachycardia at 340 milliseconds? And then all of a sudden you have ET at 340 milliseconds. Very, very, very slight. So this is just a pause and then aberration. Here's an example of a patient with some sort of tachycardia. The device paces and you have your last tachy pace here. And then you have a VAAV response, VAAV response. So some sort of atrial tachycardia. Here's a patient with a spontaneous VT. They induce the same VT in the EP lab. They ablate it. Patient comes back a year later and you can figure out from these differing electrograms that it's a new VT, new VT issues. What do you do? Complex patient management questions. When you have a patient with atrial tachycardia. Here, their atrial tachycardia cycle length is about 340 milliseconds. And then you see they have ventricular tachycardia with VA dissociation. Here again, the tachycardia sort of gets organized to 340 milliseconds. So you have two tachycardias, very similar cycle lengths. What are you gonna do? Well, you're gonna ablate at least one of these tachycardias. Maybe both of these tachycardias is the appropriate management because ATP will go crazy trying to treat this. And then these patients will end up getting shocked a lot for their atrial tachycardia and or their ventricular tachycardia. Here's an example of wobble. There's wobble in the atrial cycle length. Focus on the wobble. The AA drives the VV. So this is an atrial tachycardia. The AA drives the VV. Now it's not gonna drive it absolutely perfectly to within 10 milliseconds, but you see a long ADA cycle length and now a longer VTV cycle length. Here's an example of a pacing maneuver. We have some sort of tachycardia. We pace, we get a V, we entrain the atria to the cycle length of pacing and then end with a VAV. VAV and A's are accelerated. A VAV, this turned out to be AV node re-entry. This is a much more complex tracing. It shows a tachycardia at a cycle length of 290 to 320 milliseconds. The VA interval here is rather short. It's about 40 milliseconds. So the atrial electrogram actually falls into the post-ventricular atrial blanking period. So what happens here is the patient's gonna get ATP, is gonna be delivered and the AA interval is not affected. Upon termination of the pacing, the tachycardia results in, upon termination of pacing, you can see the tachycardia results in two to one AV conduction. And here's another example where every other A falls into, I'm sorry, with every other A falls into the PVAB. And this was interpreted as sinus rhythm at a rate of 98 beats a minute, when it really is some sort of atrial tachycardia. And finally, every A is finally detected here and now it appropriately mode switch. So you look at this and you say, my gosh, it looks like some sort of atrial tachycardia. There are a lot of A's and a lot of B's and they're not, the cycle lengths aren't that different, but they are different enough. And if you look closely, you'll see the A and B's are completely dissociated and one moves past the other. This is an example of AV node re-entry in a patient with an ischemic cardiomyopathy and a dual chamber defibrillator. This episode actually starts as VT, VT with one to one retrograde conduction. However, you can see later in this tracing, the VA times shortened dramatically. You can see that here. In fact, you can see a change in the shock electrogram. You can see the VA times shortened dramatically and the QRS morphology now changes. It changes to the QRS morphology, probably in sinus rhythm, suggesting some sort of supraventricular tachycardia. And eventually the tachycardia terminates here with a V and then an A and then a no V. So terminates on A followed by a junctional beat, followed by a junctional beat. And you can, before sinus rhythm ensues. And you can of course see that the sinus rhythm electrogram is very similar here to the electrogram during SVT. So that's what we have here. This is an example of a patient who had a very complex electrogram, a very complex rhythm. And you can see the patient's in sinus tachycardia at the beginning. And then the patient eventually goes into here into as the electrogram changes, you'll see the patient goes into ventricular tachycardia with one to one VA conduction. So the atrial rate speeds up one to one VA conduction. So sinus tachycardia here, the A's drive the B's. And then if you look closely, there's a transition here into this ventricular tachycardia and a transition to where the B's drive the A's. So it's important to look closely, particularly in these cases where you started out with sinus tachycardia and ended up with a strip showing ventricular tachycardia. Here's another example. Again, I'm asking you what's going on. This is a beautiful example, I think, of pacing. This is a patient who has, here is a marker channel. Here's an atrial electrogram, a ventricular electrogram. Patient is in tachycardia. They have a dual chamber ICD. They're atrially paced at 180 beats a minute. They're in a tachycardia about 160 beats a minute. They're atrially paced at 180 beats a minute. Here's the last atrial pacing artifact. You go from atrial pacing to ventricular sense B to another ventricular sense B. So an A pace, B, B, A, A, B, B, A. B is controlled by atrial pacing. So again, A, B, B, A. And so this patient, and the maneuver is repeated again now with 200 beats a minute, A, B, B, A. And what do you see? Well, A, B, B, A is diagnostic of what? It's the opposite of B, A, A, B. It's diagnostic of ventricular tachycardia. So you know from using only the patient's implantable device that this tachycardia was a VT and not an AV node reentry and not an atrial tachycardia. It's important when we take care of patients to think about, and what we see all the time is patients have come into the hospital because of ICD shocks. And the differential diagnosis, the immediate differential diagnosis should be, do they have a tachycardia? And if so, is it SVT or VTVF? And could we have avoided the tachycardia with ATP or ablation or drugs, or do they not have a tachycardia, but they're over-sensing either intracardiac or extracardiac signals? What are the intracardiac signals? Well, they can be non-cyclical and physiologic such as mild potentials, non-cyclical and intracardiac such as lead connector issues or EMI, or they can be cyclical. And those cyclical can be non-physiologic such as lead failure or over-sense P waves, T waves, or wave double counting. This slide does a great job of summarizing the most important points, I believe. Here you go. This looks at your near field and far field. And with the near field and far field, non-physiologic over-sensing, if there's a lead problem or connector problem, you have noise on the near field, error in the header, you have noise on the near field, you get inappropriate shocks. If your lead's dislodged, then you'll have double counting. You may get a shock, but look carefully, you have double counting. What are you double counting? It may vary with respiration, it may be periodic or cyclical. You're counting both the atrial and the ventricular electrogram. And of course, EMI, you should see on all near field electrograms and far field electrograms as well. Here's VF with short intervals. Here's near field, here's far field. Near field and far field physiologic. This is physiologic over-sensing. What is physiologic over-sensing? Well, the VF, sometimes VF can vary, vary short intervals. And how do I know it's really VF? Well, because you see it both on the near field and the far field. And that's how you differentiate it from a lead problem. Only noise will give you this as well, near field and far field. R-wave double counting, T-wave over-sensing and P-wave over-sensing. What are the characteristics of lead noise summarized here? Saturation of the amplifier, highly variable, intermittent, high frequency, and its absence on the far field or shock electrogram versus EMI, where it will be present on the far field or shock electrogram. Just remember myo-potentials can occur. Myo-potentials can be over sense the biggest muscle in the body is the diaphragm. So my potentials are typically over since on the RB lead, either dedicated or integrated bipolar. And they're differentiated from EMI is they're rarely rarely see on the shock electrogram, and they're accentuated by isometrics and Valsalva. You can also see my potentials. If you look at the far field from the device can. I want to show you this slide because it illustrates a typical over sensing patterns. So, in panel a, what you see is evidence of what looks like noise on the RV tip to coil lead only, but a little bit later you see it on the atrial lead as well. This was an example of electromagnetic interference from the time of surgery. This is an example of diaphragmatic over potential over sensing. Again, as I said, it's typically seen only on the rate sense lead. You don't see anything on the morphology electrogram. And this was recorded on a dedicated bipolar lead due to low frequency attenuation filter. C is an example of atypical cyclical over sensing. And you see an abrupt and sustained increase in pacing impedance due to an open circuit. And this was, of course, due to a lead related problem. This is a differential diagnosis of pace sense failure. This is for pace sense failure. These are the electrogram findings. These are the impedance findings. These are the conditions. So, rapid over sensing with normal impedance could be a fracture, could be an insulation failure, or it could be physiologic or non-physiologic over sensing. If you have rapid over sensing and high impedance, it's a fracture or the lead is incompletely inserted into the pulse generator. And this just goes to the differential diagnosis. The urgency is determined by over sensing. And please disable VF detection while you're trying to figure out what's going on. Here's an example of basically lead problems. This is normal lead impedance. Low impedance means a lead insulation problem. Here's an example of a header problem due to incomplete lead insertion. D is an example of lead conductor fracture with a very high lead insulation. This is the engineering display for lead conductor fracture. And this is exit block at the myocardial lead interface. Another example of external EMI, typical versus atypical. And I just show you the slide to remind you that there is an expert consensus. It's now quite old. I'm perioperative management, but it's worth reading or knowing or looking at some of the figures. These are all examples of atypical EMI. This is one that mimics a lead failure, although you do see it on the shock lead. Here's another one where you primarily only see it on the shock lead. Remember, it's a big antenna, so you may not necessarily see it on all the intracardiac channels to the same degree. This is clearly 60 cycles on this. And again, 60 cycles here. Atypical EMI is when it's not apparent on all leads. These are just some examples of cyclical oversensing due to intracardiac lead defects. Here's an example, and you can work through these, of a ring-to-cable Fidelis fracture, RIATA insulation breach with cyclical spikes, endo-attack integrated bipolar RV coil fracture. It's just an R-wave double counting. You see, it looks like, oh my gosh, R-wave double counting, but it's actually, if you look long enough, you'll see there's no relationship between this spike and the QRS. Now it looks like they're, it looks like double counting from R-waves, but if you look longer, you'll see it's dissociated. And on this beat, this distance between this QRS and this spike is different between this one. And this is an insulation breach suggesting or mimicking T-wave oversensing. You can get oversensing in insulation breaches because you get, where you get seepage of body fluids into the conductor and you see these sorts of noise patterns. Abnormal signals may be present on multiple channels or just on one lead. Here's an example of a Dorado lead. You see isolated spikes on both sensing, sensing and the shock channel. And here's an example where you see again, abnormal signals present on multiple channels. You can use differential recordings to isolate the source of non-physiologic signals such as, okay, here's a can to RV coil, RV tip to ring. Here's an RV tip to LV tip. And you can use it to figure out exactly what's going on. These signals were recorded from an inside out insulation breach of a Dorado lead that resulted in contact between the cable to the ring electrode and the RV shock coil. So it's likely that the contact between the cable to the ring electrode and the cable to the RV shock coil produced an indistinguishable, indistinguishable electrogram. And so here's how you figure it out. You see it on the tip to ring, you see it on the tip to ring. But as I said, it's also involves the RV shock coil and you see it also in the can to RV coil, but not the RV tip to LV tip. So next question is ICD shock while exercising. Does the patient need a new lead? Yes or no? The answer is no, because the rate sense looks absolutely fine. Patients exercising, this is the far field. They're just picking up my pectoral myopotentials is the patient was using his or her upper body when they were exercising. Here's an example of an elderly patient with non ischemic chromopathy and a dual chamber ICD who gets a shock. This patient had chronic kidney disease. These are the meds she's on. What are you going to do next? Well, the beginning part of the tracing shows AFib with a rapid ventricular response. You can see AFib with a rapid ventricular response. The device incorrectly identifies her rhythm as a dual tachycardia. So the patient receives anti-tachycardia pacing, which actually takes this patient from AFib with RVR into a sustained VT. Fortunately, she then gets a shock, which converts both the AFib and the ventricular tachycardia to sinus rhythm. So what you really want to do is reprogram the device. So it either doesn't treat this rapid AFib or ablate the AV node or ablate the AFib or control the AFib better. One of my favorite things is alternating intervals are also called train tracks. Train tracks are not pathognomonic of T-wave oversensing. You can see them with R-wave double counting. You can see them with SVT and three to two Wenkebach. And you can see with far-field R-wave oversensing. As in the atrium, atrial alternans, as you can see the train tracks with the atrial electrogram. Here's an example. What do you do to avoid a shock? The patient got a shock because they have big T-waves. How do you manage big T-waves? Well, it depends. It depends whether they have small R-waves, in which case you have limited programming options. Lead revision is often necessary. Or they have big R-waves and a large R to T-wave ratio. So good programming options. Lead revision is rarely necessary. We talked about differential recordings. This is just one more example for you to look over. This is a light-headed ICD patient due to oversensing. What happened? Well, what happened is the patient's in AFib. They're oversensing because the RV lead is oversensing atrial signal. Well, what's bad about that? Well, the atrial rate is very rapid, so you can get inappropriate therapy. But even worse than that, if the patient's pacemaker dependent, you can have inhibition of pacing. We've talked about oversensing. What about undersensing? Undersensing can occur when there's a small R-wave in sinus rhythm. You must evaluate those patients for lead or insulation problems. And sometimes it's functional due to changes in gain or sensitivity or electrogram morphology. Functional due to blanking periods, such as with rate smoothing. Watch out for rate smoothing. And VT is slowed by antiarrhythmic drug therapy below the rate cutoff. Under-detection of VT is failure to detect VT or VF. It can be by ICD inactivation or VT slower than program detection rate or misclassification of VT as SVT by discriminators or by lead-related oversensing by lead failure algorithms. Remember, marker channels tells you what the device sees. Here's an example where there's undersensing. You see a large R-wave in sinus rhythm, but the PVCs are undersensed. There's no specific therapy needed. The R-waves are just small. And if given enough time, the automatic gain or automatic sensitivity adjustment would eventually see these PVCs. Here's an example of some functional undersensing during VF. Big R-wave, small R-wave, big R-wave, small R-wave. You can see there's undersensing, but eventually the patient does sense the VT-VF because as it gets smaller and smaller, the gain of the sensing amplifier increases. Key points to remember. Atrial undersensing. If you have atrial undersensing, then everything, rapid A-fib, it doesn't see VA, so there are going to be more Vs and As, and it's going to think this rapid A-fib is VF and treat it. Atrial oversensing of far-field R-waves, and then what's going to happen, it's going to be less Vs and As, and it may think there's an ongoing atrial tachycardia or atrial flutter going on. Important to remember these basic principles of ICD programming, the prime detective. Detect and treat life-threatening VT-VF. Secondly, reduce unnecessary shocks without violating the prime directive. With MAT and RIT, there's a 75% decrease in unnecessary shocks and a 50% decrease in mortality. Program empiric ATP therapy, it rarely accelerates VT. Bursts and ramp are similarly efficacious. Very low risk of syncope by prolonging therapy. Here's a great table from the expert consensus, how to reduce shocks. Allow slower self-terminating VT to terminate itself. Minimize inappropriate detection of SVTS VT. Minimize oversensing of signals. Painless therapy for life-threatening VT ATP. Prevent prorhythmia by preventing pauses. As you can see, shock reduction reduces all-cause mortality by about 30%, but great reduction in appropriate shocks and no change in syncope. We've talked about under-detection. I'm going backwards, I apologize. This is a summary of what we just went over. For long detection times, fast VT is what you want to treat. This is a class. Remember, detection duration should be programmed to prolonged intervals to reduce total therapy. The slowest detection rate program should be 185 to 200 The slowest detection rate program should be 185 to 200 beats a minute. For secondary prevention patients, program the slowest detection rate to greater than 10 beats a minute less than the documented VT rate. SVT VT discrimination should be programmed on. ATP programmed on. For the sub-QICD, use two detection zones. Management of frequent shocks. If it's inappropriate, diagnose the SVT, treat the SVT. If it's non-physiologic, fix that. It may involve removing leads, putting new leads in. I show you this. This is to remind you about electrical storm. It's important how to treat it. This is the latest review article from Europace on the subject. I highly recommend you go over it. Think about the different treatment modes for the different diagnoses. CRT. In the last couple minutes, I'm going to cover CRT. You need to know 30% of patients are non-responders. What are the three Ps? Patient selection, no dyssynchrony, they have too much scar, RV dysfunction, AFib, comorbidities. Suboptimal lead position, the leads in the AIV, the lead doesn't capture or there's latency to capture. It's in the CS and not in the LV ventricular branch and nodal capture are very apical. Non-optimal device programming, AV timing, RV LV timing, upper rate programming is incorrect, too much AFib. Percent LV pacing is the most important predictor response, not percent AV pacing or VB or AV optimization. Also want to implant your lead at the latest QLV site. These are all predictors of poor or lack of response to CRT. You don't have a left bundle branch block. AFib, class IV heart failure, pulmonary hypertension, narrow, relatively narrow cure restoration, 120 to 130 milliseconds. Extensive fibrosis of the LV on an MRI, anterior apical placement of the LV lead, less than 90% LV pacing due to frequent PVCs or rapid AF, and your card association class II and non-left bundle branch. The next several slides talk about how to manage the patients. This is a good review for you to think about. Is the patient actually even an appropriate candidate? Is by V pacing manifest? Look at the EKG, look at the chest x-ray. Are competing rhythms present? Rapid AFib, sinus attack, PVCs, is by V programming appropriate? That's when you want to look at the AV and VB intervals, and is the lead position adequate? Here's the clinical treatments of these non-responders. These are the medical treatments. Don't forget treatment for comorbidities. The patient has severe mitral regurge, they may need a mitral clip, and then they'll do really well. Here's an example of an RV lead in the AIV. That's probably not going to help the patient. Suboptimal timing. Here, you want to have nice separation of ENA waves. Here's frequent ventricular ectopy, so V pacing is less than 90%. Okay, you see pre-AV optimization, post-AV optimization, you see nice ENA timing. Look at the EKG. The EKG is so valuable. LV pacing, R greater than S, R greater than S in V1 and or V2 and R less than S in limb lead 1. Highly sensitive, highly specific. Generally, LV capture loss before RV capture. Look at the axis. Loss of LV capture, axis shifts clockwise. Cure S in lead 3, more negative than lead 2, greater positivity in lead 1. Okay, 12 lead surface EKG recorded during an exercise test in a patient implanted with the CRT pacemaker, non-responder. During exercise, what happens? Well, you can see what happens. The patient, in this particular example, the patient became a non-responder because the patient is basically not, the patient's Cure S morphology looks pretty left bundle-ish, looks pretty left bundle-ish. There's some fusion here. So, what's the therapy? You want to shorten the AV interval to erase loss of CRT with exercise. You're just, you're just not, you can see here during exercise, the patient is either not pacing, the AV interval is too long, or you're just getting, it looks just like left bundle. So, what you want to do is you want to get this Cure S back here, and you want to get even possibly more R wave. So, maybe even shortening the AV interval a little bit more. You have the Cure S in lead 1, you want more R wave here, but you see what's happened here is when this patient does even the least amount of exercise, they're either not pacing anymore because they're above the upper rate limit, or the, you know, the PR interval is just too long. Here's an example of loss of biventricular pacing with loss of ventricular pacing spikes. Here's one due to upper rate limit. So, here's the patient at rest, and you see they have beautiful pacing spikes, but then when they exercise, they lose their spike completely. So, the key observation is loss of biventricular pacing due to upper rate response. So, get that upper rate up. Here's an example of this patient we already saw. Here's an example of a patient with a Holter, 68-year-old patient with a bi-VICD without any improvement one month after implant. Well, what do you need here? Here's what you need. You need an atrial lead that works because the atrial lead synchronizes fine, and if you have LV pacing, it's great, but you want to couple it to the P waves. What are you going to do? You need to reoperate. Is the atrial lead as dislodged? And here's an example of a patient who had a CRT device implanted, suboptimal LV pacing percentage, and even when it says there's LV pacing, you have to look at the 12 BDKG because there's so much fusion. So, with that, I'd like to thank you very much for your patience, and thank you for your time.

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