Hi everybody, this is Workshop 8, Core Concepts in EP. These are device questions. I'm Janie Poole from the University of Washington. Here are my disclosures. Case 1, a 27-year-old male has a history of syncopal VT, RV cardiomyopathy, and receives a de novo dual chamber transvenous ICD. We do an interrogation later that day, and we're looking at his presenting rhythm. You capture the tracing below. All impedances and thresholds are normal. The top tracing is A tip to ring, followed by RV tip to coil, followed by RV tip to ring, and the bottom is RV coil to SBC coil. The next best option is A, order a chest X-ray, B, continue watching, C, schedule EP lab for a new RV pacesense lead, or D, place the patient in a sling for 48 hours. The next best option is to order a chest X-ray. So the finding in this case is of over-sensing that you can see on the atrial and ventricular channels. It's very low amplitude noise. The patient just had a new implant, so a lead fracture is not likely. A header block issue could be considered. A chest X-ray may confirm that the pins are not advanced through the header. There's an example here shown, not from this case, but it's a good example of where the pin is not all the way placed carefully. So if that's identified in chest X-ray, then the pocket has to be open, and obviously the lead taken out of the header block can be placed. But another possibility, and more likely in this case, is the presence of air bubbles in the header block, because the artifact is seen on both the atrial and the ventricular channels. Air bubbles are generally transient and resolve within 24 hours. And here is an example that's a little bit more obvious than the example in this case, where there's artifact on both the atrial as well as the ventricular sensing channels. But the best answer is a chest X-ray, because you need to rule out a header block issue in order to decide what you're going to do for this patient. So answer is A, a chest X-ray should be obtained. Case 2, a 66-year-old male with ischemic heart disease comes to the ED following an ICD shock. The ICD was placed for primary prevention. The patient has a history of paroxysmal atrial fibrillation. He has been short of breath for a few days. Program parameters are shown below. Program tracings are shown in figure 1, which will be on the next slide. So you can see on the ATAF plot that towards the end of the plot, you can see this is where ATAF begins, and I've got an arrow where the shock event occurs. The patient is programmed, DDD 60 beats per minute. Tracking and sensing rates are at 115 beats per minute. Ventricular tachycardia therapy is on for a single zone at 207 beats per minute or 290 milliseconds with ATP during charge, followed by shocks, and there's a monitor zone on starting at 120 beats per minute. So based upon the available data, and I'll show you figure 1 in a moment, you conclude that there is a probable lead fracture, B, the device inappropriately delivered therapy for atrial fibrillation, C, the device detected ventricular tachycardia and ICD therapy was appropriate, or D, there was ventricular over-sensing of atrial fibrillation. So here are the strips, and these are continuous. So on the first strip here, you can see what the channels are. The top is A tip to A ring, middle RV tip to RV ring, and then the marker channels and the intervals. See how the rhythm begins, how it progresses, and here is termination with the shock. Let's go back up to the options again. A, probable lead fracture, B, device inappropriately delivered therapy for AF, C, device detected VT and ICD therapy was appropriate, D, ventricular over-sensing of atrial fibrillation. Okay, so based upon the available data, the correct answer is C, device detected VT and ICD therapy was appropriate. So obviously we know that the patient went into atrial fibrillation several days prior to the event, and here are the first two beats are shown. This is native conduction, V sense, V sense with the black arrows. The patient then has a longer interval to a V paste beat, the red arrow, followed by a short interval initiated by a PVC, the green arrow. So we have a short, long, short sequence here, and this starts a run of polymorphic VT that sort of stabilizes to a more regular cycle length VT, and the electrocardiogram of the more regular arrhythmia is distinctly different from the baseline electrogram. This then degenerates into VF. After ATP is delivered, you can see where anti-tachycardia pacing is delivered, and then a shock is delivered with successful termination of the rhythm. So this was appropriate device therapy. Case three, a 58-year-old female with non ischemic cardiomyopathy has a CRTD. She has a tachycardia noted on the most recent remote interrogation, and the pertinent information is shown. Based upon the data available, what is the most likely diagnosis? A, a left lateral accessory pathway, B, ventricular tachycardia, C, AV node reentry tachycardia, or D, atrial tachycardia. On the bottom plot is the heart rate plot. The closed circles are the ventricular intervals, and the open squares are the atrial intervals. You're provided with information about how the device is programmed with a VF zone at 300 milliseconds and fast VT, so this is a Medtronic device, within the VF zone at 240 milliseconds. Channels are LV tip to RV coil on top, CAN to RV coil in the middle, followed by the marker channels. The waveform is suspended, but you can see then the termination of the rhythm here below. So the question is, what is the most likely diagnosis? The most likely diagnosis is AV node reentry tachycardia, so let's walk through how I came to that conclusion. So let's think about analysis of a one-to-one tachycardia, any one-to-one tachycardia, not just necessarily on ICD interrogations, but we need to consider the onset, if available, what the VA or AV intervals are, are they short, long, or mid-RP tachycardias, what the electrogram morphology is, comparing the tachycardia to the sinus or the baseline QRS interval, is there so-called linking or wobble in the arrhythmia cycling, and if so, can we determine if the change in the A-to-A drives the B-to-B, or opposite, the change in the B-to-B cycling drives the next A-to-A? Looking at termination is always really helpful, does it end in an A or a B? And then in ICDs, if available, to look at the response to ventricular ATP, look at the marker channels, and of course, the device programming. So here, looking at this, and the ventricular electrograms, and the marker channels, confirms that this is a one-to-one tachycardia. There's atrial signals here, AB for atrial blanking, but there's a one-to-one relationship between the tachy sense and the atrial sense, or the AB. Both onset and termination are recorded. Device therapy was not delivered in this case, so we don't have the opportunity to see the response to anti-tachycardia pacing. Now let's continue to walk on through this. So let's look at onset first. So the tachycardia starts with a few PACs, the red arrows, and then a stable AV relationship is established with either short VA or a long AV interval. The heart rate plot is also useful because it confirms that the tachycardia starts with an atrial beat. This observation really essentially rules out ventricular tachycardia. So now looking at electrogram morphology, in this device, the marker WV refers to the ventricular morphology discriminator being applied. So this device determines that there's a good match to the sinus rhythm morphology, and the device declares this to be a supraventricular tachycardia. So the question is, is the device correct? So when troubleshooting these matches, and all the companies have this morphology match, but their criteria differ. So you need to know what is considered to be abnormal for each device and model. So in this case, a match is equal to or greater than 70%. So when the rhythm eventually terminates, the patient has atrial sense by ventricular pacing, which really precludes a visual comparison of the underlying normal R-wave electrogram morphology. So this template, we have to assume, was determined at implant using the patient's intrinsic QRS. And one tip about these morphology matches in patients with CRT devices is that when looking at morphology templates, you need to be certain that the peak is not truncated, as that can give a false device interpretation. Also in CRT devices, if the underlying ventricular morphology has not been updated from pre-implant, the match may not be accurate as the R-wave or the V-morphology might change over time. Okay, but so in this case, the device is thinking this is a good match for a supraventricular arrhythmia. Okay, next we're going to look at VA linking and then termination of the rhythm. So if you scrutinize the intervals or the cycle links here, you can see that the V-to-V intervals are driving the changes in the next A-to-A intervals. And in this device, all these intervals are rounded to the nearest 10 seconds. But the longer intervals start with the V and then follow with the A being within 10 milliseconds, so you have V-to-V and then A-to-A, and then you have a shorter V-to-V resulting in a shorter A-to-A. So you can see that the V-to-V interval is what's driving these cycle length changes. You can also see that the VA interval is constant and that it's the AB interval that is variable. So these observations are not really consistent with an atrial tachycardia. Also, we can look at the termination. We can see that the rhythm ends in an A, which is consistent with an AD nodal dependent tachycardia and effectively rules out an atrial tachycardia. All right. Well, let's take a look at the information and see what additional hints for the diagnosis that we can pull out of this. And here again, on this slide, it's LV-TIP-to-RV coil on top, TAN-to-RV coil in the middle, and then the marker channels, and then you can see the discriminator markings here. So you can use the onset of a far-field electrogram as a very rough estimate of the onset of the surface QRS to the A. So if you look at the VA interval and measure that out, it's about 100 milliseconds here. So although that's not exactly accurate, it probably would exclude a left-sided accessory pathway. So putting all of this together, there is enough information to determine that the most likely diagnosis is AD nodal reentry tachycardia. We excluded VT and an atrial tachycardia. It's unlikely to represent a left lateral free wall accessory pathway. I think that's probably fair to say. A right-sided accessory pathway is not ruled out, but was not an answer option. So of the options, C, AD, and RT is the best answer. Case four, a 78-year-old woman with a dual chamber pacemaker for complete AV block is in the ICU with sepsis. You're told that the pacemaker is not working. The patient's heart rate is 70 beats per minute, and she has become hypotensive requiring dopamine. ECG tracings from three successive days are shown in tracings one to three. So the question is, what is the best explanation for the tracing shown? A, the pacemaker is not working. B, extending the PVARP would solve the problem. C, the atrial lead was dislodged during central line placement. Or D, the pacemaker is working appropriately as programmed. Here's the pacemaker programming. It's programmed DDD with lower rate 60 beats per minute, upper tracking rate 120 beats per minute, sensed AV delay of 200 milliseconds, paced AV delay of 180 milliseconds, and the PVARP is 240 milliseconds. Here is tracing one on the day of admission. Tracing two is hospital day two. And tracing three is hospital day three. So going back up, what is the best explanation for the tracings that are shown? Again, the pacemaker is not working. Answer A, extending the PVARP would solve the problem. Answer B, the atrial lead was dislodged during central line placement, answer C, or D, the pacemaker is working appropriately as programmed. Here are the tracings again. Okay, the answer is that the pacemaker is working appropriately as programmed. The tracings show normal pacemaker upper rate behavior. So to understand this or figure this out, you need to know that the upper tracking rate is limited by the total atrial refractory period, which is the AV interval plus the P-bar. When the atrial rate exceeds the programmed upper tracking rate, it results in pacemaker winky block. If the atrial rate keeps increasing and exceeds the total atrial refractory period, it's going to result in pacemaker 2 to 1 AV block. So you can see here that the total atrial refractory period in this case is 440 milliseconds, which is about 135 beats per minute. And the sinus interval got up to 428 milliseconds or 140 beats per minute. So let's see what that does then. Tracing one, the patient's at rest and the heart rate is 75 beats per minute. And there is one-to-one asense ventricular tracking, ventricular pacing. But as the heart rate increases to around 110 beats per minute, and you can see that because you can see the P waves on this tracing, you see that there's asense followed by the pacing, but where there's this AR, it falls into refractory and that is not followed by a V paste or a track beat, and that is pacemaker winky block. And then as the heart rate continues to increase up around 140 to 150 beats per minute, then the pacemaker exhibits two-to-one pacemaker block. So just to provide some further information, you can look at this for reference on how this all works, whether or not you'll have winky block occur before two-to-one block or not, depending upon what the relationship is of the upper sensing intervals, the upper tracking intervals, and the total atrial refractory period. Case five, a patient comes to clinic after receiving an ICD shock. The pertinent portion of the interrogation and the electrogram episode is shown in tracing one. Your conclusion is A, appropriate ICD therapy, B, inappropriate ICD therapy due to atrial over-sensing, C, inappropriate ICD therapy due to atrial under-sensing or normal device function. So here is the the tracing. So we have A tip to A ring on top, we have B tip to B ring in the middle, and then the marker channels. And you can see that anti-tachycardia pacing is delivered here, and that the rhythm terminates with a V paste. So what are the options again? Appropriate ICD therapy, inappropriate ICD therapy due to atrial over-sensing, inappropriate ICD therapy due to atrial under-sensing or normal device function. So what is the answer? The answer is actually C, inappropriate ICD therapy due to atrial under-sensing. So we know that the rhythm is atrial fibrillation with RVR, because the patient has rapid atrial fibrillation, of course, with mostly tachycardia sensing, and some of the pacing occurs. But there are a few atrial signal markers, the red arrows. So there's inappropriate atrial pacing occurs due to under-sensing of the atrial fibrillation. So how does that impact the discrimination algorithms? So SVT versus VT discrimination in dual-chamber ICDs begins with a comparison of A to V intervals, and this is critical to device-determined appropriate delivery of ICD therapy. True VT will be decided if there's more Vs than As. Then further discrimination relies primarily upon morphology discriminators in order to determine if therapy will be withheld for AF, SVT, or sinus tach, or if therapy will be delivered. In this case, as atrial under-sensing was present, the device determined that there were more Vs than As and called this ventricular. Device therapy was then delivered according to the programmed parameters. So the right answer is C, and the remaining options are not supported by the electrograms. Case 6. A 48-year-old with hypertrophic cardiomyopathy in a dual-chamber medtronic transvenous ICD that was implanted in 2014. An alert, which is noted below, pops up on remote device check. The patient comes to clinic. The presenting rhythm was collected on the remote interrogation as shown in figure 1 on the next slide. Electrograms obtained with arm motion are also shown on the next slide. So the question is going to be, the best explanation for the findings is A, ventricular pacesense lead fracture of the tip, B, atrial pacesense lead fracture, C, ventricular pacesense lead fracture of the ring electrode, or D, high voltage lead fracture. You can see what the alerts are here. There's one for an RV bipolar lead impedance warning, and on the same day, an alert for RV tip to RV coil lead impedance warning. There's also some warnings about capture management and telling us that BF detection might be delayed if the detection interval is programmed high. Okay, so here are the figures. So this is first the presenting rhythm on the remote interrogation, and then it continues, and then the episode or the event terminates. So you can take a look at these markers, and then below is what happens in clinic with arm motion. So now we have the marker channels on top. We have RV tip to RV ring in the middle here. We have RV tip to coil on the bottom. Let's go back over this again. So we have alerts, and alerts are RV bipolar lead impedance warnings, so RV tip to ring, and then we have an alert on RV tip to RV coil. Options are a ventricular pacesense lead fracture of the tip, atrial pacesense lead fracture, ventricular pacesense lead fracture of the ring, or high voltage lead fracture. Again, here are the tracings. So the explanation, the best one is ventricular pacesense lead fracture of the tip. So this case is interesting. It does not present with the more typical large amplitude make-break signals that are generally seen in a for-sure lead fracture. However, there's enough evidence to make the diagnosis. The presenting rhythm showed far field over sensing on the atrial channel, far field over sensing on the atrial channel, which you can see up here on A tip to A ring, that's just normal far field over sensing. But at the end of the strip, you can see that there were some extra signals of short intervals. And this together with what happened with arm motion, you can see there are short intervals again, noted as fib senses or VS to VS of short intervals. And these findings together with the impedance abnormalities are enough to make the diagnosis of a lead fracture. So how do we know that it involves the tip? Because the noise and the impedance changes were present on both the tip to ring and the tip to coil. So in this case, despite absence of those classic large artifacts, you've got a lead fracture here that involves the ventricular pace sense tip electrode. Okay, case seven. This is a 57-year-old with a single chamber ICD who receives a shock. There's a single VF zone on at 320 milliseconds and detection that is the number of intervals where detection is programmed at 18 out of 24. Of the following, which is the most likely right answer? A, initial detection of VF is inappropriate. B, the ICD fails to confirm the shock. C, a 25 joule shock is not likely to defibrillate VF reliably. Or D, a 25 joule shock would likely defibrillate reliably. So the EGM source you can see is HVA to HVB in a Medtronic device. Here are the abnormal rhythms and here is where the shock is delivered. The energy delivered is 25 joules and the high voltage impedance is noted at 53 ohms. So which of these questions is correct? Well, C is the correct answer. A 25 joule shock is not likely to defibrillate VF reliably. So why is this and what's going on here? Well, first of all, A, detection is actually appropriate. If you look at these, I've numbered them, there are 18 out of 24 beats that fall within the VF detection zone to begin a charge cycle. What about confirmation? Well, confirmation is confirmed. How do we know that? Well, confirmation algorithms deliver a synchronized R-wave shock if one or a few intervals after completion of capacitor charging are fast. The algorithms vary by the manufacturer and model. The fact that the ICD delivered an R-wave synchronized shock right here indicates that the shock was confirmed. If the ICD failed to confirm the shock, it would have aborted it. So what's actually happening? So ICD shocks, as noted, are synchronized to the R-wave to prevent a shock landing in the vulnerable period and inducing VF. In this case, the R-wave, which is here, and therefore the synchronized shock happens while repolarization is still happening. The vulnerable period of the preceding beat extends to the second PVC's R-wave, which occurs about 40 to 60 milliseconds after the T-wave nadir after this first PVC. And you can see another PVC up here where I've got the red bracket. And so you can actually measure that out and show what's going on. So what's going on here? The principle is vulnerability and its upper limit or ULV. There is an upper limit of strength above which a shock will not induce fibrillation during the vulnerable period. This is called the upper limit of ventricular vulnerability and correlates with the defibrillation threshold. The threshold for fibrillation correlates to the threshold for defibrillation. In this case, the ULV is above 25 joules. We know that because the shock landed in the vulnerable period and VF was induced. Importantly, the ULV approximates the shock strength that defibrillates with a probability of about 90 percent. Thus, a 25 joule shock cannot be counted on to defibrillate reliably, which was answer C. And here I give you some examples. A lot of this data is pretty old, but the concepts have not changed. That's the end of this workshop. Thank you for your attention. Welcome to workshop number eight. We'll go over questions and answers from the Core Concepts in Electrophysiology and Board Preparation Course 2022. These are my disclosure of relationships. Okay. Case number one. A 68-year-old man is seen in clinic two days after reporting, receiving a shock without any preceding or premonitory symptoms. A single chamber ICD was implanted three years ago for syncope and ischemic primopathy. No abnormalities of the system have been noted during follow-up. He was seen in clinic three months ago and had normal pacing impedances and pacing thresholds. Tracing 1-1 is recorded in clinic from the shock received two days ago. He recalls walking past a power plant two days ago. Referring to tracing 1-1, the most likely abnormality that will be discovered in clinic today is, A, elevated pacing impedance. B, the time of the shock is the same as when he walked past the electrical power plant. C, elevated pacing threshold. D, oversensing with RR interval shorter than 180 milliseconds. E, decreased amplitude of sensed R-wave. This is the tracing, and you can see the patient receives a 35-joule shock right here. And here are the options, choices. Again, here are the choices. Here's the tracing. The correct answer is over-sensing with RR interval shorter than 180 milliseconds. This is a very important concept, one you should know and understand. The most common cause of lead failure, of ICD lead failure in clinical practice is a lead fracture, a conductor lead fracture. And thus over-sensing of rapid make-break potentials, not a high, not a low impedance, not changes in the pacing or sensing thresholds is the definition in many ways of the cause of inappropriate shocks due to lead fracture. Impedance and trends may be normal when tested with all lead fractures early on because these make-break connections are sporadic. They're intermittent. Probably 94% of patients are higher. Patients with lead fractures will have evidence of over-sensing, either short RR intervals or episodes of non-sustained BT with intervals that are non-physiologic. It is not EMI because there's no noise on the shock electrogram. This is an example of a patient who has a conductor fracture. You can see in this scanning electron microscope, a fracture here, right over here, the yellow arrows pointed to that. The hallmarks of a lead fracture are it's very common to see a stable RV pacing threshold. Now, of course, if you happen to measure the RV pacing threshold at the exact time at which there is that make-break point or at which time there's electricity is not flowing, then you're going to have a very high threshold. Likewise, if you are continuously, every single second checking pacing impedance by delivering a pulse, then you'll have some intermittently very high values for lead fracture. However, the hallmark is that these electrical, the electrical signature of a lead fracture is that it's intermittent. That some are not cyclical. It may occur in bursts and then go away. That they're very short R to R intervals because of over-sensing of these very rapid make-break connections. There are no non-physiological signals on the shock channel because this is looking at morphology. That is variable amplitude in morphology and frequency of the rate-sensing electrode and the amplifier can be saturated. Again, shown in this example, you see it's absent on the far field electrogram and all the typical characteristics of noise. This is from a paper we wrote several years ago and you can see in 94% of patients, there is over-sensing as measured by short non-physiologic RR intervals and episodes of non-sustained tachycardia with a very rapid cycle length. Whereas impedance elevations, not seen all that commonly, only 31%. And even if you look at changes in impedance that are specific for that patient, such as a change in impedance of more than 500 ohms, you see it's not even that common. Second question, what is the optimal device choice for a 68-year-old man with left spinal branch block? Ejection fraction of 48%, negative ETT three months ago, who presents with syncope and is found to be in two-to-one heart block with narrow QRS escape rate. His prior baseline ECG shows sinus rhythm and appear interval of 240 milliseconds, which is the most appropriate device for this patient. A, DDD pacemaker with an RV apical lead. B, DDD pacemaker with RV lead placed in the his left bundle region. C, DDD ICD. E, biventricular pacemaker. I show you this question to get you thinking about the guidelines and where our field is. The correct answer is a DDD pacemaker with the RV lead placed in the hysta bundle region or a biventricular pacemaker. What am I basing that on? Here we go. The ejection fraction is 48%, so the options are dual chamber pacemaker, dual chamber pacemaker with hysta bundle lead and biventricular pacemaker. When he has high grade heart block, he will ultimately have a high burden of ventricular pacing. Then he should have a by the pacemaker based on the guidelines and the block heart failure trial. However, we have pacemaker guidelines and they now acknowledge that conduction system pacing and CRT are both options, both class 2A options. You have to know the guidelines, especially in areas where the choice is not always so very clear. If this same question was asked, but in this case, the patient had mild mitral regurgitation and EF at 55%, the correct answer would be a DDD pacemaker with a conventional RV lead or lead in the RV apex would be fine. If you had this question in Europe, then the correct answer would probably be a biventricular pacemaker because the European guidelines just recently published in the last year do not give a conduction system pacemaker lead a class 2A indication, but give it a class 2B indication, whereas the AHA, ACC, HRS guidelines give it a class 2A indication. This is the block heart failure trial, should be familiar with this. The primary outcome was time to death from any cause, urgent care visit for heart failure requiring IV therapy or a greater than 50%, 15% increase in LV ancestral volume. These show you clinical outcomes, change in quality of life based on intention to treat by V is shown in blue, in the red or tan is shown the RV arm. And you can see there's greater improvement in quality of life, greater improvement in quality of life over time, even accounting for crossovers. You can see the event primary outcome is better with by V pacing. And then these are the guidelines. You can see class 2A in patients with AV block who have an indication for permanent pacing EF between 36 and 50%. We're expected to require ventricular pacing to a high degree, more than 40% of the time. It is reasonable to choose pacing methods or pacing modes that maintain physiologic ventricular activation, either CRT, his fundal pacing over RV pacing. Case three, a 68 year old male with history of coronary artery disease and VT, ventricular tachycardia, underwent implantation of a dual chamber ICD five years ago, is admitted to the hospital with symptoms of nausea, palpitations, presyncope and low blood pressure. The rhythm strip while on telemetry is shown in figure three, one device interrogation was done and it showed the following parameters. These are the parameters, the pacing parameters, the lower rate, maximal tracking rate, dynamic AV delay is on, AV search hysteresis is on, PVARF after PBC with dynamic PVARF and pacing thresholds are fine for the RA and very good also for the RV lead. So the patient comes in with developed symptoms and the symptoms correlate with some of these episodes shown here. This is taken from telemetry when the patient is symptomatic and so with this tracing the question is what change would correct this heart rhythm problem? A, reprogram PVARF, B, revise atrial lead, C, lengthen the AV delay, D, reprogram the ventricular blanking period. So those are your choices. This is the electrocardiogram and they're asking you what you can do to fix this problem. Choices, the correct answer is A, reprogrammed P-bar. Note, this is not pacemaker-mediated tachycardia, which typically has ventricular pacing at the upper rate limit and tracks a retrograde P wave. What is this then? This is repetitive non-reentrant ventricular atrial synchrony, or RNRVAS, plus A-B search hysteresis. The first seven beats show atrial pace ventricular sense complexes. This is followed by a PVC with retrograde atrial conduction. Note the inverted P waves in lead II, dashed arrows, we'll show you this in the tracing. So this is rhythm, this is from the recording I showed you. You can see the inverted P waves here. You can see the upright P waves here, okay? You can see there's a little bit of a positive P wave after the pacing spike, but now the P waves are retrograde, and of course, because they're retrograde, they're going to be inverted. And you can see that by the dashed arrows. So the device does not sense the retrograde P wave, right, because it falls into the post-ventricular atrial refractory period that extends to 400 milliseconds following a PVC. This is followed by an atrial pacing spike that does not capture the atrium, because the pacing spike falls into the absolute refractory period of the atrium. The pace A-B interval expires, resulting in a V pace with subsequent recurring retrograde atrial activation, and the process repeats again and again. This repetitive process of functional atrial undersensing due to retrograde atrial activation falling within the P-VAR, along with functional atrial non-capture due to the pacing stimulus falling in the absolute refractory period of the atrium, is termed RNRVAS. It may also be called AV desynchronization arrhythmia, or pseudoatrial exit block. RNRVAS is a less common form of pacemaker-mediated tachycardia or endless loop tachycardia, resulting from VA conduction, the more common form being PMT. So this is a nice example of that. This is functional atrial non-capture, followed by retrograde conduction, functional atrial non-capture. So although pacing at the upper pacing rate is not typically seen with RNRVAS, the hemodynamics are similar to pacemaker-mediated tachycardia. RNRVAS is typically presented with symptoms suggestive of loss of AV synchrony, fatigue, palpitations, dizziness, hypotension, dyspnea, and syncope. RNRVAS can be stored as automatic mode switching events because two atrial events, retrograde atrial activation, and A pacing are recorded by the device for each V pacing signal. It can be prevented by shortening the P-VAR, although this does increase the risk of pacemaker-mediated tachycardia. Shortening the AV delay, reducing the lower rate limit or sensor-driven rate, and specific algorithms such as non-competitive atrial pacing algorithm or by synchronous A pace on a PBC can actually, as I said, can actually be prevented using these specific company specific algorithms. This is a nice review paper. It's an under-recognized cause of pacemaker-related arrhythmia. It occurs when the retrograde P-Wave occurs within the P-VAR. PMT or endless loop tachycardia occurs when the P-Wave is outside the P-VAR. So this is promoted by a short P-VAR. This is promoted by a long P-VAR, a long AV delay. The treatment is algorithms are really nonexistent to terminate RNRVAS. You can shorten the AV delay. You can decrease the lower rate limit or disable features that allow rapid AV sequential pacing. Specific algorithms are present in all manufacturers to prevent and recognize these events and this loop tachycardia, but not specific algorithms to prevent or identify these RNRVAS episodes. Features that allow rapid AV sequential pacing, such as rate drop response, rate adaptive response, or atrial overdrive pacing algorithms, increase your risk of RNRVAS. Case four, tracing 4.1 is a representative stored electrogram in a patient who received an ICD one year ago for primary prevention. Interrogation reveals two similar episodes for which none of these episodes in the patient received therapy. What is the best next step? Reassurance and schedule next routine follow-up visit, B, schedule chest radiograph and perform maneuvers to check lead integrity, C, admit for lead repositioning, D, schedule insertion of a new sensing lead, E, reprogram sensitivity, and check VF sensing. This is an example of one of the episodes the patient had where she did not receive therapy. So what are you going to do? These are the options again shown here. The correct answer is reprogramming, sensitivity, and check VF sensing. So this is an example of T wave over sensing. In practice, that is in real life and on exams, it's important to remember for the benefit of our patients to try least invasive things first and test for adequate ventricular fibrillation sensing. You must also consider relative R wave to T wave amplitude. If the T waves are much greater than the R waves or very similar in size, then you need a new ICD lead to be placed or a repositioning of the ICD lead. And when possible, programming to an integrated bipolar sensing configuration is always an option that should be tried earlier on before opening the pocket and repositioning the lead. So this is an example of T wave double counting, which you see over here, even though the patient received an inappropriate shock. If you see this in clinic without the patient receiving any inappropriate therapy, you want to at least try to correct it non-invasively and do something about this before the patient actually receives a shock. Spontaneous pacing, pauses during pace rhythm or during ATP tend to accentuate the T wave over sensing, but during spontaneous rhythm, inappropriate therapy may be delivered by T wave over sensing. Small R wave and normal or large-sided T waves present clinical problems. There are limited programming options. Lead revision is often necessary because of the very limited programming parameters, possibilities. Here's only a modest size R wave, but a pretty big T wave. When you have big R waves, even if you have, you know, modest or moderate size T waves, you have good programming options. Lead revision is rarely necessary. You can program sensitivity higher, or you can try programming to an integrated bipolar sensing mode if possible. This is an example of a tracing recorded from a patient on remote monitoring after generator change three months ago. The most likely result from this finding, so this is case number five, and this tracing is taken from a patient with an ICD. This is found on a remote monitoring strip after generator change just three months ago. What are you going to do about this? A, removal of the ICD lead due to a lead fracture, or B, reoperation for an ICD sensing screw problem, C, reoperation for an ICD header problem, D, obtain a history for source of EMI, E, no further therapy is indicated. So how do you manage this finding? This is the finding. What are you going to do to manage this problem, or is it a problem? It's just noted on remote follow-up. The correct answer is E, or choice number five, no further therapy is indicated. This is over-sensing on the coil due to pectoral muscle over-sensing, or rather, it is over-sensing on the SVC coiled tachan. The coiled tachan is a morphology vector. This vector is not used for sensing in arrhythmia, however, it certainly can sense myo-potentials which are recorded under the pocket. So electrograms from a storied episode, this takes me, the most likely cause in a patient is a myo, in this patient's myo-potential source. This is from a paper. This shows an example of electromagnetic interference with EMI. You have evidence of over-sensing. These are all over-sensing from extracardiac sources. This is over-sensing on the high voltage and RV lead you see here. This is diaphragmatic myo-potential over-sensing, another cause of myo-potentials. The diaphragm is the biggest muscle in the body, and you can see there's intermittent over-sensing on the RV lead, but not on the high voltage lead, right? The proximal coil to the can, for example, because you're not by the, you're not anywhere near the diaphragm, and there's nothing, the RA lead is clean. Here is a lead fracture, this is an extracardiac source, it's a lead fracture, and you see intermittent make-break potentials that are intermittent and variable in amplitude. And here we have an example of a set-screw problem with these repetitive, very rapid high-frequency signals seen here, and unusual here. So this is a lead fracture set-screw. Here's a set-screw problem, and this was also an example of a, also an example of a patient who had a lead fracture. Skeletal myo-potentials are important to recognize in the differential diagnosis of conductor fractures. That is, this is an example, as I said, of diaphragmatic myo-potential over-sensing. You have multiple high-frequency uniform morphology signals, as you can see here and here, and may be recorded from widely spaced bi-poles of normally functioning leads. Diaphragmatic over-sensing shown here in the RV tip-to-coil, and pectoral in the bi-polar configuration, that includes the can, that is, includes a shock channel. That's where the myo-potentials are here, and here are the myo-potentials here. Myo-potentials on closely spaced bi-poles, remote from the muscle source, which can occasionally happen, indicate a insulation breach. So if all you see is coil-to-can, then it's probably pectoral myo-potentials, but if you see it on the RV tip-to-ring, you have to worry about failure of the insulation. Case 6. A 74-year-old woman with renal failure and persistent day fib underwent AV junction ablation for rate control one week ago. She underwent implantation on the leadless pacemaker prior to that. She was readmitted with dizziness. Her RV pacing threshold was 2.75 volts at one millisecond. Her device was programmed to five volts at one millisecond. The following strip was just recorded while the patient was asymptomatic at 2 a.m. in the morning. The best next management for this patient is A, STATECO to look for pericardial infusion, B, place new ECG monitoring electrodes, and if no further pauses, routine management and schedule follow-up and discharge. C, implant a transvenous VBI pacemaker from the left side, and D, extract the leadless pacemaker and implant a new leadless pacemaker. So those are the choices. Here is the incidental finding at 2 a.m. The correct answer is D, extract the leadless pacemaker and implant a new leadless pacemaker. The acute threshold rise with loss of capture, replace the device. Patient is pacemaker dependent. The threshold will not likely decrease, and the leadless pacemakers are easy to remove early on. So with that, I'm going to conclude and say thank you very much for your attention. Thank you. This is Sam Asarvadam. This workshop will just focus on some issues with device cases, radiology, electrocardiographic correlation, and some troubleshooting. So I'm going to show you ECG tracing from a patient with a CRT device that's been in about a year. Patient has not had any clinical improvement. What would be an explanation for why the patient is a non-responder? So I'll show the ECG, paced rhythm, and the options. Is it the PVCs? Is there lack of atrioventricular synchrony, failure to capture on the left ventricular lead, possible need for a left ventricular lead offset, or potentially all of the above. So it really can be any or all of these reasons. So if we look through a few things here, first, we look at the overall vector. So left bundle pattern and R wave, initial R wave, and one. This suggests that predominant activation is the right ventricles. It could be there's an issue with the left ventricular lead, or just needs an offset. Just in this 12 lead, we have PVCs. So frequent PVCs, it could be minimizing pacing from the CRT system, or enough PVCs could themselves be affecting ventricular function. We also know sometimes you can see a P wave. So this is a patient who may have had a CRT system placed without an atrial lead, because the patient was at atrial fibrillation at that time, and now is in sinus rhythm. This loss of AV synchrony can greatly diminish and completely offset any advantages that you could have from ventricular synchronization. Just an example of some potential things that we can look at with the 12 lead ECG when troubleshooting failure to respond to CRT. So we think about frequent PVCs, we think about AV synchrony, and we look at the ECG to see what we can tell about the ventricular pacing. So this is a question that I'm going to show you in EKG and chest X-ray, and need to see what you suspect about the system. So this is the electrocardiogram and an AP chest X-ray. So is what you're seeing consistent with a normal endocardial system, a normal ectocardial system, a coronary sinus implant, or an arterial implant? ECG X-ray. So this is consistent with an arterial implant. So why is that? So let's start with the ECG. We notice a right vundral branch block pattern, negative and lead one. That's consistent with left ventricular pacing. A left ventricular pacing could be an epicardial system. It could be an endocardial system, purposely placed endocardial system through a transeptal puncture, or potentially placed inadvertently, either through an artery or a PFO. Or it could be coronary sinus-based left ventricular pacing. Now it's hard to know which of those three it is looking at the ECG alone, but epicardial implants like epicardial foci or PVCs or VT tend to be very slurred up strokes on the QRS, whereas this is pretty sharp. So suggesting an endocardial implant from the left ventricle, probably inadvertently. Second thing that we can also look at when we correlate is with the chest X-ray. And the chest X-ray, the telltale signs of an arterial implant is it crosses the clavicle and goes in the center of the cardiac stem, the cardiac silhouette. SVC would be here, pulmonary artery would be here, aorta is in the middle. So arterial implant going into the left ventricle. That central location, along with the right fundal branch block, should make you think about this and hope that it's recognized when inadvertent and taken out. In this patient, unfortunately, it wasn't. Thrombi had formed on the lead and the patient had presented with unexplained stroke. So here, a pacing lead is placed at a site that I'm going to show and point to you. We want to try to correlate that lead location with what you anticipate will be an issue. So this is the yellow arrow, and this is the location, anatomically, if we were to target this location. This is looking from the left side of the heart, aortic leaflets, non-coronary and right coronary, coronal section, crest of the interventricular septum, atrial septum, mitral valve, tricuspid valve. What do you think is likely to be associated with this? Is it high thresholds? I'm sorry, least likely associated. So all of these are possible, but what's least likely associated with this site? Is it high thresholds? This bundle capture, injury to the compact AV node, interventricular perforation, or heart field sensing of atrial signals. So question is, if you put a lead where this arrow is shown, which of these do you not expect least likely to occur? So compact AV node injury would be not expected in this region. Many of you would have recognized this region is the membranous septum, fusion of the right and non-coronary sinuses at the level of the tricuspid valve. Membranous septum is home to the bundle of his. So bundle of his is the only structure in the membranous septum. If we targeted that site, we might capture the his bundle directly. Thresholds tend to be high because of the insulation around the his bundle. And if you're not having simultaneous ventricular capture, thresholds tend to be higher. You could perforate with a screw, a large helix through the membranous septum. Because this is all atrial tissue of the interatrial septum and the region of the non-coronary sinus, you could get far field atrial sensing. What you won't get is AV node, compact AV nodal damage. Unlike the membranous septum where the his bundle is located, the compact AV node is atrial and a mid-septal structure. So damage to the AV node, the compact AV node is unlikely. It's possible to damage the his or maybe even the proximal right bundle when targeting casing and locations for the conduction system at the level of the his or perihisin region. So coronary sinus angiography is what I'm going to show here. I'm going to show you the REO and lateral projections and to see what abnormality you think is being seen here. So this is the right anterior oblique projection and then the left anterior oblique projection. So retrograde coronary venography is being done perhaps in anticipation of placing a left ventricular lead. So which are you seeing here? So the fistula, perforation, prominent buccins valve, prominent trabezium valve, or a coronary sinus diverticule. Here's the image again. And this is a prominent buccins valve. So a few things we notice from this retrograde venography, CS osteum, typical position of the buccins valve or valve of the lateral vein is where the body of the CS diverges as an atrial vein, vein of Marshall, and the great cardiac vein, usually the same site you get a lateral or posterolateral vein. Now you could also get valves at mouths of other veins and the trabezium valve right at the CS osteum. These generally are not prominent and allow you to cross. The buccins valve can be prominent and difficult. Sometimes coil up here, but it is a valve that opens and closes with retrograde blood flow. So just gentle probing will usually allow you to get across that valve and you can complete the procedure. Occasionally, it's nearly occlusive. And when that's the case, if you stay on venography or do arteriography, venous phase imaging, you'll see posterior veins draining the blood from the left ventricle. And you could use one of those veins to try to get to the left heart border. So prominent valves, occasional difficulty with placing CS-based left ventricular leads. I'm going to show you an ECG and we're going to try to determine the location of the pacing lead. This is the ECG pattern. Take a look at this. And is this most consistent with the right ventricle, middle cardiac vein lead, anterior interventricular vein lead, posterolateral vein lead, or something else? So based on some of our prior discussions, I think without the x-ray you should recognize this is posterolateral vein facing. How do we know that? There is a right bundle-like pattern suggesting there is at least a lead capturing left ventricle. It's completely negative in one, completely negative in one. Free wall of the left ventricle. Free wall, but it's posterior free wall. Because 2,3-AVF are predominantly negative. Posterolateral LV is where you anticipate seeing on the LAO projection. So free wall of LV, negative in one, positive in lead V1, and closer to the feet, so negative in leads 2,3-AVF. So in this case, we're going to look at not so much where the lead is, but knowing that the lead is in the same location, and facing at different outputs from the same location. The vector for facing is the tip of the LV lead to the ICD lead. In this case, the coil, but more commonly with present systems would be the ring electrode of, could be the ring electrode of the RV. Why does this change occur? So we see here 2,3-AVF, negative. Increased output, the axis flips, positive in 2,3-AVF. So is this migration of the lead? Is it a VT we are inducing and maybe a training with facing that gives this morphology? Anodal stimulation, or it really could be any or all of the above. Low output, high output. So this is most likely an example of anodal stimulation. We haven't moved the lead, it's only output that we're changing. It's uncommon when it's the RV-ICD coil, but depending on contact, how much of the coil has contact with cardiac tissues, like with fibrosis, it's possible to get anodal stimulation. Stimulation from the anode, the coil or ring electrode, depending on the configuration, rather than the tip or the cathode. And because of that change, the coil is at a higher site, 2,3-AVF are positive when we get that anodal stimulation. So general, putting it together in terms of ECG, Bi-V pacing, two leads, lead 1 and V1. RV pacing, RV capture, predominant RV in a Bi-V system. It will be positive in lead 1, towards lead 1, negative in V1, away from V1. LV, free wall, sites that you like for Bi-V pacing, lead 1 is negative, V1 will be positive towards V1. When we stimulate from both, we like to see some fusion. We like to see something that looks in between these two, maybe less negative in 1, but still negative, maybe not quite as tall in V1. But if we saw simultaneous pacing, looks just like RV, then either we have loss of LV capture, where there's so much scar around where the LV lead is, that we need a head start, an offset for the LV lead, or there could be anodal stimulation. And in this cartoon example, if we give LV a little offset, you may get something that's like a fused vector, a hybrid vector between RV and LV stimulation. So it's a patient with chronic atrial fibrillation and a single chamber pacemaker set BVI at 70. Pacemaker malfunction was diagnosed based on this tracing, but what is it that we see? Oversensing, failure to capture, undersensing, combinations, B and C are off. So this is the tracing. So kind of basic troubleshooting, I think many of you would be familiar, but a revision. So there's evidence of all of these. So failure to capture, probably easiest to recognize, we see output here, but no captured QRS. There's oversensing because your timing cycle is reset. So you can walk back and you anticipate there's an oversensed event somewhere here. There's undersensing because this pacing is too quick. It's over pacing. So did not sense, paced and put the patient into a polymorphic PT. So sometimes when troubleshooting cases and we see one abnormality, important to look and see what else there may be, may give clues to the type of lead malfunction, primary etiology, and see whether any troubleshooting options are possible. Thank you very much for your attention.

device interrogation

troubleshooting

over-sensing

lead fracture

ventricular tachycardia

remote interrogation

AV node reentry tachycardia

RNRVAS

pectoral muscle over-sensing

complete heart block

leadless pacemaker