Hi, this is Greg Michaud from Mass General Hospital in Boston. The core concepts in EP and board prep, these are summary principles for those of you taking the boards. They're also summary principles for those of you who aren't taking the boards if you're just interested in sort of thinking about a list of things that are important to know in cardiac electrophysiology. So some of the things that are right for testing include the following principles. One is that paroxysmal AV block usually occurs with a PAC or a PVC as an initiator. It's due to phase IV block in the His-Purkinje system, and usually patients have bundle branch block at baseline, although patients with His-Purkinje disease in the His bundle itself may not have a wide QRS and may exhibit the same sort of phenomenon to a PAC or PVC. The key there would be the PR interval is completely normal or near normal, and a PVC sort of initiates a run of P waves and complete AV block. That's a dangerous scenario. It's important to be able to distinguish paroxysmal AV block as described above from vaguely mediated AV block. And the way to do that is that vagal AV block is associated with sinus slowing. So almost always, if you've seen enough people with vagal AV block, you see, and you measure this out, you'll see the sinus rate slows concomitant with AV block. Now there are some rare sort of vagal responses where you don't see that, but that's going to be the case in the vast majority of cases. Now that sinus slowing associated with AV block almost never happens with His-Purkinje disease because the sinus slowing should make it easier to conduct over the injured His-Purkinje system. And you usually wouldn't see that happening concomitantly. So you can never say never, but those are good rules to follow. If there's a long conducted PR interval in sinus rhythm, the normal conducted PR interval is long, that usually indicates block's going to be in the AV node. As we mentioned about intrahysion block, if you have a narrow QRS, a short PR, and conducted beats, and then you suddenly go two to one block, you have to be very suspicious that this is intrahys block. That intrahys block is an indication for a pacemaker. Two to one block in the AV node, usually the conducted beats would be long. What causes persistence of left bundle branch block at rates slower than narrow complex SVT? The answer is not phase three block because phase three block occurs when bundle branch block occurs at faster heart rates and not at slower heart rates. There's a certain threshold where that may happen, but when you see left bundle branch block at rates slower than some of the SVT at faster rates, that doesn't make sense. But what can happen is because during left bundle branch block, there's concealed penetration of the left bundle from the right bundle. It comes down the right bundle across the septum up and hits the left bundle from behind. Then you end up with a second hit to the left bundle and it perpetuates the left bundle branch block. That's a mechanism you should know about. If you see left bundle branch block in a PAC that normalizes the QRS, usually that is due to equal delay in both bundles. One thing to be aware of is if you're taking the boards, ECG artifact is very testable. There are unequivocal cases of it, and you can show that, and obviously it occurs frequently in real life. Most of the time, the people monitoring the telemetry will not even bring it to you because it's so obvious, but there are some artifact that mimics real life pretty well. Even times where we have arguments over whether it's artifact or not, but it's useful to know how to sort that out. Usually you look for non-physiologic things. If you have a pulse ox tracing down below that doesn't change at all, and it looks like the rhythm is changing, that's one way it could be tested. Another is that you suddenly see a lot of noise in other parts of the tracing, and then something that mimics VT, but you can march out the regular QRSs hidden in between, or you see half of a T wave cut off, or there's loss of a tracing and it looks like a complete flat line across the tracing where there's no physiologic noise at all. Those are all common ways to test that you would be tested, the tracing is artifact and not real. One thing that pops up from time to time is showing a tracing during an EP study in sort of a normal healthy individual where you have sudden onset of rapid atrial pacing, or you get long short sequences that produce infrahisc block, so A, H, block below the hiss. That is a physiological finding under those conditions, happens in normal people, and would not be an indication for a pacemaker, very important not to answer that. We went over through both lectures and multiple workshop questions, parahysian pacing, it's very important to know that, can be useful in your SVT cases as well. AV nodal response, the A goes with the hiss, so as you pull in the hiss to the pacing spike, you pull in the A and you don't change the atrial activation. Accessory pathway response, the A goes with the V, independent of whether you capture the hiss. So the VA time is fixed, whether you capture the hiss or not, makes no difference. And the mixed response, you'll see changing activation sequences, and probably changing VA times as well. Antedromic AVRT is not that common in real life, but you'll see it. It's a Y-complex tachycardia, does not have a hiss preceding the QRS. This includes decremental accessory pathways, they're usually atrial fascicular, they insert close to the apex, and therefore the RV apical catheter will record an electrogram right near the onset of the QRS. They can include non-decremental accessory pathways that insert at the base, and so some patients have, with WPW, would be the most common form of that, where you have one at the base, it's non-decremental, it can conduct both antegrade and retrograde and produce both orthodromic AVRT and antedromic AVRT. The way to diagnose this is a late PAC, or potentially atrial pacing. You can identify the same thing, that when the septal A is already committed, you advance the V and reset the tachycardia. That distinguishes it from VT, and also a bystander pathway, the resetting part. To sort out whether the retrograde limb is another pathway, or is the AV node, you can put in a PVC during it, or you can see spontaneous retrograde right bundle branch block that may reveal a retrograde pathway. Parahysian pacing doesn't really help you sort it out very much, or I'm sorry, parahysian pacing during sinus rhythm will help you sort it out, because if there's a retrograde pathway present, you should be able to tell that with parahysian pacing. Pre-excited tachycardia is often due to a bystander, and that often you can tell because you'll get block in the bystander pathway, and the tachycardia cycle length doesn't change after accessory pathway block. Frequently it's sort of the scenario where you have a post-receptal accessory pathway, and maybe you have AVNRT, and it looks pre-excited at times, and other times it looks like there's narrow complex just like a normal AVNRT, but that you block in the pathway, and the tachycardia cycle length doesn't change at all. That would be indicating that it's a bystander pathway. Atrial vesicular pathways, used to be called MEHIMES, are decremental. They have a typical left bundle branch block appearance because of where they insert near the distal right bundle, so it's sort of typical of what you see during left bundle branch block where activation begins at the distal right bundle, just like where this would insert. There's no retrograde accessory pathway conduction. AV node is the retrograde limb for these usually. Not always, but usually. To ablate these, you find a hist-like potential in the lateral tricuspid annulus. You ablate this and not the earliest V site, which is at the RV apex. That is not something you want to do. In fact, you can create incessant tachycardia that way. That is not as discrete where that inserts, so you want to get it on the hist-like potential where it is a discrete pathway. Just like we already talked about how you identify wide complex tachycardias as antedromic AVRT, late APC is given that advances the V and resets it, or it may terminate or delay the next QRS, equally useful. Very sensitive to catheter trauma, so it's best to do these with a mapping system so you can sort of mark the areas that are of interest in case you bump them. You can go back and potentially ablate them if it doesn't come back. Often just like the AV node area, you'll see automaticity with ablation. This is felt to be almost like an accessory AV node structure, and so it's not, I guess, that surprising that when you ablate it, you get automaticity, just like you do from that hisperkinegic area. Orthodromic AVRT, commonly seen in practice and on the boards, it often has eccentric retrograde atrial activation. There's a VAV response to pacing, and that is pretty much the rule. It's hard to come up with another scenario where you have orthodromic AVRT and don't get a VAV response unless you change the tachycardia during pacing, which can happen, but if you get the same tachycardia back, it's going to have a VAV response. Hiss, refractory, PVC, or fused beats during entrainment attempts are the way to diagnose these and confirm it, because you're going to accelerate delay VA or terminate SVT without conduction to VA in these cases, although if you're far from the accessory pathway, so if you're pacing in the RV apex in this left-free wall, you may not be able to reach that pathway before you get retrograde up through the hisperkinegic into the AV node, so that's a caveat. These hiss, refractory, PVCs, and fused beats during the onset of entrainment pacing are meant to diagnose paraceptal or right-free wall or things that are near your RV pacing site. If you want, if it's a left-sided conduction pattern, then pace from the left ventricle, pace from out of branch of the coronary sinus down into the LV, and that will give you the same response you expect with RV pacing in a right-sided pathway or septal pathway. RV site is fine for septal pathways, even left septal usually. It's the free wall sites that may not behave the way you expect. Ipsilateral bundle branch block during orthodromic AVRT will increase the VA interval, and that's measured onset of the QRS to the atrial, earliest atrial recording site. Ipsilateral bundle branch block always will increase VA interval during orthodromic AVRT. It will not always result in a change in the overall cycle length, and the reason that is, the reason is that you may get compensatory shortening or lengthening of AV nodal conduction time to offset the shortening or lengthening of the VA interval. So overall, the tachycardia cycle length may remain normal. Ipsilateral bundle branch block may also be necessary for initiation or persistence of tachycardia, and be aware of that. That's an easily testable concept where they would say, okay, they would show you there's right bundle branch block with initiation, and it was always necessary for tachycardia initiation. It's reproducible finding. That would indicate you may have a right-sided accessory pathway, or left bundle branch block in the left-sided pathway, or tachycardia terminates every time left bundle resolves or right bundle resolves. Those are testable concepts. The retrograde conduction, again, with parahysian pacing, we've gone over this multiple times, but an accessory pathway response is independent of hist activation when you're pacing. So it goes with the V, not the hist. When you're pacing the ventricle, and you capture the hist, it doesn't matter. The VA time won't change. Bystander accessory pathways are really rare, so rare that they're actually kind of hard to test on the boards, honestly. But it's something that could be tested. I wouldn't spend a lot of time. If you missed this one question, it's going to be one question. They're not going to give you multiple questions on bystander accessory pathways. But they could be identified retrograde by a change in atrial activation sequence without changing the tachycardia cycle. Same thing with antegrade pathways. Pathway blocks, antegrade cycle length does not change, indicates they're probably a bystander and not participating in the cycle and it's unaffected. But remember that although the accessory pathway may not participate in one form of tachycardia, for instance, you could have atrial tach conduction over an accessory pathway, accessory pathway may participate in ORT. Catheter ablation, WPW, there are some clear concepts that can be tested here. One should know that antreceptor accessory pathways can be safely ablated on the ventricular side of the annulus. So one should consider, however, a non-coronary cusp, right coronary cusp less frequently, the non-coronary cusp as an alternate site of ablation for these antreceptor accessory pathways. Probably safer from the non-coronary cusp, however, studies have shown that it's not always possible to get it from the non-coronary cusp. Aware that when you start ablating an antreceptor pathway and you get junction rhythm, QRS will be narrow. It's not going to conduct over the accessory pathway because you're going from the junction down. It skips, there's no direct connection between the junction and the accessory pathway except going through the ventricle and back up retrograde through the pathway or retrograde in the atrium and then down through the pathway. So junctional rhythm followed immediately by narrow QRS is an indication to come off actually when you're ablating. So it could show you a case of an antreceptor pathway being ablated and suddenly you get a narrow QRS. The temptation is to think, I got the pathway, now it's narrow, but you have to be careful and look and see, is this a junctional rhythm? And the answer may be that come off ablation. The ciculo-ventricular pathways are a particular form of pathway, a little twig off the proximal His-Purkinje system, gives you a fixed degree of pre-excitation because the pre-excitation is below the AV node. It's not an AV pathway or a nodo-ventricular or a nodo-fascicular. It's sort of fascicular right to the ventricle. What happens there is because when you pace the atrium, you can get prolongation of the PR interval, but you're not going to change the degree of pre-excitation because that's always going to be the same. And a junctional escape is pre-excited, unlike for other types of pathways. So I think the key with this is going to be that they don't participate in tachycardia. So they're recognized as a bystander and they're not to be ablated because they don't participate in anything. It's purely cosmetic. And you don't want to ablate these in real life or on the boards. When you do ablate and you're using a unipolar EGM, you want to look for a QS, a steep negative dvdt with a QS, and the onset of that should match the bipolar early electrocramp. Also be aware that accessory pathways have slant to them and they go in a certain direction around the mitral annulus and around the tricuspid annulus. They don't always go in the same direction so you need to figure out the slant. But one way to bring out an accessory pathway potential, which is the real target for ablation, it's not an early A or V necessarily, although that works as an ablation strategy most of the time. But if you really want to nail the accessory pathway, you can find that potential by reversing the activation waveform. So normally for a left-sided pathway, so left posterior say, you've got an activation wavefront that's going from proximal and sweeping past it, proximal to distal. That's in the direction of the slant. So often the A's and V's will be mixed together with the accessory pathway potential. If you reverse that activation from distal to proximal, the A's and V's jump out from one another and reveal the accessory pathway. So that's an actual potential way to reveal, you can take advantage of that slant and reveal the accessory pathway potential. Also, there are multiple different algorithms now to sort out 12-lead ECG identification of WPW, and morphology, and site of a potential ablation. And there's a lot of them. You can look through all of them, find the one you can remember, and it probably will be good enough to get you in the ballpark if you're pretty close. AVNRT is something we deal with very frequently. And usually for AVNRT, and actually any AV nodal form of tachycardia like orthodromic reentry, the HA is usually fixed, and the HH changes precede the AA changes. So any wobble in the tachycardia is occurring in the AV node. And if the HA is fixed, and you see the AH is what's changing, then that's an AV nodal dependent form of tachycardia. Can be both either AVNRT or a pathway actually. Obviously, AVNRT you're not going to affect by having bundle branch block, or PVCs that are fused or hysterectractory. You can have slightly eccentric conduction in the coronary sinus, particularly for atypical forms of AV node reentry. So don't go chasing a pathway just because it's slightly eccentric. You have to do the maneuvers to sort out which mechanism it is. P waves in AVNRT are narrow and inverted. Retrograde, sometimes you may have a surface ECG as a way to make a diagnosis. So if you have an upright P wave on the surface ECG, you can rule out AVNRT as a mechanism. The 12-lead ECG of two-to-one AVNRT, typical AVNRT is classic. It's usually infranodal. It has a narrow inverted P wave exactly between two QRS complexes. AVNRT, like ORT, will have a VAV response, and there's very few exceptions to that rule, so that's pretty much a given. It will have a long post-pacing interval, or STEM-AVA interval. It will have an AHA response to atrial overdrive pacing, or PACs. That's because you're advancing, delaying, or terminating the SVT over the slow avenodal pathway, in contradistinction to an AHA response that you see with junctional rhythm, and I show examples of both of those phenomenon in workshops and lecture as well. This is just something that could come up on the boards, but may be useful for an AVNRT case that it's difficult. Someone's coming back for a redo, has had ablation in the usual area of the right inferior extension. Late APCs that affect the tachycardia reset it by pulling in the hiss with the late APC. If it's later from the right inferior extension than the left inferior extension area, then it's going to use the right inferior extension, and you can just go ahead and ablate that. If it's later from the left inferior extension area, and that's probably the source, it's probably an unusual form of AVNRT, and not many people would do this for the first case. They probably would just ablate the right inferior extension, which is 95 plus, probably, percent of cases, but in the difficult ones, it's useful to know how to do this. Late APCs, where is the left inferior extension? You want to go two centimeters into the roof of the coronary sinus, and that's where you put the late APC for the left inferior extension. There is another really unusual form out of the mitral valve annulus laterally. I've never seen it, and it's, you know, again, unlikely to be tested because it's so rare. Catheter ablation for AVNRT should know that junctional rhythm is not an absolutely necessary criteria for a successful site, but it is frequently there at successful sites, so you're going to usually see junctional rhythm, and you can monitor that junctional rhythm to tell whether you're affecting the AV node or fast pathway. What will happen is you'll get VA prolongation or VA block, and that should prompt RF termination immediately. My goal is always to see that within 1.5 seconds of that first beat that VA prolongs or blocks, and you can usually get there, almost always, if you can recognize it immediately. Cryo doesn't produce a junctional rhythm with ablation, so you won't be able to monitor injury to the AV node the same way as you do with radiofrequency. You don't want to see block in the retrograde limb, so if you're doing cryo during RF and it blocks in the retrograde limb, come off because you just blocked in the fast pathway. You want to see it block in the slow pathway. You can also look for PR prolongation, which would be another indication to come off in sinus rhythm, and then you can do a little EP study while you're ablating with cryo and see that you've ablated the slow pathway. If you don't have junctional rhythm during your ablation or there's junctional rhythm with VA block, which can happen, then you need another strategy for monitoring for AV nodal damage or potential AV nodal damage. You could start isopraternal, and that may give you one-to-one retrograde conduction during the junctionals. You can pace the atrium faster than the junctional rhythm, so it wouldn't work well for fast junctional rhythm. You can use cryo, or you can say to yourself, I think this is safely away from the AV node. I'm going to ablate, wait, ablate, wait, ablate, a little longer, wait, and call chipping away, chiseling away maybe. You can consider left-sided radiofrequency when right side fails. I think left side is probably safer than going to the roof of the coronary sinus. You're probably closer to the AV node there. You can get lower on the left side and ablate. And then there are some cases where they may show you a one-to-two conduction with a tachycardia that looks irregular and actually mimics AFib because of the irregularity, where you're getting one P-wave and two QRSs. That could obviously be junctional beats, but it could also be conduction over both a fast and slow pathway simultaneously, producing two QRSs. The answer there would be to ablate the slow pathway. That takes it away. We have the unusual folks like notofacicular, notoventriculars, behinds, decremental pathways, bundle branch reentry. These are all potentially like a question, maybe, you know, one question probably. And notoventricular or fascicular tachycardias can occur with narrow or wide complex. Bundle branch block may be necessary for tachycardia to give you a long enough circuit to persist. They can be A within the V and mimic an AV and RT, or they can be dissociated. AV and RT can be dissociated. So you've got to have a strategy to figure these out. Usually you can distinguish by entraining them. So if you can entrain from the RV, the fusion, you can affect the tachycardia with HISS refractory PVCs by advancing the next HISS and resetting the tachycardia or pulling in the next A if there happens not to be VA dissociation or VA block. But often these will be with VA block. And, you know, again, you need to show that you can get into the HISS Purkinje system and affect the tachycardia, which would not be the case with AV node re-entry. So that would be the main kind of thing in the differential other than junctional tachycardia. Decremental pathways are usually septal. They're often concealed. It may show incessant SVT like a PJRT type of pattern. The post-pacing interval minus tachycardia cycle length in this case is going to be long probably because it's a decremental pathway. Stim AVA will probably be long, but you may be able to see that at the beginning of an overdrive pacing sequence, you advance or more likely delay the next day. So you've got to either put in HISS refractory PVCs or look at the beginning of that pacing drive during the periods of fusion to try to figure out whether you've got a decremental pathway. In bundle branch re-entry, the HH drives, cycle length changes. There's usually baseline left bundle branch block. Usually during tachycardia, the HV interval is the same or more than during sinus rhythm with left bundle branch block. You can see that one, depending on which direction the bundle branch re-entry is going, one bundle's being activated proximal to distal and the other is in the opposite direction. You wouldn't see that with really sort of anything else unless it's using down one bundle across and up another bundle. So that is something that also might be tested. And one could potentially ablate either the left bundle or the right bundle. So even with left bundle branch block, at baseline, you can probably still ablate the left bundle and get it because it's usually delay in the left bundle, not actually complete block. That's producing the baseline left bundle branch block pattern. Junctional tachycardia very rare as a de novo rhythm in adults, but it is often seen during an AVNRT ablation when you're giving isopryl to test whether you eliminated the AVNRT and slow pathway. And the reason probably is, I don't know, you heat that area and then with isopryl, you just tend to see way more junctional tachycardia than you do if you just give isopryl at the beginning of the case. But again, the AHA response is what you see with atrial overdrive, and that will sort out whether it's just junctional rhythm after a successful slow pathway ablation or not. Late APCs during tachycardia will have no effect on the next H during junctional rhythm. Early PACs may conduct over the fast pathway and reset it with an AHA response. That same thing could be seen with overdrive. The intricate overdrive pacing doesn't help you sort it out because it mimics AVNRT. You go up the V to the A and then the H comes back. So you get a VAHV response. Ablating junctional rhythm is not easy. Probably should be done at a center that specializes in this. It's high risk for AV block. Should probably be done with cryo. You might get lucky if it's low enough to be near a slow pathway, but often it requires more knee-knocking ablation near the AV node. VT and PVC localization is important. It's common Twitter fodder. It's also common fodder for the boards. People love doing this, looking at PVCs and ruminating about where they're coming from. But on the test anyway, it's not so simple as here's a PVC. Where do you think exactly it's mapping to? They might say, where on this electroanatomic map or fluoro images is PVC rising? Then they're asking both, can you localize the PVC and can you recognize an anatomic location based on imaging? Or they might say, what complication is most likely when ablating this PVC? Phrenic, coronary artery injury, his spinal injury. Management of patients with frequent PVCs may be tested. If they're asymptomatic and they have a normal EF and they have a high burden, the answer would not be to ablate it per se, maybe to follow and check EF. Usually it requires more than a 20% burden or so to affect the left ventricular ejection fraction. So you usually need a high burden. There's no strict cutoff, but that's sort of a rule of thumb. Coronary angiography or ice localization of the oste of the coronary arteries is necessary before sinus of Valsalva ablation, but ice is a reasonable way to do that as well. However, it's not reasonable for AIV or MCV ablation. You can't see that coronary artery well enough, I think, to be certain that you're not going to pick off the branch of the PDA that loops up near the, say, middle cardiac vein. So if you're going to be ablating in the ostium of the middle cardiac vein, you probably need to do coronary angiography first. Or if you're obviously down the AIV trying to get a left ventricular outflow tract or summit PVC, you could be right next to the coronary artery and you need to do angiography first. Non-ischemic cardiomyopathy often will have a epicardial exit, and you should know the criteria for epicardial exits, Q waves in V1, an MDI greater than or equal to 0.55, delta wave appearance. There are others that are in the lectures. For non-ischemics, periaortic, basal septal, basal and lateral sites are common. You should know the causes of cardiomyopathy and how they might differ in terms of sites of origin for tachycardia, because the substrates in particular areas, so for ARVC, more likely to show an RV tachycardia, lamin, basal septal, VT, it almost always affects the septum to some extent, often associated with heart block and AFib. So know these kind of disease states and how patients might stereotypically present. For hypertrophic cardiomyopathy, VT is a feature of late remodeling usually, because you have to have significant scar to have monomorphic VT. Apical aneurysm, the apical form, usually the aneurysmal form of hypertrophic cardiomyopathy is the apical form, and a high-risk patient, much higher risk than if they don't have an aneurysm, and much more likely to have sustained monomorphic PT. Also know that the PRKAG2 mutations causing hypertrophic cardiomyopathy is associated with pre-excitation. Substrate mapping and ablation often becomes the necessary evil for ventricular tachycardia, either because it's not tolerated in non ischemic cardiomyopathy with the severely depressed left ventricular ejection fraction, and there's multiple ways to do that. They could be tested in your knowledge of looking at classic ways of determining a VT ablation site, like entrainment, looking for late potentials, looking for lavas, looking for ILAMs. There's multiple potential ways to do that, looking for potential isthmuses with high-density mapping. You should know the classic Stevenson schema, which he presents in this course. The timing of electrograms during VT at each circuit location, response to overdrive pacing during VT at each location. Also recognize the significance of non-propagated stimulus that terminates VT, i.e. ablate there. That's a great site. Epicardial and localization criteria are less useful than when applied to patients with non ischemic cardiomyopathy that should be known. Utility of unipolar versus bipolar voltage mapping. Again, this is all covered. QRS morphology indicates an exit site, but not necessarily a target for ablation because isthmuses and exit sites can be remote. You may have to use exit sites as an indicator of looking for the upstream isthmus to that exit. So it may be a very useful reference, but the actual exit site may not terminate the tachycardia or render it non-inducible. For ischemic VT, you should still be able to recognize, they may give you a scenario where you have an ischemic cardiomyopathy, but a focal source of tachycardia. You should be able to recognize focal versus re-entry within training maneuvers or other mapping techniques to sort that out. In terms of pacemakers, we need to be able to recognize lead positions on chest X-ray or by EKG. So if you're not meaning to produce a right bundle by septal pacing and our deep septal pacing, and you thought you were putting it in the RV and you end up with the right bundle, that could be in the RV, but that would be a clue that maybe this went through an ASD or a PFO and ended up in the LV. And you should be able to identify that on chest X-ray, mainly by looking at the lateral chest X-ray and seeing the posterior location of the ventricular lead, which indicates it's in the posterior ventricle, otherwise known as the left ventricle. Obviously, need to know the indications for pacing, including ethics of implanting devices like class three indications, such as expected life expectancy, less than a year, that sort of thing. You should know the drug effects on pacing thresholds, like MEO, increasing that threshold, the fedeline, and so long lowering it. 1C will also increase the pacing threshold. Should know your CRT indications. Also, suspect sarcoid, I think this is a very good question for the boards and actually probably missed in real life too often, that you have a youngish person, 57 years old, comes in with AV block and they just get a pacemaker and sent out. Well, I think, yeah, they need pacing, but why did they get AV block at such a young age? Well, often maybe due to sarcoids. So obtaining an MRI, a PET, CT possibly, but MRI might be your best first test in addition to echo. If there's extensive scar on MRI, suggesting sarcoid or there's LV dysfunction, then one would consider an ICD instead of a pacemaker in those patients. Block heart failure, block HF. In other words, CRT for EFs between 35 and 50%. And remember always that a huge part of indications for pacing in the guidelines are due to symptoms. So, you know, bradycardia alone, sinus bradycardia alone, is not gonna be an indication for pacing in most cases if the patient's asymptomatic and has good exercise tolerance. ICDs will be tested again based on indications. Should know that there are special groups where ICDs are potentially indicated like sarcoid, inherited cardiomyopathies. These are, you know, patients not well represented in clinical studies. And so the guidelines don't reflect class one indications for these, but they're still reasonable. I should know your indications for CRT. Recognize lead fractures with short DV intervals. Be able to recognize EMI. T-wave over-sensing. Can be difficult to manage these patients, but there are algorithms to do so with pacing, you know, pacing parameters. Again, there's a lot of little tricky tracings you can show with both ICDs and pacers to look for evidence that, you know, you're losing atrial capture, you're losing ventricular capture, over-sensing, under-sensing. These are all things that are covered in the course. No solutions to loss of IV capture like multipolar electrodes, perhaps. Turning up the output, perhaps, or whether you'd have to actually do a revision. You should be able to recognize my potential over-sensing often on large antennas. You know, local bipolar electrodes at the tip aren't likely to give you that. It's usually much bigger antennas, like a coil to the tip or something that's involved the CAN in sensing. Sodium channel blockers will increase the defibrillation threshold. Amio will, flaconide will. Calcium channel blockers usually lower it. Sodium will, delphetalol, just like they do pacing thresholds. Pharmacology is something that you basically just have to know it, and you could review this list, but I would study the lectures in the course. This is just something I would say. Because a lot of it's memory-driven, not concepts that are easy to maintain in your brain, I often would do this sort of last thing that I would study the tables and a quick review before I go in. So maybe my leaky brain might hold onto it for that short time between when I look at it and the test. Same thing for the basic EP. Some of this you can figure out just being an experienced electrophysiologist, you can kind of figure these things out, but honestly, some of it is gonna take study of the lectures and just sort of kind of doing that at the last minute so you don't forget the stuff that's more amenable to memorization and understanding concepts. Inherited cardiomyopathies, there's a whole section on that, and I'll let you read this, but you can go over that list of things. It's a nice handy reference for inherited cardiomyopathies and sort of how they behave. Long QT, ARBC, CPVT, regatta, the whole bunch of channelopathies and cardiomyopathies that require, again, probably some memorization to remember what types of long QT go with one, two, and three, for instance, but how do they look on EKG. AT and atrial flutter is right for testing on the boards. You should be able to recognize focal versus reentry, both with cardiac mapping and with being able to recognize entrainment with fusion. Downstream pacing is an example of this where you can see with, you pace downstream and you drive the upstream at a full tachycardia cycle length away, this indicating there's fusion, and that tells you there's reentry, so that will definitely be tested. ECG localization might be tested for focal tachycardias, particularly left versus right. Understand that crystal breakthrough is something that can confound your mapping of CTI block when you're ablating CTI flutter. You should know how to determine conduction block with both the CTI and anywhere, really, by looking at split EGMs, differential pacing, recognizing there's incomplete Bach. If you're not close to the line with recording and pacing, you might miss slow conduction through a line. Usually the left atrial appendage is the most useful place to pace when you've got lines in the left atrium like roof line, anterior lines. Atrial fibrillation is a difficult to test concept. There are some clinical trials that could be tested for results like, for instance, cabana trial could be tested and know that the intention to treat analysis did not show benefit of catheter ablation over drug therapy. The early AF trial that cryo ablation was significantly better at preventing symptomatic and asymptomatic recurrences of atrial fibrillation. So those kinds of trials, big trials, randomized ones published in the New England Journal, big journals could be tested. You should know indications for catheter ablation. These are about to change somewhat, but usually there are not a lot of questions asking what level of indication is there. It's more ideas of, is this patient reasonable for catheter ablation? I'm not gonna ask, is this a 1A indication usually? These things change. By the time you take the test, it could have actually changed. You should recognize the complications related to AF ablation in my workshops. I showed a couple. One was pulmonary venous stenosis, sorry. One was atrial pericardial fistula, but also recognize phrenic nerve injury and diaphragm paralysis. You should know by now that oral anticoagulants are safer when they're not interrupted or minimally interrupted relative to catheter ablation for AFib. And then the old basics of recognizing when a pulmonary vein isolation is complete by being able to distinguish far-field potentials from near-field potentials. And that's usually just pacing the near-field space and seeing that that gets pulled into the spike, whereas the PVs stay out, removed from the pacing spike. That's pretty simple, but should know how to do that. Biophysics of ablation may be tested. I think it's mostly RF, probably cryo as well to some. I don't know whether PFA concepts would start to creep in. Don't think it's been around long enough. We don't know enough about it, I think, to probably throw tests. And if they do test it, it's going to be most likely a test case question, not one that would be counted. For RF though, we still use it regularly and it's easily testable in terms of sort of concepts that are myths related to RF. Ablation like irrigation alone creates a bigger lesion. It does not unless you increase power. So same size, same power ablation at the same site, everything else the same, you turn on irrigation, it doesn't make a bigger lesion. That kind of thing can be easily tested. Larger tip size would also make a smaller lesion if power duration and contact force are the same. The only way it makes a bigger lesion is if you turn up the power. Understand that you can get skin burns related to RF, particularly if the indifferent electrodes pads crinkle. And I don't think PFA is likely to hit test anytime soon. There are entrainment pitfalls that you need to be aware of and try to trick you on test and in real life. No capture with pacing is one of them. You have to be clear that you're actually pacing and capturing the tachycardia. Perhaps you didn't pace long enough to actually train it. You might be pacing from a site too close to the exit. So it would be difficult to show fusion. If you pace it too high in output, you can get nonspecific capture of structures downstream or upstream from where you're pacing. You could end up with short post-pacing intervals because you're capturing too far downstream. Pacing too fast, you don't wanna do that, create decremental conduction and you don't want to, makes it difficult to interpret. You wanna pace with some ability to sense off the catheter you're pacing from and sync it up with the tachycardia so you don't come on at irregular intervals. Irregular tachycardia can be difficult to interpret. And if you change the tachycardia with entrainment, also can't really interpret that. So if no sites meet the criteria for entrainment being in the circuit, then you may have several conditions. One is you're in the wrong chamber. That could be actually the case or on the correct surface of the heart. Maybe it's not endo, but epi. Or if there's slower decremental conduction, that can throw off your post-pacing interval. So the post-pacing interval may never be short when you're pacing a decremental circuit. Electroanatomic maps have pitfalls as well. I showed one in a workshop that showed RA septal breakthrough that was a little bit earlier in the P wave, broad breakout. But in that case, you want to map the LA. There are also fake outs for macro reentry. We see these pretty commonly. You create a line of block. It goes around through the line of block, but it takes a long time to go through. You're not mapping that part of the conduction pathway because it's epicardial. Pops out on the other side and goes around. It kind of looks like breakout on one side is a focal tachycardia and that it's up against a line of block. But usually that's reentry. You got to pace to sort that out for sure. You cannot look at that map and know for sure that that's focal versus reentry. You should know that a poor window or reference could throw off your map completely. And that sometimes you can entrain in something that has two loops with dominant and non-dominant loops and be able to potentially sort that out. That's not likely to be tested on the... It's a very complicated concept and pretty unlikely to be tested on pulse. There are some adult congenital. We're seeing more and more of those patients. When I took it several years ago, there were questions about sudden death and arrhythmic risks associated with certain lesions in common adult congenital lesions and particular surgery the patient may have had. So it'd be useful to know that because those are testable kind of concepts and these are patients that we will see. We're seeing more and more of this. So I expect over time we may see more questions, adult congenital questions. All right, that was a lot. I know, hopefully you can break it up into pieces as you're viewing it, but hopefully it also helped you, introduce you to some of the concepts that if I said something that confused you or said something that you were saying, whoa, I don't know anything about that, you might wanna go back into the course and find it. All of these concepts are in the course or the workshops. So you should be able to, by reviewing the course and the workshops, pass the board without a problem. Good luck.

electrophysiology

board preparation

paroxysmal AV block

bundle branch block

atrioventricular re-entry tachycardia

ECG artifact

pacing

ablation complications

atrial fibrillation management