Hi, this is Greg Michaud from Vanderbilt University, co-director of the core concepts in EP and board prep, and the new chairman for the core concepts in EP HRS committee. These are some summary principles of the course. In addition, they provide some testable concepts for those taking board review prep. So it's good for people who just want to get a summary, but it's also good to understand what is likely to be tested on the EP boards. So we'll start with principles of electrophysiology that we covered in this course and that are likely to be tested. Paroxysmal AV block is often seen with bundle branch block at baseline. It's due to phase four block in the Hispokinji system. Normally paroxysmal AV block doesn't just come out of the blue. It's initiated by a PAC or a PVC that causes a pause. And in that pause, phase four block creates the complete AV block that you see. So frequently what you'll see is a PVC followed by long string of P waves. Obviously that's an indication for pacing. One should be able to distinguish paroxysmal AV block from vaguely mediated block. When you see concurrent sinus slowing in the setting of AV block, that's a vagal event until proven otherwise. That combination of sinus slowing and AV block is produced by vagal output and is not usually seen in Hispokinji mediated block. When you see a long conducted PR interval with and also in the setting of second degree AV block, and the block is probably in the AV node, not in the Hispokinji system, most likely. But when you see a narrow QRS, short PR on conducted beats, and two to one or higher degree block, that's often block in the Hisp bundle and it's a pacemaker indication. Even if they're not symptomatic with two to one block, short PR on conducted beats, that is still an indication because the risk of higher degree AV block is very grave and these patients can do really poorly without a pacemaker. It's good to understand the mechanism of persistence of left bundle branch block at rates, and it can persist at rates slower than a narrow complex SVT, or it can exist at slower rates than a paced rate. When you see this, it's because of concealed retrograde penetration of the left bundle. What happens is the left bundle blocks, integrate, conduction comes through the right bundle across the septum and hits the left bundle again, retrograde, causing that persistence of block, even at slower rates than may have created the left bundle branch block to begin with. That's not phase three block, which is purely a rate related phenomenon, sinus rhythm starts to speed up, and then you see left bundle branch block. Sometimes you'll see a PAC that normalizes a QRS. This is due to equal delay in both bundles that can happen either right bundle becoming narrow or left bundle becoming narrow, pretty unusual scenario. One thing about the test is ECG artifact will be seen on that test. There is no doubt, ECG artifact, artifact on electrograms, they're going to show you artifacts somewhere on the test, because it's a real life problem. It's not uncommon at all that we get multiple consults in a week that were asking about VT and it's artifact, heart block, it's artifact, sinus pauses, artifact, and you need to be able to recognize that because treatment is not indicated for artifact. The other thing that is a frequent test question is showing evidence of infrahis block, but in the setting of rapid atrial pacing, often rapid onset atrial pacing in the setting of sinus rhythm, or there's a long short sequence that creates infrahisian block. This is a physiologic phenomenon, not a pacemaker indication. It's good to be able to recognize that again in real life, you don't want to be putting pacemakers in people with this. Now if you pace at a slow rate, not sudden onset that creates a long short and you see infrahisian block, that's a different story. Patient like that with other symptoms compatible with, say, syncope, sudden syncope that sounds rhythmic, then that's a different story, but not young patients, no symptoms compatible with rhythmic sounding syncope and you see long short or sudden onset of pacing causing infrahis block. It's good to know parahisian pacing and its responses, both ab nodal where the A goes with the HISS, so you get retrograde right bundle branch block with PVCs or with parahisian pacing you get capture of the HISS and the A goes with it. If it doesn't, it's an accessory pathway response. There the A goes with the V independent of HISS capture. And then there are mixed responses. I showed one of those examples in a workshop. Antedromic AVRT is a wide complex tachycardia and if you have an intracardiac electrograms, there's no HISS preceding the QRS. It includes the decremental forms of accessory pathways. These are usually atrial fascicular and they insert close to the apex. One of the clues about this is the RV apical recording is very early relative to the onset of the QRS because of where these insert. There are some forms of wide complex tachycardia where the pathways integrate only or integrate and retrograde and they still have antedromic AVRT using either pathway, integrate, retrograde up another pathway or usually up the AV node. The way you determine these are a late PAC, i.e. when the septal A is committed and it can't be making it through the AV node, advances the V and resets the tachycardia. Now that late septal thing, I mean, if you advance the tachycardia, you don't change the QRS at all, then it's very unlikely you're going through the AV node because you'd see fusion with that. So to be absolutely sure, they'll usually show you a late PAC when the septal A is committed, that'll advance the V and if it's part of the circuit, it'll reset the tachycardia, which distinguishes it from VT or a bystander pathway. How can you tell if it's pathway to pathway, YCOM or just antedromic, which means it goes down the pathway up the AV node or pathway to pathway using two separate accessory pathways? Well, PVC may help sort this out because you're looking at what's happening with the retrograde limb or spontaneous retrograde right bundle branch block could reveal that retrograde path is the AV node. Periacin pacing can also help sort this out for you in sinus rhythm. Antedromic tachycardia may be due to a bystander. What a clue to this is you suddenly see block in the antigrade pre-excitation and the tachycardia cycle length does not change. So in real life, I've seen this several times. This is the most common form of a bystander. Retrograde bystanders are really pretty rare. Atrial fascicular pathways show decremental conduction. They're really like having two separate AV node and Hispokingyi axes, sort of one sort of right word on the tricuspid annulus and one in the usual location. So the usual AV node and then kind of a second AV node. There's some forms of congenital heart disease where you get dual AV nodal systems. But anyway, this particular pathway can then create reentry between the normal AV node axis and this atypical rightward AV node axis. There's usually no retrograde accessory pathway conduction. The usual AV node is usually the retrograde limb of a circuit. Just like Hispokingyi in the normal location, you pick up a His-like potential on the lateral tricuspid annulus and at the base. And so you want to ablate these, not the earliest V site. You don't want to go and map the earliest V and ablate it. You can actually make tachycardia incessant because that can be difficult to map. And there may be multiple insertions into the bundle. And the His-like potential is your clear target will take care of this arrhythmia and get rid of pre-excitation back towards the base. The same thing we've already talked about, the late APC advances V and resets tachycardia. But it also, that late APC may terminate or delay the next QRS, which would also indicate that it's part of the circuit. These are very sensitive to catheter trauma. So when you're looking for these His-like potentials on the lateral tricuspid annulus, you have to be careful not to bump them. They may not come back in that procedure. It's useful to have a map, do this very carefully. So in case you do bump it, you're pretty sure where you were. So if you burn it, hopefully it's not likely to come back. Interestingly, just like ablating the AV node, you get automaticity with ablation, because this tissue is similar to AV nodal tissue. In fact, indistinguishable, really, on histology. Orthodromic AVRT often gives you eccentric retrograde atrial activation. There'll be a VAV response with overdrive pacing. His refractory PVC or fused beats during entrainment may accelerate, delay, or terminate SVT without conduction to the A. Now, again, you have to realize that when you're far from the pathway, you may not see these things. His refractory PVCs or fused beats may not affect the tachycardia, because the RB pacing site is very far from a left free wall pathway. Now, if you take that catheter and move or an ablation catheter and pace the LV, then you will see his refractory PVC or fused beats affect the tachycardia. You'll be able to entrain with fusion. The other bit is another trick would be to take a catheter and put it down an LV branch. And then pacing from that LV branch, capture V only, should also be able to demonstrate that his refractory PVCs or fused beats during entrainment affect the tachycardia. If you're close to the accessory pathway in the V, you will demonstrate it without fail. Another thing to help you diagnose and it's diagnostic is that when ipsilateral bundle branch block increases the VA interval from the onset of the QRS to the atrial recording, then there is a pathway present on that same side as the bundle branch block. And it's part of the circuit. In fact, bundle branch block may be necessary to initiate orthodromic AVRT or to allow its persistence, because the circuit may need to be big enough. So what I mean by that is when you get bundle branch block on the same side as your circuit, you have to now come down the other bundle across the septum, through the ventricle, up through the... So your circuit length is longer. You create a longer circuit, makes it more likely to be persistent and more likely to be able to initiate. Otherwise, you have to have sufficient delay in the AV node to set up that circuit. And that may not always be present. So you may actually need ipsilateral bundle branch block. That can also be a clue. If it's necessary to induce SVT and HV prolongation is necessary every time you induce it. Very strong clue that you're dealing with a pathway. In these cases with parahysian pacing, the retrograde conduction will be independent of his activation, unlike AV nodal conduction. Bystander accessory pathways are pretty rare. They're usually antegrade, from my experience. Retrograde may be identified by change in atrial activation, potentially without a change in tachycardia cycle length. So when you see either block antegrade in a pathway or retrograde in a pathway, and there's no change in the cycle length of the tachycardia, you suspect that they may have a bystander accessory pathway. But remember that despite being a bystander in one form of tachycardia, such as AVNRT, it may participate in another form. So the answer might be continue to look for other types of tachycardia once you've eliminated slow pathway for AVNRT, where the accessory pathway was a bystander. In ablating WPW, it's important to realize that an antriceptal pathway can be safely ablated if you stay on the ventricular side of the anus. Non-coronary cusp is an alternate site of ablation, and safe from an AV nodal perspective. The right coronary cusp is much higher risk and should be, you know, use much more caution when ablating. You know, use much more caution when ablating from the right coronary cusp for an antriceptal pathway. One thing that can happen when you're ablating in WPW, if you're near, say you're doing a post-receptal accessory pathway or an antriceptal pathway, and you begin to ablate, and suddenly the QRS looks narrow and faster. And you're like, good, I just got rid of the accessory pathway. Maybe not. So one of the things that could be happening is you got a junctional rhythm from your ablation, and you haven't affected the pathway at all. You should come off RF immediately. When that happens and reassess, pre-excitation with a standard A to V pathway will not be pre-excited with junctional rhythm. It's a feature of the usual types of accessory pathways. One form of variant pathway that will, where pre-excitation will remain with junctional rhythm is fasciculoventricular pathways. Now, these are little fibers that come off the right fascicle, usually high up. They usually produce very little pre-excitation, and it's absolutely fixed. All of the pre-excitation is coming after you've come through the AV node and down the hysperkinesis system. And this one little fiber bypasses the normal hysperkinesis system. It's sort of like a break in the insulation almost. And the current leaks out into the ventricle on the spot it's not supposed to and gives you this minimal degree of pre-excitation. The junctional rhythm is pre-excited when you pace faster in the atrium, still pre-excited to the exact same degree. Or APCs, pre-excited to the exact same degree when the AV node blocks, this blocks, but it won't block with, the pre-excitation won't block with adenosine. So, this is something you don't ablate though. It's always a bystander. It doesn't participate in tachycardia, at least it's never been shown. And because it's up high near the normal conduction system, there's a high risk of creating AV block. And it's not something you want to ablate. When you're doing catheter ablation for WPW, it's useful to have unipolar electrograms. They should match the bipolar electrogram and show a QS at the earliest site. So, the steepest part of the DVDT of the QS should match a sharp bipolar component. And then that component should even be earlier where you see an accessory pathway potential. Sometimes these can be difficult to identify. And particularly for left free wall pathways, there's a lot of slant involved. And so, if you're going with slant, if activation is moving in the direction of the slant of the pathway conduction, then A's and V's will tend to overlap. If you can reverse the activation, say you're going from V to A, if the ventricular activation is in the opposite direction of the V to A conduction over the pathway, then you're likely to see the V and A split out together. You'll see examples of this in the course, but an example of doing this would be normal activation over in the coronary sinus would be proximal to distal in the ventricle. And if you went and paced the RV outflow tract, you may see it goes from the ventricular perspective, distal to proximal. So you've reversed the ventricular activation. Since distal to proximal is the opposite of the slant, you can then see separation between the A's and B's, and you can bring out an accessory pathway potential. You can do that anywhere along any pathway, as long as you go on one side or the other and just get the activation to reverse direction and relative to the slant, and that reveals accessory pathway potentials. I find this particularly useful for the left free wall pathways. You should be able to identify ablation sites by 12 lead ECG. And there are several different algorithms. All of them work to some extent. There's not one that's clearly better than others. And understanding the concepts for how you determine frontal plane axis, precordial lead transition, those two things alone will often allow you to identify pathways. AVNRT, the HA is usually fixed for typical AVNRT, and H intervals will precede, or changes will precede AA changes. The HA may not be fixed on the first lead of tachycardia, but thereafter it tends to be. There's no effect on tachycardia with bundle branch block or PVCs that are fused or hiss refractory. You can have slightly eccentric conduction in the CS with AVNRT, particularly atypical forms where the retrograde limb is a slow. Pathway. P waves are narrow and inverted retrograde. So if someone's showing you a tracing and asking if it's AVNRT and they're upright P waves inferiorly, probably not AVNRT. There's a particular pattern recognition on 12 lead that shows you two to one often infranodal block with narrow inverted P waves exactly between two QRS beats. It will show a VAV response to overdrive ventricular pacing just like ORT because it's AV nodal dependent. But unlike ORT where you're pacing near the circuit, you'll get a long post-pacing interval minus tachycardia cycle length or STIM-AVA no matter where you pace in the ventricle because you always have to come back through the HISS for Kijiji system and retrograde through the HISS bundle to reach the circuit. So it doesn't matter where in the ventricle you pace, it's always going to be pretty long. AVNRT will show an AHA response to atrial overdrive pacing or PACs, in which case you might see advancement, delay or termination of the SVT over the slow AV nodal pathway antegrade. The right inferior extension versus left inferior extension may be a source of questions. You can deliver late APCs or perhaps do entrainment to sort out whether the antegrade limb is right inferior extension or left inferior extension. You could review Sonny Jackman's paper from several years ago looking at the method for using late APCs to identify which extension of the AV node you're dealing with. The latest APC is the area of the antegrade slow pathway. Also, post-pacing interval equaling tachycardia cycle length could also be another way to identify that. I think this concept is not, although it's out there in the literature and I think there's definite reason to potentially test it, I'm not so sure. It hasn't crept onto the test yet, but wouldn't be surprised in the next few years if it does. Catheter ablation for AVNRT, it's important to recognize that junctional rhythm is usually present with a successful ablation lesion, but one-to-one conduction is your safety factor. So if you see junctional rhythm and there's one-to-one conduction, you're safe, as long as there's not VA prolongation or block with that junctional rhythm. That should prompt immediate termination of RF. And if you do that quickly enough, you will prevent AV block in that patient. Cryo does not produce junctional rhythm, unlike RF, and there you're looking for potentially, if it's sinus rhythm, PR prolongation would prompt you to come off. Or if you're in SVT, you can do it in SVT, and what you'd want to see is block in the antegrade slow pathway, not the retrograde limb, unless you're aiming for the retrograde limb, in which case block will occur in the retrograde limb and then you should see the first beat back should be a normal PR interval. If there's no retrograde conduction with junctionals, because there's poor retrograde conduction to begin with, you see this often when patients have retrograde slow pathways as their retrograde limb of the circuit, and antegrade fast, they don't have robust retrograde conduction over the fast pathway. And so you can't use that to monitor for damage to the AV node. You can start isopril and sometimes improve that. You can do atrial pacing and look very carefully at the AH interval and make sure it's not prolonging. You have to pace faster than the junctional rhythm, otherwise it's kind of useless to pace the atrium. You could use cryo, or you could look at your anatomic location, chip away at it, and just do short applications, come off, make sure AV conduction's intact, go a little longer, make sure that's a little more stress-inducing. I usually use atrial pacing. Occasionally I've used cryo and then gone back and used RF at the same site when I proved that cryo was safe there. If they give you a scenario where right-sided ablation has failed and left-sided, or exploring left-sided ablation is an option, that's something to consider. Or if they give you an option to test to see whether the left inferior extension's part of the circuit, not the right. One should recognize the phenomenon of one-to-two conduction that creates a tachycardia that's often actually mistaken for a fib because it gives you irregular intervals. Every P wave in sinus rhythm gives you two ventricular beats because it's going simultaneously down a fast and a slow pathway. It's not a reentrant arrhythmia. You can ablate it and get rid of it. There have actually been a few cases where tachycardia myopathy has been a problem from incessant two-fer sort of activity. And if you get rid of the slow pathway, then you just have normal conduction. These patients have recovered their LV function. Now, these are obviously rare events in the life of an electrophysiologist to see a notoventricular fascicular pathway. There are many electrophysiologists who probably will never see one in their career, or at least didn't recognize it. So it's useful to know how to recognize that so you don't miss it. Heim fibers are otherwise known as atriofascicular. Other decremental pathways, and then bundle branch reentry. These are all covered in our course, mainly through workshops. So you can see good examples of these. Notoventricular fascicular tachycardia can occur with a narrow or a wide complex, can go down and integrate over those pathways, or it can be retrograde only. Sometimes it's necessary for bundle branch block to occur to have retrograde conduction over one of these pathways. So it wouldn't be that unusual. You can see A within V, and it can mimic AV and RT. It can be a dissociated rhythm, where there's no clear relationship of the A to the V, because the A is not necessary as part of the circuit. The circuit involves the AV node, and the ventricle, and the fascicular system, but not the atrium. So if you can dissociate the atrium from the ventricle during one of these tachycardias, then it's not ORT. You can distinguish this from AV and RT by entrainment with fusion. So because the hysperkinesia system is a part of the circuit, you can entrain it with fusion, just like you can entrain ORT, or hysterefractory PVCs will advance the next hyst A, or hyst, you reset the tachycardia. So it's fairly important to understand that if you have AV and RT, what looks like AV and RT, and you give a hysterefractory PVC, and you reset the tachycardia, that's the rare notofascicular. So that's a scenario that could come up. Decremental pathways are usually septal. They're often concealed. They may have incessant SVT. The scenario there would be the pathway that causes incessant ORT. It's called PJRT, paroxysmal junctional reentrant tachycardia, but it's not junctional at all. So it's actually a misnomer. And PJRT is probably more of a syndrome than an actual diagnosis as well, because there are some cases of AV and RT that can act similarly. PVCs during hysterefractories in a decremental pathway ORT may delay the next day or terminate SVT, which is diagnostic of participation in the tachycardia. These are pathways that can be difficult to differentiate from AV and RT. And one needs to either give PVCs during hysterefractoriness or look at the fusion zone of overdrive pacing to determine that you're delaying or terminating SVT during that period of time. So almost always these tachycardias give you a VA time, more than 40% of the tachycardia cycle. Bundle branch reentry can be diagnosed because the HH changes drive the cycle and changes. There's baseline left bundle usually. Depending on which way it's going, you'll see reverse activation in the right bundle to HISS or left bundle to HISS. And you can cure these by ablating left or right bundle usually. Again, likely to see at least one question on that. Junctional tachycardia, I've given a lot of examples on how to do atrial overdrive pacing to separate AV and RT from junctional tachycardia. By looking at an AHA response for junctional or AHA response for tachycardia. Basically, ventricular overdrive pacing is useless to try to distinguish AV and RT from junctional. It mimics AV and RT, so you have to do atrial overdrive pacing or APCs. Where it's commonly seen is after slow pathway ablation and you're getting isopraternal. Junction has just been heated and it tends to fire fairly rapidly after isoprop. Ablation of JT is high risk, should be done by probably specialized centers and maybe using cryo, but not something you should jump into without having some experience. VT and PVC localization is important from a test perspective, if you're taking the test, because there are lots of questions that have crept onto the board's exams in recent years based on looking at the 12 lead and trying to locate the PVC. So it could be a question that asks, where is this PVC arising? Pat muscle, which aortic cusp, et cetera. And another way to do it would be to say, where on this electroanatomic map or fluoro which is this PVC arising based on the 12 lead. And, or they might ask what complication is most likely when ablating this PVC? Understanding not only, okay, where do I locate this PVC and what collateral damage might I do if I ablate it? So am I likely to get the phrenic nerve or a coronary or the hiss pumple? So that's lots of variations of that question instead of just saying, where is it? Not only saying, where is it, but then what might be next to it or what does it look like on a map or what does it look like on fluoro? You may be asked to manage patients with frequent PVCs. So it depends on symptoms, it depends on burden and whether you give them drugs or ablation, they may give you options. If you're going to ablate in the sinus of valsalva, it is good to look for ice localization. There may be some, although if you're deep in the cusp, it's likely to be safe. There may be patients with odd coronary artery, congenital malformations. And so you want to be able to visualize the coronary ostea on ice, at least before you ablate in the sinus of valsalva. If you're ablating up near the AIV for a summit PVC or MCV ablation, MCV you might do for a pathway, you might do for PVC, then ice is really not easy to tell what's there. So coronary angiography would be necessary to make sure you're not near a coronary artery before you take that on. Unless you're extremely skilled with ice, we've not been able to figure that out. Non-ischemic cardiomyopathy-related VT, important to know the epicardial criteria such as Q waves and lead one, maximum deflection index greater than 0.55, delta wave appearance and other criteria like QSs in the inferior leads, there are others. The most common sites for non-ischemic are periaortic, basal septal, basal inferolateral. Those are uncommon for ventricular tachycardia related to ischemia because infarcts tend not to be up against around periaortic or just basal septal alone or just basal inferolateral, they tend to extend more apical. So that would be a clue for instance, if they show you a scar like that in someone with coronary disease, you'd have to be suspicious there may be another etiology. Certain types of cardiomyopathy cause certain types of tachycardia. So because of the scar location, so ARVC would be associated with RV tachycardia, Lamin cardiomyopathy with a basal septal VT, heart block and maybe AFib. There are others associated with others and it's worthwhile just reviewing that. Hypertrophic cardiomyopathy, when you see VT, it's usually a feature of late remodeling, there has to be substantial scar there to CVT. The F is another story. There may be an apical aneurysm and PRKAG2 is associated with pre-excitation. It's important to know that particular mutation associated with hypertrophic cardiomyopathy and pre-excitation. It's important also to try to understand some of the more popular means of substrate mapping in ablation, late potentials, lavas, ilams. Often for non-ischemic cardiomyopathy, epicardial ablation may be necessary more than for ischemic VT. For ischemic VT, Bill Stevenson himself has put together schematics for you in the course, circuit diagrams that tell you the timing of the electrograms during VT at each circuit location and their response to overdrive pacing during VT at each location. Also recognize the significance of non-propagated stimulus that can terminate VT. When you're trying to pace and make a diagnosis for location of the electrogram, occasionally you'll capture in an isthmus, terminate VT without propagation to the rest of the ventricle. In ischemic VT, epicardial localization is less useful. So that clear, good to know that. Unipolar versus bipolar voltage maps may be useful in identifying deeper targets on the other side, the identifying epicardial scar and mid myocardial scar. The QRS morphology in ischemic indicates an exit site, but it's not necessarily a target for ablation. So when you're doing substrate mapping and you get a QRS morphology similar to the VT, it may not be a good site for ablation. You may be outside the circuit completely. Almost always ischemic VT is due to re-entry, but it may be useful. It always is useful to demonstrate that it's re-entry and you should be able to recognize a focal mechanism by pacing maneuvers. In terms of pacemakers, should be able to recognize lead positions on an EKG, right bundle branch block, in someone with a right ventricular lead is suspicious or how to see that a lead may be in the LV on chest x-ray. Seeing that the lead is posterior or potentially through the fossil valus or maybe in the coronary sinus, which wouldn't be particularly dangerous for stroke, but may not be an ideal location for the V-lead. But a scenario with a patient presenting with stroke after pacemaker was implanted sometime, and then you get an x-ray and you see a posterior lead position in the V that went through a fossa into the V and is a dangerous such scenario. Should understand the ethics of implanting devices. In other words, the class four indications or contraindications. You should understand how drugs affect pacing, which drugs increase threshold, such as amiodarone, which lower them, such as dofetilide and sodalol. Know your CRT indications, like don't pace right bundle branch block is no clear indication for that, or narrow QRSs. Normal EF, again, wouldn't be an indication for CRT. And in real life, we sometimes have more nuanced positions, but on the test, there's just no indication for CRT when you have a normal ejection fraction. Suspect sarcoid in a youngish person with AV block what's young, I don't know. My perspective on that has changed over the years, but probably under 65 is a reasonable number to think about. And I think on a test form, certainly they would give you a number that wouldn't be too on the borderline, something like 50 year old person presents with AV block. Why would a person with AV block, you just put it in a pacemaker and send them home? No, you'd want to do additional workup. You might attain an MRI. If there's extensive scarring or LV dysfunction, extensive scarring on MRI or LV dysfunction, or something that suggests sarcoid, or they have a history that indicates they have a genetic cardiomyopathy, then obviously we might consider an ICD instead of just pacing. There's a block indication for CRT for patients who are going to have a high pacing burden with ejection fractions in the 30 below normal. Symptoms are a large part of indications and guidelines. And it's important to keep that in mind when you're deciding whether to pace someone. Someone with asymptomatic winky block AV block, there's no indication to pace that. If you identify someone who has high risk of intrahis block, and despite no symptoms, there is an indication to pace that. Again, ICD, lots of questions on indications. There are special groups that may merit ICDs, and those are patients with sarcoidosis and a significant scar, burden or low ejection fraction or slightly low, inherited cardiomyopathies with high risk of sudden death, hypertrophic cardiomyopathy in some subsets, depending on how old they are, how much remodeling there is, myotonic dystrophy, depending on how far along they are. Indications for CRT you should know well, should recognize lead fractures, short VV interval, recognize EMI, T wave oversensing, how to recognize it, and then management. There may be several ways to do that, programming wise, or potentially even replacing the lead. Recognize loss of A and V capture by V capture, what are the solutions for that? Recognize myo potential oversensing, and that what increases defibrillation thresholds, sodium channel blockers do that, potassium channel blockers lower DFTs. All of this can be found in Dr. Ellenbogen's workshops and other parts of this particular course. Pharmacology, honestly, a lot of this is memorization, and Dr. Poole has put together very nice tables, so if you're studying for the test, personally, I recommend, since our short-term memories are relatively limited, to study this kind of at the last minute. You have to memorize a lot of this stuff, honestly, and if you don't already know it, and it's best to kind of do this at the last minute so you don't forget it. If you study it two months ahead of time, it requires memorization. From my standpoint, I'm not gonna remember it anyway. So in this case, you can study her lectures, and the tables particularly, understand adenosine effects, understand how creatinine clearance could affect dosing of particular drugs, and particularly sotal andophetalide, understand drug interactions, adverse effects, management of maternal and fetal arrhythmias during pregnancy, what drugs are potentially safe to use, which ones you wouldn't wanna use. Basic EP, similar, I think, in that it can be difficult to remember these things if you don't have a solid grasp on it to begin with. Should know the basic current and action potentials. There's gonna be some nice lectures and figures you can look at to remind yourself before you head into the test. You wanna identify APDs at different locations, understand use dependence and reverse use dependence of drugs, because they can show you action potentials and ask you what happened to this action potential? Which of these following drugs was likely given between condition A and condition B? Understand EADs that are associated with acquired or congenital long QT, and then DADs with DIG and CPVT. Inherited cardiomyopathy, there is a section for inherited cardiomyopathies and looking at all the different types and how the types of arrhythmias associated with these. For CPVT, bidirectional VT is a big feature. It's exercise-related, treated with beta blockers, calcium blockers, or flecainide, sometimes sympathectomy. It's a reanidine receptor autosomal dominant mutation or calcioquestion recessive mutation, causes intracellular calcium overload in DADs. ICDs are problematic in this population and drug management may be preferred, just like with long QT. Long QT1 in particular responds extremely well to beta blockers, possibly sympathectomy. And like in CPVT, sympathetic surge associated with an ICD shock could just set off multiple rounds of ICD shocks and potentially a patient who didn't survive all that or a patient who is absolutely scared to death to get another shock. ARVD or ARVC is a desmosomal disease. Often PKP2 is most common. Guidelines recommend restricting exercise. One of the key features on the EKG is anterior T wave inversion, but you should know the major and minor criteria for this. Long QT, you should know the provoking factors for events in the various forms. The vast majority of these are going to be long QT1, 2, or 3. Know unusual drugs that you might use to treat long QT, such as long QT3. Indications for the defibrillator. In other words, someone who has had syncope, long QT1 and is tolerating beta blocker and has had no more events, there's no indication for an ICD. ECD, ECG criteria. There are stereotypical ECG patterns for types of long QT. Type 1 has a prolonged but normal-looking T wave. Type 2 has a bifid, funny-looking T wave. And type 3 with a prolonged ST segment. If you remember those three things, you'll be able to identify on the test. Brugada electrical storm. One of the things that you should consider in that scenario and not most electrical storms is giving isopropyl or pacing the patient, which will calm it down. Beta blockers can make it worse. So bradycardia is a precipitant of these arrhythmias. And if you can overcome that with isopropanol or pacing, that's the answer. When you screen for genetic arrhythmias, screen affected family members first, not all people. And then understand that genotypes and phenotypes don't always match. There's variable penetrance, so that a gene in one person in the family may produce severe disease and not much in another. So you may not want to treat all the family members the same, exactly the same, just because they have the same gene. AT and atrial flutter. You need to recognize the difference between a focal AT and a re-entrant one. Usually this is recognized by fusion on intracardiac EGMs. This is the concept of downstream pacing. There'll be lots of examples for you to look at in the workshops and in the lectures. You should be able to localize atrial tachycardia by P waves and recognize atrial flutter as typical or atypical based on morphology. So typical atrial flutter counterclockwise would be negative inferiorly, positive in V1. It's the opposite for atypical flutter, negative in V1, positive inferiorly. If you have positive positive or negative negative, that's very atypical for counterclock or CTI dependent flutter. Understanding left versus right when you're mapping and when you should go to the left. Showed example of that in workshop and there are others. In other workshops, crystal breakthrough for CTI flutter may confound your ability to determine block. Block on the line is what you're looking for, not what's happening in the lateral right atrium. Crystal breakthrough will create a Chevron pattern there and you may not get the complete reversal of activation along the right atrium because there's a crystal breakthrough posteriorly. So the key there is to do differential pacing right up against the line so that that's the latest and everything moving away from the line is later, even though it's coming around the back of the IVC. You should understand means for determining conduction block. So again, these means are how you to tell if there's a crystal breakthrough, for instance. You look for equal splits along the line of block. It's not perfectly equal because the way conduction gets to a line, particularly if it's a long line, it may reach the line at one end versus the other and conduct up along the line. So the splits may not be perfectly equal all the way up the line. So it hits the line on both sides, but it's not gonna hit both sides of the line exactly in the right, in the same location. One should be able to recognize incomplete block. If you're not pacing and recording near the line, then you may not be able to tell. And so that the answer may be get closer to the line and pace and do differential pacing to sort it out. For left atrial lines at left atrial appendage pacing or CS pacing may be necessary to determine and sinus rhythm alone may not be good enough. Now, mechanisms of AF are controversial. So it's very difficult to test on that, but it may not be so difficult to test on what autonomic milieus promote AFib, the shortening of action potential duration, heightened parasympathetic tone and sleeping there. So there are various autonomic questions that could be asked concerning AFib or sleep apnea and other things that might promote AFib, but the exact mechanism of AFib is unlikely because it's still controversial. Should know the indications for catheter ablation, recognize complications associated with this, such as perforation and how to manage tamponade, atrial esophageal fistula and how to diagnose that, diaphragm paralysis from phrenic nerve injury. Bridging to ablation is a thing of the past. Oral anticoagulation should be continued. And then there may be questions recognizing is PVI complete or not. Honestly, this is not something that should be too difficult because you can pace within your ablation lesion set and determine that you can't capture anywhere in there. That should be good enough, but they may show you electrograms that in the left superior pulmonary vein that are due to left atrial appendage. Far field recording, you can go pace the appendage, pull that signal up against the pacing stimulus and prove that it's not in the pulmonary vein itself. Can do that for any far field. Right superior pulmonary vein, you go pace in the SVC. You pull that signal right up against your pacing stimulus. It's not in the right pulmonary vein. Should understand the biophysics of RF. RF has not gone away yet. Electroporation is coming, but it's going to be a few years before we have it to replace RF, at least for AFib. And to understand that for RF catheter, the hottest temperature is under the tip when it's not irrigated. When it is irrigated, it moves that hotter spot below the surface. And that's only because you're cooling the surface and it doesn't necessarily change. The power put in there is not any different. The size of the lesion is not going to be any different. In fact, it often will be smaller since you're cooling the surface, it kind of constricts the lesion on top. Again, a larger tip size of your catheter electrode makes a smaller burn of power duration and contact force on the same. Understand that you can get skin burns from crinkled and different electrodes, that if you're ablating with very high impedance, you can put on multiple electrodes and split them to lower the system impedance and put more current into your lesions. And then understand some other things like potentially impedance fall as a predictor of steam pops. That's a well-established phenomenon in the literature now. The number is around 18 ohms. Entrainment is a great way to diagnose things, but it has pitfalls and they can be from your pacing, but you're actually not capturing what you're intending to. You're not pacing for long enough to actually entrain the tachycardia. You're too close to the exit from a circuit or focus and you can't show fusion if that's what you're trying to demonstrate. You're pacing it too high an output. So you get nonspecific capture, a large area of capture that can result in short PPIs because you're actually way out in front of your circuit capturing. And when it comes back around, comes back to your electrode, you put your virtual electrode so far out from your actual electrode that you develop a short PPI. And it can also result in capturing far field sites and not what you're trying to capture just under your electrode. You want to pace close to the tachycardia cycle length enough to tell that you've done something, but not too fast to cause decremental conduction. Irregular tachycardias can be a problem or if you change the tachycardia following entrainment. When you get no sites that meet criteria, that could be because you have an arrhythmia that's decremental, you're using a decremental tissue, or you're not pacing in the correct chamber or on the correct surface. So when you have that scenario, you may think about pacing another chamber or another surface. Electroanatomic maps are great, but they also have pitfalls. RA septal breakthrough can look like a focal site. If it's not early relative to the P wave, you should map the left atrium. Fake outs for macro re-entry when lines of block are present. The other thing is fake outs for focal arrhythmia that jump over lines of block. So when you have lines of block, it can look like a focal breakout on the other side. Entrainment will tell you the answer there. Understand how a poor window or reference would affect your map. And then when you have multiple loops, some may be dominant, some may be non-dominant. And train to figure that out. Don't rely on your electroanatomic map alone. There are a few questions on adult boards. I have a feeling this may increase with time because we, as adult electrophysiologists, are seeing more adult congenital patients because they're living longer. So I think these will tend to creep onto the boards more frequently in the future. So you should understand sudden death and arrhythmic risks associated with common adult congenital heart disease. Understand the surgeries to correct them. And what kinds of arrhythmias they're actually susceptible to. All right, that was a lot, I understand. And I think, obviously, this was not comprehensive to get the answers to all of these things I talked about. Need to go back and review the course for specifics. But this is sort of a, this might not be a bad refresher thing to look at. The day before you jump into the test to remind you of all the testable concepts, you can do it in an hour or watch it in an hour. And anything you don't understand as we're zipping through there, you can go back to the course and find examples of that and be able to study a little bit more in the areas that you don't feel confident. So I think this hour, although was very quick, it should be a useful way to study for the test and understand which place, things you still don't understand very well, and you can go back and kind of refresh your memory. All the answers to these things are in the course somewhere, in the lectures, in the workshops. So thank you very much.

electrophysiology

board review prep

principles

paroxysmal AV block

ECG artifacts

rapid atrial pacing

ventricular tachycardia

pharmacology

inherited cardiomyopathies