Hi, it's Greg Michaud, Core Concepts and EP. And for those taking the boards, this is for you. This is a sort of summary of all the principles that are usually tested. And this might be a good thing to look at right before you run into the test to sort of remind you of some of the concepts that are probably going to be tested. Not all of them. And they rotate some of these in and out, but this is probably worth taking a look at. These are general disclosure of relationships. Since we're talking about a lot of concepts, I'm going to show you these. So let's start with EP principles. And again, this is sort of a laundry list approach to this, and we're not going to get into tons of detail, but I think it's worth just having this because it'll jar your memory maybe right before you walk in or a week before you walk in about the types of things you might be expected to see. So paroxysmal AV block. Usually there's bundle branch block at baseline. It's set off by an APC or a PVC, and it's due to phase four block in the hysperkingy system. Distinguish paroxysmal AV block from vaguely mediated block by looking at concurrent sinus slowing. So pretty much sine qua non of vaguely mediated block is that sinus slowing occurs in the setting of AV block. That doesn't happen with paroxysmal AV block or would be very, very unusual circumstance. Now if you're looking at the level of AV block, a long conducted PR interval usually equals AV node block. And why? Because when it's in the hysperkingy system, going from an HV of 50 to a very long HV of 100 doesn't really give you that long of a PR interval. So that can happen, but that's rare. Much more likely that the level block is in the AV node when the PR intervals that are conducted are still long. Now if you see short conducted PR intervals, a narrow QRS, and two to one block, you have to be suspicious of intra-hissing block, and this is actually a pacemaker indication. So narrow QRS, short PR on the conducted beats, two to one or higher degree block, intra-hissing block, and this is a dangerous situation to leave without a pacemaker. Remember that concealed retrograde penetration of the left bundle can cause persistence of left bundle branch blocks. A left bundle branch block, it rates slower than the SVT. So you've got SVT, the narrow complex. You see left bundle branch block when it's actually even slower, and that's because of that phenomenon of retrograde concealed penetration. It's not phase three block, which is purely rate related. If it were rate related, you'd expect the faster rates to have left bundle, but that's not what's going on. They may show you a tracing like that. If you see left bundle branch block and a PAC normalizes the QRS, the answer is probably equal delay in both bundles. Remember ECG artifact is something that will pop up once or twice per test, so it's something to be on the lookout for. So whenever you're looking at a tracing, it might be best to say to yourself, could this be artifact, before you go and dive into more complicated ideas. This has been a popular concept that, in the setting of a long short or sudden onset of rapid atrial pacing, which is a form of a long short, and that causes infrahiscent block, that's not a pacemaker indication, it's physiologic. So despite the fact you're doing an EP study on someone for syncope and you see this, they're trying to bait you into thinking a pacemaker is indicated, but it's not. And they're not going to give you something that's particularly borderline there. It's going to be really rapid pacing, or it's going to be a really obvious long short. Remember the parahysian pacing responses for AV nodal conduction retrograde, the A goes with the his. So without his capture, it lengthens, shortens with his capture. An accessory pathway response, the A goes with the V independent of the his. That's a really good thing to remember, and mixed responses, you know, good luck. Those are hard to figure out, hard to test too, but it's possible they could try to throw something in and just say, is this likely AV nodal, likely accessory pathway, or likely two pathways retrograde? It could pull something like that. Antedromic AVRT, likely to be tested on the, at least a question. This is a wide complex tachycardia without his preceding the QRS. It does include decremental pathways. I showed you an example in a workshop. There are others with more classic mehymes. Usually these are atrial fascicular and decremental pathways where they insert close to the apex. Nondecremental pathways tend to insert at the base. The key to diagnosing this is a late PAC. When the septal A is already committed, you advance the V and reset tachycardia. There's no way for that A to get through the AV node if the septal A is already committed. The fact that you reset tachycardia distinguishes it from VT and a bystander. VT, just the fact that you can, a late PAC advances the V without changing its morphology, but also the fact that you reset tachycardia then eliminates it as a bystander. These can be pathway to pathway, meaning there's a retrograde pathway and antegrade, but more likely antedromic, which antedromic AVRT really is the situation where you go down a pathway and back up the AV node, which is the exact reverse of orthodromic, down the AV node and back up a pathway. And the retrograde pathway can be revealed by PVC or spontaneous retrograde right bundle branch block, because if it's a pathway to pathway, the hysperkinesia system is not part of it at all. But retrograde right bundle branch block would indicate that the AV node is part of the circuit. Pre-excited tachycardia may be shown as a bystander where the tachycardia cycle length doesn't change after accessory pathway block. So again, things that would, you're not going to be able to reset a tachycardia if it's a bystander. And obviously if you see wide and then narrow and there's no change in the cycle length, chances are that's a bystander. Atrial fascicular pathways are a particular type of AV or antedromic tachycardia where it's decremental. It typically has a left bundle branch block appearance with late QRS transition out towards V5. There's no retrograde accessory pathway conduction in these cases. So the AV node is the retrograde limb usually, although sometimes you can see pathway to pathway with this as well. You look for a hyst-like potential on the lateral tricuspid annulus. You ablate these and not the earliest V site, which is at the RV apex. In fact, you can make things worse by doing that. Again, the late APC will make your diagnosis. And another clue to these is that, and it's not at the base that it's inserting, is that the RV apical electrogram is coincident with the onset of the QRS because again, the apex is where the right bundle inserts. And so your electrogram there will, that's where the atrial fascicular pathway inserts. So early right ventricular electrogram right at the beginning of the QRS is an indication that this is an apical pathway, not a basal one. These are very sensitive to catheter trauma. If you're going to bump it, you better be prepared to record where you bumped it in case it doesn't come back. And often these have automaticity with ablation, which is an interesting thing. I don't know how they might test that, but they certainly could show the left bundle tachycardia occurring with ablation and ask you what this might be due to. Orthodromic AVRT often has eccentric retrograde atrial activation because most of them are left free wall. Post-receptal, antreceptal less frequent, right free wall less frequent. A VAV response is pretty much universally present. Hysterefractory PVC or fuse beats during an entrainment attempt may accelerate, delay, or terminate the SVD without conduction to the A. This may not apply to left free wall sites with RV pacing. Ipsilateral bundle branch block increases the VA interval, and that's the onset of the QRS to the atrial recording site. That is not local electrogram to atrial recording sites, so don't make that mistake. Ipsilateral bundle branch block may be necessary for the SVT to initiate or for its persistence, and that's a nice concept for the SVT to initiate. And the retrograde conduction over an accessory pathway with V pacing will be independent of his activation, unlike AV nodal conduction, and you've seen examples of that throughout this course. Bystander pathways are usually antegrade and not retrograde, and so they're a little easier to figure out. The retrograde would be identified by a change in atrial activation sequence with the cycle length being unaffected when the bystander pathways block. Multiple mechanisms may exist, such that an accessory pathway is a bystander in one tachycardia and participates in another. So although it's a bystander there, it still may need to be ablated to prevent other tachycardias. Really, bystanders are pretty rare test questions. Catheter ablation of accessory pathways is not an infrequent test question, so an antireceptal pathway can be safely ablated on the ventricular side of the annulus, but one should consider the non-coronary cusp or the right coronary cusp as an alternate site of ablation. This is a classic test question, where pre-excitation will not be present with junctional rhythm, and this is not because the accessory pathway was successfully ablated. You come off RF immediately is the answer, because what has happened is when you get junctional rhythm from RF, even if the pathway is present, it's going to be a narrow complex. There's no way for that junctional rhythm to be present. There's no way for that junctional rhythm to conduct directly over the accessory pathway, so you produce a narrow QRAS. It doesn't mean you successfully got the pathway, and it means that you may be getting the AV node, so you really need to come off RF immediately and reassess. Fascicular ventricular pathways are not that rare. You certainly will see these in your career, and they shouldn't be ablated, because they don't participate in tachycardia. They're identified by observing a fixed degree of pre-excitation with progressively faster atrial pacing. That is not something you see with normal pathways, because there's always a competition between pathway conduction and AV node conduction, and you can bring out differences by pacing faster, where you get decremental conduction through the node, fixed degree of conduction through the pathway, and start to get more pre-excited as you pace the atrium or put in APCs or give them adenosine. And the junctional escaporythms are also pre-excited. So these are connections between the fascicle and the ventricle. They're little insulation breaches, and they don't really create tachycardia circuits. When you're ablating WPW, the unipolar electrograms should match the bipolar timing and show a QS pattern. The action potential can be identified by reversing atrial or ventricular activation wavefront. So if you have a left free wall pathway and you're pacing the right ventricle, you can look in the coronary sinus, and what you'll see is proximal to distal. That will usually be with the slant of a left free wall pathway. You can reverse activation by pacing way up near the appendage in the left ventricle, or you can go out the PA and put it, the right PA, and pace there and capture far leftward. And reverse, you can look in the CS and see that you've reversed the activation from proximal to distal to distal to proximal, and that will often separate the Vs and the As and allow you to see accessory pathway potentials. Obviously, this was well described, has been well described by Jackman and colleagues. You may be asked to identify an ablation site on a 12-lead ECG, so at least be aware of the algorithms to identify pathway location based on 12-lead. Again, you know, if they give you something like that, they're not going to give you post or septum at 7 o'clock versus, or post or septum at 4 o'clock versus 5 o'clock. It'll be more obvious. So for AVNRT, the HA is usually fixed for typical AVNRT, and HH changes will precede AA changes because usually the wobble will be in the AV node and not in the retrograde limb. There's no effect with bundle branch block or PVCs that are fused or hysterefractory. Can have slightly eccentric conduction in the CS with atypical forms. P waves are narrow and inverted, and when there's two to one block, you can see this with the narrow inverted P waves exactly between two QRS complexes. This is a common 12-lead ECG that's shown and asks you to give the most likely diagnosis and when you have that pattern, you're expected to identify it. They, like orthodromic AVRT, they will show a VA response to overdrive ventricular pacing. There's a long post-pace interval minus tachycardia cycle length or STIM-AVA, and there's an AHA response to atrial overdrive pacing or PACs, in which case you would advance, delay, or terminate SVT over the slow AV nodal pathway. This is in distinction to junctional tachycardia, which you may be trying to distinguish that has an AHA response. In ablating AVNRT, junctional rhythm with VA prolongation or block should prompt RF termination. Cryo does not produce junctional rhythm, so if you're ablating during tachycardia, you don't want to see block in the retrograde limb, which is the fast pathway for typical AVNRT, come off cryo. Also, there are some strategies for monitoring AV nodal, potential AV nodal damage when junctionals do not have retrograde conduction. You can start isopryl and gain retrograde conduction. You can do atrial pacing and look for the PR interval. You can do cryo, or you can chip away with short lesions, check for conduction, short lesions, check for conduction. That takes the most chutzpah, I would say, the chip away approach, and that's one I would use very last if nothing else is working. Consider left-sided RF when right-sided fails, and they may ask you to go through a scenario where left-sided ablation may be an option, and just be aware that that may be something useful. Recognize tachycardias that are one-to-two conduction. These are two-fers. They may mimic AFib. In fact, the test question might say, patient sent for AFib ablation and show you a tracing where every sinus beat has two QRSs, which obviously represents conduction over both slow and fast pathway with a single sinus beat. We have unusual pathways, and these are not a big part of the test, but they usually throw in a couple. So, nodal ventricular fascicular may or may not be on the test. MAHIM probably will be on the test, at least one question. Decremental pathways and bundle branch reentrant tachycardia, these are sort of, you know, again, very unusual cases in real life, and so they're probably more usual on a test than they would be in real life, but they're not going to be a lot of questions. So, nodal ventricular fascicular tachycardia can occur with narrow or a wide complex. In fact, concealed ones, bundle branch block may be necessary for tachycardia. They may be VONA tachycardias, but frequently are dissociated because they don't involve atrial tissue, so that's not part of the circuit. You can distinguish these from AVNRT if they are one-to-one by entrainment with fusion, hysterefractory PVCs that advance the next hyst, or the A if there's no, if it's one-to-one. If it's not one-to-one, you'd want to see a hysterefractory PVC either terminating tachycardia or potentially advancing the next hyst or maybe delaying the next hyst if you can't use the A as, so that's the way, that's the type of thing you would look, you see on a test to diagnose exactly that scenario. Decremental pathways are usually septal and concealed, but may have incessant SVT. They will usually have a retrograde activation time, VA time more than 40% of the tachycardia cycloid, so if it's less than that, it's not likely to be a decremental pathway. PVCs during hysterefractory, refractoriness, and decremental pathway usually would delay the next day, which is diagnostic of participation in tachycardia or terminate tachycardia. In bundle branch re-entry, the HH changes, drive the cycle line changes, there's a baseline left bundle usually, you can ablate the left or right bundle in those cases, and you can entrain from the apex and be in. You can even entrain from the atrium if you can get one-to-one, it also entrained with out fusion. Junctional tachycardia, atrial overdrive, pacing will produce the AHHA response. Late PACs during tachycardia have no effect on the next hyst or the, and they're already after the nearby hyst. Early PACs can conduct over the fast pathway and reset junctional tachycardia with an AHHA response. Ventricular overdrive pacing during tachycardia mimics AVNRT and is not useful really for differentiating the two. It's commonly seen after slow pathway ablation plus isoproteinol. You're unlikely to see a question on ablation of JT, just something that we don't encounter, and it's probably not considered standard of care would be very unusual test question. VT-PVC localization has become a large part of the test in recent years. There's probably six or more questions. Where is the PVC arising? Where on this electro-atomic map or fluoro image is this PVC arising? So not only do you have to know what the morphology on the 12-lead looks like, then you've got to match it to a spot, an anatomic location on a map. And then you might ask what complication is most likely when ablating this PVC? So again, you identify where this PVC is likely coming from and then what are the nearby structures that might be injured? So these are the way that these PVC localization questions are formed, usually not just where is it coming from, but then going to the next level, what's nearby and anatomically, can you identify it? So the management of patients with frequent PVCs when asymptomatic depends on the left ventricular ejection fraction and to affect the left ventricular ejection fraction, it usually requires more than a 20% burden. If you're going to ablate in the sinus of Valsalva, coronary angiography or ice localization of the oste of the coronaries is necessary. Patients may have abnormal coronary takeoffs, et cetera. And so you need to really look some way before you ablate. At least that probably expect that on the test. If you're going to ablate in an anterior in particular vein or down the middle cardiac vein, ice is usually not adequate to see the coronaries and so coronary angiography is necessary before that. It may be a choice on the test. So VT related to cardiomyopathy, the epicardial criteria, Q waves in V1, maximal deflection index greater than 0.55, delta wave appearance, et cetera. There's a few of them. For cardiomyopathy, periaortic, basal septal, basal and inferior lateral sites are common. So if they show you scar from those locations it's more likely to be related to a cardiomyopathy than coronary disease. And in real life, we see this all the time. Patients come in, they have some coronary disease and they're sent for VT ablation and they're called ischemic cardiomyopathy. Even though the coronary disease may not have caused an MI. And then we see these kinds of patterns of VT and we say, no, probably it's true, true and unrelated. They have coronary disease, yes, but they also have a cardiomyopathy that's causing this pattern of scar. ARVC more likely to cause RV tachycardia, lamin, basal septal and heart block and a fib, these sort of pattern recognition of the kind of scars and other features of the cardiomyopathy that go together. Also sarcoid is a septal disease mostly. Hypertrophic cardiomyopathy may have an apical aneurysm with the late, with the apical version. Often VT is a feature of late remodeling in this disease. And the mutation PRKAG2 is associated with pre-excitation that be important to know. In substrate mapping and ablation, there's obviously late potentials, lavas. Now there's more data and publications on isochronal crowding, et cetera, that could be shown a map, could be shown looking at that particular map pattern and show where the best place to ablate. It's starting to become long enough from original publications that it could be added to the mix. For your ischemic VT, it's good to know the Stevenson schema and he's provided that for you in the course, such that within the schema, you need to know the timing of electrocrams during VT at each of these circuit locations, like isthmus, outer loop, inner loop, et cetera. You wanna know the response to overdrive pacing during VT at each location, fusion versus no fusion, post-pacing intervals expected. You also be, and this is a great test question, a non-propagated stimulus terminating VT or AT to be able to recognize that this is a critical site, a critical isthmus site, and that ablating at this site would probably eliminate the tachycardia. When you are looking at epicardial and localization criteria, ischemic VT makes these criteria less useful than with non-ischemic cardiomyopathy. Perhaps know the utility of unipolar versus bipolar voltage mapping, what unipolar may give you with deeper sites, epicardial locations or an epicardial scar when you're mapping the endo by using unipolar know that QRS morphology indicates an exit site, but it's not necessarily a target for ablation. These are almost always re-entry. They could show a focal mechanism and they would show you enough data to indicate that it was a focal mechanism. But one of the issues with looking at maps and diagnosing focal mechanisms is that they could be breakouts on one surface and much of the re-entry circuit you can't map. And so you have to do entrainment maneuvers to sort out whether it's focal or not. And that's gonna be the crux of the test question. It may look focal, but the entrainment tells you something else. For pacemaker, you wanna recognize potentially harmful lead positions like a right bundle branch block or a right bundle branch a right bundle branch block on EKG where a lead went into the LV or a chest X-ray showing V-lead posteriorly or patient presenting with stroke five years after a pacemaker implanted and now has clot on the lead. There's a lot of, there may be some questions on the ethics of implanting devices, especially ICDs. So knowing sort of patients who may be contraindicated with terminal cancer expected to live less than a year, that kind of thing. Drug effects should know on pacemaker thresholds like AMEO increasing the pacing threshold and dofetilide lowering it. One C will also increase the pacing thresholds. Know your CRT indications and that normally F is not an indication for CRT for instance, right bundle branch is not and QRS less than 150 generally from the test standpoint would be probably a no-go for CRT. Someone comes with AV block on the young side and young is anything younger than me. So, you know, less than 60 is very young but obtain an MRI and consider the ICD if it's extensive scar and some LV dysfunction but to pop a pacemaker in a young person with AV block is not the answer. The block heart failure study indicates CRT for EFs in the 35 to 50% range pacemaker CRT unless there's some other reason to implant a defibrillator. And remember that symptoms are a large part of indications in the guidelines. Again, ICD indications, you know, there are nice guides. You can look at the ICD indications published 2017 and go through that. It's an algorithmic tables that will tell you and you know, the tests are gonna stick with that. There are special groups like sarcoid and hereditary cardiomyopathies where ICDs may be indicated with normal ejection fractions or near normal. Recognize lead fractures that turn up as short VV intervals. Recognize EMI, T-wave over-sensing will be a ripe for, will be ripe for a test question. Loss of a capture, setting up, say R and RVOS, loss of bivy capture, what are the solutions to that? Recognize my potential over-sensing and that sodium channel blockers increase defibrillation thresholds and potassium blockers lower it. Adenosine is a good drug to know and it usually is on the test in one form or another. Understand which drugs are renally cleared and who you might need to be very careful about. Those with reduced creatinine clearances. Drug-drug interactions, there'll be relatively straightforward ones like warfarin and reodoran, verapamiltofetalide, the ones that we know about, but you can go to lectures in earlier in this course and look at a table where a lot of them were laid out nicely for you. Dr. Poole will do that for you. You don't have to go collect it all yourself. There'll be a little bit about management of maternal and fetal arrhythmias during pregnancy. Pharmacology, I'd say, is something that you have to kind of memorize. It's not like understanding electrophysiology tracings where the concepts are important. And once you get the concept, you can then look at lots of tracings and you really kind of need to memorize some of these. And so my advice would be to look at this toward the end. When your short-term memory is still intact and you can get from a couple of days out from it, having looked at these, and hopefully a week later, you might forget it all, but at least you'd remember it for the test. And you need to know basic currents and the action potential. Again, we have lectures that point all this out. Sotalol has reverse use dependence. Useful thing to know. Know the difference between EADs, which are present in an acquired or congenital long QT versus DADs with DIG and CPVT. You may be shown action potentials under various drug conditions, and you'll have to guess the drug. Is Sotalol most likely to produce this propafenone, et cetera, the difference in action potential under these conditions? Inherited cardiopathies. Again, as we do more and more genetic testing, these are, you know, we're starting to learn more about these particular diseases and so they may creep into the test a little more. CPVT produces bidirectional VT. It's exercise related. So PVCs increase with exercise. Beta blockers and calcium blockers, flecainide and sympathectomies are useful. Potential treatments. It's usually a defect in the ryanodine receptor and is autosomal dominant. Calsequestion is a recessive form. Both forms cause intracellular calcium overload, bidirectional VT. ICDs are problematic in these populations because the sympathetic surge associated with a shock can lead to more shocks and which could lead to death even with a defibrillator in. So many of these patients are, at least there's an attempt to manage them with pharmacology before considering a defibrillator. And that's one group where that may be part of a question. ARVC is a desmosomal disease. PKP2 is most common. There are others. Important thing to understand is that exercise restrictions is a therapeutic measure. Often the anterior T wave inversion on the 12 lead, you can know the major and minor criteria which are laid out for you in the course. Long QT. It's useful to know the provoking factors for the different forms. That ranolazine, maxillitine and flecainide could be used for long QT3. Indications for a defibrillator. Indications for a defibrillator less so now with particular long QT1 which responds extremely well to beta blockade. And so indications for defibrillator is not just having long QT1, but would be refractory arrhythmia that's not responding or poorly responsive to drugs or other things like even sympathectomy. Know the different types of ECG patterns associated with each of the long QT types. Type 1, prolonged but normal looking T wave. Type 2 is bifid funny looking T waves and type 3 with a prolonged ST segment. Brigada electrical storm is treated with isopryl or pacing but not beta blockers. Remember that one. When you're thinking about genetic testing, you screen affected members first to determine if it's worth screening the asymptomatic members. Atrial tachycardia and atrial flutter. You may be asked to recognize maneuvers that demonstrate whether the diagnosis is a focal one or a re-entered one. The diagnosis is a focal one or a re-entrant one. So you have to be able to recognize fusion on intracardiac electrograms. Downstream pacing is a question that's popped up in the last few years. ECG localization of AT or flutter is fair game, particularly left versus right. Understand that CTI flutter, when you're looking at the lateral right atrium, the crystal breakthrough can fool you. And even though conduction block may be present, the crystal breakthrough may look the CS or the crystal electrograms look funny like a Chevron pattern. Understand the means of determining conduction block. And these can be across any lines, split electrograms, differential pacing, incomplete block. You may not be able to determine whether it's complete or not unless you're pacing or recording near the line. And for left atrial line CS and left atrial appendage pacing are useful. So for atrial fibrillation, you might go a little bit into the mechanisms of atrial fibrillation, although honestly we understand these pretty poorly. So they're not gonna test controversial mechanisms of AFib, but might test what autonomic milieus promote AFib. Indications for catheter ablation, complications are gonna be definitely on there and how you recognize them and how you avoid them. Like things like perforation, a fistula diaphragm paralysis, pulmonary vein stenosis. And on continue oral anticoagulation, no bridging. This is plenty of studies that support this. And then you probably may or probably will be asked to recognize when PV is complete to distinguish far field potentials from near field potentials. And these are pacing maneuvers that sort that out for you. Biophysics, you know, there may be some test questions since RF catheter ablation is still quite new. Still quite common, and at least a pulse field isn't gonna be coming for quite a while. Certainly cryo may also be added into this. And again, so the idea of understanding how irrigation may affect a lesion, that irrigation alone makes a smaller burn if power duration and contact portion are the same, not a bigger one. That a bigger tip used makes a smaller burn if the power duration and contact force are the same than the smaller tip because the current density is smaller, spread out over a larger tip. Entrainment pitfalls, this is another ripe, so that they could ask you to interpret something, but if you're not capturing locally, then you can't interpret entrainment. You didn't pace long enough to entrain. You're, so in other words, it's just catching up and you didn't really get there. Your pacing stimulus may not have caught up with the tachycardia yet, or you may not have enough beats to show to accelerate the atrium yet. If you're pacing from a site too close to an exit from a circuit or focus, it's difficult to show fusion. Pacing at too high an output can give short PPIs and capture far field. Pacing too fast can cause decremental conduction and limit your ability to interpret PPIs. If the tachycardia is irregular, be aware that PPI may not be it. So if you're at 40, 50 millisecond changes in intervals, how do you know that what you're measuring after a PPI is not the short one or the long one, makes it very difficult to interpret. So if you see irregular tachycardia, that's a clue that you may not be able to interpret that. Or if you change the tachycardia after you pace, you can't really interpret it. Post pacing interval, unless the tachycardia resumes at the same cycle length. If no sites meet criteria, it may be that you're not mapping the correct surface or that decremental conduction is getting in the way of an interpretation. So there's never gonna be a normal post pacing interval or a short one when you have a decremental circuit, or if you're not in the right chamber, for instance. Electro-anatomic map pitfalls or a septal breakthrough is not early relative to the P wave is a big clue. So you see it breaking out in the septum. It's not that early relative to the P wave. Go, don't be afraid to map the LA on the test. There may be some fake outs for macro re-entry when lines of block are present. Pacing will sort this out for you, or a clue that the total tachycardia cycle length is not present on the map, which it may not expect it to be if you have a focal mechanism up against the line of block. Understand how a poor window or reference may affect your map. A very few questions on adult congenital, at least in the last few years, it's been related to sudden death and arrhythmic risks associated with common adult congenital heart disease defects and the particular surgeries associated with those congenital heart defects. So Fontan's and VT are probably in play since there's ample published literature on that. All right, that was a lot. I'm gonna end with one quick case just to refresh your memory about how questions are put together. This is a 46-year-old man with no significant past medical history. Presents after cardiac arrest, coronary artery showed no evidence of obstruction. Telemetry events are shown below. Which of the following is most likely to be true? Genetic screening for potassium channel mutation should be sought. Genetic screening for an autosomal dominant mutation in the cardiac reanidine receptor gene should be sought. First-line medical therapy would include verapamil. First-line medical therapy would include propanolol. Cardiac cath lab should be activated for STEMI and immersion PCI. Here's the tracings. And I think the first-line therapy, including verapamil would be the best answer here because this is Prince metals and polymorphic VT. He has no coronary disease. He's had these events off and on. So why would he be having an acute MI now and not in all the other cases? Second, there's clear ST elevation preceding episodes of ventricular tachycardia. So setting of acute ST elevation and polymorphic VT that goes away associated with chest pain is Prince metals angina. And treatment with a defibrillator may be indicated, but certainly some sort of drug treatment to prevent these episodes is gonna be key. Thank you.

cardiology board exams

key principles

paroxysmal AV block

bundle branch blocks

atrial tachycardia

ventricular tachycardia

genetic screening

catheter ablation