Welcome to Core Concepts in EP. This is workshop number six, Electrocardiographic Electrophysiologic Correlations. I'm Jeanne Poole from the University of Washington. These are my disclosures. So the first case is a 26 year old woman who was brought to the ED complaining of dizzy spells and palpitations. Her ECG is shown in tracing one, which will be on the next slide. An echocardiogram showed concentric hypertrophy. Her family history is positive for family members with WPW. Her 21 year old brother's ECG is shown in tracing two. He had paroxysmal atrial fibrillation and several family members have had pacemakers. So the question is a genetic syndrome involving which of the following genes or proteins is most likely to be responsible for the syndrome seen in this family? Here's the patient's electrocardiogram. Here's the brother's electrocardiogram. I'll go back up to the questions. So A is PRKAG2, B is plaquoglobin, C is beta-myosin heavy chain, and D is troponin T. Here's the patient's ECG and the brother's ECG. The answer is A, PRKAG2. These are rare mutations, but worth knowing about because it does cause a syndrome of ventricular pre-excitation, atrial fibrillation, conduction defects, and cardiac hypertrophy. Usually it's a missense mutation in the G2 subunit of AMP-activated protein kinase and it's autosomal dominant with a high penetrance and causes a gain of function despite reduced AMP affinity. The histology has been described as non-sarcomeric hypertrophy without the myofibrillar disarray, typical of classic hypertrophic cardiomyopathy. The early course is characterized by a short PR interval, often with a very bizarre QRS consistent with pre-excitation or can look like LV hypertrophy. Patients can have paroxysmal SVTs or atrial arrhythmias. Transmission system disease can often be noted in these families as well, and sudden death has been reported, but is rare. Case two, a 51-year-old female develops paroxysmal atrial fibrillation. She has hypertension with moderate concentric LVH on her echocardiogram and normal systolic function. Her baseline ECG shows LVH, nonspecific ST and T wave changes. Her PR interval is 180 milliseconds, her QRS interval is 100 milliseconds and her QTC interval is 448 milliseconds. She begins a new antiarrhythmic drug. Two weeks later, she has a Holter monitor for ongoing palpitations. The rhythm strips from the Holter monitor are shown in tracings one, two, and three, which I'll show you on the next slide. The patient most likely was placed on an antiarrhythmic medication with which of the following pharmacologic mechanisms, A, blockade of the rapid delayed rectifier current, B, blockade of voltage-gated sodium channels, C, blockade of L-type calcium channels, or D, inhibition of the sodium potassium ATPase pump. Here are the tracings. They are rhythm strips. The top is tracing one, the middle tracing two, and the bottom tracing three. Tracing one is at rest when the Holter monitor was attached to the patient. Tracing two is with walking and the patient was complaining of palpitations and then tracing three with continued walking when the patient complained of shortness of breath. We'll go back up to the choices. The question is, the patient most likely was placed on an antiarrhythmic medication with which of the following pharmacologic mechanisms? The answer is B, blockade of voltage-gated sodium channels. This patient's Holter monitor shows atrial flutter with a long atrial cycle length and with exercise, the AV interval prolongs and the QRS has widened. This observation can be explained with either flecainide or propanthenone, class Ic antiarrhythmic drugs. These are sodium channel blocking drugs which exhibit use dependence, and so there's a risk of bundle branch block occurring at higher heart rates. Also, these medications can prolong the atrial cycle length or decrease atrial conduction velocity, and this places the patient at risk for one-to-one AV conduction during atrial flutter. Class III antiarrhythmic drugs block IKR and exhibit reverse use dependence. Blockade of the L-type calcium channels are calcium channel blockers, of course, and inhibition of the sodium potassium ATPase pump is related to digoxin's mechanism of action, so none of those answers account for the findings. And answer B is the best answer. Case III, a 63-year-old female with a non ischemic cardiomyopathy is diagnosed six months ago. Left ventricular ejection fraction is 32%, and neocardicillization class is 2. Medications include carbadolol, 25 milligrams BID, lisinopril, 10 milligrams BID, spironolactone, 25 milligrams QD, and warfarin. The patient is referred for an ICD. ECGs over the past six months reveal baseline heart rates of 95 to 100s. Our current ECG is shown in tracing one on the next slide. Based upon the available data, the best recommendation is A, increase carbadolol dose, B, CRTP and ablation, C, cardioversion and single-chamber ICD, and D, amiodarone plus a pacemaker. Here is the tracing. And we'll go back up again to the questions. The choices are A, increase carbidolol dose, B, CRTP and ablation, C, cardioversion and single chamber ICD, and D, amiodarone plus pacemaker. So I considered that B was the best solution for this patient. These clinical scenarios, if you take them on the board exam, sometimes you will consider that there are several possible answers, but the question is, what is the best recommendation? So the ECG shows a left bundle branch block and an underlying atrial tachycardia or atypical atrial flutter. The A to A cycle length is about 300 milliseconds. And likely this has been going on for the last months as she has a history of a high heart rate on prior electrocardiograms. The patient is already on appropriate heart failure medical therapy and she has a left bundle branch block. So therefore she meets criteria for a CRT. However, she might have a component of tachycardia just worsening her heart failure and her atrial flutter or atrial tachycardia needs to be addressed and treated. Her left ventricular EF has a good chance of recovering such that she might not meet criteria for an ICD with appropriate therapy. It would be a judgment call as to whether she receives a CRTD and I did not include a defibrillator as an option or a CRTP. So of the options available, B is the best. A four 36-year-old male with no known heart disease develops palpitations and presents to the emergency room. The two tracings shown, tracing one and tracing two were recorded 15 seconds apart. Which of the following is the most probable diagnosis? A, typical atrial flutter with one-to-one and two-to-one conduction. B, SVT due to AV reentry using an accessory bypass pathway. A, AV node reentry with one-to-one and two-to-one conduction or idiopathic ventricular tachycardia. On the left is tracing one and on the right is tracing two. The choices again are typical atrial flutter with one-to-one and two-to-one conduction. B, SVT due to AV reentry using an accessory bypass pathway. A, AV node reentry with one-to-one and two-to-one conduction or idiopathic ventricular tachycardia. The right answer is C, AV node reentry with one-to-one and two-to-one conduction. So the question tells you that the tracings were made 15 seconds apart. And this implies that this is a single ongoing rhythm. The ventricular rate in the second tracing was exactly half that in the first tracing. And there was a distinct P wave that falls right in the middle of each RR interval. One-to-one A flutter converting to two-to-one could be considered but flutter waves are not seen in the second tracing. And most of the time, one-to-one atrial flutter would have aberrant conduction. Of the choices, AV node reentry with one-to-one and two-to-one conduction is most consistent with the electrocardiograms that are shown. Intercardiac electrograms are shown on the next slide. In prior studies, two-to-one AVNRT has been observed in about 9% of adults and 17% of pediatric age patients. It's always a fun rhythm to see in the EP lab. And of course the treatment is slow pathway ablation. And these were the intercardiac electrograms where you can see the initiation of AVNRT followed by one-to-one conduction and then two-to-one conduction in the right-hand panel. Case five, 46-year-old male seen for palpitations. In this case, he had an ambulatory ECG monitor which showed occasional PVCs and a 16-beat run of non-sustained monomorphic VT. His electrocardiogram is shown in tracing one on the next slide. The most likely explanation for the ECG is catecholaminergic polymorphic VT, hypertrophic cardiomyopathy, acute ischemia or long QT type 3. And this is the electrocardiogram. Again, the options are CPVT, HCM, acute ischemia or long QT type 3. So this one's pretty easy. The answer is B, hypertrophic cardiomyopathy. 12-ly demonstrates really classic LVH with diffuse STT wave segments, prominent T-wave inversion, and these findings are consistent with HCM. CPVT is wrong as CPVT does not really have a characteristic pattern on the 12-beat ECG unless the patient is having the arrhythmias where they could have polymorphic VT or alternating PVC morphologies, but that's not what is seen on this 12-beat ECG. And those arrhythmias are classically associated with exertion, although not always. Answer C, acute ischemia is unlikely to present with T-wave inversions across the entire ECG as was seen on this example, and the patient didn't present with chest pain. Although patients with HCM certainly can have ischemic chest pain that's related to coronary microvascular disease. And answer D, while the QT is often prolonged in HCM due to abnormal repolarization, long QT 3 most often has an ECG with a long ST segment and upright and pointed T-waves, although there's much variability in the ECG patterns seen amongst long QT 3 patients. And the prominent LVH pattern also would not be a typical characteristic of patients with long QT 3. Okay, six. A 17-year-old female has fatigue and a fast heart rate. She has noted shortness of breath for one year when jogging. She has a lot of stress at college and propranolol was tried three months earlier, but she became more tired. You obtain an ECG tracing one and an echocardiogram which shows mild global hypokinesis with a left ventricular ejection fraction of 46% and no other abnormalities. A Holter monitor shows a single rhythm throughout with one-to-one AV association, a long RP, and variable rates between 110 and 135 beats per minute. A cardiac MRI scan showed no late gadolinium enhancement. So what is the next best therapy? A, ivabradine. B, a tilt table test. C, schedule an EP lab procedure with possible ablation. And D, prescribe a physical therapy program. And here is the patient's electrocardiogram. Here are the questions again. Ivabradine, tilt table test, EP, plus or minus ablation or physical therapy. Okay, the best answer is C, schedule an EP lab procedure for catheter ablation. This patient has a pretty obvious atrial tachycardia, one-to-one AV ratio with very distinct and abnormal P waves that precede the QRS. By history, this is not characteristic of paroxysmal SVT and in the stem of the question on Holter monitoring, the heart rate has some variability which atrial tachycardias classically can have. So these findings really are most consistent with an atrial tachycardia of all of the options that were provided. ATs are an uncommon cause of SVT in the pediatric population. They can occur with or without structural heart disease and common locations of origin are along the crista terminalis, the coronary sinus ostium, the right or left atrial appendices, mitral valve annulus, and the pulmonary veins. The differential diagnosis is always sinus tachycardia or in the case of a persistently elevated heart rate and inappropriate sinus tachycardia or IST. However, IST is not associated with a reduction in cardiac function. Adabrodine has had favorable results in some patients with IST, which was answer A. This patient did not report syncope, near syncope or postural intolerance. Thus, this patient did not have classic symptoms suggestive of POTS syndrome for which a tilt table would be an option or a physical therapy program. So C is the best answer. A seven to 24-year-old male's admitted to the CCU after a syncope spell. Since arrival, no arrhythmias are noted. He has been treated with Ziprazidone for his bipolar disorder. He had one prior syncope episode three years ago when in a methadone program. He's recently started on moxifloxacin for a severe sinus infection. You are asked to consult and the rhythm strip is shown below. The next best next step is discontinue moxifloxacin, discontinue moxifloxacin and Ziprazidone, cardiovert slow ventricular tachycardia or give IV amiodarone. So the best answer is B, discontinue moxifloxacin and Ziprazidone. This ECG shows a really dramatic long QT interval with interesting T wave alternans. The rhythm is not BT. The patient was prescribed two QT prolonging medications, both Ziprazidone and moxifloxacin. It's possible that the patient has an underlying long QT syndrome that was unmasked in the setting of these medications and genetic testing would certainly be reasonable. This is suggested also in that he had syncope while in a methadone program in the past with the concern being that the syncope in both situations was arrhythmic. So stopping all QT prolonging medications is indicated. Case eight, a 61 year old male has symptomatic recurrent PAF. He took flecainide successfully in the past but then was diagnosed with coronary disease and had a stent to his LAD. A change in antiarrhythmic therapy to dofetilide is planned and your recommendation for dosing is requested. His ejection fraction is 48%. He has hypertension and COPD. His DLCO recently was 59% of predicted. His renal function is normal. This 12 lead ECG is shown on tracing one on the next slide. QRS and QTC are measured as indicated. The best next step is to recommend amiodarone, begin dofetilide at 250 micrograms BID and stop the hydrochlorothiazide, begin dofetilide at 500 micrograms BID or recommend catheter ablation. Here is the electrocardiogram with the intervals measured. So the next best step is D, recommend catheter ablation. This patient should be recommended for catheter ablation. That's what we do in EP of course, but just considering this from the perspective of antiarrhythmic drugs, if the patient had desired that instead of a procedure, A is not the best choice as the patient has pulmonary disease and the DLCO is reduced. So that would be placing this patient at high risk for pulmonary fibrosis. B is incorrect because there's no need to adjust dofetilide doses in a patient with normal renal function. And C is not the best option given the left bundle branch block. And the QT interval exceeds the recommended 440 millisecond cutoff for starting dofetilide. In patients who are not candidates for ablation, cautious dofetilide can be tried in the presence of a bundle branch block and a number of different adjustments have been suggested such as measuring the JT interval instead of the QT interval. Here is the dosing recommendations for dofetilide. Just as a review, dofetilide is a class three antiarrhythmic drug that selectively blocks IKR and causes a linear dose related increase in the QT interval. 80% of dofetilide is excreted by the kidneys and 20% in the liver by a CYP3A4. So adjustment of the dose is based upon creatinine clearance as you can see in this algorithm. And as noted, it's contraindicated if the QTC at baseline is greater than 440 milliseconds and patients need to be loaded in hospital and placed on telemetry. But that's the end of those cases. Thank you for your attention. Enjoy the rest of Core Concepts in EP. This is workshop number six, electrocardiographic electrophysiologic correlations. I'm Ed Gerstenfeld from the University of California, San Francisco. And we'll be going through board style questions that hopefully will highlight some of the points from the lectures you've heard. These are my disclosures. So we'll jump right into it. First case is a 77 year old woman who presented to the emergency room with rapid palpitations. A baseline ECG is obtained and I'm gonna show you this, Tracing 1-1. An IV medication is administered and then the next ECG in Tracing 1-2 is observed. And the question is the mechanism for the rhythm change observed is most likely A, depolarization of the AV nodal cells, B, action potential prolongation, C, increased potassium channel conductance or D, blockade of beta receptors. So here you have to figure out both the medication and the effect. So this is the baseline ECG in emergency room. Give you a second to take a look at that, tachycardia. And then a intravenous medication is given and that results in this effect. Again, to remind you, these were the options. Depolarization of the AV nodal cells, action potential prolongation, increased potassium channel conductance or blockade of beta receptors. I'll give you a few seconds again, if you wanna pause and look through those two options, I'll give you a little bit more time and then we'll go to the answer. ECG 1, ECG 2, feel free to pause on those. The correct answer is C, increased potassium channel conductance. And let's look at first what happened in this ECG. So on the left, I think you can make out, it's a narrow complex tachycardia. There's a two to one atypical flutter. And then again, here you've gotta take two steps. You gotta figure out what medication is given and then figure out what the mechanism is. So we see two things. Obviously we see AV block with a long pause and we also see this flutter degenerate to atrial fibrillation. So I think most people may have figured out that the medicine given was adenosine, which is commonly used to figure out the mechanism of an unclear SVT. So adenosine has two effects. Obviously one, it leads to hyperpolarization of the AV nodal cells, it leads to conduction block. And it does this by acting on the IKADOACH receptor. The second is the generation of atrial flutter to atrial fibrillation. And again, this happens because adenosine has an effect of not lengthening, but shortening the axon potential duration. And that can lead to a functional reentry and destabilization of flutter into atrial fibrillation. That's commonly seen. Let me just go through the possible answers again. So again, this is hyperpolarization of AV nodal cells. So A is incorrect, it's not depolarization. Again, adenosine, once you figure that out, causes axon potential shortening heterogeneously in the atrium. So it's not axon potential prolongation. We did not give a beta blocker. Beta blocker may have caused some slowing of the rate, but not AV block and not degeneration to AFib. And so the correct answer is C, increased potassium channel conductance. Okay. Again, the explanations are in the slide, so feel free to spend more time on those. We'll go to case two now. A 59-year-old man with prior MI and an ejection fraction of 38% was admitted for atypical chest pain. Cardiac enzymes were negative. A stress MIBI scan showed a fixed anterolateral perfusion defect. Medications include aspirin, metoprolol, and lisinopril. During monitoring, tracing 2-1 was observed. The patient was asymptomatic. The best management option for this patient is A, amiodarone, 150 milligrams IV. B, magnesium, two grams IV. C, electrophysiology study. D, implant an ICD, E, discharge the patient home. This is the telemetry strip, and again, I'll remind you of the answers, amiodarone, magnesium, EP study, ICD, or discharge home, and you can feel free to pause on this slide and think about it, and then we'll continue. So the correct answer here is E, discharge home. So let's look at a slide. Someone always points out during the course that happily the RN is aware, but, you know, again, if you're, whether this is real life in the wards or practicing for the boards, you will absolutely see artifact in the boards, and it's obviously important in clinical practice as well not to treat artifact, and, you know, the best way to know is just to march out the QRSs before this signal that, you know, you may think may be artifact, and the first clue is when you would expect the QRS to be with your calipers, you see these sharp signals, which are the QRS, and that the remaining QRS is exactly on time. So when you, you know, scrutinize this artifact, you see these sharp signals here, and this may be someone tapping on their electrode or brushing their teeth, but this is pretty typical artifact that you might see in the boards. So again, obviously the EF is 38%, so that, again, looking through the answers, I don't think you certainly would jump to amiodarone for this, and if you thought that was Torsad, you might have chosen magnesium. Again, if you thought that was VT and the EF was less than 40 by must, you could have chosen an EP study, but for artifacts, really not indicated, certainly not going to plant an ICD, and so the correct answer is to discharge the patient home, and again, recognizing artifact and telemetry is very important, both for clinical practice and the EP boards. Let's jump to a VT case. This is a 69-year-old man with a post-infarct cardiomyopathy status, post-implantable defibrillator placement and, out of the way, recurrent ICD shocks for VT is referred for ablation. During the EP study, VT is induced, and then overdrive pacing at 380 milliseconds is performed from the mapping catheter in a low-voltage region. You'll see overdrive pacing here. I'm showing you the pacing cycle length, and then the question is, this site where the catheter is is best classified as an entrance, an exit, an isthmus, an adjacent bystander, an outer loop, or a remote bystander. Some people may say, well, this is just, you know, asking questions about jargon, but I think it gets down to kind of understanding the mechanism of the VT, and you certainly might see questions like this on the boards and, again, useful to understand what this sort of response means in clinical practice, too. So here's the image, if you want to take a look at it and pause. Here's the options, and I'll give you a few seconds to think about this. Okay, continuing, the correct answer. Here is an outer loop site, option E, so hopefully many of you got that correct. So looking at the slide here, first is, you know, there is a mid-diastolic potential on the ablation catheter during VT, which is always a good sign, where overdrive pacing, and again, I'm showing you, you know, the first question always when you're looking at these tracings, particularly on the boards, is with overdrive pacing, are you capturing the VT? Are you accelerating the VT to the paced rate, right, pseudo-capture? You'll see lots of those sort of distractors on the boards where the answer is you need to pace faster, you need to pace at higher output, but here I think if you just look at the QRS morphology, if you look at the rate on the RV, you can see that the stimulus to RV is stable and that there's a longer pause after you stop pacing, so you are accelerating to the paced rate, which I told you was 380 milliseconds. We look at the post-pacing interval, which in this case is 420, but I think just measuring with calipers, you can tell it's pretty close to the VT cycle length of 410, so that post-pacing interval is within, you know, 5, within 30 milliseconds of the tachycardia cycle, I'm telling you that you are in the circuit, the, you know, looking at the answer here to the stimulus, the QRS is very similar to the electrogram, the QRS, and then the remaining question is, you know, where are you within the circuit, are you at an entrance, are you at an exit, are you at an outer loop? The important stimulus, the QRS and electrogram to QRS, the important thing here is to compare the morphology on the 12-lead ECG, and again, the mid-diastolic signal might make you think isthmus, but again, I think if you look in all 12 leads, it's pretty clear that there's fusion here between the VT and the pacing, right, if you look at the QRS in lead one, it's more negative here, it's wider here, look at V2, V3, really all 12 leads are different, and again, not saying it's not in the ballpark, but there's clearly some fusion in here, which means you're not in a protected isthmus, right, you have some fusion, and so you must be in what we would call an outer loop, again, you're in the circuit, you're close, but probably not the ideal place to ablate. If you haven't read Bill Stevenson's classic 1993 paper on VT and the response to ablation in the various sites, go back, and I encourage everyone to read that, but again, here we have entrainment with fusion, PPI, which is within 30 milliseconds of the tachycardia cycle, and that would be an outer loop site. Okay, moving on to case four, 45-year-old woman with a 25% burden of symptomatic PVCs refractory to metoprolol, and an EF of 45% is referred for catheter ablation. The PVCs shown, activation mapping showed no early RVOT sites, but sites with similarly early activation were found in the anterior interventricular vein and the left coronary cusp. On the left, we see the PVC morphology, on the right, we see the PVC with the ablation local activation mapping during the PVC from both the anterior interventricular vein and from the left coronary cusp to 13 milliseconds. This red line is at QRS onset, so about 13 milliseconds from the AIV and 11 milliseconds early from the left coronary cusp. For the ablation catheter at the earliest site in the AIV, I'm going to show you an angiogram with the ablation catheter at that site, RAO on the left and LAO on the right. The best next step is, A, ablate carefully at this site in the AIV, starting with 10 watts energy, B, perform a cryoablation in the AIV, C, ablate at the earliest site in the left cusp, if it's a safe distance from the left main ostium, or D, terminate the procedure and try fluconide 50 milligrams BID. Okay, I'm going to show you these angiograms one more time, give you a second to think about the answer, and the correct answer is C, ablate at the earliest site in the left cusp of a safe distance from the left main ostium. This was a bit of a complicated one, but important things to realize are, and again, this comes up very frequently in clinical practice, first, just look at this PVC morphology, it's positive in V1 with kind of a slurred QRS and positive across the pericordium with a negative, completely negative QS in lead I, and that should make you think of an anterior superior, basically LV summit, which one way to access that area is the anterior ventricular vein. Now, both sites essentially are similarly early, it's true, AIV is a little bit earlier, but when we look, we see that really we're right on top of the LAD. So you know, if you're on top of the LAD, you can cause injury at 10 watts, so this kind of low power, hope for the best, is not a good idea. In the case of an AIV, well, it used to be thought that the coronaries might be protected from cryoablation because of the warm blood in the coronary arteries, but we know from preclinical studies that although you may get away with this acutely, you still will have intimal, neo-intimal hyperplasia, and that you can damage the artery with cryoablation as well. So if you're right on top of the LAD, that's not a good idea. Terminate the procedure on trifleconide, well, again, the patient had an EF of 45% and not a structurally normal heart. And again, when you're equally early, you often can get these from the left cusp because as opposed to the AIV, where you're in a vein and your flow is limited, you can only give a low amount of power without getting a temperature rise in the left cusp, you can often get much higher power. So if you're equally early, I always would choose the left cusp first, and this is not just opinion. It was shown in this paper by Abu-Lurakh, basically, when you're equally early, they found that you were more likely to have success from the left cusp. And they also found that an AVR-AVL Q-wave ratio less than 1.45 suggested that you would have success from the left cusp, you know, basically that the complicated ratio, but it means the Q-wave in AVR is not more than one and a half times the Q-wave in AVL. And if you look at here, they're pretty similar, so that would also suggest success from the left cusp. OK, this is a biophysics question, so this should be straightforward. Hopefully you watched the biophysics lecture. This is RF energies applied in the same location with perpendicular catheter orientation to the tissue and the same blood flow under several scenarios. Which of the following settings would be expected to result in the deepest lesion? A, 8mm tip, non-irrigated, 40 watts for 20 seconds. B, 4mm tip, irrigated with normal saline, 40 watts for 20 seconds. C, 4mm tip, irrigated with half normal saline, 40 watts for 20 seconds. Or D, a 4mm tip, irrigated with normal saline at 50 watts for 5 seconds. So again, feel free to pause, think about this. OK, and the correct answer is C, 4mm tip, irrigated with half normal saline, 40 watts for 20 seconds. So again, we talked about this in biophysics, that because half normal saline is a lower ionic current milieu around the tip of the catheter, it channels more current into the tissue and has been shown to create about a 30% larger lesion. And as we talked about in the lecture, an 8mm tip, even though it's a bigger tip, with the same power, same duration, is actually going to lead to a smaller lesion than a 4mm tip because that power is averaged over the 8mm electrode. So the advantage of the 8mm tip is that you can give more power because you have cooling. But if you're comparing two, whether it's irrigated or non-irrigated, same power, same duration, a smaller tip. Again, doesn't matter if this is irrigated, the 8mm tip is basically irrigated by the blood pool. The 8mm will not give a larger lesion. So now we have two of the same for B and C, one 4mm tip irrigated with normal, one irrigated with half normal. And as has been shown, the half normal will give a bigger lesion, deeper lesion. And then D is using kind of the current paradigm that's used in the atrium often, which is high power, short duration, 50 watts for five seconds. This gives a wide but shallow lesion. And the question wasn't a surface area, it was a question of which of the following settings would be expected to result in the deepest lesion. So even though it's 50 watts, it's short duration, so that would not be expected to give a deep lesion. And so the correct answer is C. Again, could be on the boards, but very important to understand these principles just when performing day-to-day catheter ablation. Finally, the final question of mine for this workshop, a 46-year-old female has a history of hypertension and recurrent chest pain and syncope attributed to seizures. An ECG in the field upon EMT arrival right after one of these syncopal events is shown in figure A, followed by a second ECG 30 minutes later in B. The medication that's most likely to prevent future syncopal episodes is A, natalol, B, diltiazem, C, magnesium, D, quinidine, E, amiodarone. I'll show you those two ECGs again, a 40-ish-year-old woman with chest pain and syncope, ECG on arrival after an event of chest pain and syncope in A, and 30 minutes later in B. These are the options. Take a few minutes to look at that, then we'll go on to the answer. The correct answer here is B, diltiazem. Unfortunately, I don't get the feedback of the audience choices, but people seem to always struggle with this one, recognizing what the ECG is showing. And again, I've shown two ECGs because I think really understanding the surface ECG is very important to ECG-based questions. What's going on with these wide QRS complexes? And it's true, they're a little bit irregular, but look at V2. This is dramatic ST depression, and this is basically tombstoning. So it's ST elevation that's so tall, it's making a wide QRS, and I think the key is looking at V2 and V3. So in a woman having chest pain and syncope, you should really end that resolves within 30 minutes. You know, you should be thinking about coronary spasm. So beta blockers, right, that have especially a nonspecific beta blocker, the beta-2 effects are not ideal because that can worsen spasm. This isn't Torsades, magnesium is not going to help, quinidine is not going to help, amio, and all antiarrhythmics that might be given if you consider this VT or Bregada syndrome, perhaps for quinidine, but in a sense with a coronary spasm, you want to give a calcium channel blocker, often we give calcium channel blockers and long-acting nitrates. And again, I think if the patient has a cardiac arrest, then a backup ICD should also be considered because it's not 100% even on these medications. Again importantly, stenting these arteries doesn't help. You just spasm around the stent, so please don't have your interventional colleagues put stents in for this. Calcium channel, high-dose calcium channel blockers, often, you know, very high-dose long-acting nitrates, and if it was a true cardiac arrest, then an ICD should be discussed with the patient. Okay, that's the end of workshop six, I hope that was helpful, and we'll go on to more questions after that. Thank you very much. This is Sam Asirvatham, electrophysiologist at Mayo Clinic, discussing some cases, variety in electrophysiology, no relevant conflicts with this discussion. So I'm going to show you an ECG, it's a patient who's had some PVCs, runs of VT, and what I'd like you to think about is the most likely, not necessarily the site, but the most likely site of origin of the arrhythmia based on these choices. So here's the ECG. And here are the choices, is it free wall of the RVOT, tricuspid annulus, posterior LV apex, anterior interventricular vein, or right sinus oval server? So when we think what's most likely here, let's just try to look at some of the features of this arrhythmia. The first thing is, you probably noticed lead one is negative, completely negative, suggesting left side of the body origin. So left side of the body origin, small R wave and B1. So not entirely right on top of the heart, right below B1, but either slightly leftward or slightly posterior or both. Otherwise, it's an outflow morphology, 2,3-AVF positive, AVR, AVL, both are negative. So if we think about the choices that were presented, the one you should immediately exclude is posterior LV apex. That'll be a complete right bundle and it'll have a superior axis, nothing like this at all. When we think about all the others, we have free wall of the RVOT, tricuspid annulus, and right sinus ovale cell. They're all on the right side of the body. So right side of the body should give you a positive deflection in lead one. So of the possibilities given here, the one that you would map before finally ablating is the region in or near the anterior intraventricular vein. So this is an LAO view showing this complexity of what's right, what's left. So if we think about lying right down the middle, so left side of the body, lead one is here. So origin on the mitral annulus laterally, the anterior intraventricular vein region, the very distal right ventricular outflow tract, the LVOT region, but to the left of the body, all could have origin there, but the free wall of the RVOT, the tricuspid annulus, this bundle region will all have a vector towards lead one. V1 being slightly positive is a reflection of either origin that's a little deep in the heart or origin that's towards the left. So this is where we would place V1. So anterior intraventricular vein here, left sinus of valsalva here, mitral annulus here, all of those would give you a vector towards V1. When you're way back here, posterior annulus, LV inflow, you'll have a huge vector towards lead V1 giving a pretty much like a right bundle branch block morphology. Now it's going to be a figure from intracardiac traces. And this time have to think what you can exclude. So several of these are possibilities, but one that you really can be confident in saying that's not what we're dealing with here. So here's the tracing. ECG leads, RV, RA, is bundle region, ablation catheter with large ventricular signal, coronary sinus electrodes. So which of these can you think about excluding? AV node re-entry, junctional tachycardia, spinal tachycardia, or left pre-wall accessory pathway related tachycardia. So this is not going to be a left pre-wall accessory pathway related tachycardia. So main finding here is you have more ventricular electrograms than atrial electrograms. So V and A, V, no A. Now if we had just this beat to look at, looks pretty much like AV node re-entry. And some patients with AV node re-entry can have block to the atrium. Junctional tachycardia will produce a similar pattern and can block to the atrium. So also can origin in the HISS bundle itself, a HISS bundle tachycardia. But pre-wall accessory pathways, they're going to, first of all, have a discernible VA interval, 110, 120 milliseconds or more. The early A on those beats will be in the distal coronary sinus, would not be concurrent when you have both V and A. And it's very, very unusual, especially in normal hearts, to ever get some dissociation or change in the number of A's or V's in a pathway-related tachycardia. So a variety of reasons that we can pretty much forget about that. And the rest of the case would hinge on, do you take this as a AV node re-entry that just happens to have more V than A? Should we think about junctional tachycardia? Should we think about a HISS bundle tachycardia? So sometimes we'll see something like this, where the key is, look at the beats where there is a V and A. Looks an awful lot like AV node re-entry. But sometimes, like in this patient, you have an A, but no V. This can also happen in AV node re-entry. It's a HISS bundle signal. There's an A, but there's no V without a change in the otherwise, in the pattern of tachycardia. So AV node re-entry, although usually A and V are present, and A and V are very close together in most forms of AV node re-entry, there is no necessity for the ventricle to be the same number of the A-tree. In other words, if you took a patient with AV node re-entry and we were to just dissect out the ventricle, you could still get tachycardia. Because the circuit involves a small portion of A, parts of the AV node, and it's able to sustain that tachycardia. So you can block in some parts of the AV node that's not necessary. You can block in parts of the A that's not necessary. And you can certainly block in the HISS and the V and still continue tachycardia. So a little change in location here. We're going to think about a figure where I'm marking a yellow arrow. And we're thinking about the least likely association. Mitral valve prolapse, ventricular arrhythmia, difficulty with left atrial flutter, especially mitralismus-dependent flutter, Epstein anomaly, or abnormalities on cardiac MRI. So here's what we see here, echocardiogram. Left atrium, left ventricle, arrow. And here are the choices again, least likely association. So this is definitely not Epstein anomaly. So most of you would have recognized the classic picture of mitral annular disjunction. Mitral annulus valve leaflet should be right at that transition point between ventricle and atrium, but it's disjunction. It's getting pasted on back in the atrium. So as a result of this, some patients can get ventricular arrhythmia. Almost by definition, there's mitral valve prolapse, and there's actual association with mitral valve prolapse. Cardiac MRI can show fibrosis in the papillary muscles, submitral apparatus, sometimes at faraway sites as well. And if you were trying to draw a line, say from the pulmonary vein to the mitral annulus, if you just reach the valve here and don't ablate in this disjunction area, there may be atrial myocardium still there, and you haven't anchored this lesion. Now, Epstein anomaly is an issue with the tricuspid valve. We're looking at the mitral valve here. And the tricuspid valve is displaced towards the ventricles, almost like a mirror image. You can get a left-sided Epstein anomaly like an association with corrective transposition. However, it would still be malposition of the leaflet plus lot of leaflet abnormalities that would be towards the ventricular side. So not going to be Epstein anomaly. Watch out for ventricular arrhythmia in some of these patients. Be prepared for challenges with left atrial flutter ablation and cardiac MRI has become part of the workup for the stratification of these patients. So I'm going to show you an electrocardiogram before and after giving adenosine. Otherwise healthy patient, sudden onset, sudden offset tachypalpitation. So healthy patient, structurally normal heart. This is the presentation ECG. And this is after giving adenosine. Now, an additional maneuver is done where ventricular extrastimuli are placed. And this observation is made, no change in the atrial activation sequence and putting in the extrastimulus. So we have tachycardia, wide complex tachycardia, termination with adenosine, ventricular extrastimulation testing. And what I'd like, what I'll also tell you is at EP study, once this was observed pretty reliably that you put in an extrastim and you got this observation, which is most likely? Retrograde conduction. Is AV node dependent or is it pathway dependent? Is it fused? No retrograde conduction or is it, we really need parathysian pacing. That's the way to tell whether retrograde conduction is AV node or pathway. Key observation. Many of you would have recognized that retrograde conduction is through an accessory pathway. The way that you would recognize that is you see the HISS bundle electrogram is now clearly visible, not so visible with the drive train, but with the extrastim. And you know this phenomenon, retrograde right bundle branch block. So conduction goes across the septum, left bundle and to the HISS, giving this sudden jump out of the HISS signal. But even though the HISS signal jumps out, the atrial signals with the same activation sequence stay linked with the V. What that tells you is the way you're getting from V to A is not through the AV node. As if it was, it would come after the HISS. So it's an accessory pathway. Activation sequence is exactly the same. That means there's no fusion. It's only accessory pathway retrograde. So remember extrastimulation testing is the offensive retrograde right bundle branch block. And the simple interpretation may give you information very similar to what we get with parahysian pacing. Just to contrast with parahysian, we're always pacing near the HISS at high output where we capture HISS and ventricle, narrow complex, or just ventricular myocardium at lower output. When you capture just the ventricle, you'll often see a retrograde HISS, especially if you're using a dedicated catheter. But the telltale observation is your stim to A and activation sequence stayed the same whether you captured the HISS or not. So it's a way of saying it doesn't care about the HISS. It only cares about ventricular myocardium to get back up to the atrium. That's an accessory pathway. Only cares about the V, does not care about the HISS. Capture the HISS, don't capture the HISS, doesn't make any difference. Similarly, when we look at this maneuver, HISS pulled in, pulled out, retrograde right bundle, pushing it out. A is the same, doesn't care about the HISS. It's all accessory pathway. So remember, parahysium pacing, very useful maneuver to define the mechanism of retrograde conduction. You have to observe whether the activation sequence changes. If it does, there's fusion. There's both A-V node and a pathway or more than one pathway. If it doesn't change at all, but the V-A, so the activation sequence doesn't change, but in addition, the V-A interval is also unchanged, that's an accessory pathway. The key things in this that we have to keep in mind is when there is a change in sequence, that's when we should suspect there is fusion. And why is that important is because if there's fusion, you don't want to map at that particular drive train pacing rate because you won't be sure whether you're mapping the atrial activation as a result of the pathway or going up through the A-V node. So you may need to change your pacing rate or map during tachycardia, orthodontic reciprocating tachycardia. Now in the same patient, tachycardia was induced and each time tachycardia was induced, each time, a Hispinal electrogram could not be seen or would be dissociated from tachycardia. PACs were placed from the distal CS. And I'm going to show you those tracings. And we want to know when you combine the previous phenomenon phenomenon that you now recognized as induction of retrograde right fundal branch block, what is the most likely diagnosis? So putting it all together. So here's tachycardia in the lab, and here's putting in a PAC from the distal CS. So distal CS-PAC, distal CS-PAC, even before it reaches the septum, is bringing in the next B without a change in the QRS morphology. So PAC from distal CS pre-excites and resets the tachycardia without changing the QRS and without affecting the septal atrial activation. So we have one phenomenon here. Couple it with what you learned from the previous tracing and question. And what is your diagnosis? Pathway to pathway tachycardia. Antigrade pathway giving the white QRS, retrograde pathway completing the circuit. Avenode re-entry with a bystander pathway. Antidromic tachycardia, antigrade accessory pathway participating in the tachycardia but the retrograde limb is AV not. VT, or none of these. Two phenomena, one we've discussed. The second, PAC, distal CS, brings in the V, no change in QRS, resets the tachycardia. The PAC is delivered at a time where the septal A is not advanced. I think most of you would have got this when you think it through. This is a pathway to pathway tachycardia. So how do we know this? We know it first because we already demonstrated with retrograde right from the bench block. Retrograde is a pathway. And the same sequence we're seeing in tachycardia. Plus antigrade, a PAC advanced the V without changing the QRS, no fusion. So it's only one way to go from A to B during this tachycardia. And then you're able to reset the tachycardia. So antigrade is a pathway, retrograde is a pathway. PAC is able to reset the tachycardia without any fusion. Another key point is something that I mentioned while reading this out, is that the PAC was delivered at a time where it doesn't pull in the septal A. So it doesn't even reach the AV node. So if it cannot reach the AV node and still brings in the V, has to be a pathway. So all components are important. The QRS morphology, is it pulled in? Is it pulled in without pulling in the septal A? Does it reset? Does it change the next or subsequent beats of tachycardia? Sometimes if you put in the PAC early enough, you will terminate the tachycardia. The same thing, you terminate the tachycardia without reaching the septal A. So you never got to the AV node and yet it terminated. Why would you affect a tachycardia without reaching the AV node? Because you're blocking in the pathway. You're blocking the pathway. Another way of saying pathway is necessary for this tachycardia. So one way to think about a wide complex tachycardia SVTs, here I'm using the example of AV node pathway is on the right free wall and illustrates the concept of placing PACs. Place the PACs where you suspect the pathway may be. So if it's the right free wall pathway, place the PACs in the right atrium free wall. If you suspect the left free wall pathway, right bundle morphology, distal CS is early B. Then place the PAC from the left atrium free wall or the distal coronary sinus. When you place the PAC, watch for a few things. Does that PAC bring in the next V? Does it do it even without bringing the septal atrial electrogram? Does not reach the septum, but still gets to the ventricle? That has to be pathway. And does it reset the tachycardia? Then you have proven there is a pathway and the pathway participates in the tachycardia. How do we know there isn't another pathway or simultaneously another arrhythmia? Two main things, is there fusion? If no fusion, there's only one way you're going from A to B, the QRS looks the same. How do we know it's not a bystander? Because you not only pre-excite the V without getting to the AV node, but you are able to reset the tachycardia, perturb the subsequent beats, make it later, earlier, every time that you put in this PAC.

palpitations

chest pain

ECG

wide complex tachycardia

adenosine

fusion beat

accessory pathway-mediated tachycardia

AV nodal reentrant tachycardia

mitral annular disjunction

coronary artery spasm