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Session I: Basic Science and Fundamentals of Elect ...
Sinoatrial and Atrioventricular Nodes and His-Purk ...
Sinoatrial and Atrioventricular Nodes and His-Purkinje System: Anatomy, Evaluation, Autonomics and Therapy
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Hi, I'm John Miller from Heart Rhythm Society and representing Indiana University as a professor of medicine and director of electrophysiology training. I'm going to be talking in this session about sinoatrial and avianodal conduction and the Hispokingyi system, their anatomy, their evaluation, autonomics, and therapy. So let's go. These are my conflicts, as you can see there. Sinus and AV nodes and Hispokingyi system. We're going to be looking at a variety of aspects here. First, understanding the anatomy and physiology of cardiac impulse formation and conduction, how it works, and therefore understanding how it doesn't work. Be familiar with genetic abnormalities that affect the cardiac impulse and conduction physiology. Correlate abnormalities of cardiac impulse formation and conduction with anatomy and the clinical implications arising therefrom. And review different types of testing for abnormal cardiac impulse formation and conduction using both the ECG as well as intercardiac recordings and provocative testing. That's a lot to cover. First things first, a clear understanding of cardiac anatomy is absolutely pivotal for today's practicing electrophysiologists. When a lot of us started, it wasn't so important, but now we're doing ablations and we need to know where we are and understand not only where our electrodes are, where we can put pacing electrodes, and what areas we should try to avoid with ablation if possible. Most of the evaluation of the conduction system function centers on asking the single question, is there an irremediable problem with the conduction system that warrants an implanted pacing system? That's what we're asked dozens of times a day. Here's a strip. Here's an ECG. Do we need a pacemaker or a defibrillator or not? Most of the time, decisions regarding indications for pacings are made rather easily from ECG and clinical findings. Intercardiac testing is not necessary in most cases. However, there are incidental findings at EP study that warrant pacemaker implantation, or at least consideration of it when the conduction system seems to be jeopardized. Here is a rendition of the inside of the right atrium looking at it from the septal aspect, right ventricle, from the McAlpine series of the heart and coronary arteries. Coronary, coronary arteries. Here's superior vena cava. Again, this is looking outwards from the inner aspect of the right atrium towards the right side, right ventricle here. And all these pectinate muscles, which are familiar, they all gather together and go perpendicularly into the crista terminalis. And here's the superior vena cava here. Here's your tricuspid annuus along with the dashed lines there. And the sinoatrial nodal region, it's not a site, it's not a spot or a single cell or cluster of small cells. It's a region. And it occupies the uppermost portion of the crista terminalis as it abuts the superior vena cava, the hyposterolateral right atrium. Portions of it extend on down the crista terminalis in different representations and different individuals, but it hangs out mostly up here. The anatomy of this region is the sinus nodal cells that are histologically distinct and they're clustered at the junction of superior vena cava and crista terminalis, typically on the epicardial surface. This makes it difficult to reach if the crista terminalis is very thick from the inside of the heart. The source and spread of impulses from different parts of the sinoatrial nodal complex account for slight variations in the P wave. You'll see this particularly in ambulatory monitors. Overnight, the P wave tends to become sometimes inverted and much slower. That's coming at its exit is then from the lower portion of the crista terminalis. It's not necessarily a subsidiary atrial pacemaker. It's just a portion of the sinus node that's firing a little bit more slowly. The physiology of this is a tale of two clocks. We have the membrane voltage clock and we have the composed of the outward potassium current versus the inward currents, the phony current, pacemaker current, as well as others. Then there's a calcium clock governed by rhythmic spontaneous oscillations of calcium released from the sarcoplasmic reticulum. Elevated intracellular calcium concentration activates the sodium calcium exchange, which leads to net depolarization of the cell. Now there's an interplay between these two and one might entrain the other. That's the term that the basic electrophysiologists use. It's different than how we apply that term in pacing during arrhythmias, but one kind of interplays with the other. And the net result is our intrinsic heart rate at any given moment. The maximum achievable heart rate in any given individual with exercise propagation and not exogenous catecholamines is roughly about 200 or 220 or 225 minus the age in years. So a 70 year old person with pedal to the metal might be able to reach a heart rate of about 150. If that person ends up with a heart rate of 190, that's not sinus tachycardia. A 70 year old cannot reach 197, 190 beats a minute with just inherent sinus tachycardia. That's an atrial tachycardia. Okay, there are some problems with sinus node conduction that are inherent and intrinsic to the sinus node. These are idiopathic degenerative changes, inferior ischemia or infarction can affect the sinus node itself. Amyloidosis, sarcoid, other infiltrative diseases, collagen vascular diseases, and surgery, clamping the atrial appendage, heart transplant, transecting the sinus node artery, et cetera. There are problems extrinsic to the sinus node and autonomic dysfunction or hyperfunction, excessive vagal tone, remodeling following atrial tachyarrhythmias. We're somewhat familiar with that in all of our everyday practices. Ablation, if you ablate on the atrial tachycardia from the top of the crista, it can affect the sinus node. It's a tall order to eliminate the sinus node function with that, but it can occur. Superior vena cava isolation, getting it from the top as opposed to the bottom with the crystal atrial tachycardia. The left atrial roof ablation and transecting the sinoatrial nodal arteries that comes across from the circumflex artery in many cases. Drugs can certainly affect sinus node function. We're all familiar with these, beta blockers, calcium channel blockers, digitalis, clonidine, type 1 and type 3 anterior rhythmic agents, and iverbrating, metabolic factors, not as commonly considered, but very important ones to at least pay attention to in the ICU setting. For instance, individuals with hyperkalemia will quite often have a slow sinus rate and seeming sinus node dysfunction. They don't necessarily need a pacemaker. They need dialysis or calcium. Hyperbilirubinemia, those people don't necessarily need a pacemaker. They need a new liver, and it's not a common indication for temporary pacing, but sometimes we have to do that in the liver unit. Hypothyroidism, sepsis can slow the heart rate. Sleep apnea, typhoid fever, haven't seen a case of that in a couple of weeks, but it can do it. Brucellosis, same thing. There are arrhythmias that are inherent to the sinus node, inappropriate sinus bradycardia that's defined operationally as a resting heart rate less than 40 beats a minute. Now, a lot of people have a resting heart rate less than 40 beats a minute. I do right now. I'm pretty cool and calm, maybe not 40, but it's pretty low at much of the time. That's not dysfunction. That's just sinus bradycardia. If it's inappropriate for the circumstances, then we get excited about it. There's such thing as chronotropic incompetence. That is a situation, again, an operational definition in which the individual, despite going as rapidly as they can, say on a treadmill, cannot reach any more than 75% of their age predicted heart rate with exertion. This is in the absence of medications that could affect sinus node function. Individuals can have sinus pauses or a sinus arrest. That is an interval on the ECG that has no sinus P wave and is not an integral multiple of the sinus cycling. This is hard words, but harder to put into words, but easy to see in examples. We'll see some. One can have a sinus exit block, first degree, second degree, and even third degree sinus exit block as possible. Third degree, of course, is no P waves. No sinus P waves at all. Second degree is tough. You have to look at PP intervals that are clustered, grouped as an avian nodal winky block. First degree, really hard to pick out because then we have the input or the output of the sinus node, and then it gets to the atrium with some delay, unless you have sinus node recordings. You can't see that. Brady tachy syndrome or tachy brady, depending on your perspective, pauses after a cessation of atrial fibrillation more typically than flutter because flutter usually doesn't just stop. It usually goes through a transitional stage of fibrillation and sinus node suppression with that. Atrial quiescence is a rare disorder. I've seen it a little bit more commonly recently with people living longer with some very odd myopathies. This is a situation in which there is no spontaneous atrial rhythm, and it is sometimes mimicked by very wide, very low voltage P waves. So you take a normal 80 millisecond P wave and stretch it out to 400 milliseconds of total atrial activation, there's not going to be much of a bump on the baseline of the ECG. So it looks like it's atrial quiescence. And then there's some non-pathologic rhythm disturbances, sinus arrhythmia, respiratory or non-respiratory. Younger people are prone to have this. If you think this is what you're seeing in an 85 or 90 year old sedentary person, probably not as PACs or some other of no greater physiologic import. And then there's a ventriculophasic arrhythmia in which individuals with high grade or complete heart block have a shorter PP interval surrounding the QRS that is seen. And there's no VA or AV conduction. But this curious shortening of the PP interval, we'll see an example of this. This is sinus bradycardia. I think we'd all recognize this. You can define it as one beat per lead. So here's AVR. It only has one beat in it. That's bradycardia. There are better ways to measure that. This may be normal for the circumstances such as a profound deep sleep or well-trained athletes. It's not necessarily pathologic. It should generally be associated with symptoms of fatigue, shortness of breath, lightheadedness, that sort of thing, syncope in order to warrant pacing. And we'll see about pacing indications subsequently here. Inadequate heart rate, sinus rate with exertion is, again, another way of saying chronotropic incompetence for the circumstances. Here's an example of Mobitz 2 sinus exit block. These are hard to come by, at least in the current era. They used to be pretty frequent when the days of digitals. We don't see that so much nowadays. I put the PP intervals up here for you. And here it is relatively, relatively regular. This is slowing a little bit of the sinus cycle length. And here we have a situation where all of a sudden it seems like there's almost a doubling of the sinus cycle length. Oh, I'm sorry. A doubling of the sinus cycle length here and again down here. And there's no discernible P wave in the midst here. And since these are almost double the prevailing sinus cycle length within a little bit of play, this is a good indicator of intermittent failure of conduction from sinus node to atrium, Mobitz 2, sinoatrial exit block. Here's a sinus pause here, coming along in sinus rhythm. There's no PACs, no nothing. It just pauses. And this is not an integral multiple of any prevailing cycle length. So this is just a sinus pause. It's not X block of any sort. Brady Tachy syndrome. This is one of those rare examples of atrial flutter or atrial tachycardia just suddenly stops as a sinus node cut by surprise. And it doesn't come back until about four seconds or so. Here's four seconds to the P wave here. This is carotid sinus hypersensitivity. You should see the no P waves, no QRS escapes here. And the patient's starting to swoon a little bit, indicating that, yes, it is important to have cerebral blood supply after all the Y chromosome is standing. Here we have sinus node behavior in the ventricular phasic fashion here. I have these RR intervals measured here. They're all the same at 1180. And here we have the PP that surrounds a QRS shorter than the PP between QRS complexes. It depends a little bit on when the P wave occurs, if it's within the first 60 milliseconds or so of the PP. If the QRS occurs within the first 60 milliseconds of the PP interval, tends to be a little bit shorter. A couple of theories on this. There's been some good experimental work many, many years ago in several laboratories. And there is probably some influence of both of these. The shortening of the PP interval, the PP is shortened from its baseline due to increased sinus node artery supply with ventricular systole versus a baroreceptor reflex shortening or increasing the PP interval. So they're probably both of these influences. So is the basic interval 690 and it's shortened to 610, 640, or is the basic interval 640 and it's shortened or it's lengthened to 690 at some point? It's difficult to know what these are. And it's not real important to know what these are. It is reasonable to know that this does exist. It's normal behavior of the sinus node. It's not odd behavior at all. And it has no pathologic significance. Sinus node function can be assessed at EP study if one cares to do this. There are many tests that were formulated in the early days of electrophysiologic testing that can be used. They have reasonable reflection of sinus node function. I don't think anyone should place a pacemaker based on a prolonged sinus node recovery time in the absence of any symptoms. But here's how you do it. Sinus node recovery time is the interval from the last phase complex to the first sinus complex. You pace for about 30 seconds or a minute, slightly faster than the prevailing sinus rate, and then stop pacing suddenly, wait, and measure to the first sinus complex. It becomes a high-speed sinus complex, not an escape junctional rhythm. So that should be less than about 1,500 milliseconds. Secondary pauses can be quite long. And sometimes they're more important than the primary because it can get the first one out, but it doesn't know what to do with the second complex there. To account for varying heart rates, very, very slow heart rates, or very, very rapid heart rates at rest, the credit sinus node recovery time was devised. And that is the measured sinus node recovery time using the common methods that I described, and then subtracting the sinus cycle length from it to get an index of what the sinus node recovery time is on a level playing field, taking the sinus rate, the basic sinus cycle length out of the equation. That should be less than about 550 milliseconds. Sinuatrial conduction time is normally in this range, 45 to 125 milliseconds. That's from the sinus exit from the sinus complex out to the rest of the atrium. This can be measured either using the single extra stimulus method or short circles, cycles of overdrive pacing, the Strauss and Nerula methods, respectively, or a combination of these with quite a bit of stress overdrive pacing plus an extra stimulus by Kerkori and Tabool. I'm not going to go over this any further here than just to show it took a long time to make this figure, so I'll really show it. This is sinuatrial conduction times and looking at the various zones of what happens as you make the premature stimulus closer and closer and closer. We go from collision of the impulse coming out of the sinus node and no change in the prevailing sinus cycle length here. Or this is exactly twice, the 590 plus the 730 is exactly twice, so we don't have any net effect on the next depolarization sinus node. It can be reset, brought in sooner than it would ordinarily have appeared. It can be interpolated and not seeming to be affected any more than it was with the collision, or it can actually be brought in a little bit by sinus node reentry. I'm not sure how often this latter occurs. I'm not sure I've ever, I'm sure I've never recognized a case of sinus node reentry, but sustained variety, I'm not I'm not confident that it exists. It may. So that's aligning this beat where it should occur. Ordinarily, this is interpolated here. It blocks getting into the sinus node entirely here. And it's just sitting there like an interpolated PBC doesn't have any effect on the surrounding PP intervals. And then this is where that next sinus beat comes back, whether it's a little bit early, late, or right on time there. A lot of genes affect sinus node function. Therefore, there is plenty of opportunity for dysfunction among these genes and their dysfunctional protein outputs to affect sinus node function. We're all familiar with SCN5A, the subunit, alpha subunit of the sodium channel in the periphery of the sinus node. SCN4, a subunit of the protein in the funny current, because of its unusual voltage current curve. The KCNQ1, the alpha subunit of the slow component of the delayed rectifier current. RYR2 and the ryanidine receptor and CASQ2 from the calc sequestron, both dealing with calcium handling within sinus node. MYH6, atrial myosin heavy chain protein in some individuals. Connexin 40 with the GJA5. Ankerin and emrin, both membrane proteins, one in the nucleus with the emrin. A variety of problems can be manifest or no problems with variable penetration. Facing and sinus node dysfunction, a whole host of things here. There's a class one, two As and two Bs in class three. It's important to know these subtleties sometimes. Sometimes in practice, it's quite straightforward what's going on. You've got a class one indication. Beware of the class threes. We really shouldn't be delving into these at all here. It's not indicated for sinus node dysfunction in asymptomatic patients, no matter what their heart rate is. I think within reason. In patients who have sinus node dysfunction, but there are symptoms that suggest bradycardia don't actually occur when the patient is documented to be bradycardia and so on and so forth. Lots of stuff about symptoms, symptoms, symptoms, symptoms, symptoms, symptoms here. You have to have symptomatic correlate with an electrocardiographic or rhythm abnormality in order to justify sinus node, pacing for sinus node dysfunction here. All right. The one exception is that if you have a patient with syncope of unexplained origin, you've done your due diligence, done an EP study, and you find the sinus node function is markedly deranged. It is not unreasonable to place a pacemaker in that individual. Moving down the conduction system to the AV node, the first portion we encounter. Here's the AV node. This is a teardrop shaped structure at the apex of the triangle of Koch, which is made of the tricuspid annulus, coronary sinus ostium, and the tinnitus pterodactyl. Here it is, the AV node, the compact AV node up here. I've drawn it as a slightly different structure here. It has inferior left and inferior right extensions at least. Dr. Miles can consider those in much greater detail for you and much greater eloquence as well. I've shown the aortic root here. Sometimes in the old days, we used to put a pigtail catheter in the aortic root as an indicator of where the his bundle was, and therefore we can go backwards from that and find where our fossil ovalis is when doing a transeptal catheterization. There are better ways of doing that nowadays, obviously, than using a pigtail on the aorta. But sometimes we'll still put a catheter at the his to show where the aortic root is. We don't want to puncture that by accident or carelessness. Properties of the AV node are as follows. There is an AH interval that we measure. Now, we measure this. It's something that we can see on the intracartic recordings. It doesn't mean that we conduct from that A to the his potential. It means that we're measuring an AH interval. It doesn't mean that that's the AV node conduction time, but this is an index thereof. So, rough range is from 60 to 125 milliseconds. Winkybok, that is dropping a non-conducted P wave after a cycle of gradual prolongation of the PR interval, typically will occur at less than 500 millisecond cycling, but this is extremely dependent on conditions, autonomic tone, sedation, non-sedation, body position, all kinds of things, drugs. So, it's difficult to be very hard-nosed about this, although some of us are. The age prolongs progressively with more rapid atrial pacing, and that's normal physiology. There are specialized inputs from the left atrium and coronary sinus in probably most individuals to the AV node. This yields not artifactual, but actual shorter AH intervals with atrial pacing than from the right atrium at the same pace cycling. So, you'll get an AH that's shorter, and it's somewhat artifactual because, as I said, that A doesn't necessarily conduct to the H in a linear fashion. It may be that you're conducting to the AV node through some other pathway, and the wavefront passes by that atrial electrogram, and you're saying they're linear. They're not necessarily linear. So, that's maybe a little bit artifactual, but a shorter AV nodal effect of refractory period from when pacing the coronary sinus left atrium than from the right atrium is not artifactual. That's an actual phenomenon, and a shorter Winkiebox cycle by 10, 20, 30 milliseconds in some cases when pacing from this coronary sinus as opposed to the right atrium. So, it seems that there are specialized inputs that get into the AV node a little bit more easily from the coronary sinus left atrium than they do from the right atrium. We're all familiar with dual AV nodal pathways. This is by definition, an operational definition of an at least 50 millisecond increase in the AHN for each 10 millisecond, any given 10 millisecond decrease in the A1, A2, not S1, S2. That's the easy thing, but it's actually the A1, A2 input. Usually the same thing at longer coupling intervals, but if you get closer coupling intervals, they're not necessarily the same thing. There is a phenomenon called crossover in which the PR interval when you're stimulating the atrium is actually longer than the RR. So, you have a stimulus, then you have a QRS, and then you have the QRS that is caused by the stimulus that was before the previous one. It's easier to show than it is to talk about. Individuals may have multiple jumps, that is the age increase of 50 milliseconds, probably signifying multiple AV nodal pathways with different discrete inputs. So, no particular pathologic importance. There are some problems with AV nodal conduction. They're intrinsic to the AV nodus as they're aware of the sinus node. These are idiopathic degenerative changes of similar varieties, inferior ischemia and infarction. The usual suspects, amyloidosis, sarcoid, collagen vascular disease, infiltrative diseases, and surgery, especially tricuspid valve surgery. There's a rash now of tricuspid valve endocarditis, and the surgeons put in, or tricuspid repair, the surgeons put in a carpentier ring or some other ring that has an opening. It's a C-shaped ring. The opening is for the conduction system. So, sutures are not affixed in there. But if the valve is destroyed or there's been a septal abscess, the AV node is gone. And that is a big problem nowadays, pacing systems in these individuals. Autonomics with excessive AV nodal, excessive vagal tone affecting the AV node. We're all familiar with that. Drugs as there were with the sinus node, beta blockers, calcium channel blockers, digitalis preparations, clonidine type one and type three, antiretroviral drugs. Missing from this list is iverbranine, which does not affect the AV node so much. Ambiodarone should be on here as well. Others, importantly, Lyme disease. It affects the AV node primarily with antibody mediated problems. It doesn't affect the Hispokinesia system. And it hopefully is a transient phenomenon, not requiring permanent pacing. Resting AV nodal function can be tested, or AV nodal function can be tested in the baseline state with the AA general, as I indicated. And therefore, anything much over 125 milliseconds, as long as it's a clear A and a clear H, abnormally long. Pacing-induced Winkiebach should be less than 500 milliseconds paced cycling, but it's again, highly state or condition dependent. There is a disorder or a condition called enhanced AV nodal conduction, which again, by definition is an individual who has an age control less than 60 milliseconds, and whose AV nodal Winkiebach occurs, cycling occurs at less than 300 milliseconds. And over the range of conduction through the AV node, the age prolongs by no more than 100 millisecond over the entire rate of pace cycling. That's an interesting group of people. Again, they conduct rapidly during atrial fibrillation or other atrial rhythms, but it doesn't have a whole lot of pathologic significance otherwise. One can stress AV nodal conduction with worse pacing, finding a block of long cycling, score extra stimuli, looking for dual AV nodal pathways. Here's an example of our normal intracardiac recordings in surface ECG. Here's the onset of the curious. We measure the age from the earliest depolarization of the A and the AVJ to the earliest depolarization of the HISS. In this case, it's 90 milliseconds spot on in the middle of our normal range. This is AV nodal Winkiebach. It's hard to get this all on one figure because it's a long cycle Winkiebach. Here we have stimuli being conducted to the ventricle. This gets shallower and shallower and shallower until finally we have one that fails to conduct, and then the cycle continues. This is with regular input to the AV node, and it's a repetitive pattern of age gradual prolongation until conduction fails and the cycle repeats. It should not be composed with loss of atrial capture along in here. I have trainees who want to declare Winkiebach when they've actually had loss of atrial capture. Again, it's highly variable during the procedure depending on the autonomic state of the patient, their wakefulness, sedation, effects of drugs that may have been given that either improve or retard AV nodal conduction. This is an example of dual andrograde AV nodal pathways in which we have extra stimulus coming after a 500 millisecond drive. 260 millisecond extra stimulus gives rise to an AH interval of 145 milliseconds. Just bringing in the extra stimulus by 10 milliseconds here sends the AH out to 210 milliseconds. There's a hiss there that's more than a 50 millisecond increase in the AH interval for a 10 millisecond decrease in the input to the AV node, the AA interval. And here we have a bonus with an AV nodal echo up here. You don't have to pay for that. Come for free. This is another example of dual AV nodal pathways. It doesn't look like much. It looks like it's just conducting down the fast pathway. What's the big deal here? Well, the problem is it's not conducting down the fast pathway. The pathway is actually conducting down the slow pathway at a pace cycling 350 milliseconds. That'd be pretty skating down the fast pathway, but it's actually not. And then in fact, this stimulus to A is the same as the rest of these stimulus to A's. This is that so-called crossover pattern where this stimulus leads to that QRS, this stimulus leads to that QRS crossing over this stimulus, and this stimulus crosses over that QRS to go to this one here. So that's the crossover phenomenon. It is common to see one or two of these beads at the point of AV nodal Winkiebach. When it's a stable pattern like this, then I think it makes great here for crossover and not just one or two beads. So there's the QRS, QRS intervals are still stuck at 300 milliseconds there. All right. That's all these evidence of dual pathways here. Let's just run through that again. This is another piece of evidence of, pretty good evidence for dual pathways. We're pacing just a little bit faster here to fixed rate. And all of a sudden, our PR interval that had already been long, gets a whole lot longer. In fact, moving into the QRS complex and the age is substantially longer on this side over here, A to his, then it is over here, A to his. This is another manifestation of dual at AV nodal pathways, perhaps the least common manifestation. This is one atrial complex giving rise to two QRSs or so-called double fire here, two for one phenomenon here. This is sinus rhythm. In fact, you can see the sinus P waves here, and we'll just start here. This conducts down the fast and the slow, this conducts down the fast, or just the slow, this conducts down fast and slow, slow only, fast and slow, and so on and so forth. So this erratic pattern of QRSs with a stable sinus rhythm, it's not junctional rhythm. It really is conduction down to AV nodal pathways. And ladder diagrams of this are sometimes helpful in this regard. This is one from the prior case here I showed. And quite often, or I should say most often, these individuals don't have AV nodal reentrant tachycardia because the mere fact that they can conduct down both pathways means that they did not conceal into either one in either direction. So you don't go down a fast pathway and conceal up the slow, preventing it's being able to conduct. There's no connection there. So it makes sense that these people would not have AV nodal reentry, but some patients can put it all together and have AV nodal reentry. So this is known as a dual AV nodal non-reentrant tachycardia. A lot of people just call it double fire. I'm done with it. So all this stuff here, it's often mistaken as atrial fibrillation because of the irregular QRSs and the kind of, I don't see a P wave real well phenomenon. As I said, some people can have AV nodal reentry. It's not real common, but under the right conditions, they can. And this disorder, if it's symptomatic, can be pretty readily treated by eliminating slow pathway and toward influences on the unsuspecting QRS complex. The gap phenomenon. This is not a disorder. It's a phenomenon. It's an observation. And it is on the principle that proximal delay engenders distal recovery. Here's an example of an extra stimulus in the atrium at 350 milliseconds resulting in an AH of 106 we conduct with coming in by 10 more milliseconds, we block and the AV node, there's no result in his potential here. However, coming in by another 10 milliseconds beyond that, we have reconduction. How does this work? Well, the input to the AV node was prolonged by virtue of an increase in the AA interval here. So that's proximal delay. So the AV node says, oh, well, I can take an input that's the same as it was over here. I just can't take it at that. So when we prolong the AA interval to a degree that the AV node can now take it, it accepted it does, and we have reduction on the AV node. There are multiple types of this, at least two or three anterograde, at least two or three retrograde gap phenomena. I don't think these are, it's certainly not important to know which one it is. I don't know which one it is, which one I know anterograde and retrograde, but I don't know if it's type one or type two or type three. I don't want to sleep over that. It's not the same thing, however, as the excitable gap that's seen in re-entrant circuits. Dr. Stephenson, I think we'll talk about that with you. Moving further down the conduction system to the His-Purkinje system, we talked about the AV node and here's the His bundle. It goes through typically the bottom of the membranous septum. I have it shown through the top here. Here's the membranous septum. It typically goes through the bottom of it. And again, there's the aorta in the background. If you really can't find the HISS potential, no matter what you do, sometimes recording from the non-coronary sinus of the valsalva, sometimes the right coronary sinus of the valsalva as well, will give you a pretty good HISS potential along the way. The bundle branches are further extensions of the specialized conduction system. Here's the right bundle branch. It comes down from the HISS bundle region around the tricuspid scuridium, tricuspid annulus, and diving into the ventricular muscle midway, and then coming out on the moderator band to exit to the lateral free wall with epicardial mapping during sinus rhythm. The very first point activated is this surface of the right ventricle just opposite the moderator band insertion. The left bundle has a couple of different fascicles, the anterior fascicle and the left posterior fascicle. You see one is very thin. The other is rather thick and quite duplicated. So it's difficult to block the left posterior fascicle, much easier to block the left anterior fascicle with a small lesion of some sort. In many individuals, there's a septal fascicle. Maybe we're all born with a septal fascicle that degenerates with time. A variety of things have been conjectured about this, including the slowly conducting portion of right bundle left axis VT, for apneal sensitive ventricular tachycardia. Don't know that for sure. Anatomy of the HISS bundle is that it exits from the distal portion of the AV node with a rather abrupt transition. It's about a centimeter in length, the HISS bundle proximal. It's well insulated from the surrounding muscle. So it doesn't get blown over in most cases with insults along the way. It's about a centimeter in length and can be recorded from the HISS bundle septum or the aortic non-coronary sinus valve, typically. Once it leaves its one centimeter length, it divides rather quickly into the thin right bundle branch and the much thicker left bundle branch block. The right bundle is a pretty discreet, a superficial fiber in its proximal distal portions. It dives into the muscle about halfway down the ventricle and then exits out the moderator band. It is very easily injured with catheter trauma or ischemia or infarction on the anterior circulation. I think all of us have had the experience of somebody with a left bundle branch block and you put her in a swan gantt catheter at two in the morning and all of a sudden you've got another problem, you've got a complete heart block because you just banged it to the remaining conducting fascicle. Left bundle branches early to a thin anterior limb and a thick posterior limb and of a fascicle that may be a variable size and presence septal fascicle. Anterior fascicle is more easily injured and damaged by a variety of things, ischemia and infarction, maybe even just hypertension. Think of all the ECGs you see with a left anterior fascicular block on it. Septal fascicle is blocked with increasing prevalence by age alone it seems. There are dedicated fibers, it could be dedicated fibers in the his bundle going to the left bundle branch block. So they start in the his bundle and they may be damaged there. And the rest of the his bundle that contains these fibers downstream from there and the left bundle itself are perfectly fine. Pacing distal to the side of block can normalize the QRS. Absolutely, totally normal in there. Sometimes there's some contamination of ventricular activation as we're all familiar with conduction system pacing. Here's a normal HV interval of 47 milliseconds. You see that there, the range being 40 to 55, quite a narrower range than there is with avianola conduction. Then you see also that his Purkinje conduction comprises only a very, very small portion of the PR interval. So you can have pretty bad conduction in his Purkinje seismic and even double the HV interval out to 100 milliseconds and really not seriously affect the PR interval in some cases. Here are recordings from the tricuspid annulus region, as well as from the non-coronary sinus valve salvo in these cases here. This is what the sinus valve salvo look like here. In each of these cases, the his bundle from the sinus valve salvo. It's a better recording in some cases. Aberrant conduction occurs in the his Purkinje system in a variety of situations. It is a transient or conditional block in a bundle. It's not permanent all the time. Then it's permanent on a branch block instead of aberration, aberration is situational. It may be, it is refractor, it is dependent. Not maybe, it is refractor, it is dependent. It just depends on how you get there. It may be physiologic or unphysiologic. Physiologic aberration occurs in a normal his Purkinje system that has a certain effective refractory period. And when you encroach on that with premature stimulation, you get block. This occurs typically at higher heart rates or very early premature atrial complexes and occurs in the right bundle branch more than the left. So a normal person with a structural normal heart who suddenly goes into a rapid supraventricular arrhythmia may have right bundle branch block initially as their QRS complex instead of a narrow QRS. It's unusual to have left bundle in a young, healthy person. That's a clue that there might be something else going on that it's not actually supraventricular tachycardia, that's actually VT, or that it's SVT using a right-sided accessory pathway that kind of looks like a bundle branch block. Non-physiologic category, the his Purkinje refractory period is definitely prolonged in an unusual way, much longer than normal. And block is encountered at lower heart rates, not higher heart rates, in fact, in bradycardia in some cases. Sometimes a premature atrial complex that blocks in the his Purkinje system doesn't have to be very closely coupled at all. And the most effective bundle is the left rather than the right bundle in these circumstances. Being as how the right bundle branch has the longest refractory period at standard heart rates, right bundle branch block is the most common ECG abnormality seen during supraventricular arrhythmias. When you see apparent left bundle branch block aberration in young patients, you should think of orthodontic reentry in patients with the left lateral concealed pathway in whom the extra time to get through the left ventricle because of the left bundle branch block having to go down the right bundle and across the septum allows for all elements of the reentrant circuit to recover and so much so that elimination of that bundle branch block may result in some portion of the circuit being premature by the next advancing wave front terminating itself. One should also think about an atrial fascicular pathway as well as bundle branch reentry and other forms of VT. Cellular electrophysiologists talk about phase three block. Sometimes they don't like our terms a whole lot, but it's probably better called acceleration dependent. And this is most commonly observed in individuals with a long short sequence. So you've got a long RR interval and then a PAC comes along or the avenode lets an atrial fibrillation complex through and you end up with a short RR interval. That may well aberrate. And that typically aberrates with right bundle branch block pattern and is the cause of the Ashman phenomenon during atrial fibrillation. Phase four block is contrary wise deceleration dependent and characterized by a short long sequences if you see them. And its basis is that an impulse coming down from through the conduction system encounters ongoing phase four depolarization which is partially depolarized. The cell membrane not enough to have regenerative action potential so you don't get a phase zero upstroke, but the sodium channels are therefore inactive at that point, inactivated. And so basically nothing can happen until some new perturbation comes along such as another PAC or PVC to kind of reset the phenomenon here. Typically this has a left bundle branch block pattern and the probable basis of the dread paroxysmal AV block lies therein. There are individuals in whom they aberrate with a certain prematurity but then as the rate slows after that during the rhythm, the rhythm is still ongoing. The abnormal rhythm is still ongoing but the rate slows a little bit yet they continue to have aberration. This is concealed perpetuation or linking phenomenon. And we'll see an example of that in a second here. This is a rhythm strip with a long short sequence here and we have aberration. We have another long short sequence here. Long, we get rid of our aberration and then shorter again, we get it back. This is an example of the short long activation sequence. And we're coming along with a sinus rhythm. We have a PAC that's only seen in one lead here. It causes a sinus pause. And by the time that sinus beat comes back, we have now left bundle aberration along the way there. Same thing occurs over on the far right over here. Now, this is an example of the linking phenomenon or concealed perpetuation of block. This is a rather extraordinary example. We have a patient in whom we're pacing the right atrium here and at 480 milliseconds cycling, left bundle branchal block occurs. Should be right, it's left, I'm sorry. Occurs at 480 milliseconds. And we would anticipate that we conducted normally at 490 over here when we were coming down on the cycling. So if we go back up to 490, we should conduct again. Well, we didn't. We went up to 500 and it's still aberrating. We go to 550, it's still aberrating. 600 milliseconds, still aberrating. 650, still aberrating, 690 milliseconds. It goes down the right bundle, conceals up the left and the next complex comes down and it tries to go back down the left and counters the block from the other direction. It goes back down the right until that level of block is cleared and now you can conduct down. So that's a range of 170 milliseconds in which we had a conduction block there. The block in the hysperkinesis system can be permanent. So it's not going to vary. That is Lennon's disease, Lenegris disease. These are sclerosis, calcification, fibrosis of the hysperkinesis system. It can be injury from aortic bowel surgery or transcutaneous aortic bowel replacement. The ischemia infarction can affect the hysperkinesis system as well. Anterior circulation affecting the left anterior descending and blocking the right bundle or anterior fascicle. They're both relatively narrow in that area. It's subject to ischemic injury. Inferior infarctions with either right coronary or circumflex vessel disease can typically affect the left bundle, not the right so much. And cardiomyopathy usually affects the left bundle. When it affects anything, there can be just a nonspecific interventricular conduction defect as well. The frequency of blocks in the hysperkinesis system, far and away the most common is left anterior fascicular block followed by right and then left bundle. And then finally, posterior fascicular block. This is a very distributed interdigitating structure. It's hard to conceive when you look at diagrams of it, how it could ever be blocked. It's just got so many ways to, so many fail-safes for conduction. What looks like block may not be actual block. It may be just very, very slow conduction. We see this in cases of bundle branch re-entry in which the individual has a block that has a persistent conduction down the left bundle, but it's faster down the right bundle. So it just looks like left bundle branch block. We'll see an example shortly here. Here's a person who has a proximal right bundle branch block. It takes a long time to get from QRS onset down to the right ventricular apex, which is close to where the right bundle inserts. And so this is block further up. Now, if you get what looks like right bundle branch block, but the signal gets down to the apex on time, then the block is somewhere distal in the right ventricular outflow tract or right ventricular out of east car or so, some such. Now, here's an interesting paper from a PADI in Chicago regarding what looks like left bundle branch block and what may or may not actually be a block in the left bundle per se. This is 4Real321. This is definite intra left bundle disease here. And this is a very, very slow delay down the left bundle, just like everything is very slow. And this is a little bit more normal over here. This is a patient who had bundle branch reentry. We decided to kill off the right bundle because it was easy to do, and we were already recording from that area very largely. And so here we come along with a left bundle branch block beat during sinus rhythm. Another one, this is during RF. We actually accelerate this complex here a little bit, accelerate this complex a little bit more. And then we end up with P waves conducted now with a longer PR interval and right bundle branch block conducting down the left bundle that we thought was blocked, but it's actually not blocked. It's just slow conduction. And a much longer HV interval ensues than we had the baseline state over here. This is an example, not a very good example, but it's an example of narrowing of the QRS, normalizing a QRS complex with pacing the HISS bundle by taking advantage of pacing dedicated fibers of the HISS that are interrupted proximally in the HISS bundle. We pace a little bit more distantly, and we can bypass that location. And the QRS looks just fine as we're pacing the HISS bundle here. Okay. This is an example from the early 1990s. That's why I show it with a lot of noise on it there. It was kind of fun that we were doing that even back then. The HISS-Burkinje system can be tested by making some baseline observations at rest. The HV interval should be somewhere between 40 and 55 milliseconds. Different laboratories have their different cutoffs. I think that's a reasonable cutoff. So over 55 milliseconds is abnormal. 20 milliseconds longer than that, 75 milliseconds or more is poor conduction, tenuous conduction. 100 milliseconds, this is one small box on a surface ECG. And it's 55 plus 40 milliseconds on a small box is up to 100 milliseconds. That's a HISS-Burkinje system that is in very serious trouble and may not conduct the next beat. And we can barely measure that with standard calipers and standard sweep speeds on an ECG. One may have intra or infra-HISS block. It may be difficult to see a split HISS. I think a lot of these are actually intra-HISS block, but we only see the distal HISS, and we say, oh, that's where it's blocking. It may actually be in the HISS itself. One can stress the HISS-Burkinje system instead of just making observations by doing burst pacing and showing the block below the HISS at a cycle length that is longer than 450 milliseconds with fixed rate pacing. It should be able to conduct even shorter cycle lengths than that is a warrant for considering a pacing system or significant prolongation of the HV interval during pacing. It should not prolong. It should be nice and short as it was during sinus rhythm. For kinemined administration, if it doubles the HV interval from baseline or yields an HV interval that's in excess of 100 milliseconds, that's way abnormal and constitutes a reasonable indication for pacing, or if you develop intra or intra-HISS block under those circumstances. Atropine and isoproteranol can be used to stress the HISS-Burkinje system. Sometimes stimulation from the atrium is blocked by the AV node, so it's protecting the HISS-Burkinje system. Really want to get at what's going on, so go ahead and give atropine or isoproteranol epinephrine, something that enhances AV nodal conduction and really tests the HISS-Burkinje system. Here's an example of intra-HISS block. not easy to see. We have a His recording here. And then this electrode, we have another His recording. They're both represented here. And again, just one up there. And rarely observed phenomenon. It probably occurs much more commonly than we recognize, but we put in pacemakers in these people. We don't put in electrode catheters to measure their His-Purkinje physiology. These may have a normal PR interval and a relatively narrow QRS on ECG, unlike the Infra-His or Bundle Branch people. These folks can be difficult to manage, with difficult to convince that they need something when their intervals look pretty normal. Sometimes these are catheter-induced. You have to be careful when you're waving catheters around left ventricle or right ventricle. The left ventricular conduction system is perhaps more resilient than the right, unless it's diseased, and then it's less resilient. It's easy to block the His entirely from the left system, and certainly the left bundle. Infra-His Winkie block is demonstrated here. We have atrial pacing. Just showing the His reports, not the atrial electrograms. We have an HV of 60 milliseconds. The HV gets gradually longer. And then gradually longer. Accelerates or drops on this beat, and then resumes a roughly normal HV interval here. So that is His Purkinje Winkie block. It may also be catheter-induced in some cases. And one of the problems with making this diagnosis is being able to have a really good recording. These are always damaged His Purkinje systems. Therefore, the size of the His potential is much reduced from normal, and may be very difficult to see. So stressing the His Purkinje system with burst atrial pacing. Here we're going at 330 milliseconds. That's pretty fast. We're going one-to-one through the His Purkinje system, but the HV interval is substantially longer than it was at baseline over here, indicating a sick His Purkinje system that is a little bit on the ropes and may need the consideration of a pacing system. This is an unfortunate person with a pulmonary sarcoid and a syncope, and it was found out right bottom branch block left axis deviation. We did an EP study many years ago to try to figure out what was causing this. And we gave her procainamide, and lo and behold, she has infra His block here. After a challenge with only about 500 milligrams of procainamide. She went on to have a pacemaker. Back then, we weren't smart enough to figure out that she might need a defibrillator also, and ended up passing presumably from ventricular arrhythmia with a working pacemaker. This is an example of retrograde conduction in the His Purkinje system. We thought anterograde was hard. This is a little bit more difficult sometimes. When we are stimulating from the right ventricular apex, the impulse rather quickly engages the right bundle and goes very rapidly up, inscribing the His potential before the local ventricular electrogram that is mediated by muscle-to-muscle propagation. There is no direct connection in the vast majority of individuals between the His Purkinje system up here and the ventricular muscle. After all, you want your ventricles to contract from apex to base for the semilunar valves. You don't want it to start contraction here and lead bulging towards the apices. So here we have a stimulus that goes slowly up the conductions, rapidly up the conduction system, and slowly up the muscle-to-muscle that's finally inscribed here. Okay, that's great. How about when you have right bundle branch blocked to begin with? Well, you don't conduct very well up the right bundle. You conduct, you block there and go across the septum and come out somewhere. And through the AV node. And in this case, the muscle-to-muscle propagation accounting for the ventricular activation around the His bundle is the same. It's slow, methodical, and it gets there. But because the impulse from the right ventricular apex couldn't go up the right bundle because it's blocked, it has to go transeptally. And then it can skate up the left bundle, but it comes out the back of the, so-called His out the back, behind the local ventricular activation. So this is the His after the AVJ ventricular activation. Here it is before with normal conduction up there. So it's quite common to see it there. This is an example of first-degree AV delay. It's not first-degree AV block because block means something didn't get through. This always gets through. Otherwise it would not be just first degree. In this case, the PR is healthy or hefty, 280 milliseconds. Most of that is the age interval, and you see the HV as normal. One can also have first-degree AV delay, not due to AV nodal problems, but due to atrial problems. This is His potential in the AV node region of one guy who was repaired congenital heart disease is atrium to energy recorded once was about 300 milliseconds or so. In this case, the AH intervals, 310, but depending on which A you use, it could be much, much longer. Here's an individual who has first-degree AV delay in the Hesper-Kinge system. That's a long PR interval, but it's instead of being in the AV node, which has a conduction time is top normal, 120 milliseconds, 125 being top normal. This HV is massively prolonged here. And this is just hanging by a thread to see how small these potentials are relative to other ones I've shown. And this is kind of gained up as well. So this is a very diseased Hesper-Kinge system. Many elements are lost. And so it says, go ahead and conduct me. And with this low PR, it can, but it's very tenuous. I'm going to leave this to your further reading on account of time. This is being able to tell from the ECG or rhythm strip whether block is likely to be in the AV node or likelier to be in the Hesper-Kinge system. Here's an individual who has high-grade AV block. It looks like it's maybe two to one block here. And he thought anyway that he was conducting on an every other beat basis, a lot of us did. But we decided to press on his carotid sinus and see if we could slow the atrial input more than we slowed the AV nodal input from each beat and thereby get some clues as to what was causing this. And it turns out that when you slow the sinus rate a little bit here, it now escapes ventricular refractoriness and now the patient can conduct just fine, albeit at a slower rate here. So vagal stimulation effect on AV conduction is as follows. If the problem is in the AV node, conduction worsened at least transiently. If the problem is in the Hesper-Kinge system, conduction can improve. It's not a very adaptive thing to go walking around like that all the time just to avoid a pacemaker, but at least you can illustrate it. This is a different disorder entirely. This is paroxysmal AV block. This is worth recognizing as a very dangerous disorder. This is a string of P waves that are not conducted here and they're heralded by this case of PVC. This is distinguished from vagal AV block and another disorder paroxysmal. Paroxysmal AV block is distinguished from vagal AV block from several important and easily recognized varieties. With vagal influence, it affects the sinus node typically as well as the AV node. The amount of effect on one or the other may be variable, but it typically will affect the sinus node as an indicator. That's just what's causing the AV block as well. So the sinus node slows significantly at a point when the AV block is occurring and the PR is gradually increasing and during the episode or at its end, the PR gradually decreases, the sinus rate increases. Adenosine levels tend to be relatively high in these individuals. And if you give adenosine to try to provoke it, it doesn't. Prognosis is benign in these individuals in most cases. Depends on how long their pause is. Paroxysmal intrinsic AV block is a bad disorder. It can come on suddenly, there's no change in the sinus rate or it may be increasing instead of decreasing. It is typically heralded by a PVC or PAC. I talked about this a little bit earlier when you have a disease-hit Purkinje system and a PAC that comes along and finds a portion of it with partial depolarization of the membrane and most of the sodium channels being inactivated at that level. It just is frozen there. Nothing can happen. No impulses can get through it. Until another typical PVC comes along and interrupts the cycle and lets things conduct again. That need not happen. It could perpetuate in a complete AV block and the individual may perish with that. So this is something with a poor prognosis. It's in the His-Purkinje system and they have normal adenosine levels. And if you give adenosine to try to provoke this, it doesn't work. This other disorder, more recently described, Paroxysmal Idiopathic AV Block. There, again, is no change or a slightly increase in the sign of cycling. There's no obvious trigger. You don't have to have a PAC or PVC to come along. There are no characteristic findings at the end of an episode to herald when it's going to stop or that it has stopped and it's not going to come back. Adenosine levels in these individuals are low. And if you give them a little bit of adenosine as a challenge, they will show this phenomenon and they should undergo a permanent pacing. There are a lot of hazards along the way. Adeno-echoes while your atrial pacing can make it look like Winkie-Bock has occurred when it actually hasn't. Cancer-induced AV blocks, when the time is they occur, can make it look like conduction is worse than it actually is, left to its own. In the AV node, this is relatively uncommon. There are cases, we have a series of catheter-induced AV nodal block. It's not very common. In the HIP bundle itself, it's rather rare. I've only seen a few examples. Right bundle, diamond does it, it happens all the time with RV catheter placement. And it tends to be pretty reversible even by the end of the procedure. Left bundle branch block is uncommon and it typically occurs with left ventricular mapping and not with ablation of the left bundle, but just bump, bumping that area. And in some cases, it's a permanent fixture. Really be speaking of very disease, hyperkinesis has just had a little bit left in it. In a patient with left bundle branch block and syncope presenting for evaluation, it's good to pace the lateral right atrium and assess AV block before placing anything large out there. It just avoids confusion as to, confusion as to, we'll start at three, two, one. And people with left bundle branch block and syncope who are undergoing EP evaluation, it's very wise to get a single catheter up the lateral right atrial wall. Get well away from the conduction system, pace the atrium to assess winky bite before getting any electrodes in the vicinity of the conduction system and thereby eliminate any question as to, well, I may have bumped into the conduction system and caused it to worsen. That way you have your answer out front. An individual may have an apparent hisperkinesis disease and therefore you think conduction system is okay. It's because it's a split hiss and you only see the distal hiss. So the HV interval measured from that is actually normal and any block that you have will look like AV nodal block when it's actually not. This is pseudo AV winky buck, pacing the atrium here, capturing. And here we don't seem to capture the atrium here and yet we have a pause. So one might think, okay, it's getting longer and longer and there's a pause there. So this is our winky buck cycling. It really isn't. This is interrupted by AV nodal echoes that occur there and there. And there's no atrial capture here to be able to say whether we had AV nodal winky buck or not. So this is an indeterminate conduction at least as well as this, perhaps not much better because it is definitely quite prolonging there. This is a case of catheter-induced AV nodal block coming along with an individual that's a large tip electrode and can do some AV nodal damage work on this young person. And if you know the modification or a slow pathway destruction, and we get the catheter in the region of the compact AV node and lo and behold, we get this little lump here and a complete AV block that might last for a few minutes. It usually doesn't go much longer than that. It comes back and you're gonna ablate the slow pathways in these people very readily without much problem. Catheter-induced right bundle branch block is shown here. We're trying to adjust the hiss for some reason. It looks like a pretty decent hiss, but we're trying to adjust it. And here we're doing some work on the houses somewhat blowing a little bit in this, seems like in this situation, banging into electrodes here with mapping catheter and causing that complex there at the beginning of the QRS to be shifted out. This is proximal right bundle branch block. Remember, taking longer to get from the QRS onset out to the primary apex is an indicator of proximal right bundle branch block. I'm not gonna spend any more time on this particular figure here or this table. It just shows you what normal intervals are, what the effects of different types of stimulation, pacing stimulation and autonomic manipulation are on the conduction parameters shown there. There are a variety of genes that affect AV conduction. Therefore, there are a variety of ways this can go wrong. You see these common players here. We have the very interesting PRKAG2, the syndrome of pre-excitation, but AV block as well. You know, it seems like you have an extra conduction pattern pathway. It's actually very prone to blocking. Musculoskeletal disorders, such as type 1 mitotic dystrophy, Steinert and Henry-Dreyfus syndrome, Kinshera syndrome, Duchenne. Pacing in acquired AV block, not so important to have symptoms in this setting. This is the 2018, 2019 revision kind of distilled down here. Not quite as complex either. So a lot of this is regardless of symptoms. You can go ahead and justify pacing a lot of these different situations here. So in summary, a clear understanding of cardiac anatomy is foundational for the practicing electrophysiologist. Know where problems can arise that can affect the conduction system, both impulse formation and conduction. Knowing that in the vast majority of cases, the evaluation of the conduction system is hinging on asking the question, does the person have some abnormality of conduction that can't be mitigated in some way? A drug that's affecting this, ischemia, so on and so forth, that they're going to need a pacing system of some sort. Most of the time, these decisions can be made based on a clinical situation, as well as ECG rhythm strips or full ECGs. Intracardiac recordings are not necessary for this. However, occasionally there may be incidental findings acquired at EP study for evaluation of syncope or for other reasons. And one finds that there's some incriminating evidence that says that the AV node, his bundle, Purkinje system, or even the sinus node are in a bad way and are subject to failure and will need some help with pacing system. For a board review and board prep, you need to know indications for pacing, factors that influence the conduction or block in different portions of the conduction system because there are slight differences, how to differentiate sites of anterograde and retrograde block from surface and intracardiac recordings. Thank you very much.
Video Summary
The video features two segments, the first by John Miller and the second by Dr. Stephenson, discussing different aspects of the conduction system of the heart. <br /><br />John Miller focuses on sinoatrial and AV nodal conduction. He discusses the anatomy, evaluation, and therapy related to these conduction pathways, emphasizing the importance of understanding cardiac anatomy for electrophysiologists. He explains genetic abnormalities that can affect cardiac impulse and conduction physiology. Miller delves into the evaluation of abnormal cardiac impulse formation and conduction using ECG and intracardiac recordings. He highlights the conditions and factors that can affect sinus node and AV nodal conduction, as well as various disorders associated with these conduction pathways.<br /><br />Dr. Stephenson's segment concentrates on the AV node, His bundle, and bundle branches. He explains how to record the His potential and discusses the anatomy and function of the His-Purkinje system. He talks about the different fascicles of the left bundle branch and possible injuries to these branches. Stephenson explains conduction block in the His-Purkinje system, the difference between transient and permanent block, and the phenomenon of phase three and phase four block. He provides examples of conduction abnormalities, including AV block and bundle branch block. Stephenson emphasizes the importance of stress testing the conduction system and the potential use of drugs to assess conduction. He also discusses the hazards associated with conduction block and the importance of careful evaluation and pacing system placement in patients with conduction abnormalities.<br /><br />Summarizing both segments, the video provides a comprehensive overview of the anatomy, evaluation, and therapy of the sinotrial and AV nodal conduction pathways, as well as the His-Purkinje system. The speakers discuss genetic abnormalities, various factors affecting conduction, and different types of conduction abnormalities. They emphasize the importance of understanding cardiac anatomy, careful evaluation, and appropriate therapy in patients with conduction system abnormalities.
Keywords
video
segments
John Miller
Dr. Stephenson
conduction system
cardiac anatomy
genetic abnormalities
conduction physiology
His-Purkinje system
conduction abnormalities
evaluation
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