Transcript for:
Understanding AV Blocks and Sinus Node Dysfunction

okay so we are 10 minutes past the hour I uh want to make an apology to everyone watching this recording uh we did have to shift the time up a little bit just because of some urgent things that came up uh however we will be back to our normal scheduled 6m West African time um next week so uh today speaking on AV blocks and sinus talks we have Dr eono from uh the University of Texas she's an associate professor in card electrophysiology and she is going to be kicking off our week two talk if you want to take it from here okay so I've unmuted yes yes I am all right fantastic thank you so um like AJ said um I'm Caro I'm one of the um cardiac electrophysiologists at UT Health in Houston Texas as well as being part of the cardiovascular Education Foundation um part of the EP group with that um and I've been involved in um education for the cvf um since a little bit after its infancy so I'm really excited to be here again um so um thank you guys for coming we'll be talking today about um AV blocks and sinus talks basically talking about um sinus um the sinus node sinus function and why do we talk about putting in pacemakers what is the normal function um of the sinus node and a node what would you expect to see with um abnormalities there and so um you know and this will kind of build up a little bit on Dr pic's talk last week um there might be some slides that you've seen before so um don't hold that against me it was deliberate and we'll just kind of be going over a little bit of what um was discussed last week so um I want to start off with a few few questions um you know you don't have to answer them right now we'll go over them again at the end um but basically um I want you to kind of have an idea of why the concepts that we're going to be talking about today um will be important in your clinical practice so let's start off with question one um a 75-year-old man with a history of hypertension who presents for his annual followup he's feeling well without any complaints but he's found to be braed cartic with an irregular Rhythm on examination and his EKG is shown um is going to be on the next screen a hter monitor confirms this and shows multiple episodes similar to his EKG with heart rates in the 30s during sleep an echocardiogram is unremarkable and his heart rate increases appropriately with exercise and so this is what the EKG looks like I want you to take kind of a picture in your brain of what it looks like um and then um basically the question is what's the next next best step in managing this patient a would you put in a pacemaker um especially with that heart rate that gets down to the 30s B would you do some Imaging try to figure out exactly what's going on C continued observation d a cardiac um pet scan or E an implantable loop recorder and that's basically a monitor that we put underneath the skin to monitor the heart rhythm to determine if we're going to do anything else so that's your question one question two we we have an asymptomatic 72-year-old man who's referred to the emergency department by his opthalmologist because he was found to be braid cardic on routine examination and in the emergency room an EKG rals sinus rhythm with 2 to1 AB block which finding would be consistent with an infranodal AV block and so there two things that we're going to be kind of talking about here you'll be able to answer this question after the Talk number one you know what kinds of a blocks are significant number two what do you exactly mean by infranodal AV block so we'll talk about that but a theop philin would improve AV conduction B atropine improving AV conduction C leg exercises improving AV conduction D Val Salva maneuver worsening AV conduction and E kateed sinus massage improving AV conduction okay and then the third question we have a 76 year old woman all these people in their 70s having problems 76 year old woman with a history of two prior ablation procedures for aib presenting with recurrent symptomatic paroxysmal aib refractory to fide and delm therapy EKG shows atal fibrillation with ventricular rates in the 160s to 180s and an echo shows normal LV systolic function with dioic dysfunction and left atrial dimension of 5.5 CM she converts the sinus rhythm spontaneously after initiation of sodol 120 milligrams bid load after three doses she has sinus brto cardia with a ventricular rate of 40 beats a minute she notes increased fatigue in sinus rhythm what is the next best step in man management a a dual chamber pacemaker B A leadless ventricular pacemaker C switch to amiodarone D switch to propanone and e a pacemaker and AV node oblation so those are three questions I want you to kind of consider we'll come back to these at the end um but basically the objectives here we're going to be talking a little bit about the conduction system we'll talk about um different levels of heart block and then we'll also kind of touch into the management of brto cardia so we talked about this last week about what the conduction system entails and what it looks like basically you know you have your sinus node you have your interatrial conduction system that allows you to have those fast um conduction to the right and the left um Atrium and it all coalesces into the atrioventricular node um from which it goes through the bundle of hiss and down the pingi fibers into the ventricles and so you know this constitutes the backbone of the conduction system of the heart that is innovated by um your um anomic um function so you could um by the vagus nerves as well as um by um your sympathetic um inovation as well um so when you have um you know a normal sinus rhythm you expect your heart rate to be between 60 and 100 beats a minute um your AV conduction if let's say the sinus node gets knocked out and your AV node has to pick up then number one you'll see that you'll have a junctional rhythm so you won't see that atrial contraction um and your heart rate would be expected to be between 40 and 60 beats a minut minute so that Junction has is a backup pacemaker to the sinus node um and you'd expect that to be between 40 and 60 beats a minute um and the reason why it's slower than the sinus node is so that it doesn't overtake the sinus node at any point and then The ventricle is also capable of being a cardiac pacemaker but by the time you get to The ventricle it's not really a reliable partner and so once we get to a ventricular Escape Rhythm that at that point we're really worried that you know we need to work um really um fast and so um but the ventricular Rhythm usually sits at less than 40 beats a minute and um it's usually a wide complex if you see that then um we need to start working on putting in a pacemaker so um going back to the EKG and what the EKG looks like um as we made mention your PR interval um is or your P wve basically talks about what is happening in the atrium and your atrial depolarization your p-wave typically lasts about less than 80 milliseconds and that's how long you expect for your activation to go through that conduction system and also for the atrium to contract and basically the p-wave is um what you see that um signifies atrial depolarization the PR interval is the time from the sinus node for the your impulse to get from the sinus node to the AV node and that typically should last about 200 milliseconds us usually with that PR segment you'd expect it to be about 120 to 200 milliseconds if it's less than that then you're worried that you might have some ventricular preexcitation maybe the presence of a bypass tract that you can see in wpw um um but if it's longer than that then you expect there to be some um delay either in the atrium or in the AV node um followed by that you have your QRS which signifies um depolarization of the ventricles it by itself is about 80 to 100 milliseconds maybe 120 milliseconds if you have some intervent um interventricular conduction delay um and then of course your ST segment shows you the depolarization of the ventricles and your T um wave is your repolarization of the ventricles um such that your QT interval um typically just um tells us what's happening in The ventricle both depolarization and repolarization usually usually it's corrected to about 440 to 460 milliseconds if it's greater than that then we're a little bit concerned um and then your uwave um is supposed to be depolarization of the interventricular septum typically we don't see it however sometimes you do see it um it can be a normal variant um sometimes when you have electrolyte abnormalities you can actually see that a little bit more um but um it's something that we don't really pay close attention to without other things that would make us a little bit more concerned now we have the EKG that basically tells us what's happening you know from the chest it's a non-invasive test and it can tell us what's happening in the AV node if you want to do a deeper dive then the EP study is the way to go and this is basically the gold standard for determining um a rhythmic causes of Syncopy um including the most um common the sinus node um sin no is function um his pingi block and also Tachi arhythmia we're going to be uh talking about the causes of bra cardia um and so I just wanted to give you an example of what an EP study should look like um previously people who were smarter than me would um actually take um a catheter and put it on the epicardial surface of the heart and that's where they were able to get information about what's happening in the sinus node um in the um modern iteration of the EP study you actually don't see what's happening in the sinus node that is determined by what happens on your EKG so if you see a p-wave then you're like okay this is where the cus node should have started um and then we're able to see exactly what is happening on the inside of the heart so after um your depolarization or your signal comes from the sinus node into the atrium then we're able to determine all of that um the reason why that becomes important is that it's able to tell us hey this is what's happening um in the atrium when it goes through the heart as well as when um what's happening in The ventricle um we're able to see exactly how the conduction is happening through the heart so when we put in our catheters we put in four catheters typically for an EP study one in the highride atrium one in the coronary sinus one in the his area and one in the right ventricular Apex or the outflow tract um basically we're looking at um you know what's happening in the atrium and this is going to be determined by what happens in the highr atrial catheter as well as the Cs catheter um your highr atrial catheter will tell you what's happening in Atrium your right ventricular ecal catheter will tell you what's happening in The ventricle what's happening in the Cs basically tells you what's happening in the atrium and The ventricle and it's um basically relegated to what's happening in the left atrium so you're able to tell how conduction is going from the high right atrium which is where closest to the sinus node um to The ventricle and then this hiss catheter becomes really important because it tells you what's happening in the hiss and happening in the AV node so you have your ah interval and your HV interval your ah interval tells you what's happening in the AV node your HV interval tells you what's happening in the hisper kingi system um your ah interval usually is a little bit longer about 50 to um you know 100 milliseconds your HV interval is about 30 to 55 milliseconds typically really short um the combination of the two give us a rough estimate of what your PR interval should look like and then um this is just some kind of views um to let you know what's supposed to happen um or what your um catheters are supposed to look like um when you go into x-ray this is your r view that's your l view and you can tell your catheter is on the right except for your CS catheter that goes to the left side so let's get started so your left um when we're talking about block we should talk about two things number one um let's talk about levels of block everybody knows you know when we're talking about first deegree block second degree block third degree block you know the second deegree block seems to be a little bit um more um difficult to kind of um recognize or um a little bit more difficult to explain um first-degree um block typically talks about prolonged conduction so whether we're talking about you know um in the sinoatrial block which I'll explain to you later or the atrio ventricular node basically what ends up happening is that there is a delay in conduction so it's not really a block per se it's just basically a delay right third degree basically means that there is no conduction between the higher level um um the higher level area and the lower level area so if you're talking about the Sino atrial area you're talking between the sinus node and the atrium if you're talking about the atrio ventricular area you're talking between the atrium and The ventricle basically those two areas just have no um communication with each other and so typically what happens in the lower end you have an escape Rhythm that kind of kicks in so um you know and second degree basically means that you have intermittent conduction type one will tell you that there's Progressive prolongation between the higher um level and the lower level and type two means the sudden failure so all of a sudden you know you're conducting and then all of a sudden there's nothing there now um there are different locations of block right so AV block we talk about it all the time it's very easy to see because you see a p-wave and then you see you see a QRS or you don't see a QRS um the H AV node um when you're talking about block you can actually have it be in the AV node and that's considered to be super hisian or above the level of the his it can be at the LEL of the his which is intra hisian or it can be below the level of the his which is infra hisian and that you can only Define by doing an EP study on the EKG it kind of looks the same but the um reasons this is really important in determining if the patient will need a pacemaker or if you want to wait a little bit longer because if it's super hisian or in the AV note then there's a possibility that there's something systemic that's causing that block um and it can be reversible if it's inisan or infian it's less likely to be reversible and it's more important for you to rush through that and um put in a pacemaker a Sino atrial block basically what we're talking about is conduction between the sinus node which sits at the um the epicardial portion of the heart and the rest of the conduction system basically the atrium right and so all of those um types of block you know the first degree second degree and third degree can happen between the sinus node and the atrium the same way that it happens between the AV node um between the atrium and The ventricle with the EV node being the location of the block and so um I do want to um you know kind of touch on this a little bit more because this is a type of block that we typically don't really recognize and then we also don't recognize how important it is uh for us to um place a pacemaker if it's needed and sometimes the EKG can give us an idea that hey there is something here going on that we need to address um a little bit more than not or a little bit quicker than we typically do so when we talk about sinus node dysfunction what we have to understand is that the sinus node um consists of pacemaker cells which we call P cells and then the perinodal cells or the transitional cells which we call the T cells and the P cells basically are where um you generate the impulse right that sinus node and Dr pazik talked about you know the action potential that basically you know self- regenerates or self depolarizes um for you to continue having your um sinus bead um that originates in the sinus node itself the transitional cells basically transmit the electrical impulse from the sinus node to the right atrium and so the transitional cells are not able to generate that recurrent beat um the sinus node the pacemaker cells are the ones that do that now when you have um sinus node dysfunction um you could have a sinus node arrest which basically means that there's a problem in impulse generation or you could have a sinus node a um exit block where you have problems in transmission from the sinus node pacemaker cells to the right atrium and typically that's because there is some sort of dysfunction in the transitional cells um that go through um the ad so um as this diagram shows you like you'll have the um pacemaker cells and then you'll have the transitional cells and then you have the you know the atrium right and so if you have your impulse being generated here and there is some sort of dysfunction in the transitional cells then there's going to be a problem getting that impulse from the pacemaker cells to the rest of the atrium and that will affect where your p-wave um actually appears on um your EKG so in talking about disorders of the sinus node the first one we'll talk about is sinus arrest um basically is also um referred to as a sinus pause and there is a failure of the sinus node to generate an Impulse so basically the sinus node is not working and again you might ask me well how do you know that this is the case well like I mentioned there people who are much smarter than me before the times you know before now who basically put in that catheter that is able to determine um basically acts like an EKG on the um inside of the heart um they put the catheter where the sinus node was and they were able to Define these different kinds of block and so when you have a failure of the sinus node to generate an Impulse basically you will not have you know a p-wave so sometimes um you can see that the way that you can recognize it is that the pp interval so the um interval between the p waves is not going to be a multiple of the preceding p-wave interval it's not um and I'll defi I'll also talk to you about another time when we see that um if it's greater than 3 seconds is considered to be abnormal so um what you might see is something that looks like this where the p-wave is just kind of marching along and then um p waves marching along and then all of a sudden you don't see any p waves so that's basically what you should be looking for is that it's not an AV block because if it was an AV block You' see a p-wave no QRS here you actually don't see any of the p waves and so that's basically what becomes important so for Sino atrial block also known as Sino or rular block sometimes um the sinos node function is normal but transmission to the rest of the atrium is blocked so there's a problem with those transitional cells there's different types the same way that you have it with AV block you have sinoatrial block so your first degree second degree and third degree you can have that in sinoatrial block as well as having that an atrial ventricular block for first deegree sign of atrial block it really doesn't show up right in your EKG because remember the PVE only tells you what's happening in the atrium so whenever it is that the atrium gets that um first impulse that's basically when it is so you're not going to see it on the EKG so this is not it's not a theory because again somebody much smarter than me put catheters up into the heart so they're able to Define it but for us for all intents and purposes we're not going to see it on E so we're not even aware that this is going on but basically what's happening is that there's a delay in conduction from the sinus node impul um from the sinus impulse um from the node to The Atrium so this is normal sinoatrial um conduction where you have this denotes the impulse um from the sinoatrial node so you have your Sino atrial node impulse and then it basically goes into the atrium so immediately you see your key wve immediately following when you have a first deegree signo atrial block there's a little bit of a delay again on your EKG you don't see it but if you were to put a catheter up into the sinus node you'd be able to see that there now second degree is able to be seen and why because you see a difference in the way or in the relationship between the pp intervals so for type one you have a progressive delay in the sinus impulse so basically where you have your sinus impulse transitioning going through the transitional cells to um The Atrium there's a progressive delay there and what um this causes is a progressive decrease in the pp interval and then you'll see a pause and then the pause will have a duration that's less than two PP intervals so that's number one and then the second thing the interval the pp interval after the pause is going to be greater than the pp interval before the the pause so I'll give you an example in this EKG right where you have these p waves so you have these p waves that kind of marching out and you can see the p waves are getting closer and closer and closer together and then all of a sudden you see a pause and then it starts again and starts getting closer and closer and closer together so there sometimes you might see it and you'll be like huh maybe this is sinoatrial um this is sinus arhythmia right well yeah I guess it could be but then the problem is when somebody comes in and like oh I they have this EKG but then they're complaining about sometimes having Syncopy sometimes they have pauses that are greater than three seconds right if that were a sinus arhythmia that should not happen this is a lad diagram that basically tells us what we're actually seeing so if for instance this is the sinus node right the sinus node is coming on time and then basically this latter diagram here or this area here talks about what's happening in the transitional cells so basically here your sinus node impulse is generated going through the transitional cells there's a little bit of a delay a little bit of a delay and then there's block what ends up happening is once it gets into the atrium it conducts the way it normally would conduct but what ends up happening is that because that delay is going on you have these PP intervals getting shorter and shorter until it blocks off and then it's starts all over again so if you see your sinus node um or p waves getting closer and closer together and then all of a sudden you don't see a p-wave and then you see it starting over again then you should suspect a Sino atrial block most um consistently a sinoatrial um exit block type two um second deegree sinoatrial exit block type one okay sin atrial block a second degree type two um it's similar to what we see in type two and ab blocks basically the pause is going to be a multiple of the pp interval there's no change in the preceding PP interval and all of a sudden you just kind of see blocks happening right so for instance here you have your PP interval you'd expect to see something here this is a junctional Escape but then you see the P wave coming in where it's supposed to and then again um there's a drop right there's no change in you know your PP intervals here but then also this between the p-wave and that P wve is a multiple of the pp interval that happens beforehand um this again is basically what it looks like where you have intermittent failure of the sinus node impulse to transmit into the atrium here you have One PP interval there you have a blocked impulse um this equals 2 PP P intervals before it gets restarted sometimes it can be up to three or four like a multiple of pp intervals that get blocked um but this is you know when you see this and you see this sudden block where you don't see a p-wave then you should be concerned that there's a second deegree type 2 Sino atrial Block in which case you know if this patient comes in with symptoms you know this is typically not something that's um you know as a result of adrenic tone or lack thereof and this is something that you should be putting in a pacemaker for now for third degree sin tril block this is complete failure of the sinus node impulses to exit the sinus node um it's indistinguishable from um sinus arrest and so basically all you'll see is no p waves maybe you'll see a junctional Escape Rhythm um but typically you don't in that um epicardial space to determine what's happening in the sinus node at the end of the day you know what's going to end up happening is you know the same thing you'll see a sinus pause um and basically you'll need to put in a pacemaker what will happen on your EKG you'll see a junctional Escape Rhythm um you might see um some pauses you might um not um but if you see a junctional Escape Rhythm because we don't exactly know what's happening with that sinus node we typically would recommend that you put in a pacemaker at this point so I know sinl blocks are a little bit complicated um does anybody have any questions and the chat is open if you have questions feel free to chime in as well uh one thing so I guess I'd never done a deep dive on cro blocks before so it it very much correlates to what you're going to talk about next I guess with AV blocks where you have a type one which is kind of like a winky boach with the transitionary tissue allowing like a delayed transmission you have a type two that is almost like a two to one or a drop but you don't actually have a delay and then exact third interesting exactly so basically what's happening you know when you look at hro ventricular blocks typically what we'll tell you is like there different ways to Define it if you're talking about second degree um you know you can either look at what's happening in the PR interval or you can look at what's happening in the RR interval right but signo ho block you don't have the equivalent of a PR interval because we don't have a catheter in the sinus node all the time right um so all you can tell is what's happening with the p waves and that's basically what will determine exactly what's happening um with your sinoatrial block so I'm going to go to the AV um node um Dr pazik did a great job in explaining you know what happens um with the AV node the anatomy of the AV node and how you should um you know or where you should be expecting to see it and also the um you know Associated structures problems with Associated structures that can result in problems with the AV node particularly if you see you know for patients now that we do a lot of you know tavers um or for those patients people that you refer for um calcific um a um a or aortic valve um disease um It's Not Unusual for you to see that same fibrosis or that same um calcification actually infecting the E node just because of where it sits and it sits at the head of the um this um triangle um basically we're looking at um this triangle that is formed it's called like H's triangle um which is um formed by the tendon of Toro the um CS o which is starts at the um inferior border and then also the tricuspid valve um which is anterior so once you um lay that out at the head of that is your compact AV node typically what you'd expect to see is um you know on your EKG a PR interval that's 120 to um 200 milliseconds um on the intracardiac you measure this AV conduction using your his catheter um with your ah interval um representing the conduction time from The Atrium through the AV node and then your HV interval representing conduction through um the his pingi system your age interval usually sits between 55 60 and 125 milliseconds and your HV interval between 30 and 55 milliseconds so um this is typically what you see in your his catheter um this is what you know if you have your atrial catheter just kind of walking through your ventricular catheter corresponding to um your QRS for um the his catheter you should see both the atrium and The ventricle as well as the his um deflection there and um your ah interval plus your HV interval is roughly a little bit less than the PR interval on the surface EKG um for first degree AV block um it could be as a result of different things um a lot of times like I mentioned you know when we talk about your locations of block for um your AV node um you're talking about superian which is in the AV node intra hisian which is within the hiseni system and infra hisian which is below the hiseni system um if you have it in your AV node your ah interval is prolonged if you have it within the hiss pingi system then you actually have two hisses and you'll see kind of a delay in those presence of two hisses is not normal so when you see that that's automatically um an intra hisian block and then if you see if you don't see that but you see a prolongation in your HV interval then that will tell you that hey there's something going on infra hisian so for us when things are happening in the AV node that could be as a result of many different things it could be as a result of you know sympathetic or parasympathetic tone it could be as a result of hormones basically because that has more adrenergic um you know um activators we're not as worried about it as we do get when we see something infr hisian infra and intris those are all a non events so basically if anything gets to the hiss if it gets to any impulse gets to the H or to whether it's generated by itself or it comes from the sinus node it should pass on to the ventricle so there isn't a delay there so anytime time we see any kind of delay and then a patient comes in with symptoms that's a little bit more worrisome so how do we test for this well your EP study is a great place to do that for your AV block you note um a prolonged PR interval typically that's greater than 200 milliseconds now there's sometimes that you don't necessarily see that and that's where it becomes a little bit technical I'll talk to you a little bit more about that as we go on your AV um your Prime uh first AV block could be secondary to conduction delay at any level like I mentioned um your AV node so that will give you a prolonged ah interval your intra his that will give you a fractionated hiss in his signal infra his will give you a prolonged HV interval so for instance here your um first degree AV block that's super hisian you know remember I told you that you would expect this to be about one um 100 or 60 to 120 20 milliseconds you have an ah interval here that's 250 milliseconds so that's clearly within the node your ah interval is prolonged um and so it's and it's usually the most common cause of first-degree AV block and this is particularly the reason why most of the time if we see a first-degree AV block we just watch it unless the patient is symptomatic we don't necessarily put in a pacemaker um so here you have a PR interval that's um greater than and um 300 well is 320 milliseconds so that's a little bit you know worrisome but if the patient doesn't have symptoms we don't really worry about it um if you have an AV block that's inra hisian so this is kind of an example here where you see a hiss that's um looks at the it's connected to the atrial signal and then you also have a hiss that's connected to the ventricular signal when you have that inra hisian delay then that basically tells you hey there's something going on here the presence of that just tells you okay look there is a first deegree um inisan block so there shouldn't be any delay you shouldn't see to his signals if you do then um that's considered to be a delay um for infer hisian block you can have it happen with a normal PR interval or prolonged PR interval and that's because the HV interval is such a small part your PR interval that even small increases can tell you that hey there's something wrong here we might have to put in a pacemaker we're seeing it a lot in patients who have um tavers because you know initially they come in they don't have any problems with their hiss signals and then once you smash that calcium into the um hiss then all of a sudden you have um episodes where you actually would need to put in a pacemaker um here you have a HV interval that's 80 milliseconds that's prolonged however the PR interval is normal is 175 milliseconds you can kind of suspect that there's a problem because your surface EKG shows that your QRS is wide here right here we also see the same thing HV interval is prolonged QRS interval is wide um and your HV interval is really prolonged here it's 300 milliseconds your PR interval is going to be greatly prolonged because your h in is already pronged right um for your second degree AV block you have intermittent failure of um conduction through the AV node might sorry Dr can I ask a quick question sure yeah so um so if what happens in the patient Clinic when you've got a patient who has a profound first degree block so um so for instance maybe the the the pr intervals about 300 milliseconds um and they've started to become um maybe slightly symptomatic like breathlessness and things um and would you consider maybe um pacing pacing your ventricle if they've got normal LV function like so you shorten the AV delay um instead just leaving other oh yeah for sure so that is one of the indications for um placement of a pacemaker is if you have a significant PR interval that is um if you have a significant PR interval that is um causing what we call pacemaker syndrome and the reason why the patient becomes symptomatic is because you know the by the time your your impulse has gone through The Atrium right and it squeezes it's squeezing against a closed AV valve and so that's the reason why they're having all those symptoms so they'll have shortness of breath they'll have this flushing um and they'll just feel really tired with exercise um so when we see that yeah you definitely want to put in um a pacemaker for sure brilliant that's fantastic and does that depend on their ejection fraction the LV function all what what would you no right okay so the reason why you would put in the pacemaker is more because of what is happening with the patient so the only indication for putting in a pacemaker in a patient who has first bav block is symptoms so even if if the patient is walking around they have a PR interval that's 500 milliseconds and the patient is like no I feel great then there's really no indication to put in a pacemaker yeah fantastic well so but very very quickly so this I've come across this in a in clinic so what if the patient is not symptomatic may maybe they've got a sinos no disease and they're pacing the a a lot but for a long time they've been a pacing V sensing um and say for instance they've got arguments they've got 20 260 or 270 milliseconds um and and you're thinking so is there a case to be made um like for instance um to past the V if um would that would that help your heart function for instance because I'm thinking about Echo here E and A like in terms of the early ventricular feeling and active ventricular feeling is there like would you because the the bigger the Gap the bigger the Gap the more are they going to eventually is that going to lead them to heart failure because of the prolonged pial or we just treat the symptoms once once they get they start to get to M that's when we we will consider pacing the V yes so basically I mean so previously right and you guys would know more about this previously you know we were a little bit restricted in programming AV delays but now we have those variable AV delays that you can go up to 400 milliseconds um in which case you know and the reason why we you do that is because we want to Pace The ventricle as little as we need to because there's more of a risk of um RV pacing induced um cardiomyopathy than not and so we'd rather not pace The ventricle having said that you know if somebody comes in PR interval is two like they're pacing in the A and their PR interval is 260 milliseconds right um you know as long as they're asymptomatic that wouldn't be a problem like first degree a block typically is well tolerated until you get to the point where the atrium is squeezing against the closed ventricle and then that becomes a little bit of an issue brilliant fantastic thank you that was really good thank you no no problem so um like I made mention you know when you have second VAB block um it could be pathologic or it could be normal you could have increased vehical tone um you know which would be normal um if you have an h rhythmia a second degree AV block is actually expected so that sometimes you'll see a p-wave going at 150 beats a minute and then you see this AV block and you're like hm the second de AV block well the other thing that you should be thinking about is well why is this sinus node going at 150 beats a minute sometimes it could be an arhythmia and in that case you know your AV node is basically protecting your heart the reason why that happens because the AV node has this property called decremental conduction and so if you know it has all these inserts from you know like I mentioned and Dr P mentioned has all these inserts that come from the brain basically telling it hey you know I'm about to run now so we're going to increase conduction through the AV node AV node says great let's go or it says oh you know there's a lion chasing me need to go if know says also now there sometimes the atrium just goes off on its own either because of atrial attack cardia atrial fibrillation atrial flutter the AV node will say well I don't know about this sinus node didn't tell me anything the brain didn't tell me anything the hormones aren't telling me anything I think I'm just going to stick to not doing that much and basically it does So the faster you Pace In The Atrium the slower The ventricle the slower the AV node will conduct So the faster you Pace the slower the AV node will conduct and you will have this period where you will have actually uh normal AV block so that's the reason why most of the time when we see a second deegree type one we're not really very concerned you know because we think it might be normal it might be either because of increased veal tone or it's because in that situation the um the sinus node or whatever Rhythm was going on in the atrium wasn't supposed to be going that fast right now that sometimes it's abnormal if you have an inferior wall Mi you could affect blood flow to the um AV node um sometimes drugs can do it right so your beta blockers calcium channel blockers they do it in which case your um heart rate will go down as a result and then they can sometimes be reversed by altering your bagel tone so if you um increase or if you exercise right that increases your veal tone so for instance if you see yourself being in a 21 AV block all of a sudden you're exercising and then you notice conduction actually improves then that tells you okay this is happening in the AV node this is physiologic this is not really something to worry about if you see the opposite happen then that means that there's something going on with the AV node itself and we should be a little bit concerned okay Dr car just a quick question you'd mention detrimental properties of the AV node in retrograde do you still see can you see detrimental or is it always pretty consistent conduction timing no so with retrograde it's pretty much the same you can see it retrograde you can see it any grade yes okay so you don't see retro It'll Be steady all the time no so grade you actually do see detrimental conduction well okay and so that's how we Define and this is more a discussion for like EP studies and such but when we Pace In The ventricle for an EP study that's how we Define what's going on in um if you have a bypass tract or if you this is normal AV no conduction one of the things that we look at is detrimental conduction so if we're pacing in The ventricle we expect there to be some delay in VA condu ction um until it kind of goes into that two to one okay thank you that's yeah all right so sorry that's fantastic that's great really great presentation that's why you've got me fired up that's why I'm asking loads of questions so really really quick question um ask you did ask a question at the beginning which I caught their end off with with their AF um so I wanted to ask while you're on the AV conduction um what how so somebody with AF and rapidly um AF with rapidly conducted ventricular response rate and AF with slow ventricular conduction rate so when they ening what parameters are are play there to differenti it to cause to make one go faster or one go slower and what happens what what what sort of mediators are play when when somebody's exercis with AF and things like that what was dominating the AV conduction so that you get a ventri well so AV conduction in um in atal filation and atal flutter and atro rythmia in general is basically it's warped and that's the reason why you can't really kind of determine that right so with all exercise you will have some effect to the AV node from the sympathetic inovation so if somebody has ho fibrillation and they're usually sitting at a rate of I don't know 80 to 90 beats a minute once they start exercising that's going to increase right but the degree at which it increases is going to be much faster why because the atrial activation instead of it being 60 beats a minute I don't know 70 beats a minute 90 beats a minute is actually 300 to 400 beats a minute right so you're going to see a jump so if somebody is at 80 to 90 at Baseline all of a sudden with minimal exertion they're going to go up to 130 beats a minute but that's because number one you have your sympathetic Innovation increasing your conduction right and then also you have this Baseline electrical activation from The Atrium is really fast so it's it's the same thing that does it in sinus node and um sorry in sinus node function um sorry in normal function and atrial fibrilation um it's the same mechanism for you know AV noal conduction it's just that there's an enhanced or an increased degree of ventricular response as a result of the Baseline rate all right answer that question yeah yeah it does so I'm I'm taking it so for instance I can use that to explain why maybe some patients might have um AF with a slow V response rate and AF with fast V responsory purely because not really um all right sorry so I was thinking maybe also um refractory properties of of of the AV node is quite unique to the person as well is that right yes exactly yeah so that has more to do with why folks have some people have a slow some people have a fast um yeah atrial fibrillation ventricular rhythms they're not as simple you know as well we'll talk about that more on yeah sorry yeah that's fantastic thank you that was really thank you so I do want to make mention right that if you see groups being right you should think to yourself second degree whether it's atrioventricular or sinoatrial so if you see groups you should think second degree think about it like this whenever you have first degree your qrs's are going to be the same either because your p waves are the same or your qrs's are the same you know because the AV block is going to be consistent right if you have third degree what you're seeing is an escape Rhythm which should also be the same so anytime you see group beating you should think to yourself hey there's some sort of second deegree going on either it's sinoatrial or it's atrio ventricular I just need to figure out what it is okay so here we have an example of what group beating looks like right so you have see this group of four all of a sudden there's a block see this group of four then there's a block you know sometimes you'll see a group of four then a group of three then there's a block but basically just looking at this EKG I should basically say second degree and then I will now look a little bit closer closer to figure out what kind of second degree is it right in this particular case I know it's a second degree type one because your PR interval after the block is shorter than the PR interval before the block and if I were to be more technical you see the PR interval gets longer longer longer longest and then it blocks off but the easiest way to look at it is identify where your block is look at the interval before the block look at the interval after the block and then if your PR interval after the block is shorter than your PR interval before the block then that is a type one um second degree AB block otherwise known as winky block okay and inferior posterior am as well oh yeah for sure so for for those of you who the interventionalist that's when you know the interventionalist because they like oh my God there's an in M need to do that and the EPS are like yeah what's up up with that block so one doesn't necessarily need to be the other now the causes of that again can go between intr hisian infra hisian all the things and you know the reason for or whether or not you'll put in a pacemaker I mean we don't typically um do EP studies for this again um anymore um but um we typically use symptoms most of the time however it is you know great testable material and so you will you know for those of you who will take like EP boards or anything like that you will see things like this where they'll ask you okay is it infr hisian or intran and that's why we kind of I I wanted to spend a little bit more time here and so in this particular case we have an example of where you have you know your hiss you know signals here you have your a your H your V you have your a increased ah interval and then the V and then you have an a no h interval and no V right so what is this this is going to be a super hisian type one block why because the block happened at the before you got to the hiss right and you also see a prolongation in your ah interval okay for the infra hisian what happens is what's happening below the hiss right so you have your ah your HV is already long it's like 110 milliseconds here then you have your ah that is increasing it's 190 milliseconds and then here you have your block but you have an A you also have an H you have no V so here it's infra hisan because it's below the level of the H now it's much less common to to see this like than a type two or two to one block but if you see the progressive prolongation of the HV interval then you should really be concerned and this is a patient that you'd want to put a pacemaker in right no matter what the PR interval is and that's because what you have demonstrated here is that there is a disease in the HV interval or INF Frisian Dr Carol your your cursor is not showing up you is there a way you can turn on the um oh well there it is sorry I thought you were pointing at things earlier never mind I was pointing at things but I guess it doesn't show up when I do it on my other screen so I will put it over here but basically here is where I was talking about your HV inal your HV interval is um increased and then here you have your hiss but then there's no V this is what your EKG typically looks like if you have inisan disease um when you see um that you have um infr hisian block most of the time your QRS is usually wider um sometimes you see it a little little bit like less than 120 milliseconds but normally it's wider than that it's usually um you know wider and so when you see that then you're a little bit more concerned in this particular situation um you can see that your PR intervals don't change right you have a p and a dropped beat and your PR interval after the block and the PR interval before the block are basically the same so that tells you hey this is a second degree AV block a type two um and then I suspect that this will end up being infra hisian because your QRS is lower so here again we have an HV interval your HV interval is you know prolonged here so that's number one the second thing is where you have your blocked beat you have your a you have H you have no V so therefore that means that this is INF fresian this is a second degree AV block type 2 that's infian and this is somebody who you'd want to put a pacemaker in um and you should be concerned about that block now when you have your two to one blocks it becomes a little bit difficult for you to determine if it's you know first of all you can't determine if it's a second degree type one or a type two there's certain things that tell you that it is um in the AV node your block is in the AV node um certain things that tell you it's at the level of the hiss um when it's at the level of the hiss you're a little bit more concerned you want to put in a pacemaker if it's not at the level of the hiss then it's basically might be physiologic and it might be something else that you need to um take care of um a lot of the time like if you have a patient who has um for instance um severe COPD or sleep apnea is not unusual for you to see a two to one block there even if the heart rate is in the 30s there was one patient that I had who had like a 9sec pause um but it was in the setting of sleep apnea um a pacemaker really wasn't um indicated and actually what they should be getting is CPAP um but that's why it becomes important to determine if this is you know in the AV node versus if it's um infra hisian and so um when you see it you should be concerned that there's some disease of the AV node but sometimes again it could be physiologic um if you have a prolonged um HV interval then you're more concerned if you have a prolonged ah interval which is most of the time what we see um then that means a lot of times it's physiologic sometimes you can have impaired function but most of the time it's physiologic and then if your PR interval is less than 160 milliseconds when you do have AV noal conduction then it's something that um you should be a little bit more concerned that it is um intra or infra hisian so two to one block this is an example of what you would see here the PR interval is prolonged your QRS is relatively narrow um so you should be thinking that oh this is probably superian at this point um if it's intra hisian same thing happens where you have intermittent conduction um qrs's might be narrow you might have um fragmentation of the his signal um and so in um when you have isoproterenol you actually um have decrease in your um QRS um improving um versus if it's in the AV node if you give any um agents that are going to increase conduction in the AV node then that will actually improve conduction so a patient who is exercising or you gave is ISO prot panol you give um dopamine you give atropine that typically will improve conduction in the AV node um that will actually improve and then that should tell you hey this is somebody who has superh hisian disease might not need a pacemaker if any of that does not improve conduction or actually worsens conduction then you should be a little bit concerned that hey this is a person that needs a pacemaker sooner rather than later so in this case this is two to one block you see this fragmented hiss which already should give you a hint that hey this person probably needs a Pacer um and then when you see the block you actually see only one hiss you don't see the second hiss so this tells you that this is an atov ventricular block 2: one that is intra hisian here it's superian so basically where you see your a and you see your dropped beat you don't see a hiss you don't see a V when you do see the hiss um the H interval is prolonged HV interval looks normal when you see the a dropped beat there's no hiss so therefore this is superian so how do you determine if it is happening at the level of you know the AV node or if it's happening below the level of the AV node look at your QRS width if it's wide typically it's happening you know down um further down if it's normal then it's typically happening in the AV node look at the PR interval of the conducted p-wave if it's greater than um 200 milliseconds and the block typically usually is in the AV node if it's less than 200 milliseconds then the block is usually in the hisper kingi system um if atropine or exercise improve conduction then that means that there's Block in the AV node so think about it like this anything that improves your sympathetic tone improves conduction through the AV node then that and that improves you know conduction then that means that your original defect would have to be in the AV node if it worsens conduction then that means that your block is actually in the his pingi system and so that is actually somebody who needs to be um have a pacemaker alternatively if you do something that is supposed to slow down conduction in the AV node and it actually improves conduction then that means that there is Block in the his pingi system and that means actually that person needs a pacemaker so you have somebody with two to1 AV block you do a cored massage which slows down conduction through the AV node and it actually causes your EKG to get better that means that that person actually has AV block that's worse and that person needs to get a pacemaker okay so you're basically saying by slowing down the AV node you're allowing the hisper kendi system to kind of recover and conduct indicates that the problem is below the AV node versus anything stimulate the AV node and improve it indicates that's your issue perfect yes so and then of course retrograde conduction um if you have retrograde conduction the block is typically in the hisper kingi system but it could be anywhere so um this number five we typically don't use we typically use number four easy quick and dirty you see2 to1 AV block tell the person to flap their legs and ific gets better then you basically say okay this is in the AV node we need to figure out what's causing you to not have a heartbeat um but if they do that and they're like they faint then just say okay yeah we need to do something about this and then there sometimes it gets a little bit confusing right so you have a patient you know you put them on either isoproterenol or dopamine or anything that would increase the heart or atropine and then you're like well the heart rate went from 40 beats a minute to 45 and then you're like oh this is Nole let's Let It Go actually if the heart rate the ventricular rate went from 40 to 45 but the sinus rate went from 80 to 160 then that's an issue so it becomes a little bit you have to look at your EKG and have to see the degree to which the Improvement happened and that will tell you a little bit of what's going on okay all right keep it moving high grade AV block that's basically for those patients who you see a lot of p-waves and not that many qrs's but they come in like intervals and you see more than two Q waves between qrs's right it could be one of two things it could be either complete heart block or it's a high-grade AV block how do you differentiate between a high-grade AV block and a complete heart block typically a high-grade AV block you would have one to one conduction and then all of a sudden you have p waves just running away and no qrs's those are the patients who will come in typically their EKGs look normal and then all of a sudden they just pass out um I've the couple of times and there very few EP emergencies this is one of them because this person will need a pacemaker ASAP now for degree a v block that basically tells you hey there's no connection between what's happening in the top chamber the bottom chamber whether it's superian infr hisian inisan you still have to put in a pacemaker however the way you define it depends on the EP study I'll show you some examples um typically because these patients usually come in with an escape Rhythm they typically don't have come in with Syncopy they just come in that they're really tired and then they look at their EKG and their EKG shows you a v Block in this particular situation you have your A's marching out you have your V's marching out your a doesn't have a hiss attached to it but everywhere you see the V you have the hiss attached to it what does this mean this AV um this block is in the AV node so it's superh hisian but it's still a third degree V block so this again for treatment purposes it doesn't really mean anything for testing purposes it could mean something so this is just the way for you to define the different levels of block so inisan block same thing um you basically have a situation where you have your fragmentation but then where you see the a you'll see a hiss wherever you see the V you also see a hiss so basically this tells you that your third degree of V block is at the level is within the hiss either way again you still will will put in a pacemaker um for infra hisian block this also is defined by the EP study here the his follows the a instead of following the V and typically your Escape rhythm is just going to be a ventricular Escape Rhythm your qrs's are typically wider again you know I think the only difference that it makes here is that whenever you see a wide QRS as your Escape Rhythm then that Q RS is typically less reliable than one that comes from the junction so when you see an H that goes with the V the um pacemaker is coming from the junction and typically a junctional rhythm is a little bit more stable than a ventricular Rhythm and so when you have a junctional rhythm you want to you know put in the pacemaker ASAP for I'm sorry if you have a junctional rhythm then you have a little bit of time those are the patients who come in and you know that doctor will say oh they've had this heart rate for the last five years and then you put in a pacemaker and that Junction is like finally and it's quits and it never works again right um for your um wide complexes those are the patients who will die suddenly and so you want to get those patients in as quickly as possible because the Escape rhythm is ventricular versus The Escape Rhythm being junctional and you still have inra hisian block with an escape that is lower in the conduct like could the block still be within the hiss but then your Escape is actually disassociated and below the hiss exctly it would just show up as infra hisian because you don't see this the proceeding h no so anytime it comes from the his is going to be narrow so whether it's intra hisian or suah hisian is going to look narrow because it's coming from within the conduction system but when you don't have a hiss so when it's when it's in Frisian that your Escape rhythm is going to be from The ventricle and that's going to be wide yeah sorry I just meant like because you can have a disassociation between the side of the block and the side side of the Escape which kind of convolutes okay yes so com things a little bit so um what about um isthmic AV dissociation then is that like is that so isor rythmic AV dissociation is just more of a condition where we you we don't know what where the block is right because for you to Define AV block your sinus node has to be faster than your AV node or whatever is happening your Escape Rhythm if your Escape rhythm is faster than your sinus node then that's a junctional tacac cardia or ventricular Tac cardia and there really isn't a problem with the AV node when you have rhythmic AB dissociation that means that the atrium is going the same as The ventricle so we don't really know which is which we don't know what's happening and why it's dissociated it just describes a phenomenon okay brilliant thank you no problem and so you know when we're talking about diagnosis and treatment you know we just kind of go back to the guidelines right the most recent guidelines were in 2018 um basically what it says is that for you to diagnose you know um sinus node dysfunction um if you have somebody who's symptomatic with Syncopy um where sinus node dysfunction is suspected um and a lot of times sinus node dysfunction becomes very difficult to diagnose because you know you typically don't see it on the EKG unless they have it on the EKG presenting then an EP study um is a Class one indication actually now um if you just want to study you know what's happening with the anade and retrograde conduction um or if the patient um has Syncopy and you want to exclude any other mechanism for instance maybe they have like you know some substrate for VT or you know you want to make sure they don't have any AB block then it's reasonable um for you to um do a EP study but you don't want to do an EP study in patients where their symptoms are clearly related to sinus node dysfunction right so if there's a question then yes do an EP study is already clear and you just want to like satisfy your curiosity don't do it because with every um procedure that we do as you know there's always risks right so for sinus no dysfunction you know when we're um looking at the Patients you want to first of all see hey is there a reversible or physiologic cause you want to treat the underlying cause you know a lot of times you'd be worried about sleep apnea um sometimes you can have some like hypothyroid for instance you know that could cause you to have a sinus no dysfunction um and then if the treatment is effective then all you need to do is observe um if it's not then you want to make sure that they don't have you know some sort of structural heart disease um one thing that you should make sure of if you see somebody with sinus no dysfunction hey do do they have some infiltrative heart disease um sometimes you can see that in patients who have um you know sarcosis um or you know amalo that could be um also an issue but less so um if they have symptoms though you know you want to make sure that you interrogate that a little bit more and um if they have problems with your EKG or exercise EKG then you definitely want to go towards treatment and when we talk about treatment we're talking about either putting in a pacemaker directly or going through towards invasive diagnosis um to see if they need to be treated for your um atro ventricular nodal dysfunction um if you have somebody where you are suspecting that they have his pingi block and these days it's typically in the context of somebody who has had a Taver for instance we see a prolonged QRS interval but don't really know if we should be putting in a pacemaker or not those patients um we typically will do an EP study possible right um the patients that you do not want to do anything for are the patients where you already know that they have AB block so if you already see it then don't do it um if you have a patient who has you know AV block but it's asymptomatic then there really isn't anything for you to do you basically the EP study shouldn't change your management right again this is a schematic that's also in the guidelines Pretty much telling you hey if you see something you know first of all you want to evaluate is it symptomatic is it not um if it is you might want to do an EP study but um if you see it apparently then go ahead and treat it and if you don't see it and you don't see anything with further testing then please don't so what is the treatment well the treatment is a pacemaker you know yes people talk about giving theop philin it's not really the greatest medication for you to um treat um either sinus node dysfunction or AV block and it's not always um you know something that you can actually um predict and so you do want to put in a pacemaker when you're putting in pacemakers we talk about you know the indications for placement of pacemaker class one indication symptomatic bra cardia symptomatic sinus pauses symptomatic chronotropic incompetence so there sometimes somebody comes in heart rate is 60 you put them on the treadmill they only go to 80 and then all of a sudden they're like I can't do it I can't and they jump off the treadmill and usually it's very traumatic when you see somebody with chronotropic incompetence first thing you should do when you see chronotropic incompetence number one should be making sure they don't have any medications that could affect that um I had a patient who was on a beta blocker for her heart failure and her heart rate could not go above 90 and so every time she would walk from here to there couldn't do anything because she had heart failure and because she needed to be on a pacemaker she ended up having a device placed and she needed a device anyway because her EF was low but um she ended up having a device plac sooner rather than later because she needed to be on the beta blocker and she can't live her life not being able to do things because you know um we're there right so the other thing um would be um symptomatic um sinus node um radoc cardia that um results from drug therapy for medical conditions so for instance that lady that I talked to you about with heart failure or if we're talking about um you know that um somebody who has hual fibrillation you know that could be um a cause as well um a class 2-way indication so that basically means hey you should do it if you have sign of no dysfunction with a heart weight less than 40 with a history of symptoms definitely put a pacemaker in if you have Syncopy of Unknown Origin and then you find abnormalities of sinus node dysfunction um of sinus node function on an EP study um you want to put an a pacemaker in um and then of course um consider it in patients who have a heart rate of less than 40 even if they have minimal symptoms you don't want to put in a pacemaker is an asymptomatic patient we see that all the time patients will come in heart rate in the low 40s but they're asymptomatic you put them on a treadmill they're able to walk please don't put in a pacemaker because you have introduce something to their lives that they don't necessarily need um if you have documented symptoms that were not that were not there when the patient had brto cardia then you shouldn't put in a pacemaker because pacemaker is not going to improve their symptoms okay and then also um if you have symptomatic Ric cardia in the presence of non-essential medical therapy then the treatment should be take away that therapy and you know theoc cardia should get better so they should have a pacemaker plac at that point for AV noal dysfunction function you know if you have third degree or second degree with symptoms or ventricular arrhythmias if you have asymptomatic third degree or second degree with pauses that are greater than three seconds asymptomatic third degree or second degree with aib and pauses that are greater than five seconds um all of these things should necessitate plus one indication for placement of a pacemaker so and usually what you'll find is that for guidelines class ones are usually with symptoms so either you have sinus node dysfunction Aven noal dysfunction with symptoms they also make mention of some neuromuscular diseases infiltrative diseases you know um that would be is an issue and then this one here where you have asymptomatic um thir degree AV block with heart rate less than 40 but you have LV dysfunction you should definitely put in a pacemaker for that for your um class twos if you have you know basically if you have third degree V block then you should put it in um if you have a narrow QRS second degree type two any evidence of infra hisian disease definitely put it in um if they're asymptomatic but with intra or infra hisian disease on an EP study you definitely want to put that in a 2B um would be um all of this plus if they have drug use or toxicity even if the effect is expected even after the drug is withdrawn um that's very rare that that happens but when it does you do want to put a pacemaker in um afterwards um and then for um your class three if it's asymptomatic and the patient has maybe AV block but basically is superh hisian or is first deegree or in cases where where you're expected to resolve and not return um don't put in a pacemaker and the reason why you know these guidelines are really important is because whenever you put in a device you have a patient who's going to have a device in them that they're going to have for the rest of their lives right so somebody's going to be depending on you initially putting in that device for you to have known what you were putting it in for and for it to be an indication an accepted indication you know and they're going to change the generator regardless right um you want to make this as easy as possible for the person moving forward so that they don't have to there's no question about oh was it indicated you know oh I don't know you know because most people once you have a device they're not going to take out the device without a very good reason so that's number one placement of a pacemaker does have increased risks during the procedure but more importantly also has increased risk after the procedure right the risk of infection the risk of you know fracture to the device the risk of valvular abdom alties that does happen with placement of the device and so you only want to put the device in in patients where it's absolutely necessary so back to our questions so you had mentioned um for example Lyme disease and things like that what what's your thoughts on temporary pacing as a bridge so so temporary pacing um it really depends like so in the two cases of lime disease that I've seen um when you started treating them with doxcycline it basically came back in a couple of days so temporary pacing is good for that um most of the time if you expect it to like the the most temporary pacing or reversible questionable reversible um you know AV block that I've seen is mostly in the cases of surgery where you know after AV Noles um AV aortic valve surgery you notice that they have like a transient block that goes away um usually we'll wait probably till posttop day number five and then we'll make a decision so if after postop day number five the patient the heart function has not or the heart rate hasn't come back then it is what it is you put in your pacemaker even though let's say okay after I don't know 30 days the patient doesn't need the pacemaker anymore that's not to say that the patient won't need it later and so nobody will say oh we've put it in but we're going to take it out after that if that's your question yeah no exactly that are are using like an JJ as a bridge or something like that typically we do that in patients who you know we have a reasonable expectation of them being able to for us making that decision within that hospital stay so and what I mean is like less than five days if we're thinking more than five days then we're putting in a permanent because even if it comes back at day number six you know do I trust it right because nobody wants somebody to go home and then you know you finish this heart surgery and then they die of a v block that would be a bummer so back to our questions our was 75y old man history of hypertension no symptoms regular rhythm on exam EKG shown in figure one and noted his heart rate increases appropriately with exercise so first things first what do we think that this rhythm is and either you can write it in the chat or second degree type one yes so this is the second degree type one right so what would the next best step in imag managing this patient what would it be sorry I have to make moves otherwise my light might turn off um so I think if I remember reading the description earlier it was asymptomatic correct yes yeah so I think that you know symptoms always take you know precedence over a lot of this so type one asymptomatic probably continue to observe maybea loop recorder so and me the old ref move Contin to observe says loop recorder exctly continued observation exact to M so basically you know what this shows is uh you know second degree type one um patient is asymptomatic and you know the patient had a heart rate that increased appropriately with exercise most of your symptoms were during rest suggests increased veal tone so you just kind of observe the patient and see what happens excellent so next patient we have an asymptomatic 72y old man and he was found to be bardic sinus um EKG showed sinus rhythm with two to one a block now they said which of the f following would be consistent with infranodal AV block would be we some dror oldi says e as well exactly so basically we me mention of that that anything that's slows down AV conduction but improves um you know if it improves your AV conduction that's supposed to slow down a conduction and actually improves it in this instance then that tells you that this is infranodal and this patient even though they're asymptomatic they should be getting a Pacer everything else is actually a sign of super noal disease so in summary um basically if you look at your we talked about this you know we're talking about differences when you see 2 to1 AB block here if you see you know for kateed sinus massage if you have an improvement in your um um his bundle um conduction and that tells you that that's infr hisian and so that tells you that you know the patient actually has a worse um a block than not and then for um question number three we have a 76y old woman history of two prior ablation procedures as atrial fibrillation um on sodol um actually had sinus biocardia with a ventricular rate of 40 beats a minute and now she noted increased fatigue and sinus Rhythm what's your next best step in management what do you think you could argue probably a given that with SLE all she's uh insanus Rhythm so I'd probably option A at the moment exactly I agree so pretty much you know in this particular case we have somebody who has a fib with very fast heart rates needs the medication you know yes could you switch to amone sure but nobody really likes Amo right um secondly you know would you do um propanone it actually works worse than um sodol and so sodol would be the better it seemed to work really well but instead you know you had really bad braid of cardia so a door chamber pacemaker in this particular patient would satisfy that class one indication for somebody who needed um very necessary treatment for the arhythmia but um you know would also um had a symptomatic braic cardia with the medication and so you would do um a dual chamber Pacer in this so in summary you know patient with first deegree AV block or C hual block you know if the intris or infr would you put in a pacemaker yes with symptoms questionable without symptoms you know but it really depends and then AV noal definitely not the second degree where you have intermittent condiction remember the groups everywhere intris or infr yes AV noal only with symptoms really and then third degree basically the same thing but most of the time we end up putting in a pacemaker in just because depending on whether first of all number one patients sometimes don't know when they have symptoms or not and secondly also depending on what the Escape rhythm is so if it's intris or infr his we definitely want to put one in um if it's AB noal we'll see but most of the time we end up putting one in okay and that's it any questions monitoring the chat for any questions I know we had one from uh Dr Oli was wondering about the P2P uh interval speeding up during sinoatrial you talked about oh the pp yes could we bring that slide up to revisualization as well because that was that was great see I'm sure there's an easier way of doing this no it's it's a nice retrograde review all right there we go here so basically when you're um looking at it just think about it like this right it's the same the reason the reason for your P2P getting shorter is the same reason that your r r gets shorter with second degree type one if you blow right so if you have your P if you have your PR interval right increasing but your p wve is coming when it's supposed to all the time it's just your PR interval that's increasing your RR interval gets shorter because your PP interval stays the same so when that happens your like so we're talking about second degree type um one for a noal conduction right and actually let me let me see whether I can kind of pull that up all right so see here right your PR interval goes from your PP interval stays the same right your PR interval gets longer and longer but your PP interval stays the same so your RR interval gets shorter so everybody sees that so it's a similar situation here with your um it's a similar situation with the um sinoatrial block here so I'll go here where you have your p p interval so if you think about your sinus node right coming in on top of this right so basically the p-wave is basically a sign that hey the sinus node the sinus node impulse has gone through the transitional cells and gone to the rest of the atrium right but let's say here the sinus node impulse is here here the sinus node impulse is there because there's a little bit of a delay it comes to this P here the isul oh sorry there we go do you see it now yep okay so let's say here sinos node impulse is here right and then it gets to this P wve here sinus node impulses a little bit over there but it goes over here right here your sinus node impulses back here and then it gets even longer over there let's look at the ladder diagram right sinus node impulse sinus node impulse sinus node impulse all of these are equal right however the delay gets longer right so your PP interval the interval between this and this and that actually gets short because the interval between this which is your sinus nodal impulse and your atrial conduction is actually getting longer and is the combination of two things your sinus node impulse is your PP or your sinus node your sinus nodal impulses are coming at the same rate right but your transition to to The Atrium is getting longer so therefore the pp the P interval which is basically the um manifestation of what's happening in the atrium actually gets shorter so marinate on it think about it a little watch this video again and I promise you it will make sense or you can just basically cram it and say hey if we see shorter PP intervals and we see a dropped one the sign atrial blog perfect St long enough you'll begin to believe it and then tosen looks like you had a question uh you can either put in the chat or or say it out loud if you'd like hello um Dr thank you very much for this wonderful um presentation so um my question exactly is if we have a patient for example we not dependent on them pacemaker before implants let's say type two um um second degree type two AV block and then we this patient got a pacemaker and GE over the years they became dependent on this Spacemaker what's the mechanism behind dependency in this patient like the electrophysiology mechanism what H what has happened to the conduction system I just wanted to understand I mean so the older you get I think Dr pazik showed a um really good um slide where he talked about fibrosis with time and so a lot of times you have increasing fibrosis with age and that just happens with I mean normally it's there in patients who need pacemakers you know it's there so it's just that increasing fibrosis typically will end up causing you to have increasing dependence does that satisfy the question yeah thank you very much no problem so I have been told in the past that there is you know a mechanism where the tissue just kind of gets lazy uh because of you know concurrent pacing is that have you seen or observed anything like that or do you think it's just Progressive well it definitely happens with it definitely happens with complete heart block where you have uh underlying pacemaker right so the sinus node is not working and so is the junction that's taking over or the AV node is not working and either the junction or The ventricle is taking over basically once you come in with your extra beat rather then whatever the Escape rhythm is is like okay great I don't have to work anymore and it basically checks out um if it's in the junction typically you know at least in a pinch it will come back in um but most of the time it it's there's a long pause before it comes in for the um for The ventricle typically that doesn't come back and so those are the ones that we want to put in the pacemaker sooner rather than later perfect thank you any other questions from the group pause for dramatic effect well I really appreciate you taking the time today I I know you have a busy day ahead of you still so um thank you very much for for this talk it was very engaging and I I really am going to watch this a couple more times before I understand that that sin atal stuff we'll get to the bottom of it um for everyone else for jumping on uh I apologize for bumping up the timing we just had some uh something we really couldn't control for so we wanted to make sure that we stay with our current curriculum and we'll continue through on to next week so if you didn't catch the first half of it I will get this posted on YouTube in the next um 12 hours or so it should be available for everyone it just takes a while to upload and then uh we'll go from there any questions you know feel free to to reach out to us and we're happy to answer whatever you may have and thank you very much Dr Carol for your time and this was uh this is fantastic thank you so much I really appreciate it thank you Dr Kuro really appreciate you really good thank you no problem take care bye thank you everyone [Music] um