Our next topic is bradyarrhythmias. Here are some readings for you to review. There are several different topics we can cover as it relates to bradycardia. We have sinus bradycardia, sinus arrhythmias, chronotropic incompetence, carotid sinus hypersensitivity, sick sinus syndrome, and atrioventricular block. As we work through this, there are clear recommendations and guidelines that the American College of Cardiology gives. I just want you to be aware of things like the class of recommendations. Class one is a very strong recommendation, along with quality of evidence. Level A is a very high quality level of evidence. These are the reasons that we use to make these recommendations based on who gets a pacemaker or who we recommend for additional monitoring. This all comes from the American College of Cardiology. When you're first evaluating a patient with bradycardia, the easiest thing to do is look for things that are reversible. There are a lot of medications that can induce bradycardia, and wouldn't that be nice if we could just stop a medication and someone's heart rate improves? Some of these are very obvious, like beta blockers or calcium channel blockers, certain antiarrhythmic drugs, and other things you may be less familiar with and maybe cause bradycardia to a lesser degree, but it can still occur. Things like SSRIs or tricyclic antidepressants can contribute to bradycardia as well, along with other things like anesthetic medications. Always look at a patient's medication list to see if there's anything reversible. There are certain conditions that are associated with bradycardia. Things like cardiomyopathy or ischemia can contribute to bradycardia because we can start affecting the cardiac conduction system. We know that infiltrative disorders, some of those rheumatologic disorders can do this, or sarcoidosis, rheumatoid arthritis, lupus can contribute to this. Evaluating a person's past medical history can give you clues as well to things that may or may not be reversible, but are helpful to consider when you're determining an etiology. Let's start with sinus bradycardia. So we can define this as a heart rate less than 60 beats per minute with a normal appearing P wave with an associated QRS. So here's an example of sinus bradycardia. This can be physiologic. Some people have a slower resting heart rate. For instance, highly trained athletes have an excellent cardiac output and they tend to have resting sinus bradycardia. People with increased vagal tone, medications, or ischemia should also be considered. Increased vagal tone can occur in situations such as vomiting. So patients who are vomiting or straining to have a bowel movement can increase their vagal tone and have bradycardia as a result. Clinical presentation is quite variable depending on their underlying physiologic reserve as well as how slow their heart rate is. Some patients are completely asymptomatic while others may complain of things like fatigue, shortness of breath, or exercise intolerance. The management depends on their presentation. No intervention is needed unless cardiac output is compromised or if patients develop arrhythmias as a result of their bradycardia. We can use atropine initially if we need to acutely manage them, but that's certainly not a good long-term plan. So we can also consider the possibility of a temporary pacemaker or a permanent pacemaker. Next is sinus arrhythmia, and this is quite common. It's very typical to see this in younger healthy patients, and this is defined as a variation in the sinus cycle length. Often occurs in young healthy patients, and you can create, you can induce your own sinus arrhythmia if you palpate your radial pulse and you take a big deep breath in, you'll feel your heart rate speed up because you're increasing venous return with inspiration. As you exhale, you'll feel your heart rate slow down a little bit. So that's normal to accommodate increased venous return from inspiration. So you'll often see this on an EKG, and what I'll do is I'll look for a pattern. So if I see a gradual increase in the heart rate and then it slows back down, an increase and it slows back down, maybe that person's just breathing normally. Oftentimes they're asymptomatic and we don't need to do anything for this. Most patients, if they have some increased automaticity, may have some dizziness or palpitations as a result. Most of the time, we don't need to do anything other than evaluate for symptoms, and then the management ends up being really the same as sinus bradycardia. Other times when this can happen that you won't see as often is things like digoxin toxicity that can also do this. Sinus pause. This is a pause in sinus rhythm and a failure of sinus node discharge. So there's an absence of atrial depolarization and possibly subsequent ventricular asystole that occurs. In this example here, this strip, you can see two fairly normal beats. It's a little slow. And then we have a failure of a sinus node discharge, a long pause, and then everything picks back up again in this strip. This could be maybe a person who's sleeping, who has some underlying sleep apnea. It could also occur in the setting of acute myocardial infarction. The sinus node can get fibrotic with normal aging, or this can also be excess vagal tone. So in sinus node dysfunction, there's no established minimum heart rate or pause where permanent pacing is recommended. It really depends on their symptoms, but the longer the pause, the more likely someone is to be pretty symptomatic from this, and patients can sometimes pass out if it's long enough. So you really need to try and establish that temporal correlation between their symptoms and their bradycardia, and then figure out if that person needs a pacemaker. And remember, always look for reversible causes. So it depends on the length of the pause, how they're going to present. And if a pause is occurring, if it's greater than three or four seconds while they're awake, they're usually going to be symptomatic from that. If someone is standing and they have a pause of more than four seconds, that can even be enough for them to pass out. Sinus exit block is kind of interesting. So this is an arrhythmia that you see a pause that results from an absence of a normally expected P wave. And so you can determine a sinus exit block by the duration of the pause is a function or a multiple of the atrial cycle length. So if I take two calipers, I'll get my marker here, so if I were to take calipers and I were to measure from maybe this one, this QRS to this QRS, and I keep that a fixed, fixed measurement, and then I slide that over to where that pause is, it's going to be the same. So it'll be a function of that atrial cycle length. That's what that means. So this could be from excess vagal stimulation, like nausea, vomiting, constipation. You can see this with myocarditis that starts affecting the conduction system, certainly a myocardial infarction or fibrosis, and then always consider their medication list. It's usually transient and no treatment is required. We can also see this under normal circumstances and well-trained athletes, or we can see this in some medications, particularly antiarrhythmic medications like flecainide or procainamide. Chronotropic incompetence. This is one of my topics I like to mention because I think we underappreciate and we under-diagnose chronotropic incompetence. So this is defined as an inability of the sinus node to effectively increase the sinus rate and allow for the physiologic demand that's present with activity. So this will be your patient that says, you know, I feel okay when I'm at rest, but then I get up and I try and do anything and I'm just so tired, which of course, you know, your differential diagnosis is very, very long when someone says that. But when we're considering the potential for a rhythm disturbance that might be contributing, you should consider the possibility of chronotropic incompetence. So it's frequently overlooked as a lifestyle limiting condition and a potential indication for a pacemaker. So we overlook it because oftentimes their heart rate at rest is fine. It might be a little slow, but it's not bad. The key there is that it doesn't increase with activity. So sometimes you can test for this, certainly with a Holter monitor, put a 24-hour monitor on them and tell them to be active, and you can look at heart rate trends and see if they're pretty flat. The other thing you can do is put them on a treadmill, hook them up to an EKG, and then gradually increase the speed, increase the angle, and you should see a heart rate increase. And if you don't, maybe there's some issue here. This can occur with patients with fibrocalcific conduction disease and patients will complain of fatigue and exercise intolerance. So sometimes these patients end up needing permanent pacemaker. It just depends on how you can correlate their symptoms to their rhythm output. Next is carotid sinus hypersensitivity. This is always an interesting one to work up to because there's so many different things to consider. So as you know, we have baroreceptors in our carotid arteries, and if you stimulate and apply too much pressure, you can have bradycardia occurring as a result. And normally if you can induce that, it's transient and it doesn't cause any problems, but for some people they have hypersensitivity. So they have reflex syncope when you massage their carotids. Certainly you want to make sure your patient doesn't have a big brewie or carotid stenosis before you start doing carotid sinus massage. But these are patients that have an abnormal autonomic response to sinus massage, and they'll have a ventricular pause for at least three seconds, and or they'll have a systolic blood pressure drop of greater than 50 millimeters mercury. So there's two different types. We say that these patients have cardio-inhibitory type, which is where they have the ventricular asystole, or they have vasodepressor type, where they have the blood pressure drop. Some people have a mixed type, so you have to make sure you understand which type they have because the treatment is very different. So vagal activation and or sympathetic inhibition, and we think about this a lot in maybe older males with coronary artery disease, and it's a type of neurally mediated or reflex syncope, which is a fairly large umbrella term. There's a lot of things that fall under that, vasovagal syncope, carotid sinus syncope, situational syncope are all types of that. But in this case, we can clearly draw a connection there to carotid sinus hypersensitivity. So suspect in syncope in a patient with maybe a history of turning their head, so they say they feel dizzy, you're going to pass that when they're turning their head, or maybe if they're wearing a tight collar, they don't normally wear like a shirt and tie, and it's too tight, and they have some dizziness or syncope, or if they're shaving, then that can simulate that hypersensitivity. So to evaluate this, we can perform carotid sinus massage, looking for a pause or hypotension. We can get things like certainly an EKG, blood count, basic metabolic panel to make sure there's no reversible cause there. And then tilt table testing is really helpful for differentiating between neurally mediated syncope and orthostatic hypotension. So as part of your evaluation, you should check their blood pressure in your office, lying, sitting, standing, and remember, you always want to pair heart rate and blood pressure and compare them. Carotid sinus syndrome, you would consider a pacemaker if it's cardio-inhibitory or if it's mixed. So if they have asystole in response to a tilt table test with recurrent unpredictable syncope, that would certainly be an indication. Now remember, pacing is not going to prevent a blood pressure drop in the vasodepressor form, so that's why it's very important to distinguish between the two. So in that case, when it's a pure blood pressure drop, then we want to think about things like maybe sodium retaining medications, compression stockings, lower extremity weight training to try and increase muscle mass and increase venous return. Sick sinus syndrome, we see this a lot in the electrophysiology world. So this is persistent spontaneous sinus bradycardia alternating with periods of rapid atrial tachyarrhythmias. So the classic patient will be someone that comes into the office and they have rapid AFib. And so you put them on medications to try and slow their heart rate, and now they have bradycardia. And then you take the medication off, now they have rapid AFib. So one of the key points to mention when you're talking to patients about this, because a lot of times they end up needing a pacemaker, is that the pacemaker doesn't fix the arrhythmia. It just allows us to treat the arrhythmia, the fast stuff, without making the slow stuff worse. That's the way I always explain it, because patients really struggle with that. And it's important to let them know, no, you can't stop your other medications, this will actually allow us to use medications to try and make you better. So the epidemiology, fibrocalcific disease, coronary disease, it can also happen in just healthy individuals. Patients will often present with tachycardia, palpitations, dizziness, near syncope, fatigue, and then management really depends on the underlying rhythm problem. So if they qualify for a pacemaker based on their underlying rhythm, their bradycardia, their pauses in combination with their symptoms, then a pacemaker is sometimes the best treatment for these patients. And it really allows you to more effectively treat their rhythm. So recommendations for permanent pacing techniques and methods for management of bradycardia attributable to sinus node dysfunction. So this is from American College of Cardiology. In symptomatic patients with sinus node dysfunction, atrial based pacing is recommended over a single chamber ventricular pacing. So if you can clearly identify that the patient has intact AV conduction, and the problem is purely isolated to their sinus node, then all you need to do is stimulate their sinus node to pace and capture, and then let that conduction go through as normal to the AV node. Anytime you can minimize ventricular pacing, that's the best way to manage these patients. Now if they've got sinus node dysfunction, and then they also have some degree of AV nodal dysfunction, then those patients end up needing a dual chamber pacemaker. So you really need to evaluate the individual patient and the clinical scenario. And then you can see how things change as you go through the different clinical scenarios there. But those are the common situations. We also have a nice flow chart here from American College of Cardiology, American Heart Association, and Heart Rhythm Society. So someone with sinus node dysfunction, the first step, confirm symptoms, rule out reversible causes. So if they need that goal-directed medical therapy, and their bradycardia is a result of that, like our techie brady syndrome person, or maybe it's someone with advanced heart failure that needs certain medications that can slow their heart rate, then that's a class one indication for permanent pacemaking, for a permanent pacemaker. And then you can see as you progress down through that flow chart where you go from there. So always consider reversible causes, and then think about what am I trying to fix here? What is the indication for a pacemaker, what are their symptoms and what's the end result I can expect to see from putting in that pacemaker. After you do that, you need to decide, do I need a single chamber or a dual chamber pacemaker? And I explained the rationale there. Atrioventricular block, we've got first degree, second degree type one, second degree type two, third degree, and then we also have what we call high grade AV block. So we talked about sinus node dysfunction and the different varieties there, indications for pacemaker. Now let's talk about some other types of block, heart block, and when these patients might need a pacemaker. So a first degree AV block is really a delay. It's not so much a block. It's a delay in the spread of an impulse from the sinus node to the AV node. So this is like you're the sinus node and you're standing and you're talking to someone and it just takes a little longer for them to hear what you're saying, but they hear it. So this could be from fibrocalcific changes. So just normal calcification within the heart with aging or medications can do it. And these patients are usually asymptomatic. So they have to have a pretty significant first degree AV block for them to have symptoms. So management, we don't normally have to do anything for them unless they develop symptoms. One thing I always make a note of is to, if they have a first degree AV block, I want to always look for a concomitant heart block they might develop in the future. So that's the patient who's got an asymptomatic first degree AV block, maybe a year down the road. Now they've got a left frontal branch block. When I have a combination of those two things, it's something that I want to watch closer. So here's a first degree AV block, just a delay in the conduction of spread from the atria to the ventricles. And you can eyeball this really easily by finding a QRS as I have marked here, that falls close to a thick dark line, and then look at a P wave that starts, remember it's the start of the P wave, more than one large box before. So 200 milliseconds, that's a first degree AV block. Second degree type one. So this is the sinus node standing and talking to the person in the ventricle, and they're just walking farther and farther away. And then all of a sudden the ventricle can't hear them. And now we have a drop B. That's the second degree type one or a wanky box. So progressively lengthening PR interval from cycle to cycle prior to a dropped QRS complex. So in this example here, your eyes are going to be drawn to that dropped QRS. So we see right here, there's a dropped QRS. So I've got lots of things going through my mind of what this could potentially be. But when you consider a Mobitz type one or a second degree type one, always look at the PR interval immediately after and immediately before. If you see the PR interval is a little shorter, and then it's a little longer before it's dropped, now you're thinking of Mobitz type one. And then what you do is just trend that pattern out. So after that drop beat, you should see the PR interval get progressively longer and longer until the cycle repeats itself. So something that makes this one a little different that you want to consider is the possibility of sleep apnea. I always think about obstructive sleep apnea in patients with heart rhythm disorders of any kind, but certainly patients with heart block and this type of heart block in particular. So that could also be from those fibrocalcific changes. You can see this in an inferior MI or really any type of MI, but when we have an inferior MI, that right coronary artery, we're thinking about the possibility for adenodal conduction being disrupted. And then clinical presentation, they might just have some mild dizziness. They may have fatigue. They can have near sycopy depending on the number of drop beats that they have. So if they start dropping beats more and more frequently, they're more and more likely to get symptoms related to this, but usually they're fairly asymptomatic unless it gets progressive. So we treat a reversible cause if it's present, we treat with a pacemaker if they have significant pauses and then we weren't for monitoring. It warrants monitoring for progression to see if it's getting worse. So this is someone that you're not going to say, well, we'll see in five years. So you want to make sure that you're monitoring that on a routine basis to see if it's getting worse or if they're developing symptoms. Now, in contrast to a MOBIS type one is a MOBIS type two second degree AD block. So this is more serious, less common, and it's associated with a punctual P wave. That's not followed by a QRS complex. So there are a couple of keys here to differentiating between these two. So step one is that you'll see just a drop beat that comes out of nowhere. So your eyes are drawn to that drop beat right here. But then if I follow the same pattern where, let me look at the PR interval before and after you'll see that it's completely normal. So in this case, the PR interval is long, but there's no progression. So it's normal relative to each other. So I see a PR interval that is fixed and it doesn't change whether that's wide or whether it's normal, it doesn't change. So that PR interval is fixed. There's an unpredictable dropping of a QRS that I cannot say, oh, it's going to come sometime after this one. And you'll, the other thing you'll notice about this is that the QRSs are wider in this one because it's located in for Hisian. The lower in the conduction system a block is, the more likely it is to be associated with a wide QRS. So these patients are more likely to present with things like near syncope, syncope, dizziness. They're not usually asymptomatic and these people need a pacemaker. So that's why you can't miss it. And then the last type of heart block is third degree AV block. And this is defined by AV dissociation. Now we talked about AV dissociation as it relates to ventricular arrhythmias. But in this case, what happens is you have a P wave. Just remember the P wave just does its thing. And then it doesn't care about anything else. It takes the rest of the day off. So with this one, the P waves are just going to march on through, and then you'll see there's a lack of conduction from A to V. So what happens is an escape rhythm takes over. So AV dissociation means I see P waves that look normal. And then I see QRSs that are regular, but there's no association between the two of those. So in this example here, we'll see a P, I see a P wave here. So if I just look at this beat right here, I might think, oh yeah, I mean, the QRS looks wide, otherwise it looks pretty normal. But then I see this one and I think, ooh, I don't know that that's a physiologic PR interval right there. That doesn't look like it is. And then I get down here and I see a P wave, nothing, a P wave, and now I should start being suspicious of third degree AV block or complete heart block. So what you want to look for is P waves that are normal and regular, QRSs that are regular, but there's no association between the two. And the atrial rate is almost always faster than the ventricular rate. Common mistakes I see people make with this is they will look at this and just call it a left bundle branch block or a right bundle branch block. Now, remember, think about what's happening. This is an escape rhythm. So it looks, it will oftentimes, if it's coming from the ventricle, it will take the appearance of a left bundle branch block or a right bundle branch block because it's an escape rhythm that's occurring in the ventricles. Sinus node works, AV node doesn't work, nothing else works until now we get down somewhere in the ventricles. And the lower in the ventricles it is, the wider the QRS and the slower the rate. So you always want to make a note of that because if a patient has complete heart block or third degree AV block and their heart rate is very slow, I should be much more concerned about that patient because I know there's nothing else left after that. Their presentation will depend on the ventricular rate. I've seen patients with complete heart block that are asymptomatic at rest. Their heart rate's 55 beats per minute and they're fine until they start trying to do something. And then they have no increase in their heart rate because their sinus node is not conducting to the AV node. So they're unresponsive to that activity. Then I've seen patients who come in just with syncope and their heart rate is 20. So it really is variable depending on that individual person's conduction system and where in that cascade they're at. What line of defense are they at? The management, always treat reversible causes, otherwise permanent pacemaker. And that goes for any of these patients with heart block. So always treat reversible causes. If someone's on a medication that you can take away and their symptoms get better, then that's great. But usually things like a Mobitz type 2 and a third degree AV block, they're usually not reversible, but you certainly want to look for things like hyperkalemia. That's something you can sometimes reverse and they don't need a pacemaker. So always look for those things, but most of the time they need a pacemaker. So how do we evaluate the bradycardic patient? Step one, look for reversible causes. Then we always want to get a 12 lead EKG and we're doing that to get more information. So if one lead is good, 12 are better. So always get a 12 lead EKG to look and see exactly what's going on. I want to get as much information as I can about that patient to make an accurate diagnosis. An ambulatory monitor is a great next step. We want to try and correlate their symptoms to their EKG findings, because remember American College of Cardiology says this is how you decide on whether or not a patient needs a pacemaker for a lot of these rhythm disturbances. So get an ambulatory monitor and we'll talk about some options for that here in a minute. There are indications for an implantable cardiac monitor as well. So a lot of the ones we use are ambulatory that we put little patches on their chest, or we have these little cards that they can hold over their heart to record things. But we also have implantable cardiac monitors. So maybe you've got a patient with syncope, but it's not occurring that often. And we've tried ambulatory monitors and we can't really figure out what's going on with this patient. We can put an implantable monitor in, which goes right underneath the skin. And then I can interrogate that just like I would a pacemaker at regular intervals. And I can see if there's any underlying rhythm disturbances that we haven't been able to catch. So think about other things that you can do as well, like an exercise EKG for chronotropic incompetence, someone that has two-to-one AV block. So two-to-one AV block is this picture right here. So with this one, I can see for every two P waves, there's one QRS. So P wave, P wave, QRS, P wave, P wave, QRS. So two-to-one AV block, we call high grade AV block. It could be a Mobitz type one. It could be a Mobitz type two. There's some things you can look at, like if the QRS is wide, it's more likely to be a Mobitz type two, but the bottom line is they're dropping every other beat. That's not good. So in someone with the two-to-one AV blocks, sometimes if you exercise them and you can get their heart rate to change a little bit, that means they have some type of conduction from A to V that might improve. So that can be helpful. An echocardiogram should be done in a patient with heart blocks, certainly if they got like a new left bundle branch block, or if they've got advanced heart block, or maybe you're concerned about the potential for some drop in their LVEF that might be contributing their left ventricular ejection fraction. A sleep apnea screen is done, particularly in patients with things like Mobitz type one heart block. And then electrophysiology study or EPS, this can be done if they have symptoms that are suspected to be due to bradycardia when their non-invasive evaluation is non-diagnostic. So this would be certainly a later step in your evaluation. Cardiac monitors, there's lots of different types, and I feel like we're constantly making amazing advances in different things we can use. So different types of monitors and when you might select them. The common ones we use, a 24-hour Holter monitor is great, and I always think about what information am I trying to get from this? How is this monitor going to change my treatment plan or help me with my diagnosis? Think about the patient themselves, what kind of symptoms are they having? If you have a patient who says they have near syncope once a week, well, a 24-hour Holter monitor might not catch that. Maybe you need something that they can wear for a week or two at a time or longer. So a Holter monitor is really nice though if you want to try and correlate their daily symptoms with an underlying rhythm. So I can get a daily heart rate range, I can get a total number of premature beats, for example, over 24 hours, and I can calculate a percentage. If someone is having symptoms that occur every day, a Holter monitor is a great option. Patient activated transtelephonic event monitor is something that we can use for patients that are having symptoms that occur less frequently, and that's similar to an external loop recorder. So these sorts of things, if you record with loop recorders, they're going to record, they hit a button and it'll record a little bit before, a little bit after, so that gives you more information, for example. There's also external patch recorders, which are an alternative to an external loop recorder that are leadless. So those are things that might be more comfortable and less cumbersome. So a lot of these other monitors, they have to wear one or two little patches and they take it off when they get in the shower and put it back on, and so some people find that to be a little cumbersome. So there's lots of different options for what we can use. And then moving up the line here, we have things like a mobile cardiac outpatient telemetry, which is where the patient will be monitored for regular, over a period of time regularly, and then an implantable cardiac monitor we already talked about. So lots of different options for cardiac monitoring. Pacing. Permanent pacing is recommended regardless of symptoms. If someone has a Mobitz type 2, so second degree type 2, high grade AV block, third degree AV block that's not reversible. All other types of AV block, in the absence of progressive AV conduction abnormalities, pacing should be recommended only in the presence of symptoms that correlate with their AV block. So you've always got to, number one, document the rhythm disorder and then figure out does it correlate to symptoms if they have symptoms, and that's how you make your decision. If their LVEF is less than normal, and there's clear guidelines for this, and they have some type of AV block with an indication for pacing, and you expect them to require ventricular pacing more than 40% of the time, so this is someone that does not have intact AV conduction, where I think they're going to need to pace from their ventricle, we want to provide more physiologic ventricular activation as opposed to just right ventricular pacing. If you put just a pacing wire in the right ventricle, and you constantly pace the right ventricle before the left, you end up with two ventricles that are a little bit out of sync, and if someone already has heart failure, then you could potentially worsen their LV function, and you can worsen their heart failure over time. So those patients we consider for cardiac resynchronization therapy, where sometimes we can put an additional wire over into their left ventricle, and now we force those ventricles to beat together, and doing that, we can oftentimes improve their symptoms, and sometimes improve their LVEF as well, so it's a great option, and there are clear indications for who should be considered for that. And here's my last slide. I just wanted to put everything in one place, as I did for the sinus node dysfunction. Here's some ACC recommendations for AV block, so we can see the different types here. The first degree AV block, second degree AV block, different types of heart block, and then what types of symptoms they might have. Are they responsive to your initial line of treatment? What are their symptoms? And then you can go on the line, down the line from there, and then once we decide that someone does need a pacer, then we can think about what type of pacemaker do they need, single chamber, dual chamber, or resynchronization therapy. When we discuss pacemaker and defibrillator therapies during a later lecture in this module, we'll go into that in a bit more detail. So that concludes my discussion on Bradyarrhythmias, and I hope you found it helpful. Thank you.

bradyarrhythmias

slow heart rate

sinus bradycardia

sick sinus syndrome

atrioventricular block

pacemaker placement

EKG findings