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MFFD: Cardiology 2

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Summary

This medical teaching session is relevant to medical professionals and covers cardiology, with teaching from a clinical fellow in the field. The session focuses particularly on atrial fibrilation and bradycardias, and how best to approach patients with either condition. Attendees will learn how to correctly document and diagnose arrhythmia, as well as review key guidelines and discuss practical approaches to management.

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Learning objectives

Learning Objectives:

  1. Understand the definitions of paroxysmal, persistent and permanent atrial fibrillation.
  2. Recognize atrial fibrillation symptoms and be able to accurately document them in medical records.
  3. Understand the appropriate next steps for working with a patient experiencing atrial fibrillation symptoms.
  4. Describe the medical management strategies for atrial fibrillation.
  5. Analyze the benefits and risks of various therapies for atrial fibrillation.
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Computer generated transcript

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The following transcript was generated automatically from the content and has not been checked or corrected manually.

All right, guys. Thank you for coming again. And today's the second lecture on cardiology that doctor cognitive is doing for those who were there yesterday. You know him already? Those who don't who are not that he's a clinical fellow in medicine with a special interest in cardiology. And that's the second lecture we are doing today on cardiology with me as, um, in terms of the six. PM serious. I'm sure most of you know, but you can find us on instagram, Facebook, twitter and, um also big. Thank you. Tour expenses that m D u I'm now going to like, Teo condom take over and present. Thank you already. Well, how everybody? Yeah. So I'm kind of I've ah, I'm a clinical fellow. Medicine and teaching as well, unless Severe said I do have an interesting cardiology. Um, I have been working very recently in cardiology department in core More hospital, with time on on the card in the care unit and of also had some experience in critical cast. So I've got really good mixture of experience with cardiology, and at the moment, I spent a lot of time in EDS. Well, so see people coming through the door. So let's talk a little bit about what we're going to talk about. So the context of today's lecture it is slightly contrast ing it zoo finish off. Talking a little bit about tachycardia is with a focus specifically on actual fibrilation, which deserves a really section of his own. It's something that you get quest on a lot. It's very, very, very common on If you understand it well, you can get yourself some good points in exams, and also you can really make a difference when you're looking after patients on the ward's. Um, we're also going to talk about bradycardias. So Bradycardias as a as a sort of set of material, has less content than tachycardia. So it does occupy less volume than the previous lecture. But it does have some really key points in it, and I try to distill those down for you and talk about how you would approach somebody with the bradycardia on again. We'll be using some really robust guidelines from the less um, they I had a team. Um, really, I just want you to feel a bit more confident about from Bradycardias by the end off this lecture. So what does it matter? Well, we talked about it that this yesterday there's loads. People with a f is loads of people who you will see where it really makes a difference to their life on There's a lot of drug treatments on suppose Importantly, really, for you guys, it comes up in exam, so it's definitely worth knowing. Um, so we're going to start with a bit of ah, sort of warm up a bit of a question. So this is the first case. It's a case off a 68 year old man. He came in to me two days after elective D C C cardioversion for a F. Onda. He thought that this cardioversion was gonna basically cure him of atrial fibrilation. He obviously how this explained to him, but not necessarily understood it as well as he could have done on you was quite upset. He was examined on D in the GP surgery and the C G should he got atrial fibrilation on. We did everything we could for him in general practice at that time. Um, when I was working in in Coral in a general practice on, unfortunately, he remained in a F on. We had to proceed to a rate control strategy instead. So really, this is about Namenda future. So how would you describe this patient? Say arrhythmia. Is this paroxysmal left persistent F permanent F p atrial flutter or don't know. So you might wonder the my think this is very strange question to start on and it doesn't matter what day it does. So this is very, very similar or better copied often MRC Peapod One question so it does come up on is important in correct documentation in the notes and misunderstanding. The fundamental bit will make it harder to understand why we're doing what we do in later on. So a little slightly easier started for for 10. Really? Um or great got lows. People answering already fantastic on that. See what we've got. So we've got sort of a split between and see with about 15 to 20% on each of those. And then we've got most people going for persistent atrial fibrilation. Very good. So the answer is permanent Atrial fibrilation and I will explain why that is the case in this particular scenario. So class fine, f You've got paroxysmal persistent and permanent A. F now parents is small, so this is based on the nice guidelines and how they defy their terms, which is taken from the European site of cardiology guidelines. Um, so paroxysmal A f is atrophic relation, which is defined as to warm or episodes, which terminate spontaneously so they have to stop on their own, which means, without pill in the pocket treatment without DC cardioversion on. But when patients in those episodes, they have to have been thought to last less than seven days, which is usually determined by how long the patients describe their symptoms for, um, or more. More commonly nowadays, sometimes it's been picked upon smartwatches on they, they demonstrate. People have had a f for, you know, a few hours in multiple periods of time, persistent a F and permanent F, or mortification to explain. The difference is between, but they're very well, the tips of defined in in the documentation. So if something's is described as persistent again, it's two or more episodes, but in this case, it doesn't self terminate. So this is an A an atrial fibrilation, which can come and go on doesn't go away on its own on. Usually these episodes last more than seven days on this is the your patients who come into e. T. Um, have some treatment. Managed to go back into Sinus rhythm through tablets through direct cardioversion on. Then within the year they represent a CT again in another episode which needs resolving on. Although you can resolve it, it seems to seems to keep coming back. Um, so permanent F then is continuous atrial fibrilation That has to have happened for for more than a year, period. And it has to be very difficult and resistant. Cardioversion. Um, typically, we use rate control strategies in these patients, although there are some methods of really trying to to revert somebody in Sinus rhythm in extreme circumstances. But we're going to talk about some of those options later on. Right. Then let's move on to the first sort of full case. So the question is, what is the most appropriate next most appropriate step? So we've got 58 year old retired Laurie driver, and he's commences after he's experiencing episodes of Palpitations, which he describes is lasting about 30 minutes at a time. They occur on most days on, he describes them as his heart racing, So he thinks he's got fast heart. He gets them for about 30 minutes. Most days he's not dizzy with them, is not lightheaded. And he's very clear that he's not lost consciousness or collapsed on. He admits he was bit nervous telling us about all this in the context of him being a lorry driver. Um, he's got Type two diabetes, high BP and gout in his background. When you see him, he's overweight with a raise B M I of 39 on you palpate his radio ports, and he's got a rhythm which now appears to be regular with the rate of 80 on. So you perform any C. G. And he does have a normal Sinus rhythm on his STD with the rate of around 80. So, in general practice, what is the most appropriate next step? So you're gonna order an echocardiogram? Are you going to order an outpatient 24 hour tape? Are you going to arrange for a two week cardiac monitoring or you're gonna refer to cardiology? Well, I don't know which is equally acceptable on a Friday afternoon. Ah! Oh, I got got loads of response is already great. We're gonna give you guys about 40 seconds to respond on each question, just so that we've got time to get through the content. So I'm sorry if that feels a little bit quick. For some people, it's just a balance, really, To try and make sure we can get through everything and he will have access to the slides. Well, after, of course. Fantastic. So we've got a really self predominance feel uncertain. Be which is correct. So why is that correct? Answer? Well, let's talk about what the wrong answers. Our first so referring to cardiology F. It's so common that simple management of a F and see what just just described a simple air for a half without a complex problem, um, is usually managed in primary care. Wasn't referred to cardiologists. If it waas, you would need a lot more cardiologists in terms off the next steps. Then you're really choosing between whether you're doing the functional heart scan like an echocardiogram looking at the pumping function of the heart, or whether or not you're going to monitor somebody's heart rhythm and in the context of a half the first thing is to determine that they've definitely got rhythm abnormality. So that brings you between the 24 hour tape on the two week SCG. Nice guidelines will tell you that the first line things do is a 24 hour tape on. In this patient's case, that is sensible because he's having episodes every day. So it's likely that you will capture something in that 24 hour period with regards to the echocardiogram that does end up being part of the management of atrial fibrilation, but you need to confirm it first. So it's confirmed first on electrical monitoring through through a 24 hour EKG, Um, that you'll see here. This is part of the nice guidelines on they describe a baseline echocardiogram. So it's a non urgent outpatient echo, basically just to measure heart function in part of the work up. But it's not the first line thing to do, so why put together here? Hope puts a little bit of what we've talked about together into a bit of a framework that will help you just remember the basics of how you type on investigate a F say if you've got patient who has presented either with symptoms or with something that sounds like it could be a F on. Do you think that they need investigating for a F. U? Examine the patient If they've got an irregularly irregular pulse. At that point in time, do a 12 lead e c g. If that shows that they've got a tree fibrilation by which by features of atrial fibrillation's the absence of peewee waves and irregularly irregular rhythm wandering baseline, Um, then you can diagnose f there in that if someone has presents to you, but they don't have an irregularly irregular pulse, but their symptoms have described is approximately daily, like our gentleman than a 24 hour EKG is likely to be first line investigation on that will either confirm or or not confirm atrial fibrilation if the patient doesn't have symptoms daily. So this might be somebody who's having occasional fast heart rates or occasional sensation that they've got palpitations. Maybe once a month. The olds of you capturing it on a 24 hour recently quite low but in the community often toe access to week E C gs or longer methods of observing someone's heart rate. You have to start by performing a 24 hour E c G as just part of the referral protocol. So they really still need a 24 hour east. In some practices and in some parts of the country, you could go straight to arrange in a two week EKG. And in fact, in some places you could even go to referring to cardiology. Things like a leap recorder, for that's unlikely. So in terms of examines, it's 2024 hour EKG, and then an echo laid down the line. If you confirmed atrial fibrilation. So once you've confirmed after what you're gonna do well, there are kind of two things you can do face to fibrilation. There's rhythm control, and there's rate control. Rhythm control refers to you trying to get the heart rhythm out of atrial fibrilation. But in Sinus rhythm, great control refers to reducing the patient's heart rate whilst it's in a tree fibrilation to a level which means the patient is asymptomatic on delouse, their heart function as normally as possible. Um, we'll talk about which types of preferred and when solid later on. But we're going to start with with, um control. So there are kind of two ways of trying to put someone's heart rhythm back to normal. You can either do it with drugs and tablets and medications, or you can do it with electrical means. So that includes things like giving people DC cardioversion. But it also include clued things like ablations on base makers and that kind of thing in the context of rhythm control. When you're thinking about exams, they're kind of a few different ways they can present these questions. Essentially, you've got either your patients with new F who had never known to have had a half before who were managed on a specific pathway. Or there are patients. You've got no Nayef who have existing treatment in place. They're manage started differently. But we're going to talk through protocols the day which I hope will help you to answer both of these questions when they come up. So they already in control then? Well, the nice guideline say that actually, rate control, which is just to put a heart rate into a comfortable zone, is the first line for all patients except in these four clinical scenarios. So if there's a known reversible cause, um, so, for example, patients who have taken drugs. Patients who've had extreme stress is patients who have had some sort of previous electrical abnormal electrolyte abnormality, which you could reverse if they've got heart failure and they develop a F, then we know that they're mortality. Outcome is worse, so in those circumstances, it's better to try and be back into a Sinus rhythm if it's new onset. So if this is the first episode of New F, they should be tried to put back into normal science rhythm. Oh, if I Rhythm control is felt to be more appropriate based on clinical judgment, which is kind of a get out clause of way of saying that if you think there's a particular case is, it's more important for them to be rhythm control, then that may be the case. Andrea Lee The cases that I've seen where that happens is where patients who were in a F have really extreme symptoms that they just can't manage. So I've seen three or four ladies in GP who their lives there, so debilitated by the sensation of palpitations it makes him very anxious, makes him very worried, quite frightened about stroke on, although actually, you can do a lot to try and alleviate those concerns. For that, I'm trying to get them back in Sinus rhythm. Rhythm was the right thing to do, even though they they've had multiple episodes of going back into a F despite rhythm control treatment. So they were. They were put down sort of more complex pathways. Right enough of me talking, that's to another case. So what is the next most appropriate first line management? So this is similar to another case, which I've seen Reese Well, not recently. About last year, 48 year old fireman came into TD. He'd had palpitations, and he knew exactly when they came on. It was six PM the previous day, after he'd had a really hot curry. He described this really fast, funny feeling, heart Pete's, which he tapped out for me on the desk in an irregular pattern. He was otherwise very fitting. Well, it had a work medical, a spot of his fireman, sort of training and general care, including an echocardiogram, which was amazing, which was completely normal four months ago. Um, I examined him. He was slightly high B M I, although I think part of that's from? Because he's very muscular. Uh, it got heart rate of 138 but he got a normal BP. 128 over 68 is respiratory. It was 18 year normal saps. He had a normal temperature on the nurses. Did Niecy gi for me, which demonstrated a drop in relation with a rate of about 1 38. And at that time, I tried some vagal maneuvers, so I tried rubbing his neck. Um, just to see if that would make any difference. I think in that circumstance, what we should have done wasa a blowing into a 10 mil syringe in doing a modified valsalva. But we did do it. But we did do carotid Sinus massage on him, and it was unsuccessful. So what is the next most appropriate first line management for this gentleman who presented with new A F as it Digoxin? Is it by supper? Low is the amiodarone. Is it flecainide adenosine? Okay, have ago. Some always worth a guess. You learn more from getting things wrong. I need if you can things right. Good. Okay. So sometimes this teacher is really nice to see people get the right answer, but sometimes is actually really nice to see people getting a spread of answers or getting it wrong, because there's a lot to be learned when you know the context of what you're teaching is is hard enough. So so it's good to see the people have got B is mostly the correct answer bomb. I'm not disappointed that people have also got some of the wrong answers I'm going to talk through. Why Theanti is are. The answer is that they are so digoxin is not correct, so it's not typically first line for new New A. F is occasionally used in a F with heart failure. On If patients are immobile with a F and elderly, then occasionally digoxin is more appropriate first line treatment. But that's not necessarily on guidelines. The first line is by supper low, Um, and in a muscular large gentleman of 5 mg dose is appropriate. You could go lower and try to 0.5 and then slowly increase, Um, but 5 mg sounds about right for the man that I make the visualizing in my mind Amiodarone, same utterance. Love by cardiologists pretty much always reverse people. Sinus rhythm but it takes about 24 36 hours in patients. You've got really resistant arrhythmias, and it's got loads of horrible side effects. It's worth reading about it, just come up in exams. But that's actually third line, so that's even further down. Um, so flecainide then. So you may have heard that this is a tablet. Sometimes people have a sort of pill in the pocket at home way of putting them back into normal Sinus rhythm. Uh, that's considered a second line treatment, um, in a structurally normal heart. So I think the other one of the high aren't It was it was the dentist seen and I think people are thinking about the treatment pathway with the F tachycardia ls guard line from yesterday. So adenosine is used in S V T. But but more specifically, a F as a form of SPT is treated with beater blockers. And if you follow that pathway down, if it's irregularly irregular and it's narrow, complex than first line is recontracted, which is which is by stop along 5 mg, and that may also revert in Sinus rhythm. So I put a little protocol together, which I think you might be able to get a copy off afterwards if you complete the feedback. So this really is what can talk through today I've covered up a little bit off because I'll give you the answers away for later on. But if you've got a patient with new A F who's got no adverse features, which is something we talked about yesterday, then you need to think about whether they've got any of those four things that we talked about, whether or not you should choose rhythm control. So did this one of a reversible course. Yes, he had a curry yesterday. That was way too hot. Um, did you have heart failure? No. Is a new onset? Yes, it waas. So that's another reason we should put him back into normal Sinus rhythm on diet. Think you know the clinical judgment is that written control is appropriate for this month. Did it take us more or less than 48 hours? And this is really important because if someone is thought to have bean in a for more than 40 hours, there's a very significant risk that because off the poor flow in the atrium, that clot may have formed. So when you've got all that turbulent flow from the atrial atrial, not contracting normally o'clock informed on Gwen, you put someone back into Sinus rhythm. There's a theoretical risk that that clot will then get thrown out of the heart and cause a stroke. We know that this gentleman had a curry and then had symptoms at six PM yesterday. So it's within 48 hours. So what we would do is we'd give him some heparin on, then would consider a B two blocker, which is what we did. Three only sort of caveat to that which some harder questions my ask, although I hope it wouldn't be in your fifth year finals, but it is certainly coming up in, um, RCP. For those you want to do. Medicine is you've got to be cautious, given be two blockers to asthmatics because, um, you may know salbutamol is beat two agonist antagonist. So be two blockers cause consistently asthma attacks is there's a risk of be two blockers in asthma and in those patients who use calcium channel blockers instead, if I eat, a block has failed. We talked about this. Our second line treatment is to consider flecainide Flecainide you have to be careful with because there are some really significant risks that can happen with flecainide if you have an abnormal heart. We know in this gentleman he had a structurally normal heart because he had an echo formula months before. So if the B two blocker it failed, we could have considered flecainide. Um but there are some really risks of flecainide, which we don't have time to talk about today, but worth reading about if you're interested on flecainide and amiodarone would only really be considered in secondary cast. You wouldn't be giving them in GP, and you certainly wouldn't be given them without any senior support. Ondas, a junior doctor. You'd be more than confident if you're safe and you were doing appropriately to give a B two blocker. But I wouldn't expect any of you started giving flecainide around me around on your own. If all of that fails, or if we think this has been over 48 hours. What we really need to do is to antique regulate somebody for three weeks and consider them for a DC cardioversion as an outpatient. We talked a little bit about DC cardioversion yesterday for those who were here. But I'll quickly run through what that is today. So DC cardioversion is providing an electrical shock across the heart, which is time specifically along with the patient's rhythm, so that the shock happens on the R wave off their heart rate. And the idea is that that puts them back into normal Sinus rhythm that differs from defibrillation, where you apply shock across the heart, uh, in no relation to their existing rhythm. Okay, and that's usually done under light sedation because it's not very pleasant for the patient, So that's move on. We do. You ever break a little bit of the way through, so if it is going to get first, we will have a little little break in a while. So the patient asks you what else can be done? So this is a 78 year old retired vet who has come into GP to discuss symptoms off what he knows to be persistent atrial fibrilation, and it's had this diagnosed for a long time. Now, um, he's out of routine echocardiogram, which demonstrated that he's got a large left atrium on days, got a normal heart ejection fraction of preserved ejection fraction but a large dilated left atrium he's on and regulation with warfarin, and he's on 10 mg of bar soap opera or check and tell you was the maximum or all dose previous treatment that he's tried. He's hard episodes of DC cardioversion on more than one occasion, which have worked for a short while. But then he goes back into a F on. When he's in normal Sinus rhythm, he feels like a new mountain. He feels really well, and he really wants to be in normal Sinus rhythm. Um, is even tried to jocks in as well, which was unsuccessful. When you examine him, there's no evidence of heart failure on his heart rate is 78 it is irregular. So you confirm is in a uh so the patient asks you whiles can be done, So let's give people to go on this one. So we're gonna add in verapamil. Are we gonna offer him pill in pocket flecainide we're gonna add in diltiazem we're going to start amiodarone or we're going to refer him to cardiology. That's great. See everyone answering even That's Friday. Hold on. Okay, good. So there's a bit of a spread, but there's a predominance for referring to cardiology, which is the correct answer. And the intention in this question is less about necessarily knowing exactly what to do. But knowing went to escalate to to an expert. There are a couple of things I just wanted to highlight with this case just about safety and medications around a half a swell. So let's start at the top then. So adding in verapamil, why can we not do that? There's a risk that if you add in a rate limiting house channel blocker like verapamil in context with by stop roll that you can have a complete heart block so you can't have the both of those very particular medications together. There are some medications that you can mix with Barcelona also rate limiting, but no verapamil. Um, which you may know from doing your prescribing exams and that kind of thing. So do just be careful about that. Bye, Connie. Offering flecainide what we talked about this before. He doesn't have a structurally completely normal heart, has got dilated in large left atrium on. The risk is that if he's developed some alternative conduction pathway as a result of his heart muscle dilating If you give him flecainide rather than his heart's signal going down a normal um, normal is normal conduction pathway down through his atrial down, his bundle of hiss and office back injury fives. There's a risk that that can go down and alternative pathway by giving him flecainide. And in doing so, you can trigger really dangerous. It with me is so he can't have flecainide. Um, we could add in diltiazem. But in his particular cases, rate is actually quite well controlled, so it's probably not gonna make him go into a Sinus rhythm. Andre, his rate is already at 78. Um, can we consider on the odor and, well, this deceptive? There's a potential that amiodarone might be an option for him, but that can't be started in primary. Care has results in secondary care, So you're gonna refer him to cardiology on. He needs a consideration off these things. We're not going to go into them in detail because they're beyond the scope of what you'll get examined on a Z 1/5 years in a junior doctor level. But it's worth knowing about them. So the thing on the left demonstrates what happens in ablation. So atrial fibrilation. One of the options is to try and find that night. It's off our office of abnormal signal in the atrium and try and burn it so that you don't get that spontaneous arrhythmia happening. And the idea is, if you correctly have late all of the bits of the patient, um, that there's of generating the fibrillator, we waves that you could potentially stop him having extra fibrilation. It's actually less successful than you might think on. I think it's I couldn't tell you an exact stuff, but a lot more patients done is desirable. Go back into a F after having a f ablations. Um, ablations are more successful in cases of flutter on congenital heart problems, so they are used fatal fibrilation. But they're not always successful, which is why they're much further down the line. You have to pick the right patients for that procedure. Um, this medication in the middle so too low so medication ends in law, so you might think it's a B two blocker. It does work, uh, to be to block it, but it's also got lots of other effects and on actions on the heart. It's 1/5 line option, which is only started in secondary care, and occasionally that medication can keep people in normal Sinus rhythm better than something like buy salt prolonged can. So that is an option that secondary care can start, although it's not usually start in primary care. And then that thing on the right is a pacemaker on. It's probably on your screen. Bigger than one is in real life, I imagine so. Pacemakers are sort of less than half the size of a deck of cards now in terms of surface size and in terms of thickness that probably part a size again of a deck of cards and thickness. They sit in the patient's prepectoral pocket on the side of the chest, and they usually used for patients who have got bradycardias. We'll talk about later in episodes of really severe, a F, which aren't responsive to treatment. Um, occasionally you can use something called it a blood on oblate and paste pathway. So what you do is you completely disrupt the signal from the Atria and the ventricles, Bible ating, all of that conduction tissue on, But that means that the patient no longer is able to stimulate their own heart rate. And so you knock off all their own rhythm and you give them one by putting a pacemaker in and stimulating one. So you kind of take over. Um, it's really obviously quite late down the line in terms of treatment, cause it's a significant procedure and it carries risks. But for patients with severe, debilitating A F or patients with a F with significant heart failure, it can be an option. Okay, so we're moving onto Ah, quick, quick one. Really? So you just come to this lecture tonight? You've thinking everything about if you go into the ward's tomorrow on DA. Well, not tomorrow. So Saturday is that you go into the awards on Monday morning on drily mean cardiologists says, Oh, well, you think you know if they have I f Then by what mechanism does, uh does amiodarone work? And you think, God, I didn't learn now on Friday. So why I'm asking this question while it comes up in exams on, but it's really helpful to know bit off pharmacology. So is it by a bee two blockade, Is it via calcium channels is advice Sodium channels? Or is it five potassium channels, or does it work through transient blockage at the A V node on, I think sort of countrywide. We know that teaching in pharmacology is no. Always has good as some of the parts of the curriculum. So it's useful to just give you a little bit of a top upon this. Walls were talking about it. Okay, okay, so we go predominance for D. Good news, people. Do you know symbolic ology? So why is that the case? Well, put this together, which I will let you guys read over in your own time in the context of this finishing on time on a Friday. But you can break down a lot of the basic drug mechanisms that are used in atrial fibrilation management and also in other types of hypertension on a rhythm years into the von Willebrand's calcifications, which, although they're a bit old on. But there is some overlap, they are actually quite helpful, even just for finding a method of putting things in boxes to help you remember things on that means, you know, So type one s sodium channels, type two or be two blockers. Type three work on potassium channels and type before work on calcium channel blockers. If you want to learn a set of medications, I think knowing maybe one or two key examples in each of those is worth knowing on also notably knowing that how digoxin and then Dennis in work is very helpful. And you don't need to dwell on the cardiac conduction and exactly how it works. With this pathway I've drawn at the bottom, but I find it makes it easier for me to understand it. If I can imagine how these medications are plugging into this action potential through a cardiac, my sight. So I'll leave that for today. But in your own time, I'll be worth having a quick read or see what you can find online. I do think knowing a bit about pharmacology will will score some points on, but certainly helps in in understanding what's going on. Um, so I'm going to move on to rate control now that tightens up what we talked about with rhythm control, so it controls Rekey to manage an F. It's something that you'll do. A lot of the junior doctor people will say I should give him a bit more time to do this. And I think you pick it up quite quickly once you've been working on doing it on. But what does it mean? What rate control refers to control in the ventricular rate of the heart? So, you know, actually necessarily controlling the atrial fibrilation itself. The bag of worms that's going off in the atria you're controlling how much of that signal is converted down the conduction pathway into the ventricles, which ultimately is what's stimulating your heart to your ventricle to contract and the blood flow around the body on Do the E. S. C. Guidelines say that if you don't give somebody any rate control, the average rate in a half is almost 160 which is pretty dramatic because you know it's double what someone's, um, you know, resting heart rate should be Really, boy, you need to remember is that rate control is a tradeoff pressure. So if you lower someone's rate too much, there's a risk that you can drop the BP, really, and that increases the risk of falls. Um, we know in the elderly that risk of forces very high under can be very debilitating, so it's something to consider. So let's start with this next case. So what is the most appropriate drug to manage this patient rate? So you've got an 84 year old man he lives in Supported living. He's been recently diagnosed with a F after he had an ischemic stroke on. There's a really good anti coagulation plan in place for him on the stroke team. Have basically asked you to help review his rate control. Now he's back in the community. He's got background of guard high BP. You've got severe asthma and early onset dementia on the district. Nurses have been checking his heart rate over a week. They found it to be up to about 130. Um, he's currently on clopidogrel. He's on simvastatin is on salbutamol is on clinical modulate, which is a steroid inhaler. He's on Allopurinol for his gout, and he's on ramipril 5 mg. So what is the most perfect drug to manage his rate? Is it by supper alone? So too low for up mill diltiazem or amiodarone? Just checking how we doing for time, And I think we're going to be until I'm hopefully great. Some really good responses. Thank you so much for getting stuck in with questions. It really does make a difference. Teaching when you know people are out there. Listings there. Thanks for doing that. Great. So I've got a good spread, which is what I wanted, because this is a difficult question on. It's difficult for a reason the majority of people have got got the answer. Well, nearly nearly the majority. 26%. And I'll talk about why the answer is what it is. Um, on brunch through it. So we just talked about first time management for F in rhythm control, setting on back early in a rate control setting. The same answer is, is valid by so Prolia is typically first line. Unfortunately, this patient's got severe asthma, and there's a risk if we put him on by supper, little that where it is going to make his asthma really poor on. Actually, in terms of his life, you know, his quality of life is probably best. He's not on by sample. Um, we talked about Sotalol before. That's not first line. He's not classic Be two blocker. It's just not the right. Answer. Um, could it be amiodarone? What? Amiodarone is used in rhythm control, not rate control. Onda, In this particular scenario, we're not. Our treatment goal is not to put his britches rhythm back to normal is to keep his rate normal. So that is incorrect. So then your answer is between these two calcium channel blockers and I fed a peanut and diltiazem. If you want to go away and read a bit about calcium channel blockers, then there is worth doing a little bit about. Although I wouldn't worry about it too much. Essentially, you've got different types calcium channel blockers, a diehard parodying and nondihydropyridine on. They work in subtly different ways. On some of them are more late rate limiting than others on diltiazem is typically more rate limiting than fed A peen on is us such to use for rate control in a F, whereas Nifedical mean is typically more used for hypertension management instead. So sorry to interrupt. I think the questions, the answers were there a family will see was Oh, is it gone near the way around? Oh, yeah. Fine. Okay. Sorry about that. I don't know why that happened, but The answer is Diltiazem s apologies for those who have done that, that is probably because you're up Melas. Also inappropriate. Answer this question, which is why it's been changed. So I'm sorry about that, guys. Um but yeah, so diltiazem on verapamil are both good rate limiting calcium channel blockers, whereas nifedipine isn't so That's why nifedipine is room. But for those of you put for a pill, that would be inappropriate. Answer. So that's Yeah, sorry about that. Um, let's just move on to this flow chart than to kind of tightly things up. So we've gone through the left half of this page which talks about rhythm control. We now. So I've got the full picture together when we talk about rate control. So if somebody has gone through these questions that we talked about before and we think it controls appropriate, the first line treatment is typically a beater blocker. Um, unfortunately, this patient can have a B two blocker because, as we talked about before, he's very asthmatic. So the next option is a rate limiting calcium channel blocker on that would typically be diltiazem. There's also in some circumstances, digoxin is an option. I wouldn't get hung up on that too much because it is is based on patients. Risk factors side effect. Profile on I don't think you get asked that. And an exam. I think the limit of what you would get Quist on about F Break Control Management junior level would be. Can you give them a beach blocker? If know, give them a calcium channel blocker. And if you're gonna give him a course in China Bacho. Make sure it's a rate limiting one rather than one that's more you typically used in hypertension on. You'll get accessible this at the end as well. So we're about we're not. We're really a little bit over time, but we'll give everybody a 32nd break to get a bit of water and have, ah, minute to just think about what we've gone through. Bit of a stretch, Defoe's and we'll go again from here. We're sort of moving towards the end of the better bite defibrillation, and then we'll talk about Bradycardias. So give everyone self 30 seconds. All right? We just had a question on case. One to clarify. Um, I think it was the question was whether it was not a new episode off Tech was successfully terminated the previous time. That was about persistent in permanently and okay, I'll have a look at the questions at the end and types of answers for people, because without going back through the slides, I can't remember the whole case of stuff. But I will learn. I'll answer that question. Who ever asked it on Do ask questions in the chat? That's absolutely fine. Um, do you think that we're all right to keep moving? Sphere? Yeah, yeah, yeah, yeah. Okay, let's do that then. So what I want to talk about now is anti coagulation in a F, which is the other kind of the third arm in the treatment of age fibrilation on Diz Really important that we manage our patients stroke risks when they've got a tree fibrilation because it is very significant. You may have heard of the chads of asked Tool, which came out of a research today. Um, I put here, it's worth living for finals. I don't think you need to know every detail of Judge Vask, but I think it's worth knowing that if you've got high chance of ascor, you should be on a regulated on some of the letters in chance of asked, quite easy to remember. So it sometimes is, you know, is not hard to learn a very quick, brief bit of reading over it. So maybe just eyeball that at some point, if you wish pre pre finals, Um, and you can see it does make a big difference. So somebody used 69 he's a man, and he's got a bit of high BP. His stroke risk in the years. About 2.2%. Somebody used 75. So perhaps his wife and she happens Subdartos eighties. She's got, you know, almost three times a risk that he's got. So some risk factors are significantly mawr, um, applicable than others. And age is a big factor. So if that man had been 72 that I would have put his risk upload more so it is worth thinking about, and it should be reviewed by GPS because those are aren't on regulation that obviously age their risk does increase. Maybe that through their life they might need to go onto regulation if they're not already on. It's about balancing that risk of stroke against the risk of bleeding, which used to be the house blood score. In our trust, we use the orbit score, um, again, Have a quick read over those if you wish, but they take into consideration that risk of somebody having a ninja cranial hemorrhage. Essentially, nowadays, we typically prefer prefer direct or Lantus regulant drugs or used to be turned on neuron to regular drugs over warfrin. But warfarin does have its place, and it hasn't disappeared completely, and it is worth knowing about Well, So what is useful is junior is knowing which is used in which scenario, I think, and understanding the differences between them. So I've put a case together for that. So we've got 69 year old lady. She wants to discuss her and regulation after she has recently been diagnosed with a F following a preoperative anesthetic, a check for a routine hernia, repairs. We didn't know she got here. She's gonna have hernia repair, she went, See in the States, they found that she got a F got background of recurrent urinary tract infections, simple hernia, mild osteoarthritis of the knee. For the context of this case, let's assume that it's been decided that she's having rate or rhythm control and that that is done. What you need to do is talk about on regulation with her. So she's a retired tennis coach. She exercises a lot. She avoids doctors because she doesn't really have any medical problems that she needs to see anybody. Four. And she lives quite away from the practice on. She's not really keen when he talked to her on taking tablets. Should really not have to take too many issues in half Do. And you calculate a chads Vasko, which is two. And I have blood score, which is one. So I'll tell you that a score of two is enough to say that you should be discussing and suggesting the patient starts and regulation. So which of these drug options would you choose? You're going to choose warfrin, apixaban, rivaroxaban, dabigatran or aspirin. So So I've got a mix on the no accident we've got mix on the picks about it in the mix on rivaroxaban, which is what I expected, I think, on diffuse people going for warfarin. So why have I said what I said? Well, in first thing to say is this is a patient choice. So you offer the patient all of the information on the differences between the drugs and they choose. Um, in this case, she's given us lots of information, which would help us point her toe one choice or another. So warfarin is an option. It's not now considered to generally be used first line because it requires lots of drug monitoring. So she'd have to come in for a finger prick blood tests. And she's already said she just like seeing doctors and she lives far away on Warfarin is needs more monitoring management, so it's probably not the most appropriate choice for her differences between Apixaban and Rivaroxaban. Traditionally, the evidence had shown that there's a better bleeding profile and apixaban compared to Rivaroxaban, so it was thought that picks Obama's better choice. Overall, however, there since been post trials data on lots of research by companies of rivaroxaban under picks. Bone too, essentially demonstrate the opposite so you can read into as you wish. But pharmacists will believe different things, and really the difference between apixaban and rivaroxaban is very minimal. Although there's one very hard thing which which is different, which is that apixaban is a twice daily drug on Rivaroxaban is a once daily drug. So if she doesn't like taking tablets and rivaroxaban is probably more appropriate for us, it's just one tablet Once a day, the bigger Tran we'll talk about in a moment on aspirin. You should not use a single agent prevent stroke in those with a F because that's an anti platelet rather than an anticoagulant on. I put together a little bit of a comparison table here. I'm going to run through this pretty quick because we only got about 10 15 minutes left. So what's good about warfarin? Well, it's reversible. If someone comes in with a hemorrhage, you can potentially reverse the warfarin using bear plex and vitamin K. Disadvantages needs a lot of monitoring. It's affected by your pee for 50 enzymes. Anything that interrupts those is going to make your warfarin management really difficult on for older people. Warfrin comes in different tablets, so you get 1 mg tablets, 2 mg tablets and 5 mg tablets. Onda. If you're gonna have to give them those to take one every small, you have to be quite dextrous in holding them and taking them and two. It's really easy to get confused between a two and a warning. A five when they're out the box there quite similar. So can be really difficult people to know exactly what amount they're taking. Um, something that's very key, though for warfarin is it does have some really good, um, indications that only warfarin his license for so things like metallic heart valves on some postoperative surgical situations. And it's got quite a long half life. So if somebody forgets to take one tablet or probably still be under curricula eight the next day Rivaroxaban, then it's great because it 11 pill a day doesn't need monitoring. The only advantage is there's evidence to say that the hold amount, the whole volume of the Volkswagen isn't absorbed unless it's taken with food. So in older people who don't eat regularly you or who potentially skip breakfast, if they're taking, rivaroxaban should be having it with dinner rather than in the morning On occasionally, that leads to more doses being missed. Rivaroxaban is off non reversible. There's no technically no on. The doses need slightly adjusting in renal failure, renal impairment picks about them. We've already said very similar to have rocks. Bun doesn't have to be taken with food. There's no monitoring. Disadvantages are. It's two pills a day on there are dose adjustments for renal, and it's also dose adjustment by weight is it's subtle. The dose adjustment. So is not just one factor. It's one of three things, and you have to meet multiple criteria to dose adjust is no actually that difficult all that complicated to do? Um, but if your patients got renal impairment has very low b m I. Then the dose is interested. Um, and then the bigger Trans See, I don't really think I've ever seen anyone on the difficult terrain. Actually, it's not used very much. Is one pill a day there's no monitoring. Traditionally, it's been sold. Is this great drug because it's got an anti dose? So there is a There is a a fix for the bigger trying if you come in with an intracranial hemorrhage, very expensive or so I'm told. It just doesn't have as many licenses, is rivaroxaban on apixaban, so it tends not to be prescribed asthma. Partly for that reason, although it does have a ninja cation in post stroke patients with very high bleeding risks. So it's worth knowing about. So I'm gonna put together everything we talked about on a F in one slide. You obviously have access to all of this in the end, but we've talked about how you investigate f. We've talked about types of a F. We've talked about what you're gonna do with someone in F if they've got a new A f and then we need rhythm control. We've talked about be two blockers, calcium channel blockers and we've also talked about rate control and whether or not he should use be two blocker or written it in calcium channel blocker and if he'd block it doesn't work. Then you're gonna move on to adding in another type, we'll titrate to give you the book and then adding in a really um, 10 Kallstrom, but later on, if appropriate, on days, no increased risk of heart block on, then We've also talked about the anti coagulation which can see up here. So I think in this one slide, if you went back and had a bit of time to read through some of this go over it, I think it actually really have a really good understanding and a really good base. Knowledge of eight for fibrillation's would carry you through most off what you need to know. Okay, so I'm aware of in about 10 minutes left, I'll keep going for those of you who need to leave If I'm really in a bit late, then I won't be offended if you need to. But I think bradycardia is worth of spending a little bit of time going over. So why does it matter? Most common cause of collapse, it causes non vertiginous dizziness. So not spinning dizziness is a sense of lightheadedness. It can be really life threatening in some circumstances. On again, it comes up in exams. So I talked a bit about investigating arrhythmias yesterday, so I won't dwell on this too much, and most of it stays on the slides. Essentially, the first part of any patient, whenever you see them, is always gonna be your history. Taking in the context of someone with palpitations or anything cardiac related, you need to always think about the drugs, so that includes I extra cardiogenic drugs. So things we've given them are there are loads of by stop low are there are loads of antihypertensive medications. Could the patient had an accidental overdose? All their taking, any recreational drugs, etcetera? It's worth thinking about previous cardiac history, of course, on gonna examine them. We talked just a bit day about whether or not they are stable or unstable on it's worth knowing what to find. Someone is stable or unstable. Does that lead you down to different treatment protocol pathways? If you've achieved all of that, you've examined the patient. You're gonna get to the nurses or yourself taken any C g on. Really. When you see that you see GI, you're looking at the rhythm strip on. What you want to know is what the PR interval is on. What that he wave relationship is to the curious on that will give you a lot of the information that you need on looking to see if there are any signs of ischemia, so T wave inversion or ST elevation later on down the line. You really need to think about electrolytes because they're common causes of everything years on. That needs to include magnesium and calcium, as well as potassium and sodium. You need to check someone's TSH because thyroid problems concurrently cause arrhythmias on drug levels. So other people have got high levels of things, like digoxin and that kind of thing, although that probably be led by somebody senior. If you need to do those, you may lead on to have an echocardiogram to look at the pumping function of the heart, see if there are any valvular problems on in the long term. It might be appropriate to look out what the blood flow to the heart is through angiography on whether or not there's any inherited cardiac diseases. So that's we want to first bradycardia case then. So I think yesterday some of the feedback was that people would like to see the full e c g before we give them the answers. So I will try if I can feel it to put the fully see GI up. But I don't know if that will work with you doing the pole, but I'll try. So we've got 78 year old man. He's coming TD with lightheaded episodes. When standing on you had a general sense of fatigue for about two weeks. On one occasion, he thinks he passed out completely, But you can't really remember it. And it was when he was having dinner. Andi didn't think he bang his head. Uh, you look at his personal history. He's got high BP. You had a previous non ST elevation myocardial infarction in 2002. At that time, you had to drug eluting stents. He's got osteoarthritis and type two diabetes on. The nurses have given you any CG. Um, because his heart rate, they say, is very slow. So what's the most promising heat? Prominent HCG finding? Is it second degree heart block mobitz talk to Is it complete or third degree? Heart block is atrial fibrilation where the slow rate is it second degree, heart block mobitz type one or Sinus bradycardia. And I'm gonna put the fully CGM for you the so you can have a bit more of a look at what's going on. Yeah, and I'm sorry you can't see the questions. I'll bring them back up in a second. I'll just give you another sort of 10 seconds to look at the EKG and then I'll flip back so you can see the questions. Um, I'm afraid the slides were already made before I got the feedback yesterday, but they will change the next time. Okay, now, just quickly, Flick. But if I can to their We also was a was secondary heart block be was third hot degree c was a half with a slow rate on D was second degree with type one, and he was Sinus body. Great. Okay, world and everyone for answering. So the actual correct answer is that this is complete third degree heart block, and I'm gonna walk through. Why, that is the case in a moment. Um, but first, I want to just talk about third degree heart block. So the fundamental. So when I go through these, I'm gonna talk about fundamentals, and I'm going to talk a few of the bits. But if you take anything away is the fundamentals so complete heart block? Is this complete absence of conduction in between the atria and the ventricles on. Therefore, your ventricular rhythm or rate is determined by an escape rhythm, which basically means that the electrical signal that happens through the ventricles it started in the ventricles and is determined by the ventricular myocardium on its own, irrespective of the atria. Which is why it's so slow. Um, it can be really, really dangerous. On can result in cardiogenic failure and even death. Um, so why does this happen? Well, it's either due to so over time, progressive and complete failure of your A V node. So, you know, getting a stimulus at the top of the heart or it's because of complete problem with the conductive pathway after that down the bottom of the heart on Depicor. You see this in the context of a scheme year. So patients about previous heart attacks like our patient has, um, in some cases, drugs or congenital abnormalities on what determines the C G. Well, what you see typically is this P wave, which is very regular Onda QRs complex, which is regular but that the two don't speak to each other. And I appreciate you had to look at the CT on a computer, so you probably didn't want to draw on it. But if you got bit of paper, went all the way across the screen, lined up all your P waves lined up or your your s complexes and move them across, you would see that all of the P E waves line up on all of the curious complexes line up, but they don't talk to each other. Sometimes it could be really, really hard to know if it's a mobitz type heart block where you get slowly increasing P to cure US complex and then a dropped beat. Or if this is complete, heart block on. Be honest. Answer is, you just need to look at loads on, get a really, really long rhythm strip, if you can, to try and identify what's going on. And in some cases you just don't know because it is so difficult to tell cause ultimately you are just looking at a very small, um, bit of someone's heart beat. Some things that do really help is up generally in complete heart block the curious complexes broad because the signal is originated in the ventricles, it takes longer to contract. So for that reason, you have a big, broad complex, whereas in a mobitz type heart block, the signal is, at least in some of them being conducted from the atria. So it tends to be narrow. Er is really hard, but the more you do and the more you see, the more you'll get correct and actually in exams and in context of med school. They tend to give you easier ones, so you should be able to get it. I'm gonna ways onto case nine, because I know we're running late. So in fact, I might walk you through this one because we've not got so much time. So this is a 78 year old man. He's come TD. Yeah, these lightheaded episodes. We've talked about his background. You look at this thing, you confirm that it's complete heart block on. He's got these observations now that the nurses have done for you while you're seeing him. So it's hard. It was 30. This BP was low 86/56. His breathing and his oxygenation was fine and his temperature was fine on. Do you need to decide what to do? And this is something that I've seen in recess over the past week, even on the correct answer is to give this patient atropine and I will walk you through by. That is the correct answer. So you can't unfortunately called over somebody back into a normal Sinus rhythm when they're in this rhythm s. So that is just not going to be successful. Adrenaline is not first line treatment for extreme bradycardia on insulin circumstances is initiated by anesthetists, but not as first line and certainly no by anyone. Junior I am adrenaline is to be used in case is off. And if Alexis, that's where lots of destructor came from, Transcutaneous pacing might be an option, but certainly not. First line is not first line because France cutaneous pacing through the skin is really uncomfortable. It's quite painful on. Although it might solve, your problem is easier to do first line things with drugs, then, usually with bits of kitten machinery, which aren't always that easy to find a dentist sing. That's a medication we talked about before in interrupts the conduction in between your atria, any ventricles. Someone's in complete heart blocks and they do anything. So that's not right. So this is a less guidelines. So we've talked about this yesterday in sense that you manage someone 81st. We talked a little bit earlier about what that process is. Let's say you've identified whether this patient has adverse features. Well, to me, this patient is in shock. He's got a low BP on. He's described episodes of syncope I can't tell you about my cardio scheme. You have any blood test. Back is easy. Didn't show any obvious ST Changes. Does he have far heart failure? Possibly, I think even with one of these, which he has, which to me is shock. He should be having some atropine on the dose is 500 micrograms IV. Now this guideline flows onto this one further down, and, it says, has there being a satisfactory response on usually after being work really quickly. So it's over, like 30 seconds to a minute. They used it on the stroke ward about two weeks ago. A tonight, and it's quite dramatic, and it makes really big difference. Patients feel better. The numbers look better. You feel better on diet works. If it doesn't work at 500 micrograms, you can keep repeating that up to 3 mg in total. I would say that if you're ever in a situation where you feel like you need to give up to pee and you should be asking for senior helpers, not something she's doing as an F one. But in the context of exams, you will get ask these questions it's worth knowing what your seniors would suggest that you do so you can keep going up to a maximum of 3 g, 3 mg. Sorry. If that doesn't work, then transcutaneous pacing is considered as your next line option on. But there's always in this protocol because it depends what kit you have available. So transcutaneous pacing might be appropriate. Isoprenaline might be appropriate, or adrenaline might be appropriate. Certainly, Transcutaneous pacing should be available in all hospitals and should be available through the defect, which is on your recess trolley, so that should be a possibility. Isoprenaline and adrenaline are always available on coronary care unit and in critical care, but might not be straight away available in the drug cabinet or your drugs trolley. So they need to be drawn appropriately by somebody who's experienced. You'll see here on the right that even if I give him that medication and his heart rate had got better and he felt better and we felt better, it might still be appropriate that if we're worried about him, he could still need a bit more. So that includes things like if he's had in a systole recently. So if we've watched his heart go into a systole on the monitor. Even if his heart rate is now normal, we might just decide to take over and pace him. If he's got known mobitz Type two heart block in some circumstances, you might just want to pace them rather than risk anything changing, Um, or if they're if they're being complete heart block. And that curious is really, really broad, because that increases the risk of him going into ventricular fibrillation or from a systole on. These patients should be managed on a cardiac monitor and typically are taken to hire care and have underlined here. Consider, because these are things that should be don't missing one senior. So I was gonna quickly talk about atropine and how it works out. Pretty inhibits the Moscone. It's eat our Colin receptor. Try memorized out if you can come spinning Sam's on in the heart specifically inhibits the vagus nerve, so you might remember that the vagus nerve normally slows down your heart rate. So if you're inhibiting the thing that usually slows your heart rate, that will allow your heart rate to increase on uneasily of remembering that the vagus nerve slows your heart rate is you do vagal maneuvers in somebody who's going to fast you trying to stimulate a vagal response to slow somebody down. Least that helps me remember it anyway. Uh huh. So I'm going to quickly compare the heart blocks so you've got first degree heart block that is really not necessarily like a hot blockers such, but that's what it's called on A V B stands for a V block atrioventricular block, so you get this prolonged PR interval that has to be over 200 on. There's a delay in the Atria and the ventricular signal conduction, which suggests there's some abnormal conductive pathway. But it's always consistent, and it always happens on it can be actually caused by having a high vagal tone or just being athletic so it can be very normal can be caused by skinny. It can be caused by drugs. Clinically, it's usually an isolated finding, and it's not usually treated on its own. This is sort of a typically see GI that you might see of a first degree heart block where actually everything else seems to look fine, and they just seem to have this slightly long PR Ondas, you see more and more and more. E C G is often the EKG will interpret things for you. Usually that slowed rubbish, and that's just ignoring it. But it doesn't measure things quite well, so heart rate it will give you is usually correct. UTI and for gives you it's usually correct on PR Interval. It gives us usually correct, and often it will say la Long PR on. In those instances, you might have just diagnosed first degree heart block. So yes worth worth thinking about that brings it on two second degree heart block. You will know hopefully by your level of train that there are two types. There's Mobic. Start one moment. Start to in mobitz type one. You have this sort of malfunction in a V nodal cell. So over time the conduction is coming from your eight s. A note to the top of your heart. I'm going down to a V node on rather than your A V know, listening to your signal every time. After a while, it just gets tired and doesn't listen on. Then it wakes up and listens again, and that's why you get this slowing down and then it's certainly working again. And sometimes you hear this being called the Winky back phenomena on. This is your progressive prolongation of the PR interval. There's a lot of things that can call this cause this drug's high vagal tone again. Athleticism. Typically, you see this in inferior. My body form of ischemia can cause it on in some surgical situations. Clinically is really important because actually, it's usually benign, and it's got a really low chance that this will transform into anything more harmful on diff. Patient is asymptomatic, then usually you don't treat it, and you just keep an eye on the patient. They have they have on their GP records and really know a lot else gets done. Course you check things like electrolytes and family history, but you don't necessarily need to do very much. It'll if someone's symptomatic with that with top second degree mobitz type one heart block. Then you treat them along the same pathway that we showed before, and you give them up to 15. And this is an example off a first degree heart block, a CG. So if you look a lead to the bottom on the rhythm strip I think it demonstrates it quite nicely that you've got this sort of normal looking P r. And for then slightly longer PR and for then slightly longer, then slightly longer. And then there's just nothing on. The P wave is actually slightly hidden in the T wave off that fourth beat, Um, and it goes along like that. Usually it's in this usual repeating pattern, but occasionally it can be sort of three and then a drop and then four. And then I drop rather than it necessarily being the same every time that brings it on to the heart block, which is slightly more concerning. So you've got a second degree heart block moments. Type two, which is as concerning almost as 30 re heart block on, is generally complete failure. All that history. Kinji system a day bottom of your heart, that fast conducting pathway. And it's usually in the context of people who have got previously known bundle or fasciculus blocks of some previous injury to that conductive pathway know loads of causes on Meskini, a fibrosis, etcetera. Why does it matter what clinically It's really serious because there's quite high risk of that will transform into complete heart block. When those last bits that conducting stop working, there's a really risk of sudden cardiac death on If you look over a period of a year, there's a 35% risk of these patients going to a systole, so you need to do something about it now on. It is an indication for a nerve agent permanent pacemaker. This is just a rhythm strip from the life in the fast lane website that demonstrates that actually, the P waves or in relationship the curious, they're normal. And then they dropped. And that's because it's not the IV node that's broken. A V note is listening to the Atria. It's the conduction after that, which is broken, which is why you get these, these sort of beats and then a completely ignored beat. And so that brings me on two third degree heart block, which we talked a little about already. But that's this sort of complete absence of any relationship between the atrium ventricles on. But again, it's either due to this progressive failure or complete ab note or failure. And again, that's a indication for a permanent pacemaker on, as you saw move from like two left. You have increasing concern, but I would say both those on the right hand side should be managed very, very seriously under, typically managed on a cardiac monitor in a high dependency area under considered for pacemaker. This is the last case. Be great. We just get one round of answers for this one. It's a good question, I think. So. What's the most appropriate first line management is this is a 73 year old lady. She's got really onset dementia. She's coming to ET on. This is a case my colleague told me about, which is why I put it in. She was found to be quite drowsy at home. She was with her relatives on when they found her. She got her blister pack medications and they were all empty, even though her daughter and he collected the scripts about a week before. Um, so it looks like she taken on accidental overdose on D. When you read the blister pack information, it said that she was on by supple aspirin, paracetamol on codeine. She was managed any day, and she was given treatment doses. Seven Alloxan, which is the reversal agent for opiates in case it was the codeine that was making her drowsy. But she just remained drowsy. Should paracetamol levels and they were normal on an e C G was performed on. The question is, what's different but most appropriate first line management, So is a DC cardioversion. I am adrenaline vagal maneuvers blue Gone or atropine on. I'll bring the fully see gi up for you there. So thinking and look at those peewee Aves. Look at where the cure us complexes are and things like thing laterally. I've already talked to you about the heart block. So what else could be causing a bradycardia? Really? Um, I'm gonna just flipped back to the question for those of the you want the letters again? So a year is DC cardioversion be was I am adrenaline C was very good Maneuvers. D was glucagon and he was out for pain. Just give you another so far, about 10 seconds. Great. Thanks, guys. Okay, so people have gone for atropine, which is perfectly reasonable. Answer. The a new second most common answer was glucagon and that's correct. Answer. So the point I'm making here is there are some circumstances when you're in extreme bradycardia where alternatives might be appropriate on. I don't think that atropine is the wrong answer in this case, because to give these patients after peen is down the guidelines and will probably make work and might will make them better. But if atropine doesn't work, or if you are very confident that this is a beater blocker or calcium channel blocker overdose, then Glucagon is thought to be more effective on days. No hard evidence on this. There are a lot solved, Case reports. The reason why I glucagon is an answer is it's thought that Glucagon bypasses the beater receptors on increases calcium channel movement, which causes depolarizations despite the be to blockade. So there's a risk. There's a thought or theoretical thought that atropine might not work because the beater receptors are so blocked that the bradycardia will persist even if you try and give them loads of atropine to make it work. Um, to stimulate their heart by vagal tone, but it might not work because they're so be too blocked. But if you can bypass the B two blocker using glucagon, and that might increase the heart rate and resolve their symptoms, um, so that brings on to our last summer. It's like, Thank you. Got so much for making its fine over a bit late. I'm sorry about that. So initially gonna take your history and I think about all those things we talked about. You going to do your examination? You're going to think, Is this patient stable or unstable? And then you're gonna choose your guideline. You're gonna take any C g on. You're gonna look at the relationship between the P waves, the curious complexes and the PR interval on. If there are any signs of ischemia on the first thing, I think you should always think about which is the most common cause of extreme bradycardias. Is this second degree heart block mobitz type two. Is this the degree heart block? Unless you're confident you can roll over out, show these dudes someone senior on making management plan on potentially consider giving them out for pain. You can think about other causes of extreme bradycardias, one of which is ah, you know, a Sinus bradycardia. Because of a drug overdose. There are other causes. A swell which you might want to go and read about things like atrial fibrilation with a slow ventricular rate on which has its own treatment. But again, if you saw this patient, you're worried they had adverse features. Give much pain. Um, so thank you guys so much for listening. I hope you found that helpful. I know that was a lot to go through, but I hope that with all the content from yesterday, all the content from today a little bit of reading around it, you'll actually have a little basis of what you need to know for going to fast going to slow and going irregular. See, I think you guys for listening. And please, do you give me some feedback? We're going to try and keep improving these lectures. Onda. We'll probably have some more for you in the future as well. I think if Sofia will help me back, of course. I'm sure it was very interesting for me as well as an F one. So I'm so everyone else will want to have you buy. Good. Good. I'll hang around from an Elvis, have a look at those questions in the chat on all meat myself. Um, thank you. So I can see some question now the very first one on the chart. So was this not a new episode if it was successfully terminated the previous time? So it was a new episode, but it wouldn't be turned new. F. So a new episode? Yes, but it's not new a half because they're known to previously have had a f um yeah, and I'm sorry about that. Makes it with the questions. That must have just been a problem with the slide. So, yeah. Um, sorry about that, guys, Um can use docks. So can you. Darks in my ankle heart valves. So there are some circumstances where ducks could be used in place of warfrin on more and more licenses, air coming out for them. As the drug companies try and sort of spread, they're they're tablets. More and more. I think it's a good thing. So I think warfarin is poorly tolerated in los cases. It's got loads of problems associated with it, but is a Z. Far as I understand, there aren't many indications in mechanical heart valves for doakes, I could be wrong. You might want to look that up, but I've never seen anyone on a mechanical heart valve on the dose pack. They're always typically on warfarin. Um, then there's there's lots of messages. Uh huh. Is by supper. We used to rhythm control rate control. So by supper, log can be used to put someone back into a Sinus rhythm from from a defibrillation. But it's also a rate limiting medication, so it's also used in rate control. So it's used in both. Um is the answer to that question? Would verapamil have bean correct in the previous question? So that's talking about the rate limiting calcium channel blocker questions. So typically, diltiazem is the first line, so yeah, so sorry about that. Diltiazem would have been the correct answer. Uh huh. Yeah, well, I think I've answered the questions. It's Friday. Thank you all so much for listening. Please fill out feedback hand. I hope you have a good weekend, guys. Is there anything more you wanted from me? Sophia, It'll No, I think we're good. Fantastic. Well, have a good weekend, everyone. Thank you. Thanks, guys. Bye.