Join the QUB CardioSoc weekly teaching series and delve into arrhythmias! This session is aimed at preclinical students embarking on their cardiac studies, and clinical students seeking a refresher. Enhance your understanding and enrich your medical knowledge base in this peer-to-peer learning platform.
Common Pathologies - Arrhythmias
Summary
This interactive on-demand teaching session, led by Steven, a final year medical student from Queens University in Belfast, dives into the world of cardiology, with a focus on arrhythmias. Through engaging discussions, Steven provides an in-depth authenticity on understanding the heart's rhythm, something all medical professionals can appreciate. His session starts with an overview of the basics of the cardiac conduction system and the interpretation of the ECG, continuing with specific types of arrhythmia like extra beats (PVCS and PA CS) and the key differences and identifying criteria for each of them. You will also have the opportunity to participate in ECG quizzes to test your learning. This lecture is a valuable opportunity for anyone in the medical field to enhance their understanding of arrhythmias, their implications and management. Attendees will receive a certificate of completion following the submission of feedback. There will be an opportunity to ask questions during the lecture itself and receive immediate answers. This session is set to last about 45 minutes, providing attendees a comprehensive understanding of arrhythmias in a concise and engaging manner.
Description
Learning objectives
- Participants will understand the basics of cardiac conduction system and the role of different parts of the heart in this system.
- Participants will grasp the role of electrocardiogram (ECG) in measuring and mapping the heart's electrical activity and recall the normal ranges for each segment of an ECG.
- Participants will learn how to identify normal sinus rhythm in ECG readings.
- Participants will gain an understanding of different types of arrhythmias, including sinus bradycardia and sinus tachycardia.
- Participants will identify and understand the significance of premature atrial contractions and premature ventricular contractions in ECG readings.
Speakers
Similar communities
Similar events and on demand videos
Computer generated transcript
Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.
All right. Hello. Um good evening everyone. Thank you for tuning into our cardio set lecture series for this academic year. Can you please just let me know if you can hear and see me? Ok, in the chat? Just a thumbs up will do anything. Just a message from anybody. Ok, good. Fantastic. Thanks very much for that. Um Right. So today we with Steven, a final year medical student from Queens University, Belfast who is going to be doing a talk on cardiology, specifically arrhythmias. So, um I'll just be in the background answering any questions you guys may have in the chat and at the end we'll send out a feedback form for you all to fill out so they can get so that you can get your certificates if that's ok. Um So Steven um the stage is all yours. Take it away. Good stuff. Thanks. Um Abdu. So um give me two seconds. So I share my screen share screen. Mhm tire. Um and can you just confirm, can you hear and see? Yeah, just give me a thumbs up and then I'll share the the thing, the slides. Great. Cool. So if there's any issues. Um There's a couple of lads in the chat that can give me uh a text. Um But yeah, so I'm gonna talk about arrhythmias tonight guys. So um yeah, so as a, as a said, I'm Steven and I'm um fine here in, in Queens in Belfast. Um this is gonna be quite um didactic. Um because there's only 111 question that I've built into this, there's a couple of bits and pieces. If you want to put stuff into the chat, he can, but please feel under no obligation to do so because sometimes I know it's nice to just sit back and then listen. Um, well, we're not at the cinema, like, but it's, um, it's just nice to sit back and just listen to somebody talk without having to engage that much. So if you want to engage, you can, um, and don't be worrying if, um, you don't want to engage. Um, first test is, has anybody noticed that I actually spelled the title wrong. I noticed this about 15 minutes ago, but I just wasn't bothered to change it. There's supposed to be it in there. But anyway, um, so yeah, so these are my, um, times guys, I'm going to cover a wee bit of theory very, very briefly and then I'm gonna talk about bits of arrhythmias and I've put these like maximum times here. Um, so that I don't, um, I don't straight too. Hopefully I won't stray too far from them, but hopefully, we should be done in about 45 minutes maximum. Um And if you have any questions as we go along, put them into the chat, I'll answer them at the end or one of my very helpful colleagues will answer them on my behalf and I completely entrust them to do. So. Um So basically I'm gonna start with some theory if that's OK. Um And this is real, first year, second year stuff um about the cardiac conduction system. So, as everybody knows, um this um essay node here, this is where the, the cardiac um cycle starts. Um The impulse will originate there, it'll travel across the atria, it'll pause in the A V node for a short while about 0.1 of a second. Um And then they'll travel on down through the interventricular septum and the bundle of hiss and all that stuff. Um the left or right bundle branches and then it gives off Perkins fibers and goes up the, the ventricular walls um as, as you all know. Um and it's sort of just important to have that in your head as we move through. Um And how do we measure that? We use? Obviously, we use the electrocardiogram and the ECG. Um and this would be a normal ECG, well, it sort of mo mostly normal anyway. Um and this would be a standard sort of ECG printout you would get um across probably 95% of hospitals and GP practices in the country. Um just be worried that everything's maybe not always in the same place. So, um sometimes EC GS are just printed a bit differently. Um And just to, obviously everybody knows what an ECG looks like, but just to draw it to your attention, just what these sort of axis are. Um They're not really axis as such because they're not really labeled like that. But along the X axis axis across X, along the bottom, we've got speed and normal calibration will be 25 mills per second millimeters per second. Um On the why axis. So w up so this um way it represents voltage. So 10 mill millimeters represents a mill vote. So um there's sort of important to have in your head. So if, if you ever get an E CG and the, the paper is printed, not this big or voltage, the E CT might look a bit funny. Um So they don't actually have AAA tachycardia or severe body cardia, maybe the calibration is just wrong. So just be attuned to that. So as everybody knows one big square, so one of these big squares I've zoomed in here is 0.2 of a second. So 200 milliseconds and one of these wee tiny, tiny wee squares um is not 0.4 seconds or 40 milliseconds. Um And just to, to sort of contextualize everything, uh a full page is 10 seconds and that's important if you're calculating rate in an exam or, um, I suppose even on the ward, um, if you're not reading it off the, off the, the, the, the cheat sheet at the top. Um, so that's a bit about C GS and what the ECG show you'll get a nice PQ RST. Um, if the person's reasonably healthy. So, um, it's important to understand what each of these means, um, in terms of arrhythmias because there's issues with these um these waves or observations between these different, these different points in the tracing. Um It might indicate that there is some sort of arrhythmia or there's a, you know, an electrolyte abnormality leading to an arrhythmia or, you know, you know, yourself. So, um a peak wave of this first little hump here represents atrial depolarization. And you've got QR S which is just sort of beginning bulk, middle and end of ventricular depolarization. It's not necessarily linked to the um anatomy. And then you've got T wave um shortly after that at the end and that just represents ventricular repolarisation which allows the heart to um go back to the start and um depolarize again um between these sort of points in the E CG, you've got um intervals in segments. So the Orangeville is quite relevant in, in terms of arrhythmias and that just represents a nodal delay between the P and the um the R technically. So this sort of area here, um and the ST segment which everybody loves is around here. Um, and it's important, um, or, well, it's important but it's, um, maybe less relevant for, um, arrhythmias but more relevant in, in, in, in heart attacks and MRI S. Um, and it's sort of that period of time between ventricular depolarization, I should say and repolarisation. So, it's important that, you know, um, what each of these sort of these segments or these, um, bits, um, how long they should last because as I said, if they're too long or too short, it could indicate that there's some sort of um underlying pathology. So your QR S complex should be less than three small squares. So it should be less than 0.12 seconds or a 0.12 seconds, which doesn't really make sense, but um it should be less than three small squares. Anything greater than that is a broad QR s and that is indicative. Usually you have some sort of um ventricular problem. Um Qt lessens 11 small squares, but that's not really, um that commonly known. And then APR should be a bit less than, than, than five small squares and that's relevant for um uh a V block. So that's the theory done. Hopefully, um, you can understand where I'm coming from with that. Uh I'm gonna talk again. This is spelled wrong by the way, now about the arrhythmias. So, could I ask just an open question? It's not a trick question, please. Three words What is this or two words? What is this? It's not a trick question. There's no hyperkalaemia. The rate is normal. The rhythm is normal. If somebody wants to type in the chat, I can't see the chat. But let me see. Can somebody please put under the table? What that was? It's not a trick question. Give me five seconds. Somebody please type something. Yeah, it's so it's normal sinus rhythm. Exactly. He's all solid anyway. So, not a trick question. This is normal sinus rhythm. Um And I'm going to talk very, very briefly about normal sinus rhythm. Um It's quite common, normal sinus rhythm as you, you might um understand. And it's just sort of defined a bit funny in um in which it's a cardiac rhythm in which depolarization of the cardiac muscle begins of the essay node, which is quite vague. But um what you'll see in normal sinus rhythm is that you'll have ap wave preceding each of a, each normal QR s which is not um not broad, it'll be a narrow QR s so less than 0.12 seconds. And um following that, you'll have this nice repolarization of a, you know, a nice T wave. Um The rhythm will usually be regular, will hopefully be regular and the rate will be between 60 100. It'll have a normal pr interval as well. Um If it's going too slow, so less than 60 you, I know this anyway. Um that's a sinus bradycardia and greater than 100 BPM is uh sinus tachycardia. I don't think I need to really say anything else about normal sinus rhythm. Um So I'm gonna move on to extra beats. So it's actually quite interesting. It's really, really straightforward and easy. But um there are terms that are actually, they're really, they're thrown about quite a lot and you sort of have to understand what each of them means. They're not, they're not difficult to understand, but I think sometimes it's easy to overlook what these actually mean. So, um, there's different, um, types of beats. This one's really, really commonly seen in, um, like E CG quizzes and stuff. I don't know if you do E CG quizzes, but if you do ECG quizzes, um, commonly you'll see this. Um, I think it's just because it's so identifiable, er, and people are very, very quick to say, oh, that's a PVC and that's correct. And, um, that's grand, but it's actually pvcs are actually less common than PA CS. So premature atrial contractions, premature ventricular contractions. And there's another type called premature junctional contractions, but I'm not going to talk about them. Um, and just very quickly PA CS, as I said, are more common actually than PVCS, but they're more difficult to identify in an E CG, which is why I think they're probably, um, not, not so common for the, the good old E CG quizzes. So, what you'll see in an E CG with APAC, you'll have an abnormal P wave, um, preceding, uh, you know, a normal Q RSA normal being normal, um, length of a QR S. Um, because it's an atrial problem, I'll talk about this later. There's gonna be a, it's not gonna be broad, it's gonna be a narrow QR S. So you can see here this is your T wave finishing off after this P or this, um, QR S complex. And you've got this funny looking very, very narrow, but very, very, um, high in its amplitude, this very bizarre looking P wave. Then you've got your Q RST, then you've got the snore sets itself normal PQ RST. And then you've got, again, this abnormal looking P wave here with QR S and that's just premature atrial contractions. It's just when the Atria fire off. Um, not in a, not, not when they, when they should really, um, on the pvcs, as I said, these are more identifiable in act S. You'll see these big broad QR S complexes, they're not going to be preceded by any sort of, um P wave because the, um, the, the atria are, um, not implicated in this. It's a premature ventricular contraction as opposed to an atrial contraction. Um, and for those really smart academic people among us or cardiology registrars, if there's any on the call, um, er, what you'll see in the ECG as well is that the RR interval in APAC is gonna be quite long. Whereas, um, between, er, RR interval between, um, two regular curious complexes with a PVC in the middle will be twice the normal RR interval if that interests you. I don't know if I explained that correctly. But, um, that's, that's just some theory if you're really that interested. Um, these are terms, that's what I was sort of talking about. These terms are really, really commonly, um, you know, thrown about, especially in the cab. I don't know. Not that I spend my whole life in the cla but the few times that I've been there a lot on my, um I did a cardiology elective and a lot of my elective they were saying, oh, there's patients and patients showing bigeminy and whatever. But um if so to explain that if every X beat is a PVC, so a premature ventricular contraction, this big thing here, every second beat um is a PVC. It's called by Gey. Third is Trigemini and fourth is quadrigeminy. Um As you can see in these tracings here and there's X number of pvcs in a row. So two in a row is a couplet and three in a row is a triplet or it's technically also nonsustained. VT because you don't really know what this is. The ventricle is, um contracting, um like completely, um uh what's the word not, not related to the, the atrium? Um And it's nonsustained because it's less than 30 seconds, I'll talk about all that later. But, um, it's greater than three, contractions. So that's a couple and that's a triplet. So they're just terms, they're very, very straightforward to understand, but you just sort of need to be aware of them. Um So now this is the bulk of my talk tachyarrhythmias, which is when the heart is going too fast and in a, um, strange sort of um, rhythm irregular. Um So this is a really, really helpful diagram I made and it sort of allows you to categorize the different kinds of tachycardias because I feel like tachycardia or I feel like all of arrhythmias are taught sort of a bit, you know, bitsy py because they cover cardiology, they cover emergency medicine and anesthetics. And also you'll do a lot of arrhythmia, you'll do a lot of a atrial um fibrillation and that sort of stuff will be um dealt with in general practice. So you'll, you'll sort of see it all over the place. Um But it's sort of nice to put it all onto the one diagram. So you've got a tachycardia. Um Somebody presents you with an ECG, first thing you want to look at is if it's narrow or if it's broad and it's QR S so a narrow um QR s and normal QR S if, if you want to call it, that is less than 100 and 20 milliseconds as I've been talking about and a broad QR S would be greater than 100 and 20 milliseconds. And this is important because if it's narrow and you've got a, a tachycardia, the chances are that there is a issue with the Atria, if it's broad, that indicates that there's an issue with the ventricles and that sort of stands the sense because if you think about what the QR S actually um represents, it represents ventricular um depolarization. So if you've got a um issue with ventricular depolarization, it's usually a ventricular arrhythmia, the QR S is gonna be broad because that's what the QR S sort of displays electrically. Whereas if it's narrow, um and it's irregular, it indicates that the problem is a bit above that at the atrium. So the narrow curs um it can be regular or irregular and I'm gonna talk about sinus tachycardia. I'm gonna talk about S VT supraventricular tachycardia of which, by the way, there are several which I don't think people appreciate. And then um on the irregular side, you've got atrial fibrillation, which as everybody knows is incredibly common. And then on the other side, on the broad curious, the ventricular issues, you've got ventricular tachycardia, which can be monomorphic or polymorphic. And we're gonna talk about those and ventricular fibrillation. Um So, as I said, narrow atrial problem, broad ventricular problem. So I'm gonna talk about atrial fibrillation. First of all, as I said, it's incredibly common. Um So it's characterized by rapid and irregular beating of the atrial chambers of the heart. So, in this normal diagram, this typical heart, normal heart over here, um you've got a impulse which travels across the atrial atrial contract. There's delay there if you know blood fills in the ventricles in the right left ventricles and then the um impulse moves down the ventricles, ventricles contract and you have a cardiac output um in atrial fibrillation. Um what happens is you'll have ectopic atrial pacemaker activity. Um So there'll be, instead of having your nice um A sa node, your nice A V node and everything's very organized, there'll be sort of impulses coming from all over the atria or from elsewhere in the atria. It's very commonly at the root of the pulmonary valve. If anybody's ever seen uh an ablation of somebody with um permanent af that's really symptomatic. Um They'll usually um have a bit of their um so the basal p, the base of the pulmonary vein will be ablated. You'll see it in the, in the cab um or development of reentry circuits, which I'm not really going to talk about. But if you're interested, I would recommend Googling it. It's quite straightforward, but um cut a long story short. Um What happens is the atria will fibrillate. So fibrillate just means to quiver or to shake, I suppose. Um So they don't relax and contract nicely. There's loads of different causes of af um no wonder because it's incredibly common and um it can be transient. So people take too much coffee or take too many medications or take illicit drugs. Pregnancy can cause it, it can be idiopathic very commonly or people with bad heart people with ischemic heart disease or hypertension valve disease, et cetera. Um, so patients will present in all sort of manners. Um There's um, you know, loads of patients, actually loads of patients, not that I've seen loads of patients, but I've actually seen loads of patients that have incidentally found that they have um atrial fibrillation because they get an E CG done when they come to the emergency department or they had an E CG done by me and um GP for whatever reason and they were found to be in af um and then at the sort of other extent um patients um that are symptomatic you um palpitations, shortness of breath, all those sorts of things, um or they might manifest as um strokes. So they might not know that they've got atrial fibrillation and atrial fibrillation as everybody knows, um makes patients more prone to um thromboembolic events or stroke because of um stasis of blood flow, usually in the um the left atrial up here and commonly in the left atrial appendage. But um I don't know, I don't know how, um I don't know how you would know that. But anyway, um so what happens is the blood instead of being nicely moved on, it becomes static here it stays here for a good period of time. Um Because of that it's prone to clotting. Um It clots, what happens is the, the, the clot will move from here into your left ventricle. Um, and then be sent up into your, um uh your systemic circulation anyway. So, um yeah, so I wanted to say, what are the 2 g changes classically associated with? Af again, I'm not going to insult your intelligence by um making you type in the chat what the two CG changes are. Um But lo and behold, they are, the, the, the um rhythm will be irregularly irregular as you can see here, this is very, very irregular and you'll have lack of P waves. So you'll get this quivering, you'll get this fibrillating all along the isoelectric line between QR S complexes. Um And you'll have no discernible P waves. So that's caly atrial fibrillation that's really, really common. I think I got an a in third year with the atrial fibrillation. Um There's always something to do with an ECG and an OS because it's so easy to test. So atrial fibrillation, I think is really, really good for that. There's different types, this is important, but at the same time, it's also maybe a bit academic. So you can have parts as more persistent. Um Longstanding, maybe not really or permanent and it just represents um just I would, I would recommend just go away and, and, and reading about what each of them sort of mean. Um It's maybe just a bit academic um in terms of um management, management of atrial fibrillation. So there's loads of guidelines. And um I remember one time a doctor said to me, I think it was only about this story. It was quite recently and he said to me, um that guidelines are guidelines and the key word is guide. So they're, they're there to guide. So they're not hard and fast rules. They're, they're, they're good because it gives you sort of a structure to work through. But um it's not necessarily what you must do in every patient that you have to take each patient and um sort of consider everything about them before you decide how you're gonna manage them, which I suppose it was good advice and I suppose that's, that's talked about an awful lot, but you don't really appreciate it until you, until somebody says something like that to you anyway. So in order um to assess and diagnose atrial fibrillation, you get 12 A DCG, of course. Um after that, because the risk of stroke is so high, you need to carry out what's called a chad Vas score. Um which is a really common M CQ question. I don't know if we got it in our finals or like our final written paper of MLA, I think, but I think we maybe got it, maybe got it in a previous exam somewhere, I think. There was something to do with Chad Vas previously, not knowing the score but knowing that it was called the Chaz Vas score. Um because stroke is so important, um you have to, you have to calculate that and Chad VSC is um it allows you to decide whether or not a patient with atrial fibrillation needs anticoagulated or not. In order to help you make that decision. Um there's the has bled score or the orbit score which people use more. Nowadays, I believe the orbit score um to assess how likely they are they are to bleed on their anticoagulant. Um So it's sort of a balance that you have to strike. Um and just for any absolute nerds out there, the um chad Vas score is actually, I think it's been changed. I think they're removing the um the sex category. Yeah, there's a female sex, I think they're removing that. I think um there's a, there's an, the only really um the E se published stuff about that fairly recently within the last six months, I think. Um So if you just want to look that up, you're more than welcome to. Um I think also people overlook this but a patient with atrial fibrillation is hemodynamically unstable. So what does that mean? That means if they're presenting with low BP or they're in shock or heart failure or peri arrest, um They probably need DC um cardioversion and you just treat them in line with the um the er Rus Council um Tachycardia algorithm which you'll see in all emergency departments, all um um resources um et cetera. Er, and you should probably know it very well. Um I would recommend knowing it very well. Um So after you do your chad vas um you get a score out of it for men greater or than are equal to two and women greater than are equal to three and anticoagulation. It's strongly recommended. Most people will meet that score. Um So they get anticoagulated, er if it's men or one or one or two consider anticoagulation. Um And that's when the orbit becomes more important, some of those sorts of things. And here we usually use Apixaban. So we use a Doac first line to treat that unless um A doac is contraindicated or um you know, they've had a valve replaced or something and they're already on Warfarin um because it more or less does the same job. So then actually managing the disease only comes sort of third in the list. So um this again is very sort of academic, you have to decide whether you want to rate control them or rhythm control. Um And there's different sort of criteria for deciding sort of mentally. Ok, which is best. So rate control um is first line for most patients unless their af has um been ongoing for less than two days. So it's recent onset. Um they've tried the rate control and they're still really symptomatic with it or if they, if they're younger it's their first presentation or if it's secondary to something else and rhythm control is more suitable. Again, that's not a decision probably for you to make as an F one or F two doctor, but probably would be more um medical registrar, cardiology, reg cardiology consultant, electrophysiologist, sort of decision to make. Um And in terms of rhythm control, that's the other um side of things. Um, rhythm control involves either cardioversion or um, well, involves cardioversion and keeping them there. Um So that can be either electrical or pharmacological. So cardioversion, electrical is um not as dramatic as people think it is. It's um, usually patients don't really, um, well, they do react but like they, um it's not as dramatic as people think it is. Um, that's the, you know, people you put pads on and you charge and all that sort of stuff or pharmacological is just using um, medications that you can, you can take, you can ingest orally, um, consider antiarrhythmic drugs. Um That's again by, by specialists. Um If anybody's really interested, there's um there's loads of different kinds of antiarrhythmics and, um, I don't know if anybody's a classical musician um in the, in the audience. Um, if there's anybody there. But, um, the classification is called the Vaughan Williams classification of antiarrhythmics. And um, Vaughan Williams was also, uh not the same person I don't think, but he was AAA composer, anybody knows any of his music. So, um and then you can also consider ablation. Um again, as I said, at the root of the pulmonary vein, it's very common to see that for refractory cases. Just what drugs do you give them for, for rate control. So beta blockers are very common by soprol rate limit. It just means rate limiting calcium channel blockers like dilTIAZem as an example and digoxin in elderly people, or I think if they're quite sort of sedentary, I think you give digoxin there, it's sort of recommended, which is actually quite a good drug drug digoxin. And you're aiming for a rate less than 100 and 10. So as I've talked, I've talked all through that, but um it's a bit academic. Um so just sort of have an appreciation I think is, is good enough. So moving on to um atrial arrhythmia number two, I'm going to talk very, very briefly about atrial flutter because it's very, very similar to um atrial fibrillation and its sign symptoms and management. But the difference is that it's um it's usually regular and um you have these so with flutter waves between QR S complexes. Um so you can, this is sort of a nice diagram, you can compare the two. It's technically an S VT which I'm going to get on to talk about very soon. But S VT just means obviously supraventricular tachycardia and that just means any tachycardia arising from the atria. So time, the atrial ft and atrial fibrillation are both types of SVT um on an atrial flutter, you'll have this really fast atrial rate. Not all of the um atrial impulses will be conducted to the ventricles. As you can see in this one, this is probably probably two, well, two or 3 to 1, it's hard to know because there's this T wave and you don't know that there's ap wave buried within that. But, um, yeah, it's um, very common. You'll see a ventricular rate about 100 and 50 in atrial flutter. Um, so that's atrial flutter. Um Here's another question for you about something that I've just talked about. Um, have a quick look at that and please type into the chat. What do you think? It is? Three letters, you know what the answer is? Um I want to please put it in the chart. I'll give you five seconds. It's three letters. Yeah, it's S VT but S VT is actually, um S VT is interesting because S VT is actually an umbrella term for loads of different, um, arrhythmias, loads of different issues. Ok. So it's, it's maybe not as broad as saying, ok, this person has an infection but it sort of is because so I could have a chest infection or I could have orbital cellulitis or I could have like an cephalitis or I could have, um, you know, an Osteomyelitis. I can have loads of different infections or if I a big abdominal collection or just a skin cellulitis and they're all technically infection and they're all usually treated with antibiotics. But um, they're different organs that'll affect the person in a different sort of way. So, infection is an umbrella term. Supraventricular tachycardia is a bit of a smaller umbrella, but um it's still an umbrella term. So it's just an arrhythmia where the heart beats very fast in a regular rhythm. Usually with the arrhythmia arising above the ventricles ie in the atria. So there's loads of different types. So af you probably know this anyway, but af atrial flutter technically are S VT S, there's loads of different types. Um, I'm gonna talk about these ones in bold. So I'm gonna talk about a VN RT and a VRT. If you aren't interested, you can switch off for five minutes and then come back. I'm also going to talk about Wolf Parkinson White, which is, I suppose technique is an inherited type of, um S VT. And then after that, there's loads and loads of different, um, types. But that's be beyond my understanding, to be honest with you, um, S VT, if a person presents in sort of sort of one of these kinds of S VT anyway, usually they'll, they'll feel quite, quite unwell with it. Um, I've seen a lot of Children with it for whatever reason. I don't know. Um, but they, they'd be quite unwell they feel quite unwell Children. I don't know, they, they just look quite scared, sort of. Um they'll have palpitations, potentially presyncopal or syncope, which just means collapse or like um fainting could be short of breath. I might have chest pain. Um And S VT S are interesting. Um I have a question in the chat um just based on the management. So if somebody doesn't mind activating my question, my question is, what's everybody's favorite vagal maneuver? Sorry, this is extremely nerdy, but I'm gonna vote here. Actually, I'm not, I wanna see what everybody's favorite V maneuver is interesting. I'll give it another five seconds. Maybe I won't. I've got eight responses. That's good. It's got a Valsalva. Valsalva coming out on top. OK. With, with 50%. 0, ok. That was, that was, that was a great response guys. Um So Valsalva coming out on top guys, I have to say I'm gonna vote for a modified Valsalva. I think it's um not that it really works better, but um I've seen it done and it actually worked. Um So Valsalva is you get them to blow in into like a singe. It's like a, it's a bagel thing. Modified Valsalva is when you get them to blow into the syringe and then you throw their legs back. So you get them to sit up like 90 degrees and that their head and that their legs and you tip them back so that their legs are up and it's supposed to increase venous return or something like that. I'm not exactly sure, increasing venous return and it does something to something somewhere, um, which, which causing them to come out of S PT carotid sinus massage. You've got bors and stuff that can be stimulated in that way, the diving reflex is just, um, put a, you wouldn't try a carotid sinus massage in pre hospital environment. I probably wouldn't either, To be honest with you, I would um refer to my senior in any of these cases. Um But yeah, the diving reflex is interesting. I saw a child um have their um their head submerged in water and it didn't work, but they, they tried it and I don't, I don't really know why because people often say don't do it. But anyway, and then coughing, that's just sort of similar to Valsalva. It sort of just increases that pressure. It's a vagal thing again. Um OK, back to this, so vagal maneuvers. Um That's your first sort of line with your choice of VL maneuver. Um Adenosine is the, the medication that's, that's given for that um in line again with your um uh tachycardia algorithm. Um And you give the doses are 6, 12 and 18. Um They're very commonly known numbers. I've never seen them in MC Qs, but um they've thrown about an awful lot. It used to be 6, 12 and 12, I think, or 66 and 12 but anyway, um, but I remember uh an eg a consultant telling us as a group one time that, um, usually if it doesn't work after the first one, the chances of it working after 12 and 18 are also quite low. So, um, and the, the adenosine has a very, very short half life as far as I remember. So, um, you have to give it in the flush. So you actually put it in the flush and, and, and, and give it rather than giving it by the time you get that out and put the flush in and inject the flush, the it's half wasted. Um So yeah, consider then as well synchronized DCC um DC cardioversion up to three times and then consider catheter ablation in circum certain circumstances which I'm gonna talk about as well a wee bit. Um And then finally, as I've said before, all S PT S because their atrial will demonstrate narrow QR S complex and ecg unless you've got co coexisting ventricular disease because then there's a ventricular issue as well. Um So give me two minutes. I'm gonna talk about a VN RT and A VRT. If you don't want to listen, you don't have to. So VN RT that just stands for atrial atrioventricular nodal reentrant tachycardia. So it's really, really common in terms of S VT S. Um And what happens is the arrhythmia will originate within or next to the V nodes, the A V nodes it's a bit here as you all know. And what happens is there's um two pathways, there's a slow and a fast, this is maybe a bit theoretical, but there's a slow and a fast pathway. And um if you think about it, the impulse traveling via the fast pathway can go very, very quickly. Um And the slow one maybe hasn't even started by the time the fast one has reached sort of the end of its, of its road, if you, if you want to imagine it that way, um And the impulse can then travel back up the slow pathway and that sort of goes around in a bit of a roundabout. And because of that, the sense sets up what we call a reentrance circuit. So they're, they're not that difficult to understand reentrance circuits and it underpins an awful lot of um uh arrhythmias and, and, and cardiology. So it is worth, I think having a wee read up on. Um So just know that A VN RT is most common. Um And then there's a VRT, an A VRT um is an arrhythmia which originates in the A V node, but the reentrant circuit is via a ventricular um er accessory pathway. Um So the, the impulse will travel down and around and down and around, but the heart will still be going very, very fast. Um And just if you just want to look up, it looks like homework, but if you are really interested, look up reentrance circuits, how they form, how they lead to these different kinds of S VT and the ECG changes. So, you'll get, like, I think it's pseudo R waves and pseudo S waves they talk about. Um, and then there's a thing is it, I think it's the RP interval. Yeah, it's not pr, it's opposite of that. So, it's, it's RP interval. If it's short it is a VN RT and it's long, I think it's a VRT, something like that, but that's, that's not medical school, sort of standard, I don't think. Um, so, yeah, so moving on to Wolff Parkinson White, which is, I actually think Wolf Parkinson white is really, really interesting and it's supposed to be rare, but I've seen an awful lot of people and I actually know a few people that have had Wolff Parkinson White and had ablations for it. So, Wolf Parkinson white is a bit like, um, before, in which you have this path that goes down and comes back up, but you have this little thing here. Um, I don't know if anybody knows the name of it, if you just want to rack your brains for five seconds and then I'll give you the answer to what this, um, accessory pathway is called. So, 54321, it's called the bundle of Kent. Ok. So, uh, there's an accessory electrical pathway between the ventricle and the atria ie bundle of bundle of Kent and there's no delay at this so it can conduct very, very quickly. Um And as a result of that, um a person, if you can imagine the impulse will go round and down, travel via the bundle of Kent, back up to the Atria and go round and round and round and round. And because of that, their heart beats very fast. So as as a result of that, especially when, uh for whatever reason, again, I've seen a lot of Children with it. Um They'll present especially during exercise with the tachycardia. Um I saw a child one time with um a massive heart rate. It was 226 or something. It was very, very fast. Um And then I had Wolf Parkinson white. Um The patient again, feel quite unwell with it probably with palpitations, shortness of breath and maybe presync or thinkable. Um The E CG. Um I don't know how likely this is to come up in an exam, but I think it's very, very straightforward. Um And you can see um this is supposed to be Ap QR S and T but in this QR S, you've got a delta wave. So a delta wave um obviously delta is just this letter here. And um Greek, I presume Greek or Latin probably Greek. I don't know. Um You get the slurring um up stroke before the, the QR S or at the start of the QR S after the, the P the P wave. And because of that, obviously, you, you then get a short pr so you've got a short pr and this up, up stroke slurred up stroke in the QR S, that's a delta wave and the, the person probably has got wolf Parkinson white and they might require an ablation. Um And that's, that'll be reasoning the comment, I think for Children you have to be five, I think is the minimum cut off age or minimum age for ablation. But um I don't know. Um So moving on to the ventricular thing, so that's super ventricular done. So now ventricular, so this is maybe I don't wanna say more serious, but this can get more serious. This can lead to arrest much, much more quickly. So, a ventricular tachycardia obviously is a tachycardia originating in the ventricles. Um And you'll have an ectopic foci an ectopic electrical focus in the ventricle which perpetuates this ventricular tachycardia. This VT and patients present with palpitations, pacing could be, could be chest pain, all those usual things, but it can degenerate into a VF arrest. So, as everybody knows, a VT and VF are your um shockable rhythms and cardiac arrest. Um And as such, this needs to be treated very seriously as per the adult tachycardia um or a LS guidelines um on your E CG, it's ventricular. So it's kind of a broad QR s and it'll be going very fast and actually what causes it it's mostly caused by scar tissue. Interestingly. So people with, again, bad heart, so, ischemic heart disease, same just means cardiomyopathy. So, um, I did a, a project on, um, this actually looking at patients with, um, dilated cardiomyopathies and, um, I looked at their, um, their MRI, their cardiac MRI and looked at the amount of scar that they had in their, their myocardium and looked if they ever ended up having VT or VF. And actually, there's, there's a lot of that actually out on it that um patients with those sorts of cardiomyopathies with increased amount of scar will have VT and VF much, much, much more commonly. Um So, yeah, and just a bit of, um, I was supposed to say housekeeping isn't the right word, but just for a bit of um background or whatever VT, you need 30 seconds of VT. Um for it technically to be VT, if it's less than 30 seconds, it's NS VT nonsustained VT and you need at least three complexes. Otherwise it's just a triplet of pvcs if that makes sense. Um But again, that's a bit academic as well. So it can be monomorphic or polymorphic monomorphic mono, meaning monomorphic, just meaning form VT. So as you can see monomorphic, they all look the same and it's, I suppose probably technically a singular ectopic ventricular focus causing all of these um when you get this regular pattern broad QR S complexes and they're all identical. Um Whereas you can also get polymorphic. So, polymorphic meaning um shape, morph, whatever. Um And most commonly, you get torsades, de pointes or torsades, de pointes. Um And this is when you get, instead of having the singular um ectopic focus, you have multiple ventricular um foci um and they're just firing off at all sorts of um angles and, and, and, and ways and as a result of that, the CS looks very, very strange. Um, as, as in here, it looks, you know, broad, it's argued a bit narrow, narrow, narrow, broad and the, the amplitude is, is up and down and up and down. So, um, this is a TDP and it's Torsade de pointes and it's, um, the way I think of it is like if you have like, where's it called? So, so my phone, for example, um I don't know if you can see me but, um, so I've got my phone right. If you look at like this length is about say 20 centimeters or so, but if I like, turn it over, the length is now a centimeter. So it's like twisting. Now we're back to whatever that was 20 centimeters centimeter. 20. Do you know what I mean? It sort of, um, it twists, um, and that's where that comes from and I don't know if that makes sense to people, but, um, that's the way I think about it. That's where the name comes from because it twists around the point um if that makes sense. Um And the, the key thing with TDP is that you'll have this variable curious sample suggest, but you'll have QT prolongation as well. Otherwise, it's technically not TDP by definition. Um And it can be caused by anything that leads to P uh QT prolongation. So a lot of drugs can lead to it. For example, Erythromycin very commonly tricyclic antidepressants, um antiarrhythmics, I think citalopram, um which uh antidepressant um there's loads of different drugs that can cause it. Um and there's obviously other causes as well. Genetic disease. Um be it inherited rhythm disease or um structural cardiac disease. Um Management. A very common M CQ question is management is magnesium. Magnesium is a great drug. It can be used for loads and loads and loads of different things. But magnesium is a one of the main um or the main thing you should be given in TDP as per your adult tachycardia guidelines if you look down. Um Yeah, if you look down there, you don't see it kept magnesium. Um a ventricular fibrillation finally is probably the worst of them all because it will present an arrest because it's not really um compatible with any sort of cardiac output. Um So it represents 10% actually of all arrests. Interestingly, and you get this broad QR S and tachycardic and you can see the ventricle is just fibrillating. There's no sort of discernible, anything sort of organized there at all. Um loads of different causes and the management is just your, your A LS, obviously, because they'll, they will arrest. Um And if you get ROSC, if you get um return of spontaneous circulation, obviously, uh electrophysiologist will probably consider putting an ICD in to, to shock them out of it if it happens in the future. Um So when would VF not concern you? So it was just, this is just a question to make you think. So. I've seen it a couple of times and people aren't concerned about it. If you just want to think about it, you don't have to type in up um a couple of times that I've seen it um has been um I think it was a good analogy. Thank you. Um, a couple of times I've seen it is if you've ever been in cardiac theaters and somebody's having a, like a uh like a valve replacement or um what's it called? A cabbage? Um And they're having it on pump. So the, obviously the, the heart will be um uh what's it called? It'll be stopped. That's not the right word, but it'll be stopped for a temporary period of time. And then when the blood is pumped back into it, it usually restarts skin, but sometimes when it restarts it will fibrillate um or sometimes it needs defibrillation to restart and in that case, you can get VF. So I actually saw a patient, I saw, I saw two patients actually, um, in cardiac theaters, um, just immediately POSTOP, they were having their, um, they were having their hearts started again if you will and they had VF but they didn't need anything dramatically. So, um, so that's the bulk of, um, the talk overnight you'll be happy to hear. So I'm going to quickly, very quickly talk about Brady arrhythmias, um, and then finish off with some inherited cardiac disease. Um, so bradycardias, um you can have it again, narrow or broad QR s complexes narrow. I'm gonna talk about sinus tachycardia and ap blockage of ventricular nodal block. And then you can have broad Q RSS, which again is a ventricular problem that that rule holds true for body arrhythmias as well. Um which is your bundle branch box, right and left. So this is sinus bradycardia. I don't think there's anything I need to particularly say about sinus bradycardia, except that it's very common in people with um you know, athletes, people with high vagal tone, I think is the, the phrase they use. Um usually asymptomatic, sometimes people get dizzy or thinkable, but um usually not associated with any underlying pathology, but I suppose it can be, but usually just indicates a healthy heart moving on to a V block. Um A V block is literally blocked conduction or slow or impaired conduction of electricity from the atria to the ventricles. Hence, atrioventricular block. Um It's very straightforward and there's three sort of types of it. So you can have um first degree, secondary or third degree. So first degree is sort of the least severe where the signal is slow. I like this diagram because the signal is slow. So it's conducting through, but there's a little bit of a delay here at the note. And because of that, you get a long um pr interval. So it'll be greater than five small squares, so greater than 200 milliseconds. So as you can see there, it's a bit long. Um It doesn't get any, sorry, I'm pointing the wrong thing. It doesn't get any longer. It stays the same length. Usually. Um People are usually asymptomatic. It requires no management. It's not that um big of a thing. Most people actually probably have it if you're athletes and all that sort of stuff, um, they'll, they'll have a, a first degree, a V block. Secondary ge heavy block is um splitt again into MBIS type one and type two. Um And not all atrial impulses will reach the ventricles in this second degree IV block. So the signal is I like that word sporadic. So sometimes it gets through and sometimes it doesn't, well, it's type one, you get progressive QR widening on the ECG and then you'll drop a QR S. So you can see here it's, it's probably normal. It's getting a bit longer, definitely too long there and then you drop a QR S and then it'll go back and it will repeat the same thing. So, technically, the rhythm would be irregular then if you think about it. But, um, well, that's, again, that's a bit academic. But, um, that's, that's Mobitz type one. Mobitz type two is this, um, sort of constantly, it's usually a bit prolonged, um, pr, but you'll drop every, um, you know, regular QR s regularly. If you get what I mean, you'll drop every fourth or you'll drop every third. Um, and you can sort of come up with ratios for that. Um, moments type two is usually more serious. People are more symptomatic with it. Um, and they usually require insertion of a pacemaker. Um, and then third degree, finally, there's absolutely no conduction um relationship between the atria and the ventricles. So you get a blocked signal technically isn't right because some signal does get through. But, um, you'll have no, completely, no um, communication or no sort of relationship between them. So, if you look at this E CG, that's ap wave, that's probably ap wave, that's ap wave, that's probably a bit of ap wave, that's ap wave. But you can see they don't correspond to QR S at all. The junctional escape is what that's called. So the, the QR S just sort of get, gets through very randomly. Um, and people usually are quite symptomatic of this and require um, an A CD or sorry, require ACR like a pacemaker, a CRT or whatever. Er, finally, I'm going to talk about bundle branch block in, in this sort of block. Um So that a bundle branch block is a complete or partial interruption of flow of impulses in either of the bundle branches. So what does that mean? So you've got a right and left bundle branch and they're composed of fascicles, which is just little sort of wires, I suppose all joined together. Um an injury, injury to a bundle branch or a fascicle um causes the current to flow by a different path because the current takes a path of least resistance as you all know from physics. So an injury, be it a heart attack or a cardiac surgery or whatever, what happens? It's a bit like a, it's a bit like if the road is closed. So if the main road is closed for me going home, instead of taking an hour to get home, it'll take me an hour and 15 minutes to get home, for example. Um So the co the current flows by a different path because some something's blocked somewhere. Um If that makes sense. So because of that, um it takes me, it takes me 15 minutes extra to get home. The depolarization of the ventricle is going to be delayed. And as a result of that, you get a broad QR s complex and here's this classic um thing here, the William Morrow thing, some people say William Morrow, but I was always taught William Morrow Um So you look at your chest leads V one and V six. And you're supposed to be able to see in the left bundle branch block, it'll get this broad QR s first of all, and V one will look a bit like a W with an I faith, but I think the M is always very, very clear. So V six, you'll see an M. Um And if you see uh an M and V six and V one looks a bit broad chances starts left bundle branch block, right bundle branch block. On the other hand, is the opposite way around. So V one will show this M pattern and V six, this W pattern. Um it can be caused by loads and loads of different things, things as I've said this bundle branch block, but it could be, you know, anything from aortic stenosis to any sort of cardiomyopathy. Um I think I read about like Lyme disease can cause it like there's any sort of number of things. And then obviously new, left bundle branch block is, is classically associated with um an acute Mr as well. Um although that's sort of fall out of favor a bit, I think for um teaching and stuff. But anyway, um yeah, so that is um bundle branch Kock, that's what I wanted to say there. So if you'll indulge me for another two minutes, I'm gonna talk about inherited rhythm disease very quickly just because I think inherited rhythm disease is actually absolutely fascinating. And, um, it's very serious. It's very rare but it's, this inherited rhythm disease is what causes, um, you know, you hear of, um, you know, very high achieving sports people and stuff who, um, collapse on, you know, on a pitch or those sorts of things. And, um, they, they die as they say, they arrest on the pitch. Um, they have sudden cardiac death is what that's called um during exercise or during exertion. And there's loads of different types and most are asymptomatic. Unfortunately, until somebody presents in um an arrest and, you know, unless you get lost, that's it. So they may present with syncope, which might actually be an arrest and they come round um or it can be picked up on familial familial familial screening. So, um for patients that um will have a first degree relative that had, you know, a premature death, you know, if somebody dies age 42 um an autopsy shows that they had a um funny sort of myocardium or something and then, then you can get genetic tests and all that sort of stuff. Um And I think it's really interesting as well because it has a significant quality of life impact on people. So, margin like a 15 or 16 year old who has unfortunately a first degree relative that passes away due to one of these diseases. Um And then do you know it's the whole ethical thing. Do they go and get tested or they have the gene? Like, what do you do? Like, do you want to put a 15 year old? Do you want to put an ICD into a 15 year old? Like, what do you do? Do you, you have to tell them to stop playing sports and they don't want to do that and all that sort of stuff? So, it's sort of a really interesting sort of debate and the ethics around it. So I'm going to very, very, very quickly talk about three. Um I've seen, I've never seen Brugada or L QT, but I have seen this arrhythmogenic RBC, right? Ventricular cardiomyopathy, which I suppose technically is a cardiomyopathy but, um, people die with it or people have, um, symptoms with it because of the rhythm issues. Um, this is just an interesting paper. I didn't read it. I looked through a few of the figures. Um, and this is a really, I actually did read this one, this thing. Um It's really, really interesting. It's sort of a, it's about 14 or 15 pages maybe. Um, it's like, it summarizes an awful lot of very, well, the most common inherited rhythm diseases um for patients. And it was, it was actually really, really interesting to read through, um, if anybody's interested. Um, so very quickly talking about Brugada. First of all, it's one of the, what we call channelopathies. So, the, the ion channels that you just wanna know from cardiac physiology. Um an issue with sodium channels. Um and because of that um polar depolarization and then action potentials conduct a bit funny. Um It's reasonably rare. So one in 2000, but you know, estimates are always estimates or only estimates. So that could be more or less. It's an inherited in an autosomal dominant fashion. There's this particular gene that is associated with it, but there's tens and tons of genes that are associated with Brugada. And again, like all these diseases present, potentially sudden cardiac death, previous syncope, et cetera. So this is somebody's ECG with Brugada, which is quite a classical sort of E CG. If you ever see it, this, this would be Brugada. So you get what we call cove ST elevation. So this is the Coving of the ST segment here and it's obviously elevated of the isoelectric line and it has to be in greater than one. So two or three of V one V two and V three. And following that, you get this down sloping negative T wave um as well as that, you have to have clinical criteria that you have to meet at the tick box thing as well. Um And patients definitively, tomato just need an ICD. Um I've never seen it but um yeah, that's, that's Brugada. Um Now long QT is er, is interesting as well, I was gonna say. Um of course, it's interesting. Um QT is greater than 450 milliseconds. So you get this QT, it's very, very long. Um It's one in 7000. But again, that's only an estimate. It can be genetic or required this one. So loads of different drugs can do it. Um Again, that Erythromycin citalopram and all that stuff, electrolyte imbalances can cause it, it can be um genetic disease can, can cause it. Um and it can present in loads of different ways. So it can present with VT or TDP or previous syncope or they can arrest. Um And management is just avoid the, the QT prolonging meds. There are certain medications you can give, I'm not sure what they are. I can't remember uh or they potentially need an ICD to prevent the, the ventricular arrhythmias and arrests, et cetera and very, very, very fine. A R VC is a RV CM which means right ventricular cardiomyopathy um where you see right ventricular hypokinesis. So the right ventricle doesn't pump as well as it should. And as a result of that, um there's a lot of scar in the right ventricle and as I said, scar leads to ventricular arrhythmias. So it's about one in 10,000, although there's other studies that have said one in 2000. So again, I don't know, um it's autosomal abominate again. Um And it's an issue with the desmosome. So the desmosome is um as far as I can remember, like links the sarcomeres together or um I can't even remember if sarcomere is the right word. I haven't, I haven't used that word in about eight years. But um it's one of those structural proteins um involved in the in the the cardiac myocytes. Er again, similar presentation will be asymptomatic until ventricular with me as sudden cardiac death arises. Um And quite a classical CG you get this epsilon wave, which is this wee notch in here um followed by T wave inversion again, the chest leads. Um And this is quite um there's other criteria you have to meet as well. Um It's called like the task force criteria. It's like it's a, it's a society thing as well. I haven't read through it but II think it's quite a complicated thing. You have to meet an awful lot of points um diagnosis you need, this is obviously a structural problem. So, although the, the, the, the worst bit of this is the, the rhythm disease, the arrhythmia that comes with it, it's a structural problem. So you need sort of structural imaging. So I think the right ventricular angiography is your gold standard um for that. So that's inherited rhythm disease in a nutshell. And that's the end. So if you don't mind taking a wee snap of um that and I'll put it back up at the end as well. Um If that's OK and filling in the feedback form, um and I'll go back if you have any questions, I'm happy to take them. Um, although I don't know if I'll be able to answer them if that's ok. Uh, would you recommend learning about pharmacology of antiarrhythmics for UK MLA? No, I don't think they're gonna ask you about the Vaughan Williams classification of antiarrhythmics or? I don't think so. II didn't have one in mind. I'll put it like that. Although I'm not sure what they could ask you. You maybe could. But, um, I think that would be quite a, quite a, quite a bad question. Quite a, not a bad question, quite a mean question. But if you're really interested, I mean, it's not that hard to, to remember. I don't think, I think there's like group one is sodium channel blockers and there's a few drugs in that group two is whatever the block potassium channels or something. But um, yeah, that's my best advice. Er, will your slides be available? Er, yeah, the slides are available for anybody that completes the feedback. So please complete the feedback. Um And um yeah, do whatever you want with the slides. That's all good. Thanks very much for that, Steven. That was very thorough. No problem. And uh if anybody else has any questions, please feel free to put them into the chart. Um, otherwise, as Steven said, the slides will be available afterwards after you fill out the feedback form and get your certificate. Um So yeah, thanks very much for attending this evening and we all hope you have a good Christmas break and hopefully we'll catch you at the next lecture, which is the second week of January. All right. Oh, good. Take care. Cheers. Nice Christmas care. See you later. Bye.