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Uh Hi, everyone. Im, welcome to the last lecture of today. It was given by Rohan on pharmacology and cardiology. So, over to you, thank you, Charlene. Hi, everyone. Um My name's Em Rohan. So I'm one of the Preclinical education officers at Beer. Um It's a pleasure to give you this talk today on the Pharmacology of cardiology. Um If you have any questions throughout talk, don't hesitate to put the question in the chat. I'll be checking the chat and also if you have any, if there's any technical issues, just put that in the chat as well. So without further ado, let's get started. So it's still a little bit about me. So I um I'm a third year medical student at UCL currently in intercalating in cardiovascular science. And my research project is based at Barts NHS Trust and it's focusing on the association in deprivation scores and cardiac implants or electronic device arrhythmias specifically ICD S. Um I've got a profound interest in medical education. I'm the Preclinical Education Secretary for UCR Medical Schools. The cricket team run the CC as well as being a senior and transition mentor for first year students. So I really do like teaching. So let's start off, uh, with the topics covered today. So we're gonna look at first topic is hypertension drugs and, uh, anti hypertensive agents. Second topic, we're gonna look at drugs of heart failure. Third topic, we'll look at antidysrhythmic drugs. Ok. So let's start off with the first topic. Anti hypertensive agents. It's a very important topic. It comes a lot, it comes up a lot in exams in your first year and second year, regardless of which medical school you're at. So definitely, um make sure you know this for your exams. Ok. You might, some of you might have heard about the renin angiotensin aldosterone system, the ras very important system, OK? And it all to do with the secretion of renin from the kidney, which leads to the conversion of a protein called angiotensinogen from the liver. Again, common SS ba make sure you know that angiotensinogen is secreted from the liver that is converted by renin to angiotensin one, which is then through the ace enzyme angiotensin converting enzyme that is converted to angiotensin two. Again, a common exam question. And then that has a number of effect. Your 10 has a number of effects which we're gonna look at. OK. And there's some are listed here. So this diagram you might have seen before, very important. So I definitely spend some time going through that. All right. So looking at BP. So normal BP, first of all, is usually between 9090 is the sys systolic and the 60 is diastolic and 100 and 2080. Ok. In between that range, according to nice, every increase of two millimeters of mercury is associated with a 7% increased risk of mortality from ischemic heart disease. So, it's really important to keep that under control. And hypertension is I, is defined as having a systolic BP above 140 millimeters of mercury or diastolic above 90. Ok. Right. In terms of the causes of high BP, well, this it separates into two casualties. The idiopathic essential, which is the most more prevalent type. Ok. Um Then there's also the secondary cause of high BP, which the secondary ones can be reversed if you addressed. Uh If you address the, if the issues, for example, the co of the aorta, once you fix that, then the BP should reduce. Ok. So let's now look at the determinants of BP. So you might remember from a level when you looked at the two equations. So BP is cardia output times total peripheral resistance and cardiac output is cyst is stroke volume times heart rate. Therefore, BP is cyst er stroke volume, times heart rate times total peripheral resistance. And the goal of your treatment is to bring, as we, as we mentioned, BP back towards normal. So you could either target uh the the stroke volume, the heart rate, the heart or total peripheral resistance, the vasculature. So we'll look at some of those different drugs uh, in a moment. OK? If you have any questions, don't hesitate to put them in the chat. OK. So, so what should we treat with? So, a good way to remember this. OK. Is, well, before we look at the drug, let's first focus on the non pharmacological aspect. So, diet and exercise are really, really good er way to reduce your BP, having a low sodium diet exercise. These are all good ways that um we mention to patients first before starting them on um any er treatment. OK. So in order to remember it, I'd say the there's ABCD um way to remember it. So the the the first line drugs that you use. So a stands for ace inhibitors, which we talked about and angiotensin two receptor blockers. All right, which is involving the, the ra um system. The B the beta blocker is not really used it usually 1/4 line treatment. So don't worry too much about those. And the C is the calcium channel blockers, OK? Such as amLODIPine D is a diuretic. So the thiazide or thiodia is like and potassium sparing er drugs. There are also other classes such as alpha blockers um which also can be used and the monitor to take notes of are the ace inhibitors, calcium channel rock and the diuretic and they will be the main ones that will be used. So, first of all, starting off with ace inhibitors, OK? Ace inhibitors, the way to remember it is it ends in Pril. OK? So Ramipril, Lisinopril. OK? Um That's the best way to remember it. If you see anything that ends in Pril, it's an ace inhibitor, it's gonna work to reduce your um uh BP. OK? Then you've also got the ace inhibitors act in the conversion between angiotensin and angiotensin two. OK. So it prevents the formation of angiotensin two. So therefore, there's less vaso constriction, there's less water retention and less aldosterone if that makes sense. OK. Whereas the angiotensin receptor blockers, um for example, they act on angiotensin two, they prevent angiotensin two from binding to its receptor. It in a similar way, it prevents all these effects occurring. And you can remember those by looking at the ending. So they all end in 10 R, 10 R 10. So Losartan Candesartan, OK. That's the way to remember it. Some of the caution side effects the 4th, 1st and 2nd, you don't really need to know lots of side effects at this stage. I say the most important one to know is the cough, the ace inhibitor. OK. The that we use sometimes in a RB instead of an ace inhibitor is because the ace inhibitor can lead to a cough and that's due to the build up of bradykinin. OK? That's something I would take note of that. So often asked in questions. OK. Now let's look at beta blockers again. I said that they play a minor role in the treatment of hypertension. But nevertheless, as you know, if, if you've covered um a arogenate receptors, there's a different types of receptors and they have different functions. So the heart, there's lots of beta one receptors, the kidney, there's also beta one. So we can target these ones in red. So beta blockers, they end in um pro so for example, Bisoprolol, Atenolol, OK. These are all the beta blockers, ok? And some of them are selective, for example, bisoprolol, but some of them are not such as labetalol. So you don't need to re at this in first a second. You don't really need to know specific indications but just be aware of that the beta blockers are sometimes used, ok? You have to be careful that it could cause uncontrolled heart failure as well. So you have to be careful and cautious. You do have to be very cautious in using an asthma patient because it could cause constriction and it could lead to um to severe problems with the patient. Calcium channel blockers are the dihydride. So, amLODIPine, the most important one, the calcium channel blockers to prevent the entry of calcium into um the heart. Um I came on, yeah, we've started to can everyone hear me someone to put a message in the chart just to confirm that you can hear me. Yeah. You can. Ok. Fine. All right, great. Ok. So yeah, the calcium channel blockers. Yeah. Ok. So those are some of the, put, some of the courses and side effect. Don't worry too much about the course and side effects at this stage. Just know that we have um got the different types of drugs they end in ps amLODIPine. Ok. And they, they prevent the entry of calcium into um the heart. Ok. And therefore reducing contract um contraction. OK. So the next um thing here, but the important thing to know is that for the dihydrin, they mainly affect the um the smooth muscle contraction in the periphery. Ok. So we will come on to some of the calcium channel blockers that are specific for the heart. But what's important to know is that these particular calcium channel blockers, they target the periphery. So therefore, you're reducing the amount of peripheral resistance. So maybe there's less contraction, there's less peripheral um resistance. I hope that makes sense. We'll cover some of the other calcium channel blockers afterwards. OK. So th this one here beam pill is also a calcium channel blocker but it's used in heart failure. It targets the heart. Ok. Diuretics again, really important if you've done the kidney that would and this will help um with that there are different types of diuretics. So the first one is um the thiazides. So for example, Benzo thiazide, OK, that targets the N ACL S importer. OK. You've got thiazide like diuretics, some here in and they act in the same way and the ones that's important is the potassium sparing. OK. Spironolactone. That is an aldosterone. Um that is an aldosterone um antagonist. OK. So that prevents OK, the contract um the the amount of water to be absorbed. Ok. So, and that what you do have to be aware of that and that can cause hyperkalemia. OK? So you have to monitor their potassium level. OK? So these are some of the drugs for diuretics. Let's go on to the next one. Now, this is the algorithm. OK? They won't expect you to know this. OK. Draw this out or anything but you do need to be aware of what you would prescribe um in hypertension. So if someone has this from nice, OK? Um If you have hypertension with type two diabetes, then you automatically give them an ace inhibitor or angiotensin receptor blocker. OK? Usually you start with the ace. But if, if that says, because there's side effects as we said about with the ace, you put them on A A RB instead. However, for if they are aged 55 or over, they're black African or they're age less than 55 and not black, then you start them off. Um Sorry if you, if they're less than 55 and not a black African or uh carrying origin, then you still give them ace inhibitor A RB. But it's those that are aged 55 or overall black African or a Caribbean. You start those people off with C CBS calcium channel blockers. OK? So we'll look at this is that this is useful to be aware of. As you can see that we tend to just use the ace inhibitor A RB, the calcium channel blocker and the thiazide like genes. We don't really use the alpha blocker or beta blocker. That's 1/4 line treatment. OK? Sometimes they put beta blocker in, in the SBA just to throw you off but just make sure that um you don't get thrown off. So let's go through an SBA. OK? Um And again, they've, we'll go to this, a 63 year old black man presents for a check up at his GP. He has no significant past medical history but admits to a poor diet. His BP is 153 of 95 millimeters of mercury. And the GP wants to start medical management, which of the following medications is most appropriate. So have a think about this and put your answer in the chat. Um I'm gonna, if anyone wants, I'm gonna get the algorithm up for you. So I'm gonna show you the algorithm just have a read of that. OK? And then I'm gonna put, look at the options and I'm gonna put the algorithm here that might help you in case you're not unsure, give you a few 30 seconds of that. And if you wanna change your answer, then you can change your answer. OK? All these sides will be available afterwards. Anyone else? OK. So yeah, the answer is a amLODIPine. OK. So if you look at this algorithm, OK. The, the patient is a 63 year old black man. OK. So this patient here, OK. He, he's whether he's black, he's his patient is Black African Af um African Carib. So therefore, automatically you have to give him calcium channel blocker and obviously as well. It's age 55 as well. But because he's Black African, you have to give him the calcium channel blocker which is amLODIPine. Remember the calcium channel blockers and in P OK, I hope that helps. So this is hypertension. Best way to this I would say is just use the ABCD approach, write down the different drugs. They make sure you know an example for each um and be aware of this algorithm for revision. OK. If anyone's got any questions, please feel to, to put it into the chat and then we'll move on to heart failure. OK. So that's good heart failure, drugs of heart failure. OK. So first of all definitions, OK. Just so you're aware. So the physiological definitions, it's the failure of the heart and it's compensatory mechanisms to provide sufficient blood flow to meet at metabolic demand. OK. Clinical definition, it's a complex clinical syndrome that results from any structural functional impairment or ventricular filling or rejection of blood. Ok. Um And sometimes we do use, um we do, we tend to prefer, we tend to use heart failure over congestive heart failure. Yeah. Right. In terms of symptoms and signs, you might have heard of the terms right heart failure, left heart failure, ok. Right. Heart failure is all about the congestion of the peripheral tissues. Ok. So the right ventricle is having problems. So there's congestion of peripheral tissues. The common sign of right heart failure is edema. Ok. So if you look at someone, let's say in their legs, you'll see that they will, there'll be edema present. Um You can get gi tract con congestion, liver congestion, it's all to do with the venous system. Yeah, there would be congestion in the venous system. That's how I'd remember it. Whereas the left heart, left heart failure is slightly different. Ok. Main thing is gonna be decreased cardio out but the left ventricle is not gonna be as efficient as pumping blood. There also could be pulmonary congestion with entry, the pulmonary vein into the left atrium. There could be pulmonary congestion if the left ventricle can't pump out enough blood. Ok. The symptoms and signs and the Frank Sterling curve you might have heard about this. Ok. So the Frank Sterling curve is talking about how the initial um length, the initial length of the uh sarcomere is proportional to the amount of um contraction that you'll get. Ok. And you, it's usually illustrated by this particular curve here. Ok. The amount your preload, which is your left ventricular um your end dilic volume, that will be that will determine your stroke volume, how much blood that the heart can pump out. Ok, into the aorta. And in a normal heart, you should get this nice curve going out here. Yeah. Ok. But in heart failure, the heart is not able to pump efficiently. So you this curve will be reduced downwards. OK? And when you reach around this sort of threshold here, you will get congestion in the um in the venous system. OK. Right now, next thing is the pathophysiology of heart failure. So heart failure ought to do with a low cardiac output. OK? And what can happen is that the hearts will try to compensate for that. So you can get sympathetic nervous activation that can then go back to try and um lead to. So sodium and water retention to try and increase your preload. OK. The amount of your preload. So then therefore it will try and reduce that heart failure. Yeah. Um So with lots of comp comp mechanism and it can lead to cardiac remodeling. So you could get eventually, for example, right? Er Venular hypertrophy, the heart will try and adapt to those changes. OK. The next thing here, pharmacologies, we're gonna talk about. The main thing they're gonna test you in question, especially for the pharmacology aspect is different drugs that I use what are the different drugs use? What are their functions? OK. It's com make common SBA questions. These are some of them here. It might look a bit daunting. We're gonna go through each one in detail. So if you get thrown with this sort of complex diet, best thing to do is just break it down into smaller chunks. So let's now look at the management of chronic heart failure with reduced ejection fraction. OK. So the first step, we're gonna look at some of the drugs here. So the ace inhibitors, the beta blockers, OK. Um And then we'll look at some, we'll work our way through this. OK. So the first thing to do, let's talk about the loop and thiazide diuretics, OK? That is a first line treatment for heart failure. OK? And what they are affecting is the amount of water retention. It's gonna lead to an increased amount of water retention. So you get an increased preload. OK? And there's different parts. So the loop diuretics, they work on the thick ascending um loop of Henley. OK? You've got some of the MRA S, they act on the collecting duct, um mineral receptor, um mineral altoid receptor antagonists, for example, spirolactone, they will act on the collecting duct and you've got the Pfizer diuretic. So they're gonna act on the N ACL co transporter. It's a good way of thinking about it. OK. So when you're looking at diuretics, I'd write down, you'd have the MRA S, you have the loop diuretics and the thiazide diuretics, three types of drugs you need to be aware of. So looking at the loop and thiazide diuretics. So the first one famide is a loop diuretic. OK? You've got metalozone, it's a thiazide diuretic. They act on different places in the kidney but they all work for the same function. They work to decrease sodium and water retention. OK. Effects will be increased urine output. OK? Some of these a adverse effects here. OK. But in your, in 1st and 2nd year, you don't really need to be aware of those as much. Just be just be a yeah, just just know that they exist but they were all they're more gonna test you on the mechanism of these drugs. OK. Obviously chat with your medical school as well. So you use this in all types. So this is the new, the N yh A. Does anyone know what the N yh A class means? Do you wanna put that in the chart one? OK. It's the New York Heart Association um Heart failure classification system. There's different classes. OK. Uh II put it there. Yeah, New York Heart and there's different um yeah, there's different particular um the different particular level. So in the New York heart classification, you have one, new er N yh A class one, N yh A class two plus three plus four. And they describe different um effects of heart failure So number one is the, the least adverse and number four is the greatest. Ok? I hope that helps. Right. Next thing is the ace inhibitors. We talked about ace inhibitors lot, you'll see a lot of overlap in drugs. Ok. So ace inhibitors, um or if the ace inhibitor causes adverse side effects, you can give an A RB as well and then also beta blockers. So beta blockers are used in heart failure, They're not using hypertension unless it's 1/4 time treatment. So beta blockers, they work to for, to activate the sympathetic nervous, they block the sympathetic nervous system activation. OK. So beta blockers. OK. So you've got Bisoprolol and um Carbol, they block beta one. OK? And some of them um Bisoprolol is a selective beta blocker. So only um block beta one whereas Carbilev is a nonselective. OK. So they affect um as, as we said, they block the sympathetic nervous system activation, OK? In the heart. So it's meaning that the heart doesn't work, you have to work as hard. OK? And that will be used for all types of um New York heart association classes. OK. Then we've got ace inhibitors as we talked about ace inhibit. Again, it, it prevents the formation of angiotensin two from angiotensin one. OK. If the ace inhibitors not, if you don't need the ace inhibitor, you can use it A RB and that prevents er angiotensin binding to its receptor leading to the same effects So ace inhibitors, OK. They end in Pril, as we said, they inhibit asterone production. OK? They inhibit angiotensin two production. They decrease sodium retention, water retention. OK. Um And uh I think that's the main thing, as we said here, the side effect of cough is the one to, to be aware of, OK, angiotensin receptor blockers. So they end in artin, OK. The same thing, they inhibit allo production, decrease water retention. They do not give you a cost. That's why they are usually in the they, they patients are usually started on these instead. OK? I put a few extra things here to the indication, key trial, the clinical use, but focus on the examples mechanism and um the effect. All right. Right. This is the newest type of drug that's been used. SG LTT L2 inhibitors. OK. That's in the, it inhibits the proximal reabsorption of glucose which then defer the effect of um acting as a diuretic and an anti hypertensive agent as well. OK? And these ones here that end and flows in. So you can remember that um in that way, next thing is the vasodilator. OK. So you've got the hydrALAZINE or nitrates. So, hydrALAZINE or nitrates here you can, that will lead to vasodilation and therefore it will reduce your amount of afterload. OK? The afterload is amount of um force needed for the uh the heart to pump blood into the aorta. OK? So if you've got lots of vaso constriction, there's lots of resistance and if you're gonna need a higher afterload. So the aim is if you relax the blood vessels, then you're gonna have a low afterload, the heart doesn't have to work as hard because a high afterload is a bad thing. Vasodilators got the nitrates and hydrALAZINE, they are vasodilators, OK? And they act on the smooth muscle cells and they lead to vasodilation leading to the production of nitric oxide, OK? And they reduce preload and afterload, obviously, adverse effects hypertension. So you want to reduce it, you do want to make their BP too low. OK. Now, next thing is we've talked about is a mineral cor called receptor antagonists. OK? You'll see these is coming up a lot and we usually use these for people that are in class two to class four. OK. So everyone apart from class one. So these ones here they antagonize the effect of aldosterone, OK? Leading to less water retention. So mineral Aldo receptor antagonist, make sure you know, spirolactone, it decreases sodium and water retention acts as diuretic and prevents adverse remodeling. OK. The B1 of the main effects, adverse effects side effects is hyperkalaemia. You must monitor that. Um there you must monitor the potassium level. Yeah. And these are sometimes known as potassium sparing um drugs, OK? Because they block um the the the potassium, they block the effects of the potassium transporter which is constantly pumping potassium ions out into your urine if that's blocked. Therefore, there's gonna be a build up of potassium s inside, inside your cell. It's a new type of drug. Some of you might not have heard of this one. It's called Sacubitril. Valsartan. Now, way to look at this. Does anyone know what Sacubitril is? What does it sound like someone wanna put it in the chart? What type of drug is? Sarubbi? Don't worry about the Valsartan. What type of drug is this here? Anyone there? A few messages? Yeah. OK. So if something has in chill it has to be OK. Um Is that yeah, what people better see what people see here? Uh Let me see, see. Blood TTS. Um Yeah. Ace A OK. So in terms of this drug here, OK. So, so the Sacubitril OK, is a Neprilysin inhibitor. So that counteracts vasoconstriction. Some of you might have not heard of that. I'd definitely be aware of that. OK? So it's leading to vasodilation and some of you said um yeah, the Valsartan, this is a a RB an angiotensin receptor blocker ends in art. OK? Um It's easy one to think that it could be an ace because it ends in like Lisinopril. OK? But actually scuba is a nephrosin inhibitor. So just to recap just to recap. So, sacubitril is a Nephro inhibitor. Therefore, it leads to vasodilation. OK? So nephrosin usually leads to vaso constriction but because we inhibit it, it's gonna lead to relax relaxation Valsartan is a A RB. OK. I mean, there's a new type of drug that's used and it's used in heart failure and it's used for those that really sort of the patients that have a reduced ejection fraction. OK. Next one is digoxin. Um Some of you might have heard of this particular drug, OK. It has numerous um mechanisms, it has a positive inotropic effect. OK? That, so there's two different words you need to be aware of. So there's chronotropy which is to do with uh your heart rate. OK. Um And then you've also got inotrope which is to do with um contraction. OK. Does anyone have any questions so far? Ok. So let's carry on with that then. OK. Um And then digoxin has a positive inotropic effect. It reduces your preload and inhibits the sympathetic nervous system. It actually leads to a greater parasympathetic um effect. OK? To leading to the rare reducing of your heart rate. OK. So uh let me see. How are you doing for me to check the time? Uh OK. What time? Yeah. OK, fine. So let's look at uh yeah, these are some of the trials I'll put there just be aware of the mechanism of action. OK. And the fact is it's an antiarrhythmic drug. OK. Right. And we're gonna come onto that as well. Again, now, devices sometimes if all these drug treatments don't work, then you could use some, you could use um you can consider other therapies. You could use a cardiac resynchronization um therapy or you could use an ICD as well. Ok. So yeah, you can use cardiac arrest resynchronization devices. You could use an ICD and that would deliver a shock um if the patient goes into um cardiac arrest. Ok. So that can help. Um but these are sort of the the treatment, the last resort sort of treatments. If all the pharmacological treatments, then then we will consider devices. OK? There's some of drugs that have no effect in management. So, statins, for example, they don't have any effect. Um any of the like for example, warfarin, any anticoagulation drugs, some are potentially harmful. OK? Um But this is just for, this is what you want me to examined on this. This is just to give you some extra information. All right. Right. So we've got an SBA here. That's all made sense. D do you want to have a go at this? Everyone to spend 30 seconds on that? It does. So these are the sort of questions you're gonna get, ask you what's happened. They'll give you a passage, especially in your 1st and 2nd year. These what they ask about drug types. What does the drug do? Where does it act? Put your arms in the chat. We won um loop. Yeah, it is a loop. Which, which one is it there? Surfing the boot. So, yeah, it's descendingly good. A thick, ascending the loop of Henry. Ok. These are sort of questions you'll get right. Ok. Now let's go on to, unless anyone's got any questions, let's go on to the antidysrhythmic drugs. Ok. Um, so just to give some definitions. Ok. Um, first of all, ok, the dysrhythmia is known as the disturbances in the rate of rhythm, the rate or rhythm of, what's that? Can you explain that, uh, mechanism? Ok. Sure. Yeah. So mechanism of action for, er SGL two. OK. What's it gone? T OK. So what's gonna happen here? OK. So SGR T two T two inhibitors, they're gonna act on the proximal er proximal tubular reabsorption. Um They're gonna inhibit, they're gonna act on the proximal tubular um part of the kidney. OK. The transport of that it's gonna inhibit the reabsorption of glucose. OK. This is a new treatment and the, the mechanism behind it is that as you um prevent the reabsorption of glucose, you're going to lead to less water um reabsorption um back into the bloodstream. So, therefore acts as a diuretic. OK? There's gonna be less amount of preload in the heart. So it's all to do with the, the diuresis that it does that it causes if that makes sense. OK. But it's a relatively new drug treatment. OK. Um Let me see here. So, yeah, let's carry on with this, the anti distributed drugs. So the definition I've talked about is the disturbances in the rate or rhythm of the heart. OK. There's different types, irregular rhythms which will go through abnormally fast. So, tachycardia, abnormally slow bradycardia. OK. Technically speaking, when you do say we tend to say arrhythmia, which actually means without a rhythm. But um the technical term is dysrhythmia. OK? But we usually we use them interchange a bit. OK. So some of you might have seen this, OK? This is, this is a very important common exam question. Make sure you know the difference between a ventricular action potential and a pacemaker action potential, the ventricular action potential. OK. Here we've got this very this massive depolarization. What is this depolarization caused by anyone? Then N zero, you put it in the chart which ion is responsible for this calcium? OK? Anyone else just be careful? Calcium? I know. Yeah. So just be careful with that. So in the ventricular act man, this particular depolarization is called by sodium ions, depolarization is called by sodium ions. OK? The sodium ions channel opening. Whereas in this particular, the pacemaker to do with calcium, be very careful with that. Yeah. And this um this particular number four here is called the funny current. OK. This is the reason why it's called a pace. Why it it's a pacemaker action potential is because this particular channel here OK, readily depolarize this is OK. And that keeps only these action uh potentials um being formed. And that's why you find the pacemaker in the sr nodes. So it's important to know which arms cause these. But the biggest difference is in the ventricular act, there was a, a massive depolarization caused by sodium arms. So zero is because of sodium arms whereas in the pacemaker potential. OK. Up stroke here, the depolarization is called by calcium arms. So be just be careful of that. All right. Treatment for dysrhythmia. Ok. There's a few non drug treatments but we're gonna focus on the drug treatment um today, but some of the non drug treatments are listed here. So ICD S using catheter ablation cardioversion. OK? But we're gonna focus on the drug treatments today. So there's a classification system. You, you might have heard about this in your lectures. OK? We that we use the Vaughan Williams classification. It's a good way to remember it. I focus on learning class one, class two, class three, class four. OK. These ones here, obviously they are um they are A B and C but I want you off first time to learn it, just learn 123 and four and then go into the details about A B and C. OK? So we're gonna talk about these. Yeah. So the three groups of class one. So class one anti drugs, they affect sodium channels. That's the first thing to remember. OK. But they affect it in different ways. So one A is a moderate block of sodium channels. OK? Um And leading into a slow rise of action potential, whereas one B you might have heard of LK. It's quite a popular drug. It's used as a local anesthetic. OK. Um This leads to a mild sodium channel block and a shortened repolarisation. OK. Whereas fluide which is A1C class one, GIC drug leads to a huge and a sodium channel block. OK. And I've listed some of the side effects there just so you know, very similar. OK? Um Just one thing to be aware of is that class one, a disopromine, some of the side effects, it has similar to um the side effects are anticol um collagenic. OK. So for example, you get dry mouth constipation, urinary retention. These are all signs, these are all signs of atropine like effects. OK? You might have covered this in then your latches. OK. So this is class one now going on to class two. So class two, the beta blockers can be be covered that at the start of the literature. OK. Again, they end in OL OK. So timolol metoprolol propranolol, OK. And they block the exci effects of the sympathetic activity by blocking beta one receptors. Remember it's beta one, not beta two or beta three. OK. And by blocking beta one receptors, they reduced the inward calcium current, reduced the pacemaker activity and slow A V conduction. All right, obviously, you do have to be careful with the side effects. As I said, bronchoconstriction. OK? I have to be very careful that in, in asthmatic patients, you don't wanna give an asthmatic patient a beta blocker. Ok. Now class three anti dysthmic drugs, OK. The potassium channel blockers, for example, amiodarone, OK. That prolongs the cardiac action potentials. Remember, potassium is involved in the repolarisation um phase and also in the repolarisation phase. Ok. So what will happen here is if you block the rep, it's gonna take longer to repoise. Ok? And therefore it reduces the time window in the cardiac cycle When dysrhythmias can occur if you're prolonging the action potential, some of the side effects, one to be aware of that is often tested. Um You is hyperthyroidism, hyperthyroidism, um hyperthyroidism, this can amidone can cause um problems in your thyroid to be aware of that. If you get patients say you you in an endocrine module and you do hear about this, they can link this nicely with um dysrhythmic drugs, anti dystrophic drugs, OK. Class four anti drugs. So calcium channel blockers. So remember we said about how amLODIPine which is a calcium channel blocker have. AmLODIPine is a calcium channel blocker in the peri in the periphery. OK. In the blood vessels. Yeah, whereas veramil is a calcium channel blocker as well, but it acts selective for the heart. Ok. So because it blocks that pacemaker that that depolarization. Remember this action potential here is the pacemaker potential and because it blocks the calcium channels, um remember I said the calcium iron channels are involved in the depolarization phase. So in this particular phase here, number zero in the pacemaker is to do with calcium. Whereas number zero in the vent ventricle is to do with sodium. That's something I'd note down. Yeah. Um therefore, if you're blocking those channel, you're gonna lead to a slow rise of the acting potential. And therefore you're gonna decrease um the amount of calcium current and therefore you'll lead to decrease sino atrial node, excitability. OK? And a reduction in the heart rate and reduction of dysrhythmias. Ok. So I hope that helps. Now, let's look at before we finish. Let's look at an SBA here. Put an SBA here. A 63 year old woman was successfully cardio for an unstable broad complex tachycardia. The cardiologist decides to commence oral amiodarone at 200 mg three times a day. What is the mechanism of action of amidone? What do people think these are the sort of questions you'll get in 1st and 2nd year? Good. Yeah. So it is a potassium channel blocker. OK. So um yeah, just be aware of that. It's a potassium channel blocker, as we mentioned. OK. Um And as you can see here, OK, we talked about amiodarone. It's a potassium channel blocker here. OK. So finally, that's the final slide. So thank you all for listening. Does anyone have any questions if you do, please feel free to put it in the chat? And I highly recommend that you um fill out a feedback form and we'll put it just in the chat now. OK. So uh so could you could, you could go back to the flow chart five or the H HF structural? Yeah. So heart failure trucks. It will be take out this one here, I think. Yeah, this one here, the one we looked at. OK. Sr uh Valsartan we looked at here. OK. Um Taku is a nephrosin inhibitor. OK. Valsartan is a A RB. OK. We've looked at Digoxin. OK. Um We've looked at the, the nitrates that leads to er can we vaso er vasodilation? OK. And then we've looked at a few other beta blocker ace inhibitor. A RB. So hopefully that helps. Um if anyone has any more questions, then just let me know if an asthma patient is accidentally given a beta blocker to control hypertension and no effect is seen initially. Can we proceed to um clearly gone initially? OK. I'm not too sure about our question. I would say, I think you did the main thing you want to do if, if you did give an out patient a beta blocker, obviously you want to try and avoid that. If you did do that, you want to try and obviously reverse the effects of that beta blocker. So you give a beta an agonist. OK? And to try and reverse that effect, I'm not really sure why keep Glucagon and I think that was something you'd look at afterwards and monitor her blood glucose level. Ok. Anyone else? Got any questions? Antidote for a beta blocker? Ok. Yeah. How do we get the notes? Ok. Um These slides, I'll upload them. Um, they'll be uploaded, you'll see the recording on, er, metal, but also I'll be uploading the slides as well. Ok. Awesome. Thanks so much Rohan um for presenting today. That was amazing. Um Thank you everyone for coming as well and sitting down for the past four hours, it's been a great session and I hope you learned a lot. Uh, please fill in any feedback forms. You will get the recordings and a note um, in due course. I don't know if it's immediately available, but they will definitely be available to you very, very soon, if not immediately. Um Thank you all for coming. I'm gonna wrap up now, unless anyone else has any other questions, um, put them in the chat, I'll be around for another 23 minutes. Um But otherwise, thank you very, very much. It was great seeing everyone that room.