you've got four classes class one anti-arrhythmic s' class 2 class 3 and class 4 and the way that people typically learn them as they go through table format and they just sort of brutally memorize everything that you need to know and that might work for some people but that's really not a good way to learn anything in general unfortunately memorizing by charts is one of the poorest ways to retain information and we have research to suggest that that's true so I think that the way that I want to approach this is to use some of my really silly and stupid dirty USMLE mnemonics to help you remember key information and what we're gonna pay special attention to throughout this lecture is how these medications are altering the cardiac action potential and what are their high-yield adverse drug reactions it's not important to know every single bit of information about these drugs you don't need to know which one prolongs the ERP which one prolongs the PR interval no no what you should take away from this lecture if you're struggling to learn these medications is one how do they change the cardiac action potential and can you physically draw on a piece of paper how that action potential is changing based on your understanding of where different ions flow in the cardiac action potential the next thing that you need to know about these medications is their main adverse drug reaction and I say main adverse drug reaction because some of them have very unique side effects that are gonna come up on your USMLE or complex the third thing and this might be obvious but the third thing that you need to know is how to classify these medications so obviously class 1 our sodium channel blockers but have you ever paused for a second and thought about what that means I mean the mechanism and the class is telling you which part of the cardiac action potential these medications will work on so that's sort of an overview and a framework that we're going to use to work throughout this video again I'm gonna point out everything that you need to know as we go through it but I want you to pay special attention to the cardiac action potential the classification of the drugs and the main adverse drug reactions so with that said let's start by talking about class 1 anti-arrhythmic s' so these are the sodium channel blockers and normally when people learn these they go in order of class 1a class one B and class 1c which are the three subtypes of sodium channel blockers but I'm actually gonna rearrange this and we're gonna do them out of order we're gonna do 1c than 1a and then 1b and it'll be very clear why I've chosen to do it this way just to start the way that I want the the reason that I want to do one see 1a and 1b is because it ties in beautifully to my mnemonic and will also help us remember how these medications are altering the cardiac action potential so C a B or kab makes me think of a salty cabdriver and the salty cabdriver reminds me that we're talking about sodium right salty for sodium and Cab for 1 C 1 a and 1 B C a B so the salty cabdriver reminds me that we're talking about sodium channel blocking agents specifically the subtype of class 1c class 1a in class 1b the other reason that it's really convenient to learn them in this order is because if you learn them in the order of C a B then understanding how these will how these drugs will alter the cardiac action potential makes beautiful perfect sense so what you see on the slide are the normal cardiac action potentials drawn in with black lines now let me pause for a second and say that the purpose of this video is not to review the normal physiology of the cardiac action potential and I'm going to assume that you have a basic understanding of that physiology so if you don't really know how the cardiac action potential works then what I would encourage you to do right now is pause the video and go spend a little bit of time getting comfortable at that because you're gonna have to understand how the phases of that cardiac action potential work in order to understand how those phases will change when we introduce drugs that block certain ions so what you see here are the standard cardiac action potentials now just as a very very brief superficial refresher you have faced for depolarizing then you have a quick repolarization with phase 1 then you have phase 2 and then you end with repolarization of phase 3 and this will repeat etc etc so that is what we're looking at right now these are normal cardiac action potentials and what I'm going to do is use three different colors to show you how sub subtype 1 c 1a and 1b anti-arrhythmic s' will change the action potentials so the sodium channel blocker 1c group will decrease the slope of phase zero the most the one a group will decrease the slope of phase zero in in between C and B and then B will have the least amount of decrease in slope of phase zero so as you can see all of the sodium channel blockers are going to decrease the slope of phase zero okay they're going to decrease the slope of phase zero the question is how much is it going to happen one C will do it the most one a will then do it the second most and one B will do it the least so going in order of C a B for our salty cabdriver reminds you that you start with the most and then you just go down in descending order and I think that it's easier to learn it this way than to do a B C because if you do a B C then it's it's out of order if you do it C a B then it goes in descending order so one C will decrease that phase zero slope the most one a will decrease that phase zero slope the second most and one B will decrease that slope the least so this is the first really really high yield bit of information that you need to know when it comes to the sodium channel blockers the next thing that you need to know are the actual different agents in these different classes and I've put them on this slide here flecainide and propafenone are the sodium channel 1c agents quinidine dye so pyramide and procainamide are the sodium channel 1a agents maxilla teen and lidocaine are your sodium channel blocking 1b agents now it's really not that important to know which agents go into which group although that can certainly help you on exams but what is super important to know very very high yield are the main adverse drug reactions or ADRs that will occur with each of these drugs and I've put them in here in black text and I'm gonna give you some really cool mnemonics to remember this but let's explain them first so the 1c agents flecainide and propafenone are contraindicated in ischemic tissue so you can't use them post em i the 1a agent quinidine will cause Sencha nism which is headache and tinnitus procainamide will cause drug-induced lupus and all of those 1a agents can cause tore sad to point so the I put drug-induced lupus on the same line as die so pyramide but it corresponds with procainamide and then all three of those 1a agents can cause TDP also known as torsades the one be agents maxilla teen and lidocaine these are the best post mi they're great for our ischemic tissue so post myocardial infarction you could use the 1b agents so how do you remember all this stuff well I've got some really cool dirty USMLE mnemonics the 1c agents c4 can't use post mi or c4 contraindicated 1a so quinidine I think of quench anism so the actual term is sinchon ism but quinidine is quench anism because sinchon ism kind of scent like the c sound kind of sounds like the q Quinn cinch quench cinch quench anism whatever it's headache in senators just memorize it die so pyramide can cause de pointes or torsades torsades the point de índice of pure my d indy points and then procainamide causes prescription induced also known as drug-induced lupus so prescription induced SLE the pn prescription for the p and procainamide and then your 1b agents really the only thing that you need to know is that they're the best post mi so b4 best post mi so this is the high-yield stuff to know for your sodium channel blocking antiarrhythmics again to quickly summarize you we learned them in order of CA B because of our salty cab driver cab for CA B and salty tells us we're talking about sodium channel blocking agents if you learn them in order of CA B then as you go down from C to a to b they decrease the slope of phase zero in descending order and I've shown that here with red blue and green changes to the cardiac action potential the 1c agents are flaking ID and propafenone and C cannot use them post a my C for cannot use or C for contraindicated quinidine for Quinton ISM also known as sinchon ism which is headache and tinnitus that's a very high yield adverse drug reaction for quinidine die so pyramide as well as quinidine and procainamide can cause torsades de pointes so the d into point and the d and die so pyramide procainamide is is known to cause drug-induced lupus so we've we memorize that by saying prescription induced lupus because pee and prescription and pee and procainamide and then your one B agents be for best post mi so here's a chart and I think that we should fill this in as we go through this lecture just to be really complete so we've filled in all of our sodium channel blocking agents remember again that the mechanism here is that they're blocking phase zero which is the inward sodium ionic current adverse drug reactions I fill it in your 1c agents are contraindicated post am I your 1b agents are best post em I remember synchronism for quinidine drug-induced lupus for procainamide and torsades for all three so we've talked about our class one agents we've used some stupid mnemonics but I hope that you paid special attention to how it changes the cardiac action potential what the mechanism is and what the main adverse drug reactions are so now let's talk about class two class two are the beta blockers and beta blockers I'm sure you're a little bit familiar with these are things that end in a law right / panel of metoprolol asthma law Atena law the mechanism of the class - beta blockers is that these decreased slope of face for depolarization by suppressing AV nodal or SA nodal activity so what you see in black is the normal cardiac action potential and if you introduce a beta blocker it will shift and change to what you see in red and the reason that this happens is because you're decreasing the slope of that phase for depolarization by decreasing your AV s a nodal activity so by inhibiting the sympathetic drive into the system you decrease the slope of face for depolarization because you're altering the ionic flow of your normal currents so how do you remember all this well this one's pretty simple to be honest with you the way that you should remember this is with four letters so beta has four letters in it sa AV is for total letters so beta blockers suppress the AV SA node beta has four letters sa AV is a total of four letters all of these drugs end in O law that's four letters and they're often used in afib a flutter and I remember that because a fib has four letters also four letters tells us of course that you're decreasing the slope of phase for depolarization so everything with beta blockers has to with for the only thing that has nothing to do with that is the fact that these are categorized as class two anti-arrhythmic s-- so if you can memorize the beta-blockers are class two anti-arrhythmic s-- and then queue yourself to remember that everything has to do with four because beta has four letters si AV is four letters O Lal is four letters it decreases the slope of face for depolarization and it's oftentimes used in afib a flutter a v has four letters then you'll know everything that you need to know about beta blockers and the side-effects that you should know are things that you already know from having done your pharmacology section so I'm going to leave that out for the purposes of this discussion but let's fill in our chart beta blockers are pretty simple they block phase 4 which is your sodium potassium baseline leak current it causes COPD exacerbation impotence and hypoglycemic masking that one's really really high yield so know that if someone's hypoglycemic but they're on a beta blocker it can mask the symptoms of it this is why in an overdose of beta blocker you actually give glucagon examples or anything that end in O law and just remember again that for our class to anti-arrhythmic beta blockers everything has to do with the number 4 because there's four letters in beta so phase four olá a fib na AV so that's everything that you need to know about beta blockers again for the purposes of this discussion we're paying very special attention to the cardiac action potential the adverse drug reactions which I sort of glossed over for beta blockers because you should already know them since you've done the pharmacology section but that's really everything that you should know so we've done class one our sodium channel blockers and now we've done class two our beta blockers let's move on and talk about class three our potassium channel blockers so the examples of potassium channel blockers include amiodarone I butyl I'd dil fettle I'd and soda law and this is pretty easy to remember because it spells out the word AIDS so how will you remember that AIDS has to do with potassium well you just have to memorize it unfortunately a IDs are your potassium channel blockers your class three anti-arrhythmics so the mechanism of the potassium channel blockers are that these prolong phase three of repolarization so in black you see the normal cardiac action potential and what happens if you introduce a potassium channel blocker also known as a class-3 anti-arrhythmic is that that you're gonna prolong phase three of repolarization and what you get is shown here in blue now the way that you can memorize this is that potassium begins with the letter P and if you draw out a letter P on top of this cardiac action potential where the looped part of the letter P gets bigger or moves more to the right is how the cardiac action potential changes so I've drawn in the letter P on top of this action potential and where that curvy part of the letter P is all the way on the right of the letter P that'll move more and more to the right which is really what happens if you prolong phase 3 of repolarization now it's easy to remember this because potassium channel blockers are class 3 antiarrhythmics and the mechanism is that they prolong phase 3 so 3 & 3 line up beautifully so this has to do with the letter 3 so if and just to really show you what I mean here if I take out this P but show you with red how this cardiac action potential is changing were prolonging phase 3 of repolarization so again we're prolonging the loopy part of the letter P shown here in red so you've got your little depolarization and then the repolarization gets further and further to the right so you can draw in the letter P and make that loopy part of the P get longer and longer and longer aka move further and further to the right and that's how the cardiac action potential changes high-yield adverse drug reactions to know there's a few and of course it should be no surprise they all have to do with the number 3 so they all have 3 letters in them one is that class 3 antiarrhythmics can cause torsades and one of the ways that we write torsades in shorthand is TDP which has 3 letters for amiodarone specifically this can be toxic to the lungs toxic to the liver and toxic to the thyroid so you want to check PF tees lfts and TF teas and notice that all of those things have three letters so potassium channel blockers are class three they prolong phase three of repolarization and all of the high-yield adverse drug reactions and tidbits of knowledge that you need to know have three letters so torsades TDP has three letters amiodarone you want to check PFT LFT TFT those all have three letters and actually these drugs have effects that are similar to classes one two and three so they can block some sodium they can hit a little AV nodal and they can also do potassium so they have similar features to three classes even though they're technically isolated as class three agents and specific that's specific to amiodarone it's very very high yield so again potassium channel blockers class three prolong phase three all adverse drug reactions have three letters we remember the types of drugs with a IDs AIDS and everything that would probably come up on an exam typically it'll be about Meo Tyrone but just know all of the examples for completeness sake remember that that amiodarone has class one two and three effects PFT lft TFTs need to be checked and these can all cause torsades so that's your potassium channel blockers if we complete our chart here let's keep it going mechanism is that a prolonged phase three which is your outward potassium current so because obviously it's blocking potassium so it's blocking that part of the cardiac action potential your ADR is all with three letters and your examples a IDs remember that most of your questions will come from amiodarone because it's a pretty unique pharmacologic agent but no all of them for completeness sake so that's class three our potassium channel blockers we've now done class one the sodium's class two the beta blockers and class three the potassium channel blockers to quickly refresh your memory remember about our salty cab driver that's armand demonic for class 1 class 2 beta has four letters so it's everything to do with the number four class three potassium is everything to do with the number three and now let's wrap up by talking about class four which is our calcium channel blockers so the calcium channel blockers are probably the easiest of these four classes to memorize and that's because there's two drugs that you need to know in just two there verapamil and diltiazem and you've probably heard these names mentioned before so they're a little bit easier to commit to memory the mechanism here it may seem complex at first but I'm going to break this down and make this really simple for you so calcium is really implicated all over the cardiac action potential in too which source you read you're probably gonna see different bits of information as to which part of that action potential they affect what I think that you should know is that calcium channel blockers are class four agents are class four anti-arrhythmic s-- they decrease the slope of phases zero three and four so if you look at how a calcium channel blocker will alter the cardiac action potential it really doesn't make sense unless you memorize zero three and four and it prolongs repolarization via the AV node which is the you know the phase three part of zero three and four so what you see here in black is the normal cardiac action potential and if you introduce a calcium channel blocker what you get is the movement from the black lines to the red lines and again the only way to really make sense of this is if you understand what phase of the cardiac action potential is changing and how the calcium channel blocker acts on them so it decreases the slope of phase zero phase 3 and phase four and for phase three specifically it's prolonging repolarization by acting on the AV node and this is why you can actually give calcium channel blockers in things like atrial fibrillation where you want to suppress AV nodal activity so how do you remember this right there's a lot going on it's zero it's three it's four it's AV nodal blah blah blah I know that it's overwhelming but let's keep things stupid and let's keep things simple so these are calcium channel blockers and calcium has seven letters what do you get if you add zero three and four you get seven so it decreases the slope of phases zero phase 3 and phase four and phase zero plus phase three plus phase four is a total of seven and calcium has seven letters in it the other thing that you can memorize too to remember that calcium are your class four agents is that of phases zero three and four the highest number in that group is four so calcium is class four but the really important high you'll take away here is how calcium channel blockers change the cardiac action potential so be able to draw out the change from the black lines to the red lines and if you understand the physiology of the cardiac action potential then you can understand that phases zero three and four are really technically changing here and that corresponds to what we see if we introduce a calcium channel blocker the to adverse drug reactions to know here are the least high yield of all of the ones that I've gone over today but it's lower extremity edema and constipation so let's fill in our chart our calcium channel blockers are our class four anti-arrhythmic s-- again they block phases zero and four and prolong phase three the way that you remember that is that zero plus three plus four is seven and there are seven total letters in the word calcium the adverse drug reactions are lower extremity edema and constipation and two examples that you should recognize on exams would be verapamil and diltiazem so that's it this is your chart you refer to the end of this video if you want to just look at the chart I know that this is a little bit scary it's a lot of information but if you start this lecture by first reviewing the cardiac action potential and then going through these anti-arrhythmic syn order from class 1 to class 2 to class 3 to class 4 I think that you'll be able to tackle this really complex topic remember the most important thing to know here is how the cardiac action potential is changing so be able to draw out the normal cardiac action potential and what happens to it when you introduce any of these anti-arrhythmic agents remember your adverse drug reactions especially for all of the class 1 agents and amiodarone those are the highest yield without question but at the end of the day this is a really really terrible topic to learn and I hope that I was able to simplify this for you