Cram The Pance - S1E56 Antiarrhythmic Drugs

Episode Date: September 28, 2025

High Yield Antiarrhythmic Drugs Review:Class I (Sodium Channel Blockers)Class II (Beta Blockers)Class III (Potassium channel blockers)Class IV (Calcium Channel Blockers) for your PANCE, PANRE, Eor's and other Physician Assistant exams.Review for your PANCE, PANRE, Eor's, Physician Assistant exams, Medical, USMLE, Nursing Exams.►Paypal Donation Link: https://bit.ly/3dxmTql (Thank you!)Included in review: Pathophysiology of antiarrhythmics, cardiac action potential, phases 0–4, Phase 0 depolarization, Phase 1 initial repolarization, Phase 2 plateau, Phase 3 repolarization, resting membrane potential, cardiomyocytes, pacemaker cells, funny current (If), L-type calcium channels, T-type calcium channels, effective refractory period (ERP), conduction velocity, reentry, rate control, rhythm control, AV node, SA node, QT prolongation, torsades de pointes, post-MI arrhythmias, structural heart disease, supraventricular tachycardia, atrial fibrillation, atrial flutter, ventricular tachycardia, ventricular fibrillation, ACLS, catecholamines, cAMP, PKA, beta-1 receptors, calcium influx, nodal blockade, non-dihydropyridine vs dihydropyridine, Disopyramide, Quinidine, Procainamide, Lidocaine, Mexiletine, Flecainide, Propafenone, Metoprolol, Atenolol, Bisoprolol, Betaxolol, Esmolol, Acebutolol, Propranolol, Carvedilol, Labetalol, Nadolol, Pindolol, Timolol, Sotalol, Amiodarone, Dronedarone, Ibutilide, Dofetilide, Verapamil, Diltiazem, Amlodipine, Nifedipine, Nicardipine, Amiodarone adverse effects, blue-gray skin discoloration, interstitial lung disease, thyroid dysfunction, corneal microdeposits, hepatotoxicity, beta-blocker contraindications, asthma caution, bradycardia, AV block, cardiogenic shock, diabetes caution, CCB adverse effects, constipation, AV block, bradycardia.Become a supporter of this podcast: https://www.spreaker.com/podcast/cram-the-pance--5520744/support.

Okay, so today we're going to go over anti-arhythmics. This can definitely be one of the more complicated topics to learn in school. It can definitely be a lot more daunting compared to the other topics. So I did my best to break it down and probably throw in more mnemonics than I've had in any other podcast. So hopefully that helps you. So before we get started, thank you as always for the really nice comments, the support for the channel. Everybody who reaches out and leaves a nice comment, I truly do appreciate it. So thank you so much.

Let's go ahead and get started with antirhythics. So there's four main classes that you need to know. And that's your class, one. channel blockers, class 2, beta blockers, class 3 potassium channel blockers, and class for calcium channel blockers. So if you ever forget which class is which, remember the sentence, some block potassium channels, some block potassium channels, the letters S, B, P, C, that helps you remember class 1 S, sodium channel blockers, class 2, beta blockers, class 3, P, potassium channel blockers, C, class

four calcium channel blockers. All right, let's go ahead and get started. We're going to start with our sodium channel blockers, but before we do, I want to want to review, dun, dun, dun, the cardiac action potential, as it's the foundation to understand how this class works, as well as some of our other classes that will go over today. So the cardiac action potential is complicated, and to make it even more complicated, it varies depending on which part of the heart we're talking about. We have an action potential in our pacemaker cells, as well as our cardiomyocytes in the cardiac muscle. But I'm going to try to make this as simple

as simple as possible. Let's first start with the action potential of the cardiomyosites. Now, before breaking down each phase, there's a few simple key facts to keep in mind. First, There is five phases, 0, 1, 2, 3, and 4. Next, there's three players in the game, 3 major ions, sodium, calcium, and potassium, which are all positively charged. And finally, at rest, the inside of the cardiac cell sits at about negative 90 milliseconds, making it relatively negative compared to the outside. All right, so let's break it down, starting with phase 4, which I like to call the floor.

Phase 4 is the floor. This phase is the resting membrane potential. The cell is electrically quiet. There is some leakage of ions, but overall, to keep it simple, Just remember, phase four as the floor, as not much is happening, and it's a pretty flat phase. Then comes phase zero. This is where the action starts. Fast sodium channels open up and sodium rushes into the cell, causing the inside to become rapidly

more positive. This phase causes this rapid depolarization and creates this sharp upstroke on the graph. Phase zero, just remember, is all about sodium and depolarization. Next is phase one. A brief but important moment. Sodium channels close, and potassium, the party pooper, as we'll call him, begins to exit the cell. This leads to a slight dip in the membrane potential known as initial repolarization. Phase two potassium keeps leaving like the party pooper he is, but calcium starts to

enter the cell at the same time, which essentially balances things out, and that's why phase two is known as the plateau phase. Ultimately though, the calcium channels eventually close, and potassium, of course, keeps leaving, leading to a rapid drop in repolarization, which is phase three, this big old drop, and then eventually the cell returns to its negative resting state and more back at phase four, the floor. So to sum it up, phase four is the floor, resting state, phase zero is the sodium-fueled upstroke to start the party, rapid depolarization, phase one, initial repolarization, party pooper, potassium starts to leave.

Phase two, calcium saves the day and rushes into balance out potassium's exit. Phase three, calcium eventually gets shut down, and potassium like the party pooper is keeps leaving, big drop and repolarization. Okay, so now that we have a general understanding, let's start with our Class 1 sodium channel blockers. So the meds in this class, well, there is a lot of them. They're broken into subsections, making it even worse. Class 1A, 1B, 1C.

I know learning antirthmics really sucks. I feel you. I do have a mnemonic, though, so we'll go over that in just a minute. So class 1A is diso-pyrimid, quinidine, prokainamide, class 1B is lytocaine and maxillotene, and class 1C is flecanide and propaphenone. So how the heck can you remember all of those? They all sound different and weird. Well, there's a tried and true mnemonic that goes double-quanine,

quarter pounder lettuce, mayo, fries, please. Double quarter pounder, lettuce, mayo, fries, please. Know this mnemonic really well, as it's not only going to help you remember the meds in this class, but also some additional mnemonics that I have thrown in. So starting with your class 1A drugs. Double quarter pounder, DQP stands for Dysop pyramid, which is the D. Q stands for quinidine, and P stands for prokynamide. Now, I've got a little twist to this mnemonic that's going to help you remember a key feature

of these 1A drugs that you cannot forget. Picture your double quarter pounder, not. on a regular hamburger bun, but instead, remember, it's stuffed inside of a foot-long hot dog bun. A double-quarter pounder and a foot-long hot dog bun, it sounds odd now, but trust me, it's going to make sense and help you soon. Okay, next our Class 1 B drugs, lettuce mayo, stands for Lidicane and McSillotine, and then finally our Class 1-C-Meds, Fries, Please, which is Fleckinide and Propaphanon. So once more, double-quarter pounder, diso-pyramid, quinidine, and prokaneamide, Class 1A, remember it's on a foot-long hot-dog bun, lettuce mayo, which is

lytocaine and maxillotine class 1b and then fries please flecanide and propaphanone class 1c so that's how you remember the meds in this class now let's talk about how they work on that cardiac action potential we discussed before of the cardiomyocytes so if we think about our cardiac action potential we talked about before where do we think the main area of impact would be when did sodium the party animal join in so phase zero right our big spike de polarization so when we add a sodium channel blocker to a patient within arrhythmia, we decrease sodium influx, and it's kind of like cutting the gas to the engine and slowing things down a bit. And by slowing phase zero depolarization, we slow conduction velocity, and this can suppress ectopic beats, interrupt reentrance circuits, helping to restore normal rhythm.

Now here's where it gets a little tricky. So these meds are all sodium channel blockers, but they all impact sodium in varying degrees. Some are potent sodium channel blockers, some are weak sodium channel blockers, some even block potassium. So let's make this as simple as we possibly can. So starting with our Class 1C drugs, which bind the tightest and the longest, making them the most potent sodium channel blockers causing the steepestrediction in the Phase Zero upstroke. And even though they stretch out our Phase Zero Upstroke, they don't really change the action potential duration. The action potential duration, by the way, is just the total time it takes for a cardiac cell to complete one cycle. So from Phase Zero depolarization to the end

of Phase 3 repolarization. Next is our Class 1A drugs, which produce intermediate block A producing a moderate slowing of phase zero, but most importantly, they also block potassium. Sneaky little guys. So this lengthens the effective refractory period and the action potential duration, resulting in QT prolongation, which is going to cause some issues. We'll go into more depth about in just a few minutes. And then finally, we have our Class 1B drugs. They bind and release very quickly, so their effect on phase zero slope is minimal.

They also decrease the refractory period a bit, too, which can shorten the action potential duration. So I have an easy way for you to remember the different subclasses and their strength of impact on the sodium channel simply by remembering the more salt and the food, the more it blocks sodium. So remember our mnemonic double quarter pounder lettuce, mayo, fries, please. So out of all of these, which has the least amount of salt? Double quarter pounder, lettuce, mayo, or fries, please. And this isn't a trick question. Just think about the foods and think about what has the least amount of salt. So lettuce and mayo, right? So class 1B, lytocaine and mixilatine, have the least sodium channel blocking activity. Next, which of these foods has the most salt? The fries, right?

So fries please, class 1c, phlecanide and propaphenone exert the most potent sodium channel blocking among the class 1 agents, which finally leaves us with our double quarter pounder, class 1A, which has moderate amount of sodium. So these meds, diso-pyramid, quinidine, and prokainamide have moderate sodium channel blocking activity. So that's how I remembered it. There are other nemonics, but the salt thing just made sense for me and worked. Okay, so the next thing that I want to go over is a few high yield things to know about each of these meds, starting with our Class 1A sodium channel blockers. So Class 1A, remember, is double quarter pounder, diso-pyrid, quinidine, prokaneinamide. Now before I told you remember, this double quarter pounder is on a foot-long

hot dog bun, and you probably already have an idea of why I said that. So all Class 1A drugs are notorious for prolonging the QT interval. So things like Torsad de point, a dangerous form of polymorphic VT are possible with these medications. And that's because like we want to over before in addition to blocking sodium channels they also block potassium prolonging the action potential and they're the only subclass of sodium channel blockers that do this so class 1a drugs you have to know they can prolong the QT interval so very important and very likely a test question so the way that you're going to remember that is thinking back to our nomotic again same nomotic over and over so double quarter pounder on that foot long hot dog bun so we remember double quarter pounder

diso pyramid quinidin and procanamide you're always going to remember that double quarter pounder is on a foot long hot dog bond. And that's because all of these drugs can prolong the QT interval. So that double quarter pounder, oddly on this foot long hot dog bond helps you remember class 1A drugs prolong the QT interval. Nice and simple. Don't forget it. So let's talk about quinidine first. Now I know we just said all of the meds in class 1A prolong the QT interval, but quinidine really prolongs the QT interval. Quinidine has historically been one of the most common causes of drug induced for side to point. And the only reason it isn't still at the top of the list today is simply because we don't use it much anymore. It has a poor side effect profile and

their safer meds. There is still some utilization in recurrent VTac and Brugata syndrome and short QT syndrome. And I'll give you a second to think about why we might use this drug to treat short QT syndrome. Yeah. So, but overall, it's usually not going to be a top pick. With that being said, you still got to know it because in addition to potentially causing Torsada point, it has a unique side effect that's often tested on. So the highest you'll thing you need to know about quinidine is that it can cause something known as cintianism. Weird name, but the backstory may help you to remember it. So there is this tree called the cinchona tree native to the Andes.

It produces bark that's rich in alkaloids. This bark is not only the source of quinidine, but also the source of quinine, which you're probably familiar with for its treatment of malaria. So both of these meds, which come from the same tree, share a side effect from their plant origin, sentianism, which can cause a constellation of symptoms, tinnitus, hearing loss, confusion, delirium, visual disturbances. and we call this cintianism as it's named after the tree it's derived from the cinchona tree. So hopefully that little backstory helps you to remember.

Quinidine can cause cincionism and of course torsade to point. Next drug from Class 1A, it's much higher yield and that's procanamide. Procanymide is another effective anti-arhythmic drug that's again limited by its side effect profile. And there's two things you need to know about procanamide that are very high yield, Wolf Parkinson-White and Lupus. Let's talk about that. So procanamide can be used to treat arrhythes associated with Wolf Parkinson-White-Sy syndrome. This is a popular exam.

question, so you need to know it. Next, this drug can cause lupus-like syndrome or drug-induced lupus. So chronic administration of prokhanomide can lead to lupus-like syndrome, so these patients will have similar symptoms to those seen in lupus, rash, arthritis, etc. So these are the two things that you need to know about procanamide. It can treat wolf-parkinson white arrhythmias, and it can cause drug-induced lupus. So how do you remember that? So instead of remembering it as prokaneumide, remember it as protrainamide. Every time you hear prokainamide, I want you to think pro-trainamide and have this picture in your head of this big train rolling down the tracks at the front of the train the conductor is a wolf with bright white fur that's your cue for wolf parkinson

white and this train is circling in this continuous loop which will help you remember lupus-like syndrome so pro canomide is protrainamide think of a train being driven by a white wolf wolf parkinson white circling in a continuous loop lupus like syndrome and then our last drug in the class one a class is dysopyrid, which instead I used to remember as dryso pyramid, D-R-Y, dry, because the only thing I think you should know about this drug is it'll dry you out as it causes anticholinergic side effects, which is the most common adverse drug reaction. So it can cause dry mouth, dry eyes, urinary hesitancy, constipation. So avoid this in patients that have glaucoma, myasthenia, et cetera. So remember, instead of diso-pyramid, remember dry-so-pyramid, DRY, to remember the anticholinergic

side effects. Okay. Next is our class one. B. What are the Class 1B drugs? Remember, Class 1B, lettuce mayo, lytocaine, and macsilatine. So starting with lytocaine, when administered intravenously, can be used for the treatment of ventricular arrhythmias. Most common ADR is going to be CNS toxicity. And then we have mixilatine, which is essentially an oral version of lytocane. It can also cause CNS toxicity, but because it's a POMED, we often see GI problems, nausea vomiting or heartburn. Not important. What you should know about these two meds is when prescribed, it will be for fast and failing ventricular tissue. So if you're going to use these meds, it will be fast ventricular

rhythm, so ventricular tachycardia, ventricular fibrillation, and or on failing or ischemic tissue. So ischemic arrhythmias after a myocardial infarction. And that's because the class 1B meds preferentially binds sodium channels in the depolarized and inactivated state, which are common in ischemic myocardium and during tachythmias. So drugs like maxilatine can be used for arrhythmia suppression post-emi. Litikin can be used in our ACLS. algorithm. So main takeaway, class 1B, remember, use these drugs in fast and failing ventricular tissue, ventricular tachyrithmius and post-MI. Okay, that finally leaves us with our class 1C drugs. Class 1C, remember, fries please, which is flecanide and propathenone. So these drugs can

be used in both ventricular arrhythmias and superventricular arrhyth, like atrial fibrill fibrillation, atrial flutter. There's something known as the pill in the pocket approach, which is a form of pharmacologic cardioversion. Basically, a patient has a history of aphib, is at home, feels an episode coming on. They can pop one of these combined with an avionotinotalking agent, like a beta blocker get themselves back in rhythm. So that's cool, but really the most important thing to know about the subclass and what I want you to remember is that these drugs are contraindicated in patients with structural heart disease like post-MI. They're only to be used in patients with structurally normal hearts. Using these drugs in patients with structural heart disease, coronary artery

disease, etc., can lead to sudden cardiac death. Quite the opposite of the Class 1B drugs we just went over where that was one of their primary indications. And a very easy test, question. So how can you remember that class 1B drugs are good postaimi and class 1C drugs are bad postomai? So back to the same mnemonic again. I told you to remember it. So if you just had a heart attack and you're ordering some dinner, you're going to substitute your fries for a salad, right? So remember that class 1B lettuce mayo, good postaimi and class 1c fries please, no good postaimi. Remember after a heart attack swap the fries out for a salad. So that's your sodium channel blockers. Quick recap drugs in this class are remembered by the monic double quarter pounder lettuce mayo

fries please double quarter pounder diso pyramid quinidine and pro canomide that's your class 1a lettuce mayo lytocaine and maxillotine that's your class 1b and then fries please flecanide and propaphanone class 1c these drugs slow down the influx of sodium during phase zero and remember the more salt in the food the more it blocks sodium channels remember your double quarter pounder is on a foot long hot dog bun to help you remember your class 1a drugs can prolong the qt interval torsad etc remember quinidine can cause synchionism, procanamide, aka protrainamide, remember your white wolf driving the train on a loop track, Wolf Parkinson, White, and Lupus. Class 1B, Lidicane and McSillotine use on your fast and filling ventricular tissue, and class 1c, fleconide and propapinone. Most importantly, remember these

drugs are contraindicated with structural heart disease, post-emite, et cetera. Remember, after an MI, swap your fries out for a salad. That's your sodium channel blockers. Next, let's talk about class two, which are beta blockers. You're probably already familiar with this class as we use these meds for hypertension, as well as a number of other indications. And if you ever forget which med class is part of class two, remember B is the second letter of the alphabet, and beta blockers, which start with a B, are our class two agents. So these drugs, in addition to their anti-hypertensive properties, also have anti-arhythmic properties. Luckily, remembering the names of these meds is a whole lot easier compared to your sodium channel blockers, because all of these drugs

end in LOL, like ketanololol, propranolol, carvetololol, metoprolol. So all beta blockers end in LOL, And most, but not all, end in O-L-O-L-L-L-L. And here's something important that I want you to recognize. If you see a beta blocker that does not end in O-L-O-L, you need to know that this is going to be a unique or, let's say, a fancy beta-blocker that does something a little extra. So if a beta-blocker does not end in O-L-L-L, it's usually because it has extra properties beyond standard beta blockade, like alpha blockade that we see in Carveta-L-L-L-L-L, which end in I-L-O-L-L-L-Raspectively, or potassium channel blockade that we see in SOTA, which ends in A-L-L-L-L.

So when you see a beta-blocker, check the suffix if it ends in O-L-L-L-L-L, like Metoprol, it will act primarily through standard beta-blockade. If it ends a little differently, like Label-A-L-L-L, you'll know it has some additional properties beyond standard beta-blockade. Now, how do these drugs work? So for that, let's look back at our... cardiac action potential again but this time we're going to be looking at our cardiac action potential of our pacemaker cells so this is a little different

this action potential only has three phases phases zero three and four so let's start with phase four which before we called the floor as this was almost a flat period with not much happening but now in phase four it's a little different you're going to notice there's this little upward slope and that's because in phase four we now have this slow leak of sodium sneaking through these pacemaker channels this is sometimes called the funny current in addition and very important during phase four we also have calcium influx which is first through T type calcium channels and then a little later on through L type calcium channels which ultimately depolarize

the membrane to its threshold potential next is phase zero where we have calcium continuing to enter through producing a slower upstroke than the fast sodium driven spike of our cardiomyrosites we were talking about before and then finally phase three which is repolarization follows as calcium channels close and guess who starts to leave yep potassium the party poop flows out, which brings us back to phase four once more. And as you can see, I didn't mention phase one or two, and that's because our pacemaker cells lack a distinct phase one or two. All right, so now that we understand the pacemaker action potential, how do beta blockers influence this to help treat arrhythmias? Well, indirectly by preventing epinephrine and norepinephrine

from binding to the beta receptors. So how the heck does that help us treat arrhythmias and how does that impact the action potential? So in the heart, we have beta receptors, primarily beta one and adrenergic receptors. And when catecholamines like epi and norepi bind to these receptors, this long chain of events occurs. First, the enzyme adenolocytes is activated, which converts ATP into CAMP. CAMP activates P-K-A, which phosphorylates L-type calcium channels, causing them to open leading to an influx of calcium. So what do you need to actually remember from that? So all you really need to know is that when epi and norepi bind to these receptors, a bunch of stuff happens, which leads to more calcium in the cell. So if we block these receptors, we block these

beta receptors with a beta blocker, we block epi and nor epi from binding, which ultimately slows the influx of calcium, and this is primarily at the end of phase four, which decreases that slope, which makes it take longer for the cell to reach the action potential threshold. So we have a decrease slope of phase four in our pacemaker cells. So in turn, the SA node is going to fire less often and the AV node is going to conduct more slowly, both of which help control heart rate and are especially useful in treating tachoridemias like atrial fibrillation. Now, beta blockers also have effects on non-pacemaker cells like our cardiomyocytes. And in these cells by decreasing calcium influx, they decrease cardiac contractility, decreasing oxygen demand for these cells. So this is

really a lot of info, but really here's the main takeaway in the simple recap of what you should know in just a few words. So beta blockers stop epi and nor epi from binding. which indirectly decreases calcium influx, which flattens our phase four slope. So that's what I think you should know. Now, what are the common indications for this class of drugs you should know? Of course, beta blockers are used in a number of different conditions, but when it comes to their anti-arhythmic indications, the one you should know is for rate control and atrial fibrillation and atrial flutter.

They can also be used in SVT, post-M-I, M-A-T, etc. But please remember, rate control, an a-fib, and a flutter. That's the most common and most important. Okay, so now I want to go over some extra tips for beta-block. and of course a whole bunch of nomonics. So first, not all beta blockers are the same. We have cardio selective beta blockers that primarily just block the beta one receptors in the heart.

And then we have non-selective that also block beta 2 receptors, which can be found in smooth muscle cells, GI tract, uterus, but most importantly in the lungs, where they can induce bronchol dilation when stimulated. Remember the mnemonic beta 1 primarily found in the heart, you have one heart, beta 2, which can be found in the lungs, you have two lungs, which just helps you to remember it. Now there's a bunch of beta blockers,

So how the heck can you remember which are cardio selective and which are non-selective? Remember that a beam of light is selective to just one area. A beam, B-E-A-M is selective to just one area. So if the beta blocker starts with a B-E-A or M, it's cardio-selective. So B-E-A-M, B-Soprolol, B-Tazololol, B-Tas-A-M-B-Tal-A-B-T-O-L. A stands for Attenololol or A-Sputylol, and then M stands for Metoprol. So you really don't even need to remember all of the specific names. All you need to remember is that a beam is a direct or selective light, meaning if a beta blocker in the question starts with a B, E, A, or M, it's cardioselective.

So if they ask you a question, like, you decide to treat this patient with a beta blocker who has a history of mild to moderate bronchospastic disease, which would be the preferred beta blocker to use. So all you need to do is find one that starts with beam, B, B, A, M, as the cardio selectivity makes this a safer drug for this population. So this is great for exam knowledge, but for real life, what you should know is that even cardioselective agents can exert, some inhibition of beta 2 receptors at high doses. So if you had a patient with severe or decompensated broncospastic disease, you'd want to avoid all beta blockers in these patients selective and non-selective. Okay, next I want to segue into a mnemonic to help you remember the contraindications slash warnings of this class of drugs. So to help you remember the common and most tested on, remember the nomonic ABCD. ABCD stands for asthma, bradyacardicardia,

cardiogenic shock, and diabetes. Asma, bradicardia, cardiogenic shock, diabetes. So let's break them down. A stands for asthma, which we just talked about, so I won't go into great detail, but beta blockade with non-selective agents prevents broncholation. So non-selective beta blockers should be avoided in susceptible patients, asthma, et cetera. And in severe disease, you really want to avoid all beta blockers, even the selective agents. Next, B stands for bradycardia. These men's have negative chronotropic effects. They slow the heart rate. So they're relatively contraindicated in symptomatic bradycardia, sinus no dysfunction, and in patients with second or third-degree a.V block unless a pacemaker's present. C stands for cardiogenic shock or severely decompensated heart

failure. So while beta blockers improve survival in stable chronic heart failure, initiation should be avoided in severe acute decompensation or cardiogenic shock. As in these states, the heart depends on the sympathetic drive, the beta one stimulation to maintain output, which beta blockers shut down. So blocking beta 1 receptors reduces contractility and heart rate, which can worsen shock. Finally, the D stands for diabetes. This is more of a caution rather than a. a contraindication, but one that's important to know. So beta blockers can mask hypoglycemia symptoms like sweating anxiety, which are mediated by epinephrine, which they block. They also may delay recovery from insulin-induced hypoglycemia by blunting epinephrine's effect on gluconeogenesis

and glycogenolysis, although the studies are a bit more conflicting in this area. But the main takeaway, use these in caution with diabetics. All right, that's your beta blockers. Quick recap of the juicy details are Class 2 anti-arhyrhythics. Remember the second letter of the alphabet is B. and beta blockers which start with a B are our class two anti-arithmics. All drugs in this class end in LOL and most end in O-L-L-L-L-L. The ones that don't got something special about them. Beta-blockers block epi and nor epi from binding to our beta-1 receptors in the heart, indirectly decreasing intracellular calcium influx, decreasing the slope of phase four.

The main indication I would know is rate control and a-fib and a flutter. Remember your cardioselective beta-blockers with beam, bisoprol, betaxilololololol, etymololololol, etoprolol. Finally, remember your common contraindication slash warnings for beta blockers, A, B, C, D, Asma, bradycardia, cardiogenic shock, diabetes. That's your beta blockers. We're halfway there. Let's talk about our class three antarhythyrhymics.

Next, our potassium channel blockers. There's a few different drugs in this class, amyodorone, dronetorone, amputalide, dofedolidol, honestly, you should really just focus on amyotorone and maybe sodololol, but there is a mnemonic to help you remember all of them if you choose to. And the mnemonic is, and I'm sorry for this, but the nymonic is AIDS, AID, D-S. AIDS stands for A amiodorone, I, abutolide, D-Dophedolide slash dronetorone, and S-sodol. And to further help solidify this mnemonic and help you remember that the AIDS mnemonic is associated with potassium channel blockers, you can't remember this sentence,

can't cure AIDS with potassium, can't cure AIDS with potassium, with can't and cure spelled with a K instead of C to help you remember the chemical symbol for potassium. I apologize, it's not the most appropriate mnemonic, and the nomenics from here on out, well, you'll see. All right. So how do these drugs work? Well, for that, we need to go back to our cardiac action potential of the cardiomyosites we were discussing before, the one with five phases. So remember potassium, the party pooper who kept leaving the party and ultimately in phase three just flooded out leading to repolarization?

Well, what if we had a drug that could come in and just block the door and not let him out during phase three, making him just hang around? Well, that's our potassium channel blockers, our class three drugs which block potassium eflux during phase three, prolonging phase three repolarization. So these drugs bind and inhibit potassium channels. meaning we have less potassium leaving the cell, which leads to a slower rate of repolarization, prolonging the action potential and effective refractory period. And this increase in the refractory period helps because this essentially lengthens the period of time.

The cell can kind of hang out before being stimulated again. We give it a little breathing room, which helps interrupt reent erythmias. Now the problem with prolonging things, prolonging the action potential in particular, is we get a new problem. And I'll give you a second to think about what that problem may be. What was another med class or subclass we talked about that also blocked potassium?

It involved a footlong hot dog bun. That's right, our Class 1A sodium channel blockers. The double quarter pounder on a foot long hot dog bun also blocked potassium, and they led to the same issue we'll go over now, which is prolonged QT interval with the potential of developing Torsad to point. So a significant adverse effect that you need to be aware of for these medications. Of note, this is much less common with amioderone and dronetorone compared to the other meds in this class.

But you need to remember your Class 3 potassium. channel blockers can prolong the QT interval and so can your class one a sodium channel blockers we went over before. Please remember this as it will likely be tested on. All right, moving on, what are the indications for our class three drugs? So some indications are atrial fibrillation, atrial flutter, ventricular tachycardia. Amiodarone, really the only one you should focus on is a powerful anti-arhythmic used for both atrial and ventricular arrhythmias, limited only by its side effect profile.

Orally, it's most often prescribed to prevent atrial fibrillation and ventricular arrhythmias. intravenously, it's used in critically ill patients with a-fiv to restore sinus rhythm, control ventricular rate, or convert ventricular arrhythmias. And like Lytocaine, it also plays a key role in our ACLS protocol. So let's talk a bit more about amyodorone, because I feel like if you're going to get a question about a class three antihrythmic, it's going to be on amyotorone. And not only that, amyotorone is just a really cool drug. So first, remember amyotorone as am3 odorone instead of am e-oderon.

Remember am-3 odorone, as in the number three. So a year from now, you'll, when you forget all about this lecture and you get a test question that has amyodorone on it and you forget everything about it, if you always remember it as am3 odorone instead of am eotorone, you'll never forget it's a class three antihrythmic. Now, on that note, even though this medication is classified as a class three antihrythic, as it does block potassium channels, it also blocks sodium channels like a class one, beta adrenergic receptors like a class two, and calcium channels like a class four. Pretty crazy. Dreneterone, another class three drug, which is structural.

similar to amyodorone, just lacking the iodine group, also blocks all four channels. So maybe not super high yield, but pretty cool. Okay, next let's cover potentially the highest yield thing to know about amyodorone, and that's its adverse effects. So amyodorone is highly lipid soluble, so it accumulates in all different tissues throughout the body, which is part of the reason it has so damn many side effects. Oral amyodoron has a super long half-life, hangs around for up to 100 plus days in some cases. So this is probably the highest yield thing to know about amyodorone, its adverse effects.

So how do you remember the adverse effects of an overall? amyodorone. Well, unfortunately, all of the class three and four drug demotics are inappropriate, and it's not on purpose. It's just what works out with the letters. So I'm sorry, but all right. So for the adverse effects, remember taking amyodorone is a B-I-T-C-H. Taking amyodoron is a B-Itcich, which stands for blue skin, interstitial lung disease, thyroid toxicity, coronal deposits, hepatotoxicity. So starting with B, amyotorone can cause blue skin. Amiotorone can cause a bluish-gray discoloration of the skin, sometimes called blue man syndrome. This is going to be most prominent on the face. There's other skin issues, photosensitivity, hyperpigmentation,

but don't forget the blue skin. Next, I stands for interstitial lung disease. Amiodorone-induced pulmonary toxicity is found in up to 5% of patients. The most common form is interstitial pneumonitis. So before you start a patient on amyodorone, you should obtain a baseline chest x-ray to ensure there isn't any evidence of existing interstitial lung disease. Next is probably the most important one, and that's thyroid toxicity. Thyroid toxicity, so amyodorone contains high amounts of iodine. That's actually the reason the name amiodorone contains the letters IOD. It's due to the fact amyodoron contains two iodine atoms per molecule in its chemical structure. And since iodine is a key substrate for thyroid hormone synthesis, this iodine load can disrupt thyroid function, leading to either hypo or hyperthyroidism.

Thyroid dysfunction is actually one of the most common complications of amyodorant therapy. And because of this, patient should have baseline thyroid function tests such as TSA before starting the medication and should be monitored periodically during treatment. Next is the C, which stands for corneal microdeposits. So these micro deposits occur in the majority of patients taking amiodarone. They're typically benign and don't affect visual acuity. They result from amyelurone being secreted into the tears by the lacrimal glands and gradually accumulate on the corneal surface, but generally resolve after discontinuation of the drug. And then finally, we have H, which stands for hepatotoxicity.

So around 25% of patients taking amyotorone will have a transient rise in serum amino-transferase concentrations are liver function tests. so AST, ALT can go up. Most patients are asymptomatic. Habitatis occurs in fewer than 3% of patients. And cirrhosis and hepatic failure are rare. So add this to your checklist of the many organs you will need to check before starting amiodarone. Baseline LFT should be attained prior to initiation as well as checking during therapy.

All right. So remember taking amyodorone, as you can tell, is a BITCH, blue skin, interstitial lung disease, thyrotoxicity, corneal deposits, hepatotoxicity. One other class three med I want to briefly mention before we wrap up this class is Sotelol. So before I tell you why this med is unique, I want you to think and look at the name and think about what's unique about it. It's spelled S-O-T-A-L-O-L-L. So first, it ends in L-O-L. So it's a beta-blocker.

But remember what we talked about before with beta-blockers. If they end in O-L-L-L-L-Traditional beta-blocker, anything else, we know they have some additional properties. So Sotol ends in A-L-L-L-L. So we know there's more than just traditional beta-blockade with this med. And in this case, it's pretty obvious as we're talking about potassium channel blockers, right now, so we know SOTOL also has potassium channel blocking abilities in addition to beta blockade, and that's why it's considered a Class 3 med. But later on, when you see this on an exam question, you'll likely remember it's a beta blocker

due to the LOL at the end, but it's easy to forget it's also a potassium channel blocker. So because of that, I used to remember it instead of Sotololol as Sopodolol. Instead of Sotolol, remember it as Sopodolololol. The POT helps me remember that in addition to being a beta blocker, it's also a POT potassium channel blocker. So instead of sodolol, remember it as sopotalol. All right, that's our class three anti-arhythymicics. Remember the meds by remembering the mnemonic AIDS, AIDS, amyodorone, abutalide, dofedelide, slash dronetorone, and sod. You can't cure AIDS. Remember, they block potassium e-flux during phase three, prolonging phase three repolization.

These drugs can prolong the QT interval with the potential of developing torsades. The highest yield med to know is amyodorone. Remember instead of AME-Oterone, remember it as AM3 odorone to help Remember, it's a Class 3 anti-arhythmic. To remember the super high yield adverse drug reactions, remember taking amyodorone is a B-I-T-C-H, blue skin, interstitial lung disease, thyroid toxicity, corneal deposits, hepatotoxicity. And finally, remember, sodalolol is a beta blocker as well as a Class 3 potassium channel blocker. Remember it as Sopodolol instead of Sotolol.

Let's move on to our final class, Class 4 drugs next. So our Class 4 drugs are calcium channel blockers. So in this class, it's much easier as there's only two meds to know, and that's verapomil and Diltyism. And if you need help remembering these two meds are Class 4 meds, and I'm sorry, another inappropriate mnemonic, but remember the sentence, four negation leads to venereal disease. Four nication helps you remember Class 4. Venereal disease, which starts with the VE and DI, help you remember Verapamil and Dilakizem, which also start with VE and Deltiesm. Fournication leads to venerial disease, helps you remember your Class 4 meds of varapamyl indotizem. Now, the next question you might

ask yourself is Class 4 meds are calcium channel blockers, and we know there's a bunch of calcium channel blockers. So why are we only listing two meds? What about all of the other calcium channel blockers like amlodipine, nifedipine, etc? Why are we only discussing deltizem and verapamil? So for that, we need to quickly review the different types of calcium channel blockers and what they do. So there's two different types of calcium channel blockers, non-dhydripyene and dihydropyridine. Non-dhydripidine are dootysm and verapim, which will go over more in a moment. And dihydropyrene are all of the others, amlodotapine, nifetepine, nicartopine, etc. The nice part about this is, dihydropyriene, ends in I-N-E, and so do all of the dihydropyridine calcium channel blockers, amlodipine, I-N-E,

nipetapine, etc. The non-dihydropyodine meds are the non-I-N-E meds, Deltysm, and Verapimel that do not end in I-N-E. So a nice easy way to differentiate the two. So to keep this brief, both of these subclasses inhibit the L-type calcium channels on cells, which will go over in more detail in a second, but the big difference is that dihydropyrodin meds are I-N-E-Mads, amlodotapine, nipetepetine, etc. primarily target the calcium channels on vascular smooth muscle tissue. So they're great for treating hypertension as they cause vasodilation of these vessels

reducing systemic vascular resistance, but exert minimal direct effects on the myocardium. That's where our non-dihydropyrodin meds come in, the ones that do not end in I&E, deltisem, varapimil. These meds do the same. They inhibit L-type calcium channels, but they are more selective for the pacemaker and non-pacemaker cells of the heart, making them useful for the arrhythmias will go over. So let's talk a bit more about how these non-dihydropyroderine meds work. our class four agents.

So the main effect is going to be on the pacemaker action potential. So like we were talking about before, the pacemaker action potential only has three phases, phase zero, three, and four. And let's just do a quick recap because it's a tough subject and why not? So phase four, remember, is a slow sodium leak through the funny current, with calcium entering first through our T-type calcium channels, and then later on through our L-type calcium channels to push us through to reach the threshold potential.

Phase zero is the slower calcium-driven upstroke of depolarization. And then finally phase three is repolarization as calcium channels close and potassium, the party pooper he is, flows out. So unlike beta blockers, which indirectly affected calcium channels by blocking epi and nor epi, calcium channels directly impact calcium channels

and have an impact on phase four and zero. So they decrease calcium entering during phase four and zero. So we'll have a decrease in the slope of phase four and zero, slowing things down so the heart gets a little bit more breathing room. And just like in beta blockers, they'll decrease firing of the S-A-N. node, decrease conduction velocity through the AV node, which helps to treat our arrhythmias. Like beta blockers, calcium channels also have effects on calcium influx in non-pacemaker

cells like our cardiac myocytes, decreasing the force generated during contraction, so they have an effect not only on cardiac conduction, but also cardiac contractility as well. So remember calcium channel blockers block calcium channels, just as the name states, which affects phase four and zero of the pacemaker cardiac action potential. Now what arrhythmias do they treat, you might ask? Well, since they're similar to beta blockers, we will see some similarities. Vltaism and Vrapamil are both used for acute and chronic ventricular rate control in atrial fibrillation and atrial flutter. They're also effective for superventricular tachycardia alongside adenosine and can be used in multifocal atrial tachycardia.

But the main indication to remember is rate control in a fib and a flutter and SVT. All right, what else should we know about our calcium channel blockers? Well, of course, you got to know the adverse drug reactions. So the three adverse effects you need to know for non-dihydro perioding calcium channel blockers are constipation, cardiac block bradycardia, which luckily is, the initial of calcium channel blockers, CCB. So starting with C, which is for constipation, this is pretty common and occurs in up to 25% of patients. The next C, cardiac block. These drugs may cause first, second or third degree AV block. And then finally, B, our last letter, these drugs may lead to sinus bradycardia. So you should avoid these drugs in patients who are using other

AV notal blocking agents like beta blockers, patients with six sinus syndrome, or patients with underlying avidno dysfunction. All right, that's our class four antirethics, our calcium channel blockers. Remember the meds in this class by remembering fornication leads to venereal disease. Class four, ferapamil and dutizem. Remember, these are non-dihydroperidine agents. They decrease calcium entering during phase four and zero. Indications, rate control and a fib and a flutter, SVT. Remember your adverse drug reactions by remembering CCB, constipation, cardiac block, bradycardia. All right, if you're still with me, congrats, that was a lot. So that was your class one through four antarhythics. I'm going to do a 60 second or so recap of the highest

deal topics and mnemonics, then we'll do a few quick questions to test your knowledge. So four classes of anti-arhythmics to know, class one sodium channel blockers, class two beta blockers, class three potassium channel blockers, class four calcium channel blockers. Remember them by remembering the sentence, some blocked potassium channels, SBPC. Starting with class one, sodium channel blockers, which slow down the influx of sodium during phase zero. And remember, the more salt in the food, the more it blocks sodium channels. Remember class one has three subclasses, class one A, diso pyramid, quinity,

procanamide, Class 1B, lytocaine and mixillotine, Class 1C, Fleckinide, and Propaphanone. Remember your double quarter pounder, lettuce, mayo, fries, please. Remember our Class 1A meds, double quarter pounder are on a foot-long hot dog bun to help you remember the Class 1A drugs prolong the QT interval. Super important. Don't forget about procanamide, aka protrainamide, your White Wolf-Wark driving a train on a loop track, Wolf Parkinson, White, and Lupus. Remember, our Class 1B meds are indicated for fast and failing tissue like post-MI, but

our Class 1 C meds are contraindicated post-MI. Remember, after a heart attack, you swap the fries out for a salad. Next, Class 2 beta blockers, remember the second letter of the alphabet is B, and beta blockers which start with a B are our Class 2 anti-arithmics. All drugs in this class end in LOL, and most end in OLL.L. The ones that don't got something special about them. Beta blockers block Eppy and nor Epe from binding to our beta-1 receptors in the heart, decreasing calcium influx, decreasing the slope of phase 4.

The main indication I would know is for rate control and a-fib and a flutter. Remember your cardioselective beta blockers with beam, bisoprololol, betaxylol, esmol, atenol, ACEBudol, and metoprololol. Finally, remember your common contraindication slash warnings for beta blockers with ABCD, asthma, bradyacardic, cardiogenic shock, diabetes. Class 3 potassium channel blockers, remember the meds by remember the demonic AIDS, AIDS, amioderone, abutolide, dophedolid, tronetorone, and sodololol. They block potassium e-flux during phase 3, leading to prolonged phase 3 repolarization. U-T prolongation is an important adverse effect. to know, the highest yield med is ameotorone. Remember, am3 odorone, to help you remember, it's a

class 3 antirthmic. And to remember the super high yield adverse drug reactions, remember taking amyotorone is a B-I-T-C-H, blue skin, interstitial lung disease, thyroid toxicity, corneal deposits, hepatotoxicity. And finally, remember, Sotolol, is a beta-blocker as well as a Class 3 potassium channel blocker. Remember it as Sopodolol, P-O-T, to help you remember it also blocks potassium. Finally, our class fours, is remember the meds in this class by remembering fornication leads to venereal disease, fornication, class four, venereal disease, barapomel, and dilatizam. Remember, these are non-dihydropyodine agents. They decrease calcium entering during phase four and zero in nodal cells prolonging phase

four and zero. Indications rate control and a fib and a flutter, SVT. Remember your adverse drug reactions by remembering CCB, constipation, cardiac block, bradycardia. That's your antirithmics. Let's do five quick questions to test your knowledge. Question one. Which of the following antirhythmic drugs has the most potent impact on blocking sodium

channels in the myocardium, leading to the greatest reduction in the slope of phase zero depolarization. Again, which of the following antirhythmic drugs has the most potent impact on blocking sodium channels in the myocardium, leading to the greatest reduction in the slope of phase zero depolarization? Choice A, lytocene, B, maxillotine, C, flecanide, D, dysopyramid, E, verapamil. Again, A, lytocane, B, maxillotine, C, flecanide, D, D, Dysop pyramid, E, verapamil. So that is going to be answer C, Flecanide.

So which of these meds has the most potent sodium channel blocking activity? We have five choices, and one of them we can knock out right away. Answer E, Vrapamil is a Class 4 calcium channel blocker, so let's eliminate that option. So then we're left with four choices. Lidicane, maxillotine, flecanide, diso pyramid, which are all sodium channel blockers. And if we remember the demonic, all we have to do at this point is find the saltiest food. So let's think about the foods and how salty they are, which sounds ridiculous, but it works. So lettuce mayo, we know has the least amount of salties.

salt, which has the weakest sodium channel blockade. That's our class 1B drugs. Double quarter pounder, moderate amount of salt, moderate sodium channel blockade, which are class 1A drugs. And then finally, the meds we should be looking for, fries please, which are the saltiest and have the strongest sodium channel blockade are our class 1C. And since fries, please, represents propaphanone and flecine, we have to look for these meds. And luckily, flecanide is present in the answer choices. So we know that answer C, flecanide is the correct choice, which is a class 1C agent exerting the most potent sodium panel blockade and has the greatest impact on reducing the slope of phase zero.

Question two. A 58-year-old man who was recently started on a new medication by his cardiologist presents to the emergency department. After beginning therapy, he reports episodes of dizziness and near syncope. An ECG obtained in the emergency department shows a markedly prolonged QT interval followed by polymorphic ventricular tachycardia with a characteristic twisting of the QRS complexes around the isoelectric baseline. Which of the following medications is most likely responsible for this.

patient's presentation. A. Lytocaine, B, D. D. D. C. quinidine, D. McSillotene, E. Metoprolol. Again, A, lytocene, B, D. D. D. Mactyazem. C. quinidine. D. Mxilatine. E. Metoprololol. So that's going to be answer C quinidine. This question is describing a patient with prolonged QT and polymorphic ventricular tachycardia with twisting QRS complexes. So Torsandapoint. So which medication class that we've covered? today are most likely to cause prolonged QT and torsats. And you've got to know this. That's your Class 3 potassium channel blockers and your Class 1A sodium channel blockers. So now that we know which drugs to look for in our answers, let's start with your potassium channel blockers. We remember

those drugs with the mnemonic AIDS, AIDS, amioderone, amyoderone, diputalide, dofedelide, dronetorone, and sodol. None of those meds are present in the answer choices. So next, let's search for our Class 1A drugs. Remember your double quarter pounder on a footlong hot dog bun, which represent disopiramid, procanamide, and quinidine, And quinidine, we can see as answer C, a Class 1A drug that, as we discussed before, is notorious for prolonging the QT interval and causing Torsads is the most likely cause of this patient's presentation compared with the other medications and the correct answer for question two. Question three, a 64-year-old man was started on a new anti-arrhythmic medication several months ago.

At a routine follow-up, he reports new fatigue and notices blueish-gray discoloration of the skin over his face. Laboratory studies reveal an elevated TSA, as well as an increase in serum aminotransferase concentrations, AST and ALT. Which of the following medications was most likely initiated in this patient in the past few months? A, dophedolid, B, Sotolol, C, amyodorone, D, Fleconide, E, Vrapamil. Again, A, dophedolid, B, Sotol, C, amyotone, D, Fleconide, or E, varapamil. So that's going to be answer C amyotorone. So correct answer is answer C amyotorone. You better know this one. Remember, amyotelon messes with so many different organs in the body. And it's why the answer C amyotone. And it's why the answer C amyotone. And it's why there are so many monitoring parameters needed when initiating and continuing on this medication,

chest x-ray thyroid function test, serum amino transferase levels, etc. So amyodorone can cause a number of different adverse effects. The main ones, though, are in the mnemonic BITCHH because taking amiodron is a BITCH. Blue skin, which is seen in this patient, interstitial lung disease, thyroid toxicity, which we see here is evident by the increase in TSAs, well as the complaints of fatigue, likely secondary to hypothyroidism, corneal deposit, and then finally hepatotoxicity, which we also, also seen this patient with the increase in AST and ALT.

So don't forget, taking amyodorone is a BITCHH. The other drugs, while they may have some adverse effects seen in this patient like the hepatotoxicity, ameuroin is the only one to potentially have all of these clinical manifestations. Question four. A 70-year-old man with a history of hypertension and atrial fibrillation presents to the clinic complaining of recurrent palpitations. He is hemodynamically stable, and his ECG confirms atrial fibrillation. After failing other therapies, the patient has started on an oral medication,

that primarily prolongs phase 3 repolarization of the ventricular cardiac action potential, increasing the action potential duration and effective refractory period, which of the following medications was most likely initiated in this patient? A, lytocaine, B, metoporilol, C, dophedolide, D, Vrapamil, E, maxillotine. Again, A, lytocaine, B, metoporal, C, dofetolide, D, verrapamil, or E, maxillotine. So that's going to be answer C. Dophethylide. So this is not an easy question, but let's break it down.

So first, avoid all of the noise. The only part of this vignette that matters is the statement, which drug in this list prolongs phase 3 repolarization, increasing action potential duration, and effective refractory period. And by definition, that is a potassium channel blocker, which in this case, the only potassium channel blocker listed is dophedolide, the D and AIDS. The other meds B, metoprolol is a class 2 beta blocker,

which mainly affects phase 4. 4 of pacemaker cells, Lytocaine and maxillotine are lettuce and mayo meds, are Class 1B sodium channel blockers, which act on phase zero. And finally, D. Verapamil is a Class 4 calcium channel blocker, which affects primarily phase 4 and zero of nodal cells.

Question 5, a 64-year-old man with a history of atrial fibrillation is being managed for rate control. He was previously prescribed a calcium channel blocker, which was discontinued due to intolerance. The treatment plan now shifts to a beta blocker. His medical history includes mild, well-controlled asthma, managed with occasional albuterol inhaler use, which of the following beta blockers is the most suitable option for rate control in this patient. A, propranol, B, natalol, C, pindolol, D, metoprolol, e,

E, timelol. Again, A, propranol, B, natalol, C, Pindol, D, metoprolol, or E, timelol. So that is going to be answered D, metoprolol. So we have a patient with a history of aphib and mild bronchospastic disease. He didn't tolerate calcium channel blockers, so we're going to start him on a beta blocker. Non-selective beta blockers hit both the beta-1 receptors in the heart as well as beta-2 in the lungs, which can cause bronco-constriction, so these are not recommended in patients with bronchospastic disease like asthma. A selective agent, on the other hand, at lower doses, will hit primarily beta-1 receptors

and can be used with caution in this patient population. So the only question you need to ask yourself at this point is which is a cardioselective beta-blockers in the answers, and the easy way to know, is just to remember that a beam of light is direct, and find a beta blocker that starts with B, E, A, or M. In this case, that would be Metopor-Lol, which is a cardioselective agent, and the correct answer for this patient.

All right, that was your antirthmics. Try not to be too overwhelmed. It is a lot, but try to just focus on the highest-ealed stuff and try to focus on the mnemonics. If you can try to remember those, you'll get through the exam, and you'll be fine. Thank you so much for listening to the podcast, and thank you so much for the support.