Okay, so today we're going to go over anti rhythmics.

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 tomonics 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 anti rhythmics.

So there's four main classes that you need to know, and that's your Class one sodium channel blockers, Class two Beta blockers, Class three potassium channel blockers, and class four calcium channel blockers.

So if you ever forget which classes which, remember the sentence some block potassium channels, some block potassium channels the letters SBPC that helps you remember.

Class one S sodium channel blockers, Class two B Beta blockers, Class three P potassium channel blockers CEE, 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 review, done done, 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 possible.

Let's first start with the action potential of the cardiomiocytes.

Now, before breaking down each phase, there's a few simple key facts to keep in mind.

First, there is five phases zero, one, two, three, and four.

Next, there's three players in the game, three 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 ninety millivolts, making it relatively negative compared to the outside.

All right, so let's break it down, starting with phase four, which I like to call the floor.

Phase four 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 as 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 to Phase one, 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 and 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 in potassium like the party pooper, e is keeps leaving big drop and repolarization.

Okay, so now that we have a general understanding, let's start with our class one sodium channel blockers.

So the meds in this class, while there is a lot of them, they're broken into subsections making it even worse.

Class one A, one B, one C.

I know, learning anti rhythmics really sucks that, I feel you.

I do have anomonic though, so we'll go over that in just a minute.

So Class one A is disopyramid quinidine procanamide, Class one B is lytoicane and mixilotine, and class one C is flecinide and propaphenome.

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 quarter pounder, lettuce mao fries please, double quarter pounder, let 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 one A drugs, double quarter pounder DQP stands for disopyramid, which is the d.

Q stands for quinidine, and P stands for procaanamide.

Now I've got a little twist to this mnemonic that's going to help you remember a key feature of these one A 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 bund.

It sounds odd now, but trust me, it's going to make sense and help you soon.

Okay, Next our Class one B drugs lettice mayo stands for lytokane and mixilotine.

And then finally our Class one C meds, fries please, which is flecanide and propaphenone.

So once more double quarter pounder disopyramid quinidine and procanamide Class one A.

Remember it's on a foot long hot dog bun lettice mayo, which is lytokine and maxilotine class one B.

And then fries please flecanide and propafenone class one CE.

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 depolarization.

So when we add a sodium channel blocker to a patient within arrhythmium, 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 re entrance 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 one SEA drugs, which bind the tightest and the longest, making them the most potent sodium channel blockers, causing the steepest reduction 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 a total time it takes for a cardiaccel to complete one cycle, so from phase zero depolarization to the end of phase three repolarization.

Next is our class one A drugs, which produce intermediate BLOCKA, 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 cost some issues.

We'll go into more depth about in just a few minutes.

And then finally we have our class one B 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 in the food, the more it blocks sodium.

So remember our mnemonic double quarter pounder, lettuce, male fries please.

So out of all of these, which has the least amount of salt?

Double quarter pounder, lettuce, mao 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 mao right, so Class one B lytoicanum oxilotine have the least sodium channel blocking activity.

Next, which of these foods has the most salt the fries?

Right?

So fries please.

Class one C fleckanide and propafenone exert the most potent sodium channel blocking among the Class one agents, which finally leaves us with our double quarter pounder Class one A, which has moderate amount of sodium.

So these meds diso pyramid quinidine and procaanamide have moderate sodium channel blocking activity, so that's how I remembered it.

There are other mnemonics, 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 old things to know about each of these meds, starting with our Class one A sodium channel blockers.

So Class one A, remember is double quarter pounder diso pyramid quinidine procanamide.

Now, before I told you, remember this double quarter pounder is on a foot long hot dog bund, you probably already have an idea of why I said that.

So all Class one A drugs are notorious for prolonging the QT interval.

So things like torsade to point, a dangerous form of polymorphic vtach are possible with these medications.

And that's because, like we went 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 one A drugs you have to know they can prolong the QT interval, so very important and very likely to test question.

So the way that you're going to remember that is thinking back to our pnomonic again, same mnemonic over and over.

So double quarter pounder on that foot long hot dog bund.

So we remember double quarter pounder, disopyramid, quinidine, and procanamide.

You're always going to remember that double quarter pounder is on a foot long hot dog bund.

And that's because all of these drugs can pro long the QT interble.

So that double quarter pounder oddly on this foot long hot dog bund helps you remember Class one A drugs prolong the QT interval, nice and simple, don't forget it.

Let's talk about quinidine first.

Now, I know we just said all of the meds in Class one A prolonged the QT interval, but quinidine really prolongs the QT intervle Quinidine has historically been one of the most common causes of drug induced to 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 they're safer meds.

There is still some utilization in recurrent vtach in Brugatta 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 towards to point, it has a unique side effect that's often tested on.

So the highest deel thing you need to know about quinidine is that it can cause something known as sensinism.

Weird name, but the backstory may help you to remember it.

So there is this tree called these Sinschona tree native to the Andes.

It produces bark that's rich in alkaloids.

This bark is not only the source of quindine but also the source of quinine, which you're probably familiar with for its treatment of malaria.

So both of the meds which come from the same tree share a side effect from their plant origin, sensianism, which can cause a constellation of symptoms tinatus, hearing loss, confusion, and delirium, visual disturbances.

And we call this sentianism as it's named after the tree.

It's derived from the Sinchona tree.

So hopefully that little backstory helps you to remember quinidine can cause sentianism and of course torsade to point.

Next drug from Class one A, it's much higher yield, and that's procanamide.

Procaanamide is another effective anti arrhythmic 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 lupis.

Let's talk about that.

So procaanamide can be used to treat arrhythmias associated with Wolf Parkinson White syndrome.

This is a popular exam question, so you need to know it.

Next, this drug can cause lupus like syndrome or drug induced lupis.

So chronic administration of procainamide can lead to lupus like syndrome.

So these patients will have similar symptoms to those seen in lupus, rash, arthritis, et cetera.

So these are the two things that you need to know about procanamide.

They can treat Wolf Parkinson White arrhythmias and it can cause drug induced lupis.

So how do you remember that?

So instead of remembering it as procanamide, remember it as protrainamide.

Every time you hear procanamide, I want you to think protrainamide 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 loopis like syndrome.

So procanamide is protrainamide.

Think of a train being driven by a white wolf wolf Parkinson white circling in a continuous loop.

Loopis like syndrome.

And then our last drug in the Class one A class is disopyramid, which instead I used to remember as drysopyramid dr wide 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, my asthenia, gravists, et cetera.

Instead of disopyramid, remember dry soopyramid dr y to remember the anticholinergic side effects.

Okay, next is our class one B.

What are the Class one B drugs?

Remember Class one B lettice, male lytocane, and maxillotine.

So starting with lytocine.

Lytocane, 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 mixilotine, which is essentially an oral version of lytocine.

It can also cause CNS toxicity, but because it's a POMD, we often see GI problems.

Nausee of 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 a schemic tissue so schemic arrhythmias after a myocardial infarction.

And that's because the Class one B meds preferentially bind sodium channels in the depolarized and inactivated state, which are common in aeschemic myocardium and during tacharrhythmias.

So drugs like maxilotine can be used for rhythmia suppression.

Posts demi lytokin can be used in our ACLS algorithm.

So main takeaway Class one B.

Remember use these drugs in fast and failing ventricular tissue, ventricular tacharrhythmias and POSTMI.

Okay, that finally leaves us with our class one C drugs.

Class one C remember fries please, which is flecinide and propathenone.

So these drugs can be used in both ventricular arrhythmias and superventricular arrhythmias like atrial 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 that home feels an episode coming on, they can pop one of these combined with an av NOTAB blocking agent like a beta blocker, going to 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 POSTMI, They're only to be used in patients with structurally normal hearts.

Using these drugs and patients with structural heart disease, cornary arter disease, et cetera can lead to sudden cardiac death quite the opposite of the class one B 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 one B drugs are good post DEMI and class one C drugs are bad post demi.

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 one B let us mayo good post DEMI and class one C fries please no good post am I.

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 demonic double quarter pounder.

Let us mao fries please double quarter pounder, disopyramid, quinityde and prokanamide that's your Class one A.

Let us mao lytokane and mixilotine that's your Class one B.

And then fries please fleckenide and propafenone Class one C.

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 bund To help you remember your Class one A drugs can prolong the QT interval, torsad, et cetera.

Remember quinidine can cause synchronism.

Procanamide aka protranamide.

Remember your white wolf driving the train on a loop track Wolf Parkinson White and lupis Class one B letacanum, oxilotine use on your fast and filling ventricular tissue.

And Class one C fleckanide and propafenone.

Most importantly, remember these drugs are contraindicated with structural heart disease postami, et cetera.

Remember after an MI, I 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 arrhythmic 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 a tenelol, propranolol, Carbada law, and mitoprolol.

So all beta blockers end in l OL, and most but not all end in ol l ol L.

And here's something important that I want you to recognize.

If you see a beta blocker that does not end in olol, 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 olol, it's usually because it has extra properties beyond standard beta blockade, like alpha blockade that we see in Carvata law and Libata law, which end in ilol and alo l respectively, or potassium channel blockade that we see in sodolol, which ends in alol.

So when you see a beta blocker, check the suffix.

If it ends in olol like mitopralaw, it'll lack primarily through standard beta blockade.

If it ends a little differently like lo betalall alol.

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 depolarized the membrane to its threshold potential.

Next this phase zero, where we have calcium continuing to enter through, producing a slower upstroke than the fast sodium driven spike of our cardio myocytes we were talking about before.

And then finally phase three, which is repolarization, follows as calcium channels close and guess who starts to leave yet potassium, the party pooper flows out, which brings us back to phase four once more.

And as you can see, I didn't mention phase one 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 epinefrin and nore epinefrin 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 adrenergic receptors, and when catechola means like EPI and nor epi bind to these receptors, this long chain of events occurs.

First, the enzyme IDENTL cyclosis activated, which converts ATP into CIMP.

CIMP activates pKa, which phosphorulates L type calcium channels, causing them to open leading to an influx of calcium.

Ugh, So what do you need to actually remember from that?

So all you really need to know is that when EPI and nor rep 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 epianore 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 tacharithms like atrofibrillation.

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 us so they're anti rhythmic indications.

The one you should know is for rate control in atrial fibrillation and atrial flutter.

They can also be used in SVT, postmat, et cetera.

But please remember rate control in 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 blockers and of course a whole bunch of demonics.

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 two receptors which can be found in smooth muscle cells GI tract uterus.

But most importantly in the lungs, where they can induce broncho dilation when stimulated.

Remember the demonic beta one primarily found in the heart.

You have one heart, beta two, 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 BA or M, it's cardio selective.

So B EA, M, B stands for bisoprolol or a bitaxilol.

E stands for esmolol, A stands for a tenolol or asputle all, and then M stands from a toprolall.

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 cardio selective.

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 at bronchospastic disease, which would be the preferred beta blocker to use.

So all you need to do is find when that starts with beam b EA 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 cardio selective agents can exert some inhibition of beta two receptors at high doses.

So if you had a patient with severe or decompensated bronchospastic disease, you don't want to avoid all beta blockers in these patients, selective and non selective.

Okay, Next, I want to segue into anomodic 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 demonic ABCD.

ABCD stands for asthma, bradacardia, cardiogenic shock and diabetes asthma braidacardia 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 bronchodilation, 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 bradacardia.

These mens have negative chronotropic effects.

They slow the heart rate, so they're relatively contraindicated in symptomatic bradacardia, sinus nod dysfunction, and in patients with second or third degree av 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 de compensation 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 one 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 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 epinephrin'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 two antierrhythmics.

Remember the second letter of the alphabet is B, and beta blockers which start with a B are r Class two antierythmics.

All drugs in this class end in lol and most end in olol.

The ones that don't got something special about them.

Beta blockers block epian or EPI from binding to our beta one receptors in the heart, indirectly decreasing intracellular calcium influx, decreasing the slope of phase four.

The main indication I would know is rate control in a fib and a flutter.

Remember your cardio selective beta blockers with beam bisoprolol, bitaxilaw asmolol atenolol, aceputle law, metoprol law.

Finally, remember your common contraindication slash warnings for beta blockers ABCD, asthma, bradacardia, cardiogenic shock, diabetes.

That's your beta blockers.

We're halfway there.

Let's talk about our class three antiarithmics.

Next are potassium channel blockers.

There's a few different drugs in this class, amiodorone, dronetarone, ammutilide, dofeedolide, sodolol.

Honestly, you should really just focus on amiodorone and maybe sodolol.

But there is a nomonic to help you remember all of them if you choose to.

And the mnemonic is and I'm sorry for this, but thenomonic is AIDS ai DS AIDS stands for a amiodorone, I, abutilide, d do feedolide, slash, dronetarone, and s sotolol.

And to further help solidify this demonic and help you remember that the AIDS mnemonic is associated with potassium channel blockers, you can remember the 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 nomonic in dynomonics 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 cardiomyocytes 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 are 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 re entrant arrhythmia.

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 foot long hot dog bund.

That's right, our Class one A sodium channel blockers, the double quarter pounder on a foot long hot dog bund 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 towards sad de point, so a significant adverse effect that you need to be aware of for these medications.

Of note, this is much less common with amiodorone androneterone compared to the other meds in this class.

But you need to remember your Class three 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.

Amiodorone, really, the only one you should focus on is a powerful anti arrhythmic used for both atrial and ventricular arrhythmia, limited only by its side effect profile or only, It's most often prescribed to prevent atrial fibrillation and ventricular arrhythmias.

Intravenously.

It's used in critically ill patients with a fib to restore sinus rhythm, control ventricular rate, or convert ventricular arrhythmias, and like letocaine, it also plays a key role in our ACLS protocol.

So let's talk a bit more about amiodorone, because I feel like if you're going to get a question about a class three anti arrhythmic, it's going to be on amiodorone, and not only that, amiodorone is just a really cool drug.

So first, remember amiodorone as AM three odorone instead of am eodorone.

Remember am three odorone as in the number three.

So a year from now, when you forget all about this lecture and you get a test question that has amiodorone on it, and you forget everything about it.

If you always remember it as AM three odorone instead of am eodorone, you'll never forget it's a class three anti arrhythmic.

Now, on that note, even though this medication is classified as a class three anti arrhythmic as it does block potassium channels, it also blocks sodium channels like a class one, beta adrenergic recept like a class two, and calcium channels like a class four.

Pretty crazy.

Dronetarone, another class three drug which is structurally similar to amiodorone, 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 sealed thing to know about amiodorone, and that's its adverse effects.

So, amiodorone 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 amiodorone has a super long half life hangs around for up to one hundred plus days in some cases, so this is probably the highest heeled thing to know about amiodorone.

It's adverse effects, So how do you remember the adverse effects of amiodorone.

Well, unfortunately, all of the class three and four drug demonics 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 if the adverse effects, remember taking amiodorone is a bitch.

Taking amiodorone is a bitch.

Which stands for blue skin, interstitial lung disease, thyrotoxicity, coronal deposits of patotoxicity.

So starting with b amiodorone can cause blue skin.

Amiodorone 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 eye stands for interstitial lung disease.

Amiodorone induced pulmonary toxicity is found in up to five percent of patients.

Most common form is interstitial pneuminitis.

So before you start a patient on amiodorone, 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 amiodorone contains high amounts of iodine.

That's actually the reason the name Amiodoron contains the letter's iod It's suited the fact amiodorone 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.

Thyroidys function is actually one of the most common complications of amiodoron therapy and because of this, patient should have baseline thyroid function tests such as TSH before starting the medication and should be monitored periodically during treatment.

Next is the C, which stands for cornial microdeposits.

So these microdeposits occur and the majority of patients taking amiodorone.

They're typically benign and don't affect visual acuity.

They result from amourone being secreted into the tiers by the lacrymal glands and gradually accumulate on the cornial surface, but generally resolve after discontinuation of the drug.

And then finally we have H, which stands for patotoxicity.

So around twenty five percent of patients taking amiodorone will have a transient rise and serum aminotransfhrase concentrations our liver function tests so ast ALT can go up.

Most patients are asymptomatic, Habititis occurs in fewer than three percent of patients, and cirrhosis and hepatic failure are rare.

So have this tear checklist of the many organs you will need to check before starting amiodorone.

Baseline LFT should be attained prior to initiation, as well as checking during therapy.

All right, so remember taking amiodone, as you can tell, is a bitch.

Blue skin, interstitial lung disease, thyrotoxicity, cornial deposits, hepatotoxicity.

One other class three met I want to briefly mention before we wrap up.

This class is SODOLOL.

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 so ta l O L so first it ends in LOL, so it's a beta blocker.

But remember what we talked about before with beta blockers.

If they end in olol, traditional beta blocker anything else, we know they have some additional properties.

So sodolol ends in a lool, 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 sodolol also has potassium channel blocking abilities in addition to beta blockade, and that's why it's considered a Class three 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 sodolol as so potolol.

Instead of sodolol, remember it as so potolol so ptalol.

The pot helps me remember that in addition to be a beta blocker, it's also a pot potassium channel blocker, So instead of sodolol, remember it as sopotolol.

All right, that's our Class three anti rhythmics remember the meds by remembering the mnemonic aids aids amiodorone abutilid doftolide slash droneterone and sodolol.

You can't cure aids with potassium.

Remember they block potassium e flux during phase three, prolonging phase three repolarization.

These drugs can prolong the QT interval with the potential of developing torsades.

The highest yield meant to know is amiodorone.

Remember instead of am eodorone, remember it as am three odorone to help you remember it's a class three anti arrhythmic.

To remember the super high yield adverse drug reactions, remember taking amiodone is a bitch blueskin, interstitial lung disease, thyrotoxicity, corneal deposits, patotoxicity.

And finally, remember sotolol is a beta blocker as well as a class three potassium channel blocker.

Remember it as sopotolol instead of sodolol.

Let's move on to our final class class four drugs next.

So our class four drugs are calcium channel blockers.

So in this class it's much easier as there's only two mets to know and that's verrapimil and doltize them.

And if you need help remembering these two meds are Class four meds and I'm sorry another inappropriate nomonic, but remember the sentence.

Four nication leads to venereal disease.

Four nication helps you remember class four venereal disease which starts with the vee and d I.

Help your remember of rapimil and dultize them, which also start with vee and d I.

Four nication leads to veneeral disease.

Helps you remember your class four meds of rapamil and do tie them now.

The next question you might ask yourself is class four meads 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 m lodopene, ni fetipene, et cetera.

Why are we only discussing del tiem and vrapimil.

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 dihydropyridine and dihydropyridine non dehydropyridine are deltizem and veropimil, which will go over more in a moment, and dihydropyridine are all of the others, and lodopene, ni, fetipene, nicardipene, et cetera.

The nice part about this is dihydropyridine ends in IE, and so do all of the dihydropuritine calcium channel blockers M lodopene i E, nipetipene i E, et cetera.

The non dihydropyridine meds are the non I E meds don't tie them, and verrapimel that do not end in in E.

It's 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 dihydropyridines are I in E meds, AM, lodopen, niphetipene, et cetera primarily target the calcium channels on vascular smooth muscle tissue, so they're great for treating hypertension as they cause vasodielation of these vessels, reducing systemic vascular resistance, but exert minimal direct effects on the myocardium.

That's where our non dihydropyuridine meds come in.

The ones that do not end in in E don't tie them verrapiml.

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 dihydropyridine meds work.

Are Class four agents, so the main effect is going to be on the pacemaker action potential.

So, like we were talking about before, the pace maker 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 node, decrease conduction velocity through the AV node, which helps to treat our arrhythmius.

Like beta blockers, calcium channels also have effects on calcium influx and non pacemaker cells like our cardiac myocytes, decreasing the force generator during contractions, 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.

Fill tizim and verapamil are both used for acute and chronic ventricular rate control and atrial fibrillation and atrial flutter.

They're also effective for superventricular tachycardia alongside a dentisine 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 do 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 dihydropyridan calcium channel blockers are constipation, cardiac block bradedcardia, 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 twenty five percent 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 braidacardia, so you should avoid these drugs and patients who are using other av nodal blocking agents like beta blockers, patients with six sinus syndrome, or patients with underlying av NOD dysfunction.

All right, that's our Class four anti arrhythmics are calcium channel blockers.

Remember the meds in this class by remembering four nication leads to venarial disease Class four for rapamilandultizzem.

Remember these are non dihydropurity in agents.

They decrease calcium entering during phase four and zero indications rate control in a FIB and a flutter SVT.

Remember your adverse drug reactions by remembering CCB constipation, cardiac block braidycardia.

All right, if you're still with me, congrats.

That was a lot.

So that was your class one through four anti arrhythmics.

I'm going to do a sixty second or so recap of the highest deal topics and demonics.

Then we'll do a few quick questions to test your knowledge.

So four classes of anti rhythmics to no 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 quinidine, procaanamide, Class one B lytokane and maxilotine.

Class one C fleckinide and propaphenone.

Remember your double quarter pounder lettuce mao fries.

Please remember our Class one ameds double quarter pounder are on a foot long hot dog bund to help you remember the Class one A drugs prolong the qt intervle super important.

Don't forget about procaanamide aka pro trainamide.

Your white wolf driving a train on a loop track Wolf Parkinson white and lupis.

Remember our Class one B meds are indicated for fast and failing tissue like post m I, but our Class one C meds are contraindicated post m I.

Remember after a heart attack you swap the fries out for a salad.

Next, Class two beta blockers.

Remember the second letter of the alphabet is B, and beta blockers which start with a B are Class two antierrythmics.

All drugs in this class end in LOL and most end in olol.

The ones that don't got something special about them.

Beta blockers block epianore EPI from binding to our beta one receptors in the heart, decreasing calcium influx, decreasing the slope of phase four.

The main indication I would know is for rate control in a fib and a flutter.

Remember your cardio selective beta blockers with beam bisoprolol, bataxilol, esmolol, atenolol, aceputle lul, and mitoprolol.

Finally, remember your common contraindication slash warnings for beta blockers with ABCD, asthma, bradacardia, cardiogenic shock, diabetes, class three potassium channel blockers.

Remember the meds by remembering the demonic aids aids amiodorone, a buttylid, dohedolide, troneterone, and sotolol.

They block potassium E flux during phase three, leading to prolonged phase three repolarization.

QT prolongation is an important adverse effect.

To know.

The highest yield med is amiodorone.

Remember am three odorone to help you remember it's a class three anti arrhythmic and to remember these super highyield adrast drug reactions.

Remember taking amyodoron is a bitch.

Blue skin, interstitial lung disease, thyrotoxicity, coronial deposits of patotoxicity, and finally, remember sotolol is a beta blocker as well as a class three potassium channel blocker.

Remember it as soapotolol pot to help you remember it also blocks potassium.

Finally, our class fours.

Remember the meds in this class by remembering fornication leads to venereal disease formication Class four veneal disease, verapamel and deltizem.

Remember these are non dihydropurity in agents.

They decrease calcium entering during phase four and zero in notal cells, prolonging phase four and zero indications, rate control in a FIB and a flutter SVT.

Remember your adverse drug reactions by remembering CCB constipation, cardiac block, bradycardia.

That's your anti rhythmics.

Let's do five quick questions to test your knowledge.

Question one, Which of the following anti rhythmic 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 anti rhythmic 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 Lytokane B maxilatine, C flecanide, D disopyramid e verrapimil Again A Lytokane B maxilatine, C flecanide, D disopyramid e verrapim il.

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 ever rapimil.

It is a class four calcium channel blocker, so let's eliminate that option.

So then we're left with four choices Lytokane, maxilotine, flecanide, disopyramid, 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 let us mayo we know has the least amount of salt, which has the weakest sodium channel blockade.

That's our Class one B drugs double quarter pounder, moderate amount of salt, moderate sodium channel blockade which are Class one A 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 one C and since fries Please represents propaphenone and fleckanide, we have to look for these meds and luckily Flecaninde is present in the answer choices, so we know that answer C Flecanide is the correct choice, which is a Class one C agent exerting the most potent sodium channel blockade and has the greatest impact on reducing the slope Phase zero.

Question two, a fifty eight year old man who has recently started on a new medication by his cardiologists presents to the emergency department.

After beginning therapy, he reports episodes of dizziness and near syncopede.

An ECG obtained in the emergency department shows a markedly prolonged qt interable 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 atacine B diltiaism C quinidine D maxilotine E metoprolol.

Again a lytokine B DILTIAZM, c quinidine D, maxilotine E metoprolol.

So that's going to be answer C quinidine.

This question is describing a patient with prolonged QT and polymorphic ventricular tachycardia with twist and QRS complexes so torsa de point.

So which medication class that we've covered today are most likely to cause prolonged QT and torsads And you've got to know this.

That's your class three potassium channel blockers and your Class one A 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, amiodorone, beutilide, deftolide, dronetone, and sodolol.

None of those meds are present in the answer choices.

So next, let's search for our class one A drugs.

Remember your double quarter pounder on a foot long hot dog on which represent disopyramid, prokanamide, and quinidine and quididine.

We can see as answer ce A Class one, a drug that, as we discussed before, is notorious for prolonging the QT interble and causing torsades, 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 sixty four year old man was started on a new anti rhythmic medication several months ago.

At a routine follow up, he reports new fatigue and notices bluish gray discoloration of the skin over his face.

Laboratory studies reveal and elevated TSH, as well as an increase in serum aminotransphrase concentrations, AST and ALT.

Which of the following medications was most likely initiated in this patient in the past few months.

A dofetylide B sodolol, c amiodorone, D flecanide, e verapimil.

Again, A dofetylide B sodolol, c amiodorone, D flecanide or e verapimil.

So that's going to be answer c amioterone.

So a correct answer is answer c amioterone.

You better know this one.

Remember, amiodorone messes with so many different organs in the body, and it's why there are so many monitoring parameters needed when initiating and continuing on this medication just X ray, thyroid function test, cerum, amino transferrase levels, et cetera.

C Amiodone can cause a number of different adverse effects.

The main ones though, are in the mnemonic b itch, because taking amiodon is a bitch.

Blue skin which is seen in this patient, interstitial lung disease, thyrotoxicity which we see here as evident by the increase in TSHS, was the complaints of fatigue likely secondary to hypothidism, cornio deposit and then finally hepatotoxicity which we also see in this patient with the increase in ASD and AOT.

So don't forget taking amiodone is a bitch.

The other drugs, while they may have some adverse effects seen in this patient, like the hepatotoxicity, amiurone is the only one to potentially have all of these clinical manifestations.

Question four.

A seventy year old man with a history of hypertension and HR fibrillation presents to the clinic complaining of recurrent palpitations.

His hemodynamically stable and his ECG confirms atrial fibrillation after failing other therapies, the patient is started on an oral medication that primarily prolongs phase three 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 Lytokane B metopol law, C do fetylide, D verapimil E maxilotine.

Again A Lytokane B metopo law, C do fetolide, D verapimil or E maxilotine.

So that's going to be answered, C do fetolide.

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 three 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 de fedolided the d and aids the other meds.

B.

Motopol Law is a class two beta blocker which mainly affects phase four of pacemaker cells lytoicanum, oxilotine or lettuce and maomeds are Class one B sodium channel blockers which act on phase zero and Finally, d Verapamil is a class four calcium channel blocker which affects primarily phase four and zero of nodal cells.

Question five, A sixty four 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 and hailer use.

Which of the following beta blockers is the most suitable option for rate control in this patient?

A proprano law B natlol C pindlelal D metopo law E timil again, A propranolol B naanilol C pindlelol, D metoprolol or E timilol.

So that is going to be answered D metoprolol.

So we have a patient with a history of a fib and mild bronchospastic disease.

He didn't tolerate calcium channel blockers.

Who are going to start him on a beta blocker non selective beta blockers hit both the beta one receptors in the heart as well as beta two in the lungs, which can cause broncho 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 one 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 cardio selective 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 metoprolol, which is a cardioselective agent, and the correct answer for this patient.

All right, that was your anti rhythmics.

Try not to be too overwhelmed.

It is a lot, but try to just focus on the highest yield stuff and try to focus on the demonics.

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