Speaker 1: Okay, so today we're going to go over anti rhythmics.
Speaker 1: This can definitely be one of the more complicated topics
Speaker 1: to learn in school. It can definitely be a lot
Speaker 1: more daunting compared to the other topics. So I did
Speaker 1: my best to break it down and probably throw in
Speaker 1: more tomonics than I've had in any other podcast, so
Speaker 1: hopefully that helps you. So before we get started, thank
Speaker 1: you as always for the really nice comments, the support
Speaker 1: for the channel. Everybody who reaches out and leaves a
Speaker 1: nice comment, I truly do appreciate it, So thank you
Speaker 1: so much. Let's go ahead and get started with anti rhythmics.
Speaker 1: So there's four main classes that you need to know,
Speaker 1: and that's your Class one sodium channel blockers, Class two
Speaker 1: Beta blockers, Class three potassium channel blockers, and class four
Speaker 1: calcium channel blockers. So if you ever forget which classes which,
Speaker 1: remember the sentence some block potassium channels, some block potassium
Speaker 1: channels the letters SBPC that helps you remember. Class one
Speaker 1: S sodium channel blockers, Class two B Beta blockers, Class
Speaker 1: three P potassium channel blockers CEE, Class four calcium channel blockers.
Speaker 1: All right, let's go ahead and get started. We're going
Speaker 1: to start with our sodium channel blockers, but before we do,
Speaker 1: I want to review, done done, the cardiac action potential,
Speaker 1: as it's the foundation to understand how this class works,
Speaker 1: as well as some of our other classes that will
Speaker 1: go over today. So the cardiac action potential is complicated,
Speaker 1: and to make it even more complicated, it varies depending
Speaker 1: on which part of the heart we're talking about. We
Speaker 1: have an action potential in our pacemaker cells as well
Speaker 1: as our cardiomyocytes in the cardiac muscle. But I'm going
Speaker 1: to try to make this as simple as possible. Let's
Speaker 1: first start with the action potential of the cardiomiocytes. Now,
Speaker 1: before breaking down each phase, there's a few simple key
Speaker 1: facts to keep in mind. First, there is five phases zero, one, two, three,
Speaker 1: and four. Next, there's three players in the game, three
Speaker 1: major ions sodium, calcium, and potassium, which are all positively charged,
Speaker 1: and finally, at rest. The inside of the cardiac cell
Speaker 1: sits at about negative ninety millivolts, making it relatively negative
Speaker 1: compared to the outside. All right, so let's break it down,
Speaker 1: starting with phase four, which I like to call the floor.
Speaker 1: Phase four is the floor. This phase is the resting
Speaker 1: membrane potential. The cell is electrically quiet. There is some
Speaker 1: leakage of ions, but overall, to keep it simple, just
Speaker 1: remember phase four as the floor as not much as happening,
Speaker 1: and it's a pretty flat phase. Then comes phase zero.
Speaker 1: This is where the action starts fast. Sodium channels open
Speaker 1: up and sodium rushes into the cell, causing the inside
Speaker 1: to become rapidly more positive. This phase causes this rapid
Speaker 1: depolarization and creates this sharp upstroke on the graph. Phase zero,
Speaker 1: just remember, is all about sodium and depolarization. Next to
Speaker 1: Phase one, brief but important moment sodium channels close and potassium,
Speaker 1: the party pooper as we'll call him, begins to exit
Speaker 1: the cell. This leads to a slight dip in the
Speaker 1: membrane potential known as initial repolarization. Phase two. Potassium keeps
Speaker 1: leaving like the party pooper he is, but calcium starts
Speaker 1: to enter the cell at the same time, which essentially
Speaker 1: balances things out, and that's why Phase two is known
Speaker 1: as the plateau phase. Ultimately, though, the calcium channels eventually
Speaker 1: close and potassium of course keeps leaving, leading to a
Speaker 1: rapid drop and repolarization, which is phase three. This big
Speaker 1: old drop, and then eventually the cell returns to its
Speaker 1: negative resting state and more back at phase four the floor.
Speaker 1: So to sum it up, phase four is the floor
Speaker 1: resting state. Phase zero is the sodium fueled upstroke to
Speaker 1: start the party rapid depolarization. Phase one initial repolarization. Party
Speaker 1: pooper potassium starts to leave. Phase two. Calcium saves the
Speaker 1: day and rushes into balance out potassium's exit. Phase three,
Speaker 1: Calcium eventually gets shut down in potassium like the party pooper,
Speaker 1: e is keeps leaving big drop and repolarization. Okay, so
Speaker 1: now that we have a general understanding, let's start with
Speaker 1: our class one sodium channel blockers. So the meds in
Speaker 1: this class, while there is a lot of them, they're
Speaker 1: broken into subsections making it even worse. Class one A,
Speaker 1: one B, one C. I know, learning anti rhythmics really
Speaker 1: sucks that, I feel you. I do have anomonic though,
Speaker 1: so we'll go over that in just a minute. So
Speaker 1: Class one A is disopyramid quinidine procanamide, Class one B
Speaker 1: is lytoicane and mixilotine, and class one C is flecinide
Speaker 1: and propaphenome. So how the heck can you remember all
Speaker 1: of those they all sound different and weird. Well, there's
Speaker 1: a tried and true mnemonic that goes, double quarter pounder,
Speaker 1: lettuce mao fries please, double quarter pounder, let mayo fries please.
Speaker 1: Know this mnemonic really well, as it's not only going
Speaker 1: to help you remember the meds in this class, but
Speaker 1: also some additional mnemonics that I have thrown in. So,
Speaker 1: starting with your Class one A drugs, double quarter pounder
Speaker 1: DQP stands for disopyramid, which is the d. Q stands
Speaker 1: for quinidine, and P stands for procaanamide. Now I've got
Speaker 1: a little twist to this mnemonic that's going to help
Speaker 1: you remember a key feature of these one A drugs
Speaker 1: that you cannot forget. Picture your double quarter pounder not
Speaker 1: on a regular hamburger bun, but instead, remember it's stuffed
Speaker 1: inside of a foot long hot dog bun. A double
Speaker 1: quarter pounder and a foot long hot dog bund. It
Speaker 1: sounds odd now, but trust me, it's going to make
Speaker 1: sense and help you soon. Okay, Next our Class one
Speaker 1: B drugs lettice mayo stands for lytokane and mixilotine. And
Speaker 1: then finally our Class one C meds, fries please, which
Speaker 1: is flecanide and propaphenone. So once more double quarter pounder
Speaker 1: disopyramid quinidine and procanamide Class one A. Remember it's on
Speaker 1: a foot long hot dog bun lettice mayo, which is
Speaker 1: lytokine and maxilotine class one B. And then fries please
Speaker 1: flecanide and propafenone class one CE. So that's how you
Speaker 1: remember the meds in this class. Now let's talk about
Speaker 1: how they work on that cardiac action potential we discussed
Speaker 1: before of the cardiomyocytes. So if we think about our
Speaker 1: cardiac action potential we talked about before, where do we
Speaker 1: think the main area of impact would be? When did
Speaker 1: sodium the party animal join in? So phase zero, right,
Speaker 1: our big spike depolarization. So when we add a sodium
Speaker 1: channel blocker to a patient within arrhythmium, we decrease sodium
Speaker 1: influx and it's kind of like cutting the gas to
Speaker 1: the engine and slowing things down a bit. And by
Speaker 1: slowing phase zero depolarization, we slow conduction velocity and this
Speaker 1: can suppress ectopic beats, interrupt re entrance circuits, helping to
Speaker 1: restore normal rhythm. Now here's where it gets a little tricky.
Speaker 1: So these meds are all sodium channel blockers, but they
Speaker 1: all impact sodium in varying degrees. Some are potent sodium
Speaker 1: channel blockers, some are weak sodium channel blockers. Some even
Speaker 1: block potassium. So let's make this as simple as we
Speaker 1: possibly can. So starting with our class one SEA drugs,
Speaker 1: which bind the tightest and the longest, making them the
Speaker 1: most potent sodium channel blockers, causing the steepest reduction in
Speaker 1: the phase zero upstroke. And even though they stretch out
Speaker 1: our phase zero upstroke, they don't really change the action
Speaker 1: potential duration. The action potential duration, by the way, is
Speaker 1: just a total time it takes for a cardiaccel to
Speaker 1: complete one cycle, so from phase zero depolarization to the
Speaker 1: end of phase three repolarization. Next is our class one
Speaker 1: A drugs, which produce intermediate BLOCKA, producing a moderate slowing
Speaker 1: of phase zero, but most importantly, they also block potassium.
Speaker 1: Sneaky little guys. So this lengthens the effective refractory period
Speaker 1: and the action potential duration, resulting in QT prolongation, which
Speaker 1: is going to cost some issues. We'll go into more
Speaker 1: depth about in just a few minutes. And then finally
Speaker 1: we have our class one B drugs. They bind and
Speaker 1: release very quickly, so their effect on phase zero slope
Speaker 1: is minimal. They also decrease the refractory period a bit too,
Speaker 1: which can shorten the action potential duration. So I have
Speaker 1: an easy way for you to remember the different subclasses
Speaker 1: and their strength of impact on the sodium channel simply
Speaker 1: by remembering the more salt in the food, the more
Speaker 1: it blocks sodium. So remember our mnemonic double quarter pounder, lettuce,
Speaker 1: male fries please. So out of all of these, which
Speaker 1: has the least amount of salt? Double quarter pounder, lettuce,
Speaker 1: mao or fries please? And this isn't a trick question.
Speaker 1: Just think about the foods and think about what has
Speaker 1: the least amount of salt. So, lettuce and mao right,
Speaker 1: so Class one B lytoicanum oxilotine have the least sodium
Speaker 1: channel blocking activity. Next, which of these foods has the
Speaker 1: most salt the fries? Right? So fries please. Class one
Speaker 1: C fleckanide and propafenone exert the most potent sodium channel
Speaker 1: blocking among the Class one agents, which finally leaves us
Speaker 1: with our double quarter pounder Class one A, which has
Speaker 1: moderate amount of sodium. So these meds diso pyramid quinidine
Speaker 1: and procaanamide have moderate sodium channel blocking activity, so that's
Speaker 1: how I remembered it. There are other mnemonics, but the
Speaker 1: salt thing just made sense for me and worked. Okay,
Speaker 1: So the next thing that I want to go over
Speaker 1: is a few high old things to know about each
Speaker 1: of these meds, starting with our Class one A sodium
Speaker 1: channel blockers. So Class one A, remember is double quarter
Speaker 1: pounder diso pyramid quinidine procanamide. Now, before I told you,
Speaker 1: remember this double quarter pounder is on a foot long
Speaker 1: hot dog bund, you probably already have an idea of
Speaker 1: why I said that. So all Class one A drugs
Speaker 1: are notorious for prolonging the QT interval. So things like
Speaker 1: torsade to point, a dangerous form of polymorphic vtach are
Speaker 1: possible with these medications. And that's because, like we went
Speaker 1: over before, in addition to blocking sodium channels, they also
Speaker 1: block potassium, prolonging the action potential. And they're the only
Speaker 1: subclass of sodium channel blockers that do this. So Class
Speaker 1: one A drugs you have to know they can prolong
Speaker 1: the QT interval, so very important and very likely to
Speaker 1: test question. So the way that you're going to remember
Speaker 1: that is thinking back to our pnomonic again, same mnemonic
Speaker 1: over and over. So double quarter pounder on that foot
Speaker 1: long hot dog bund. So we remember double quarter pounder, disopyramid, quinidine,
Speaker 1: and procanamide. You're always going to remember that double quarter
Speaker 1: pounder is on a foot long hot dog bund. And
Speaker 1: that's because all of these drugs can pro long the
Speaker 1: QT interble. So that double quarter pounder oddly on this
Speaker 1: foot long hot dog bund helps you remember Class one
Speaker 1: A drugs prolong the QT interval, nice and simple, don't
Speaker 1: forget it. Let's talk about quinidine first. Now, I know
Speaker 1: we just said all of the meds in Class one
Speaker 1: A prolonged the QT interval, but quinidine really prolongs the
Speaker 1: QT intervle Quinidine has historically been one of the most
Speaker 1: common causes of drug induced to side to point, and
Speaker 1: the only reason it isn't still at the top of
Speaker 1: the list today is simply because we don't use it
Speaker 1: much anymore. It has a poor side effect profile and
Speaker 1: they're safer meds. There is still some utilization in recurrent
Speaker 1: vtach in Brugatta syndrome and short QT syndrome. And I'll
Speaker 1: give you a second to think about why we might
Speaker 1: use this drug to treat short QT syndrome. Yeah, so,
Speaker 1: but overall it's usually not going to be a top pick.
Speaker 1: With that being said, you still got to know it
Speaker 1: because in addition to potentially causing towards to point, it
Speaker 1: has a unique side effect that's often tested on. So
Speaker 1: the highest deel thing you need to know about quinidine
Speaker 1: is that it can cause something known as sensinism. Weird name,
Speaker 1: but the backstory may help you to remember it. So
Speaker 1: there is this tree called these Sinschona tree native to
Speaker 1: the Andes. It produces bark that's rich in alkaloids. This
Speaker 1: bark is not only the source of quindine but also
Speaker 1: the source of quinine, which you're probably familiar with for
Speaker 1: its treatment of malaria. So both of the meds which
Speaker 1: come from the same tree share a side effect from
Speaker 1: their plant origin, sensianism, which can cause a constellation of
Speaker 1: symptoms tinatus, hearing loss, confusion, and delirium, visual disturbances. And
Speaker 1: we call this sentianism as it's named after the tree.
Speaker 1: It's derived from the Sinchona tree. So hopefully that little
Speaker 1: backstory helps you to remember quinidine can cause sentianism and
Speaker 1: of course torsade to point. Next drug from Class one A,
Speaker 1: it's much higher yield, and that's procanamide. Procaanamide is another
Speaker 1: effective anti arrhythmic drug that's again limited by its side
Speaker 1: effect profile. And there's two things you need to know
Speaker 1: about procanamide that are very high yield, wolf Parkinson White
Speaker 1: and lupis. Let's talk about that. So procaanamide can be
Speaker 1: used to treat arrhythmias associated with Wolf Parkinson White syndrome.
Speaker 1: This is a popular exam question, so you need to
Speaker 1: know it. Next, this drug can cause lupus like syndrome
Speaker 1: or drug induced lupis. So chronic administration of procainamide can
Speaker 1: lead to lupus like syndrome. So these patients will have
Speaker 1: similar symptoms to those seen in lupus, rash, arthritis, et cetera.
Speaker 1: So these are the two things that you need to
Speaker 1: know about procanamide. They can treat Wolf Parkinson White arrhythmias
Speaker 1: and it can cause drug induced lupis. So how do
Speaker 1: you remember that? So instead of remembering it as procanamide,
Speaker 1: remember it as protrainamide. Every time you hear procanamide, I
Speaker 1: want you to think protrainamide and have this picture in
Speaker 1: your head of this big train rolling down the tracks.
Speaker 1: At the front of the train, the conductor is a
Speaker 1: wolf with bright white fur. That's your cue for wolf
Speaker 1: Parkinson White. And this train is circling in this continuous loop,
Speaker 1: which will help you remember loopis like syndrome. So procanamide
Speaker 1: is protrainamide. Think of a train being driven by a
Speaker 1: white wolf wolf Parkinson white circling in a continuous loop.
Speaker 1: Loopis like syndrome. And then our last drug in the
Speaker 1: Class one A class is disopyramid, which instead I used
Speaker 1: to remember as drysopyramid dr wide dry because the only
Speaker 1: thing I think you should know about this drug is
Speaker 1: it'll dry you out as it causes anticholinergic side effects,
Speaker 1: which is the most common adverse drug reaction. So it
Speaker 1: can cause dry mouth, dry eyes, urinary hesitancy, constipation, So
Speaker 1: avoid this in patients that have glaucoma, my asthenia, gravists,
Speaker 1: et cetera. Instead of disopyramid, remember dry soopyramid dr y
Speaker 1: to remember the anticholinergic side effects. Okay, next is our
Speaker 1: class one B. What are the Class one B drugs?
Speaker 1: Remember Class one B lettice, male lytocane, and maxillotine. So
Speaker 1: starting with lytocine. Lytocane, when administered intravenously, can be used
Speaker 1: for the treatment of ventricular arrhythmias. Most common ADR is
Speaker 1: going to be CNS toxicity. And then we have mixilotine,
Speaker 1: which is essentially an oral version of lytocine. It can
Speaker 1: also cause CNS toxicity, but because it's a POMD, we
Speaker 1: often see GI problems. Nausee of vomiting or heartburn not important.
Speaker 1: What you should know about these two meds is when prescribed,
Speaker 1: it will be for fast and failing ventricular tissue. So
Speaker 1: if you're going to use these meds, it will be
Speaker 1: fast ventricular rhythm so ventricular tachycardia ventricular fibrillation and or
Speaker 1: on failing or a schemic tissue so schemic arrhythmias after
Speaker 1: a myocardial infarction. And that's because the Class one B
Speaker 1: meds preferentially bind sodium channels in the depolarized and inactivated state,
Speaker 1: which are common in aeschemic myocardium and during tacharrhythmias. So
Speaker 1: drugs like maxilotine can be used for rhythmia suppression. Posts
Speaker 1: demi lytokin can be used in our ACLS algorithm. So
Speaker 1: main takeaway Class one B. Remember use these drugs in
Speaker 1: fast and failing ventricular tissue, ventricular tacharrhythmias and POSTMI. Okay,
Speaker 1: that finally leaves us with our class one C drugs.
Speaker 1: Class one C remember fries please, which is flecinide and propathenone.
Speaker 1: So these drugs can be used in both ventricular arrhythmias
Speaker 1: and superventricular arrhythmias like atrial fibrillation atrial flutter. There's something
Speaker 1: known as the pill in the pocket approach, which is
Speaker 1: a form of pharmacologic cardioversion. Basically, a patient has a
Speaker 1: history of aphib is that home feels an episode coming on,
Speaker 1: they can pop one of these combined with an av
Speaker 1: NOTAB blocking agent like a beta blocker, going to get
Speaker 1: themselves back in rhythm. So that's cool. But really the
Speaker 1: most important thing to know about the subclass, and what
Speaker 1: I want you to remember is that these drugs are
Speaker 1: contraindicated in patients with structural heart disease. Like POSTMI, They're
Speaker 1: only to be used in patients with structurally normal hearts.
Speaker 1: Using these drugs and patients with structural heart disease, cornary
Speaker 1: arter disease, et cetera can lead to sudden cardiac death
Speaker 1: quite the opposite of the class one B drugs. We
Speaker 1: just went over where that was one of their primary
Speaker 1: indications and a very easy test question. So how can
Speaker 1: you remember that Class one B drugs are good post
Speaker 1: DEMI and class one C drugs are bad post demi.
Speaker 1: So back to the same mnemonic again. I told you
Speaker 1: to remember it. So if you just had a heart
Speaker 1: attack and you're ordering some dinner, you're going to substitute
Speaker 1: your fries for a salad, right, So remember that Class
Speaker 1: one B let us mayo good post DEMI and class
Speaker 1: one C fries please no good post am I. Remember
Speaker 1: after a heart attack, swap the fries out for a salad.
Speaker 1: So that's your sodium channel blockers quick recap. Drugs in
Speaker 1: this class are remembered by the demonic double quarter pounder.
Speaker 1: Let us mao fries please double quarter pounder, disopyramid, quinityde
Speaker 1: and prokanamide that's your Class one A. Let us mao
Speaker 1: lytokane and mixilotine that's your Class one B. And then
Speaker 1: fries please fleckenide and propafenone Class one C. These drugs
Speaker 1: slow down the influx of sodium during phase zero. And
Speaker 1: remember the more salt in the food, the more it
Speaker 1: blocks sodium channels. Remember your double quarter pounder is on
Speaker 1: a foot long hot dog bund To help you remember
Speaker 1: your Class one A drugs can prolong the QT interval, torsad,
Speaker 1: et cetera. Remember quinidine can cause synchronism. Procanamide aka protranamide.
Speaker 1: Remember your white wolf driving the train on a loop
Speaker 1: track Wolf Parkinson White and lupis Class one B letacanum,
Speaker 1: oxilotine use on your fast and filling ventricular tissue. And
Speaker 1: Class one C fleckanide and propafenone. Most importantly, remember these
Speaker 1: drugs are contraindicated with structural heart disease postami, et cetera.
Speaker 1: Remember after an MI, I swap your fries out for
Speaker 1: a salad. That's your sodium channel blockers. Next, let's talk
Speaker 1: about Class two, which are beta blockers. You're probably already
Speaker 1: familiar with this class as we use these meds for
Speaker 1: hypertension as well as a number of other indications. And
Speaker 1: if you ever forget which med class is part of
Speaker 1: Class two, remember B is the second letter of the alphabet,
Speaker 1: and beta blockers which start with a B are our
Speaker 1: Class two agents. So these drugs, in addition to their
Speaker 1: anti hypertensive properties, also have anti arrhythmic properties. Luckily, remembering
Speaker 1: the names of these meds is a whole lot easier
Speaker 1: compared to your sodium channel blockers, because all of these
Speaker 1: drugs end in LOL, like a tenelol, propranolol, Carbada law,
Speaker 1: and mitoprolol. So all beta blockers end in l OL,
Speaker 1: and most but not all end in ol l ol L.
Speaker 1: And here's something important that I want you to recognize.
Speaker 1: If you see a beta blocker that does not end
Speaker 1: in olol, you need to know that this is going
Speaker 1: to be a unique or let's say a fancy beta
Speaker 1: blocker that does something a little extra. So if a
Speaker 1: beta blocker does not end in olol, it's usually because
Speaker 1: it has extra properties beyond standard beta blockade, like alpha
Speaker 1: blockade that we see in Carvata law and Libata law,
Speaker 1: which end in ilol and alo l respectively, or potassium
Speaker 1: channel blockade that we see in sodolol, which ends in alol.
Speaker 1: So when you see a beta blocker, check the suffix.
Speaker 1: If it ends in olol like mitopralaw, it'll lack primarily
Speaker 1: through standard beta blockade. If it ends a little differently
Speaker 1: like lo betalall alol. You'll know it has some additional
Speaker 1: properties beyond standard beta blockade. Now, how do these drugs work?
Speaker 1: So for that, let's look back at our cardiac action
Speaker 1: potential again, but this time we're going to be looking
Speaker 1: at our cardiac action potential of our pacemaker cells. So
Speaker 1: this is a little different. This action potential only has
Speaker 1: three phases, phases zero, three, and four. So let's start
Speaker 1: with phase four, which before we called the floor as
Speaker 1: this was almost a flat period with not much happening.
Speaker 1: But now in phase four it's a little different. You're
Speaker 1: going to notice there's this little upward slope, and that's
Speaker 1: because in phase four we now have this slow leak
Speaker 1: of sodium sneaking through these pacemaker channels. This is sometimes
Speaker 1: called the funny current. In addition, and very important, during
Speaker 1: phase four, we also have calcium influx, which is first
Speaker 1: through T type calcium channels and then a little later
Speaker 1: on through L type calcium channels, which ultimately depolarized the
Speaker 1: membrane to its threshold potential. Next this phase zero, where
Speaker 1: we have calcium continuing to enter through, producing a slower
Speaker 1: upstroke than the fast sodium driven spike of our cardio
Speaker 1: myocytes we were talking about before. And then finally phase three,
Speaker 1: which is repolarization, follows as calcium channels close and guess
Speaker 1: who starts to leave yet potassium, the party pooper flows out,
Speaker 1: which brings us back to phase four once more. And
Speaker 1: as you can see, I didn't mention phase one one
Speaker 1: or two, and that's because our pacemaker cells lack a
Speaker 1: distinct phase one or two. All right, So, now that
Speaker 1: we understand the pacemaker action potential, how do beta blockers
Speaker 1: influence this to help treat arrhythmias? Well, indirectly by preventing
Speaker 1: epinefrin and nore epinefrin from binding to the beta receptors.
Speaker 1: So how the heck does that help us treat arrhythmias
Speaker 1: and how does that impact the action potential? So in
Speaker 1: the heart, we have beta receptors, primarily beta one adrenergic receptors,
Speaker 1: and when catechola means like EPI and nor epi bind
Speaker 1: to these receptors, this long chain of events occurs. First,
Speaker 1: the enzyme IDENTL cyclosis activated, which converts ATP into CIMP.
Speaker 1: CIMP activates pKa, which phosphorulates L type calcium channels, causing
Speaker 1: them to open leading to an influx of calcium. Ugh,
Speaker 1: So what do you need to actually remember from that?
Speaker 1: So all you really need to know is that when
Speaker 1: EPI and nor rep bind to these receptors, a bunch
Speaker 1: of stuff happens which leads to more calcium in the cell.
Speaker 1: So if we block these receptors, we block these beta
Speaker 1: receptors with a beta blocker, we block epianore epi from binding,
Speaker 1: which ultimately slows the influx of calcium. And this is
Speaker 1: primarily at the end of phase four, which decreases that slope,
Speaker 1: which makes it take longer for the cell to reach
Speaker 1: the action potential threshold. So we have a decrease slope
Speaker 1: of phase four in our pacemaker cells. So in turn,
Speaker 1: the SA node is going to fire less often and
Speaker 1: the AV node is going to conduct more slowly, both
Speaker 1: of which help control heart rate and are especially useful
Speaker 1: in treating tacharithms like atrofibrillation. Now, beta blockers also have
Speaker 1: effects on non pacemaker cells like our cardiomyocytes, and in
Speaker 1: these cells, by decreasing calcium influx, they decrease cardiac contractility,
Speaker 1: decreasing oxygen demand for these cells. So this is really
Speaker 1: a lot of info, but really, here's the main takeaway
Speaker 1: in the simple recap of what you should know in
Speaker 1: just a few words. So, beta blockers stop EPI and
Speaker 1: nor epi from binding, which indirectly decreases calcium influx, which
Speaker 1: flattens our phase four slope. So that's what I think
Speaker 1: you should know. Now, what are the common indications for
Speaker 1: this class of drugs you should know? Of course, beta
Speaker 1: blockers are used in a number of different conditions, but
Speaker 1: when it comes us so they're anti rhythmic indications. The
Speaker 1: one you should know is for rate control in atrial
Speaker 1: fibrillation and atrial flutter. They can also be used in SVT, postmat,
Speaker 1: et cetera. But please remember rate control in a fib
Speaker 1: and a flutter. That's the most common and most important. Okay,
Speaker 1: So now I want to go over some extra tips
Speaker 1: for beta blockers and of course a whole bunch of demonics.
Speaker 1: So first, not all beta blockers are the same. We
Speaker 1: have cardio selective beta blockers that primarily just block the
Speaker 1: beta one receptors in the heart, and then we have
Speaker 1: non selective that also block beta two receptors which can
Speaker 1: be found in smooth muscle cells GI tract uterus. But
Speaker 1: most importantly in the lungs, where they can induce broncho
Speaker 1: dilation when stimulated. Remember the demonic beta one primarily found
Speaker 1: in the heart. You have one heart, beta two, which
Speaker 1: can be found in the lungs. You have two lungs,
Speaker 1: which just helps you to remember it. Now, there's a
Speaker 1: bunch of beta blockers, so how the heck can you
Speaker 1: remember which are cardio selective and which are non selective.
Speaker 1: Remember that a beam of light is selective to just
Speaker 1: one area. A beam B, E, A M is selective
Speaker 1: to just one area, So if the beta blocker starts
Speaker 1: with a BA or M, it's cardio selective. So B EA, M,
Speaker 1: B stands for bisoprolol or a bitaxilol. E stands for esmolol,
Speaker 1: A stands for a tenolol or asputle all, and then
Speaker 1: M stands from a toprolall. So you really don't even
Speaker 1: need to remember all of the specific names. All you
Speaker 1: need to remember is that a beam is a direct
Speaker 1: or selective light, Meaning if a beta blocker in the
Speaker 1: question starts with A B, E, A or M, it's
Speaker 1: cardio selective. So if they ask you a question like
Speaker 1: you decide to treat this patient with a beta blocker
Speaker 1: who has a history of mild to moderate at bronchospastic disease,
Speaker 1: which would be the preferred beta blocker to use. So
Speaker 1: all you need to do is find when that starts
Speaker 1: with beam b EA m as. The cardio selectivity makes
Speaker 1: this a safer drug for this population. So this is
Speaker 1: great for exam knowledge, but for real life, what you
Speaker 1: should know is that even cardio selective agents can exert
Speaker 1: some inhibition of beta two receptors at high doses. So
Speaker 1: if you had a patient with severe or decompensated bronchospastic disease,
Speaker 1: you don't want to avoid all beta blockers in these patients,
Speaker 1: selective and non selective. Okay, Next, I want to segue
Speaker 1: into anomodic to help you remember the contraindications slash warnings
Speaker 1: of this class of drugs. So to help you remember
Speaker 1: the common and most tested on remember the demonic ABCD.
Speaker 1: ABCD stands for asthma, bradacardia, cardiogenic shock and diabetes asthma
Speaker 1: braidacardia cardiogenic shock diabetes. So let's break them down. A
Speaker 1: stands for asthma, which we just talked about, so I
Speaker 1: won't go into great detail, but beta blockade with non
Speaker 1: selective agents prevents bronchodilation, so non selective beta blockers should
Speaker 1: be avoided in susceptible patients asthma et cetera, and in
Speaker 1: severe disease, you really want to avoid all beta blockers,
Speaker 1: even the selective agents. Next B stands for bradacardia. These
Speaker 1: mens have negative chronotropic effects. They slow the heart rate,
Speaker 1: so they're relatively contraindicated in symptomatic bradacardia, sinus nod dysfunction,
Speaker 1: and in patients with second or third degree av block
Speaker 1: unless a pacemaker's present C stands for cardiogenic shock or
Speaker 1: severely decompensated heart failure. So while beta blockers improve survival
Speaker 1: in stable chronic heart failure, initiation should be avoided in
Speaker 1: severe acute de compensation or cardiogenic shock, as in these states,
Speaker 1: the heart depends on the sympathetic drive the beta one
Speaker 1: stimulation to maintain output, which beta blockers shut down. So
Speaker 1: blocking beta one receptors reduces contractility and heart rate, which
Speaker 1: can worsen shock. Finally, the D stands for diabetes. This
Speaker 1: is more of a caution rather than a contraindication, but
Speaker 1: one that's important to know. So beta blockers can mask
Speaker 1: hypoglycemia symptoms like sweating anxiety, which are mediated by epinephrine,
Speaker 1: which they block. They also may delay recovery from insulin
Speaker 1: induced hypoglycemia by blunting epinephrin's effect on gluconeogenesis and glycogenolysis.
Speaker 1: Although the studies are a bit more conflicting in this area,
Speaker 1: but the main takeaway use these in caution with diabetics.
Speaker 1: All right, that's your beta blockers. Quick recap of the
Speaker 1: juicy details are class two antierrhythmics. Remember the second letter
Speaker 1: of the alphabet is B, and beta blockers which start
Speaker 1: with a B are r Class two antierythmics. All drugs
Speaker 1: in this class end in lol and most end in olol.
Speaker 1: The ones that don't got something special about them. Beta
Speaker 1: blockers block epian or EPI from binding to our beta
Speaker 1: one receptors in the heart, indirectly decreasing intracellular calcium influx,
Speaker 1: decreasing the slope of phase four. The main indication I
Speaker 1: would know is rate control in a fib and a flutter.
Speaker 1: Remember your cardio selective beta blockers with beam bisoprolol, bitaxilaw
Speaker 1: asmolol atenolol, aceputle law, metoprol law. Finally, remember your common
Speaker 1: contraindication slash warnings for beta blockers ABCD, asthma, bradacardia, cardiogenic shock, diabetes.
Speaker 1: That's your beta blockers. We're halfway there. Let's talk about
Speaker 1: our class three antiarithmics. Next are potassium channel blockers. There's
Speaker 1: a few different drugs in this class, amiodorone, dronetarone, ammutilide, dofeedolide, sodolol. Honestly,
Speaker 1: you should really just focus on amiodorone and maybe sodolol.
Speaker 1: But there is a nomonic to help you remember all
Speaker 1: of them if you choose to. And the mnemonic is
Speaker 1: and I'm sorry for this, but thenomonic is AIDS ai
Speaker 1: DS AIDS stands for a amiodorone, I, abutilide, d do feedolide, slash, dronetarone,
Speaker 1: and s sotolol. And to further help solidify this demonic
Speaker 1: and help you remember that the AIDS mnemonic is associated
Speaker 1: with potassium channel blockers, you can remember the sentence can't
Speaker 1: cure aids with potassium can't cure aids with potassium with
Speaker 1: can't and cure spelled with a K instead of C
Speaker 1: to help you remember the chemical symbol for potassium. I
Speaker 1: apologize it's not the most appropriate nomonic in dynomonics from
Speaker 1: here on out. Well, you'll see, all right, So how
Speaker 1: do these drugs work. Well, for that, we need to
Speaker 1: go back to our cardiac action potential of the cardiomyocytes
Speaker 1: we were discussing before, the one with five phases. So
Speaker 1: remember potassium, the party pooper who kept leaving the party
Speaker 1: and ultimately in phase three just flooded out, leading to repolarization. Well,
Speaker 1: what if we had a drug that could come in
Speaker 1: and just block the door and not let him out
Speaker 1: during phase three, making him just hang around. Well, that's
Speaker 1: our potassium channel blockers are class three drugs which block
Speaker 1: potassium eflux during phase three, prolonging phase three repolarization. So
Speaker 1: these drugs bind and inhibit potassium channels, meaning we have
Speaker 1: less potassium leaving the cell, which leads to a slower
Speaker 1: rate of repolarization, prolonging the action potential and effective refractory period.
Speaker 1: And this increase in the refractory period helps because this
Speaker 1: essentially lengthens the period of time the cell can kind
Speaker 1: of hang out before being stimulated again, we give it
Speaker 1: a little breathing room which helps interrupt re entrant arrhythmia. Now,
Speaker 1: the problem with prolonging things, prolonging the action potential in particular,
Speaker 1: is we get a new problem. And I'll give you
Speaker 1: a second to think about what that problem may be.
Speaker 1: What was another med class or subclass we talked about
Speaker 1: that also blocked potassium. It involved a foot long hot
Speaker 1: dog bund. That's right, our Class one A sodium channel blockers,
Speaker 1: the double quarter pounder on a foot long hot dog
Speaker 1: bund also blocked potassium and they led to the same
Speaker 1: issue we'll go over now, which is prolonged QT interval
Speaker 1: with the potential of developing towards sad de point, so
Speaker 1: a significant adverse effect that you need to be aware
Speaker 1: of for these medications. Of note, this is much less
Speaker 1: common with amiodorone androneterone compared to the other meds in
Speaker 1: this class. But you need to remember your Class three
Speaker 1: potassium channel blockers can prolong the QT interval, and so
Speaker 1: can your Class one A sodium channel blockers we went
Speaker 1: over before. Please remember this as it will likely be
Speaker 1: tested on all. Right, moving on, what are the indications
Speaker 1: for our class three drugs, So some indications are atrial fibrillation,
Speaker 1: atrial flutter, ventricular tachycardia. Amiodorone, really, the only one you
Speaker 1: should focus on is a powerful anti arrhythmic used for
Speaker 1: both atrial and ventricular arrhythmia, limited only by its side
Speaker 1: effect profile or only, It's most often prescribed to prevent
Speaker 1: atrial fibrillation and ventricular arrhythmias. Intravenously. It's used in critically
Speaker 1: ill patients with a fib to restore sinus rhythm, control
Speaker 1: ventricular rate, or convert ventricular arrhythmias, and like letocaine, it
Speaker 1: also plays a key role in our ACLS protocol. So
Speaker 1: let's talk a bit more about amiodorone, because I feel
Speaker 1: like if you're going to get a question about a
Speaker 1: class three anti arrhythmic, it's going to be on amiodorone,
Speaker 1: and not only that, amiodorone is just a really cool drug.
Speaker 1: So first, remember amiodorone as AM three odorone instead of
Speaker 1: am eodorone. Remember am three odorone as in the number three.
Speaker 1: So a year from now, when you forget all about
Speaker 1: this lecture and you get a test question that has
Speaker 1: amiodorone on it, and you forget everything about it. If
Speaker 1: you always remember it as AM three odorone instead of
Speaker 1: am eodorone, you'll never forget it's a class three anti arrhythmic. Now,
Speaker 1: on that note, even though this medication is classified as
Speaker 1: a class three anti arrhythmic as it does block potassium channels,
Speaker 1: it also blocks sodium channels like a class one, beta
Speaker 1: adrenergic recept like a class two, and calcium channels like
Speaker 1: a class four. Pretty crazy. Dronetarone, another class three drug
Speaker 1: which is structurally similar to amiodorone, just lacking the iodine group,
Speaker 1: also blocks all four channels. So maybe not super high yield,
Speaker 1: but pretty cool. Okay. Next, let's cover potentially the highest
Speaker 1: sealed thing to know about amiodorone, and that's its adverse effects. So,
Speaker 1: amiodorone is highly lipid soluble, so it accumulates in all
Speaker 1: different tissues throughout the body, which is part of the
Speaker 1: reason it has so damn many side effects. Oral amiodorone
Speaker 1: has a super long half life hangs around for up
Speaker 1: to one hundred plus days in some cases, so this
Speaker 1: is probably the highest heeled thing to know about amiodorone.
Speaker 1: It's adverse effects, So how do you remember the adverse
Speaker 1: effects of amiodorone. Well, unfortunately, all of the class three
Speaker 1: and four drug demonics are inappropriate and it's not on purpose,
Speaker 1: it's just what works out with the letters. So I'm sorry,
Speaker 1: but all right, So if the adverse effects, remember taking
Speaker 1: amiodorone is a bitch. Taking amiodorone is a bitch. Which
Speaker 1: stands for blue skin, interstitial lung disease, thyrotoxicity, coronal deposits
Speaker 1: of patotoxicity. So starting with b amiodorone can cause blue skin.
Speaker 1: Amiodorone can cause a bluish gray discoloration of the skin,
Speaker 1: sometimes called blue man syndrome. This is going to be
Speaker 1: most prominent on the face. There's other skin issues photosensitivity, hyperpigmentation,
Speaker 1: but don't forget the blue skin. Next eye stands for
Speaker 1: interstitial lung disease. Amiodorone induced pulmonary toxicity is found in
Speaker 1: up to five percent of patients. Most common form is
Speaker 1: interstitial pneuminitis. So before you start a patient on amiodorone,
Speaker 1: you should obtain a baseline chest X ray to ensure
Speaker 1: there isn't any evidence of existing interstitial lung disease. Next
Speaker 1: is probably the most important one, and that's thyroid toxicity
Speaker 1: thyroid toxicity, so amiodorone contains high amounts of iodine. That's
Speaker 1: actually the reason the name Amiodoron contains the letter's iod
Speaker 1: It's suited the fact amiodorone contains two iodine atoms per
Speaker 1: molecule in its chemical structure, and since iodine is a
Speaker 1: key substrate for thyroid hormone synthesis, this iodine load can
Speaker 1: disrupt thyroid function, leading to either hypo or hyperthyroidism. Thyroidys
Speaker 1: function is actually one of the most common complications of
Speaker 1: amiodoron therapy and because of this, patient should have baseline
Speaker 1: thyroid function tests such as TSH before starting the medication
Speaker 1: and should be monitored periodically during treatment. Next is the C,
Speaker 1: which stands for cornial microdeposits. So these microdeposits occur and
Speaker 1: the majority of patients taking amiodorone. They're typically benign and
Speaker 1: don't affect visual acuity. They result from amourone being secreted
Speaker 1: into the tiers by the lacrymal glands and gradually accumulate
Speaker 1: on the cornial surface, but generally resolve after discontinuation of
Speaker 1: the drug. And then finally we have H, which stands
Speaker 1: for patotoxicity. So around twenty five percent of patients taking
Speaker 1: amiodorone will have a transient rise and serum aminotransfhrase concentrations
Speaker 1: our liver function tests so ast ALT can go up.
Speaker 1: Most patients are asymptomatic, Habititis occurs in fewer than three
Speaker 1: percent of patients, and cirrhosis and hepatic failure are rare.
Speaker 1: So have this tear checklist of the many organs you
Speaker 1: will need to check before starting amiodorone. Baseline LFT should
Speaker 1: be attained prior to initiation, as well as checking during therapy.
Speaker 1: All right, so remember taking amiodone, as you can tell,
Speaker 1: is a bitch. Blue skin, interstitial lung disease, thyrotoxicity, cornial deposits, hepatotoxicity.
Speaker 1: One other class three met I want to briefly mention
Speaker 1: before we wrap up. This class is SODOLOL. So before
Speaker 1: I tell you why this med is unique, I want
Speaker 1: you to think and look at the name and think
Speaker 1: about what's unique about it. It's spelled so ta l
Speaker 1: O L so first it ends in LOL, so it's
Speaker 1: a beta blocker. But remember what we talked about before
Speaker 1: with beta blockers. If they end in olol, traditional beta
Speaker 1: blocker anything else, we know they have some additional properties.
Speaker 1: So sodolol ends in a lool, so we know there's
Speaker 1: more than just traditional beta blockade with this MED. And
Speaker 1: in this case it's pretty obvious as we're talking about
Speaker 1: potassium channel blockers right now, so we know sodolol also
Speaker 1: has potassium channel blocking abilities in addition to beta blockade,
Speaker 1: and that's why it's considered a Class three MED. But
Speaker 1: later on, when you see this on an exam question,
Speaker 1: you'll likely remember it's a beta blocker due to the
Speaker 1: lol at the end, but it's easy to forget it's
Speaker 1: also a potassium channel blocker. So because of that, I
Speaker 1: used to remember it instead of sodolol as so potolol.
Speaker 1: Instead of sodolol, remember it as so potolol so ptalol.
Speaker 1: The pot helps me remember that in addition to be
Speaker 1: a beta blocker, it's also a pot potassium channel blocker,
Speaker 1: So instead of sodolol, remember it as sopotolol. All right,
Speaker 1: that's our Class three anti rhythmics remember the meds by
Speaker 1: remembering the mnemonic aids aids amiodorone abutilid doftolide slash droneterone
Speaker 1: and sodolol. You can't cure aids with potassium. Remember they
Speaker 1: block potassium e flux during phase three, prolonging phase three repolarization.
Speaker 1: These drugs can prolong the QT interval with the potential
Speaker 1: of developing torsades. The highest yield meant to know is amiodorone.
Speaker 1: Remember instead of am eodorone, remember it as am three
Speaker 1: odorone to help you remember it's a class three anti arrhythmic.
Speaker 1: To remember the super high yield adverse drug reactions, remember
Speaker 1: taking amiodone is a bitch blueskin, interstitial lung disease, thyrotoxicity,
Speaker 1: corneal deposits, patotoxicity. And finally, remember sotolol is a beta
Speaker 1: blocker as well as a class three potassium channel blocker.
Speaker 1: Remember it as sopotolol instead of sodolol. Let's move on
Speaker 1: to our final class class four drugs next. So our
Speaker 1: class four drugs are calcium channel blockers. So in this
Speaker 1: class it's much easier as there's only two mets to
Speaker 1: know and that's verrapimil and doltize them. And if you
Speaker 1: need help remembering these two meds are Class four meds
Speaker 1: and I'm sorry another inappropriate nomonic, but remember the sentence.
Speaker 1: Four nication leads to venereal disease. Four nication helps you
Speaker 1: remember class four venereal disease which starts with the vee
Speaker 1: and d I. Help your remember of rapimil and dultize them,
Speaker 1: which also start with vee and d I. Four nication
Speaker 1: leads to veneeral disease. Helps you remember your class four
Speaker 1: meds of rapamil and do tie them now. The next
Speaker 1: question you might ask yourself is class four meads are
Speaker 1: calcium channel blockers. And we know there's a bunch of
Speaker 1: calcium channel blockers, So why are we only listing two meds?
Speaker 1: What about all of the other calcium channel blockers like
Speaker 1: m lodopene, ni fetipene, et cetera. Why are we only
Speaker 1: discussing del tiem and vrapimil. So for that, we need
Speaker 1: to quickly review the different types of calcium channel blockers
Speaker 1: and what they do. So there's two different types of
Speaker 1: calcium channel blockers non dihydropyridine and dihydropyridine non dehydropyridine are
Speaker 1: deltizem and veropimil, which will go over more in a moment,
Speaker 1: and dihydropyridine are all of the others, and lodopene, ni, fetipene, nicardipene,
Speaker 1: et cetera. The nice part about this is dihydropyridine ends
Speaker 1: in IE, and so do all of the dihydropuritine calcium
Speaker 1: channel blockers M lodopene i E, nipetipene i E, et cetera.
Speaker 1: The non dihydropyridine meds are the non I E meds
Speaker 1: don't tie them, and verrapimel that do not end in
Speaker 1: in E. It's a nice easy way to differentiate the two,
Speaker 1: So to keep this brief, both of these subclasses inhibit
Speaker 1: the L type calcium channels on cells, which will go
Speaker 1: over in more detail in a second. But the big
Speaker 1: difference is that dihydropyridines are I in E meds, AM, lodopen, niphetipene,
Speaker 1: et cetera primarily target the calcium channels on vascular smooth
Speaker 1: muscle tissue, so they're great for treating hypertension as they
Speaker 1: cause vasodielation of these vessels, reducing systemic vascular resistance, but
Speaker 1: exert minimal direct effects on the myocardium. That's where our
Speaker 1: non dihydropyuridine meds come in. The ones that do not
Speaker 1: end in in E don't tie them verrapiml. These meds
Speaker 1: do the same they inhibit L type calcium channels, but
Speaker 1: they are more selective for the pacemaker and non pacemaker
Speaker 1: cells of the heart, making them useful for the arrhythmias
Speaker 1: will go over. So let's talk a bit more about
Speaker 1: how these non dihydropyridine meds work. Are Class four agents,
Speaker 1: so the main effect is going to be on the
Speaker 1: pacemaker action potential. So, like we were talking about before,
Speaker 1: the pace maker action potential only has three phases, phase zero, three,
Speaker 1: and four. And let's just do a quick recap because
Speaker 1: it's a tough subject and why not. So Phase four, remember,
Speaker 1: is a slow sodium leak through the funny current, with
Speaker 1: calcium entering first through our T type calcium channels and
Speaker 1: then later on through our L type calcium channels to
Speaker 1: push us through to reach the threshold potential. Phase zero
Speaker 1: is the slower calcium driven upstroke of depolarization, and then
Speaker 1: finally phase three is repolarization as calcium channels close and
Speaker 1: potassium the party pooper he is flows out. So unlike
Speaker 1: beta blockers which indirectly affected calcium channels by blocking EPI
Speaker 1: and nor epi. Calcium channels directly impact calcium channels and
Speaker 1: have an impact on phase four and zero, so they
Speaker 1: decrease calcium entering during phase four and zero, so we'll
Speaker 1: have a decrease in the slope of phase four and zero,
Speaker 1: slowing things down so the heart gets a little bit
Speaker 1: more breathing room. And just like in beta blockers, they'll
Speaker 1: decrease firing of the s A node, decrease conduction velocity
Speaker 1: through the AV node, which helps to treat our arrhythmius.
Speaker 1: Like beta blockers, calcium channels also have effects on calcium
Speaker 1: influx and non pacemaker cells like our cardiac myocytes, decreasing
Speaker 1: the force generator during contractions, so they have an effect
Speaker 1: not only on cardiac conduction, but also cardiac contractility as well.
Speaker 1: So remember, calcium channel blockers block calcium channels just as
Speaker 1: the name states, which affects phase four and zero of
Speaker 1: the pacemaker cardiac action potential. Now, what arrhythmias do they treat?
Speaker 1: You might ask. Well, since they're similar to beta blockers,
Speaker 1: we will see some similarities. Fill tizim and verapamil are
Speaker 1: both used for acute and chronic ventricular rate control and
Speaker 1: atrial fibrillation and atrial flutter. They're also effective for superventricular
Speaker 1: tachycardia alongside a dentisine and can be used in multifocal
Speaker 1: atrial tachycardia, But the main indication to remember is rate
Speaker 1: control in a FIB and a flutter and SVT. All right,
Speaker 1: what else do we know about our calcium channel blockers. Well,
Speaker 1: of course you got to know the adverse drug reactions.
Speaker 1: So the three adverse effects you need to know for
Speaker 1: non dihydropyridan calcium channel blockers are constipation, cardiac block bradedcardia,
Speaker 1: which luckily is the initial of calcium channel blockers CCB.
Speaker 1: So starting with C, which is for constipation. This is
Speaker 1: pretty common and occurs in up to twenty five percent
Speaker 1: of patients. The next C cardiac block. These drugs may
Speaker 1: cause first, second or third degree av block and then
Speaker 1: finally b our last letter, these drugs may lead to
Speaker 1: sinus braidacardia, so you should avoid these drugs and patients
Speaker 1: who are using other av nodal blocking agents like beta blockers,
Speaker 1: patients with six sinus syndrome, or patients with underlying av
Speaker 1: NOD dysfunction. All right, that's our Class four anti arrhythmics
Speaker 1: are calcium channel blockers. Remember the meds in this class
Speaker 1: by remembering four nication leads to venarial disease Class four
Speaker 1: for rapamilandultizzem. Remember these are non dihydropurity in agents. They
Speaker 1: decrease calcium entering during phase four and zero indications rate
Speaker 1: control in a FIB and a flutter SVT. Remember your
Speaker 1: adverse drug reactions by remembering CCB constipation, cardiac block braidycardia.
Speaker 1: All right, if you're still with me, congrats. That was
Speaker 1: a lot. So that was your class one through four
Speaker 1: anti arrhythmics. I'm going to do a sixty second or
Speaker 1: so recap of the highest deal topics and demonics. Then
Speaker 1: we'll do a few quick questions to test your knowledge.
Speaker 1: So four classes of anti rhythmics to no Class one
Speaker 1: sodium channel blockers, Class two beta blockers, Class three potassium
Speaker 1: channel blockers, Class four calcium channel blockers. Remember them by
Speaker 1: remembering the sentence some blocked potassium channels SBPC. Starting with
Speaker 1: class one sodium channel blockers, which slow down the influx
Speaker 1: of sodium during phase zero, and remember the more salt
Speaker 1: in the food, the more it blocks sodium channels. Remember
Speaker 1: Class one has three subclasses. Class one A diso pyramid quinidine, procaanamide,
Speaker 1: Class one B lytokane and maxilotine. Class one C fleckinide
Speaker 1: and propaphenone. Remember your double quarter pounder lettuce mao fries.
Speaker 1: Please remember our Class one ameds double quarter pounder are
Speaker 1: on a foot long hot dog bund to help you
Speaker 1: remember the Class one A drugs prolong the qt intervle
Speaker 1: super important. Don't forget about procaanamide aka pro trainamide. Your
Speaker 1: white wolf driving a train on a loop track Wolf
Speaker 1: Parkinson white and lupis. Remember our Class one B meds
Speaker 1: are indicated for fast and failing tissue like post m I,
Speaker 1: but our Class one C meds are contraindicated post m I.
Speaker 1: Remember after a heart attack you swap the fries out
Speaker 1: for a salad. Next, Class two beta blockers. Remember the
Speaker 1: second letter of the alphabet is B, and beta blockers
Speaker 1: which start with a B are Class two antierrythmics. All
Speaker 1: drugs in this class end in LOL and most end
Speaker 1: in olol. The ones that don't got something special about them.
Speaker 1: Beta blockers block epianore EPI from binding to our beta
Speaker 1: one receptors in the heart, decreasing calcium influx, decreasing the
Speaker 1: slope of phase four. The main indication I would know
Speaker 1: is for rate control in a fib and a flutter.
Speaker 1: Remember your cardio selective beta blockers with beam bisoprolol, bataxilol, esmolol, atenolol,
Speaker 1: aceputle lul, and mitoprolol. Finally, remember your common contraindication slash
Speaker 1: warnings for beta blockers with ABCD, asthma, bradacardia, cardiogenic shock, diabetes,
Speaker 1: class three potassium channel blockers. Remember the meds by remembering
Speaker 1: the demonic aids aids amiodorone, a buttylid, dohedolide, troneterone, and sotolol.
Speaker 1: They block potassium E flux during phase three, leading to
Speaker 1: prolonged phase three repolarization. QT prolongation is an important adverse effect.
Speaker 1: To know. The highest yield med is amiodorone. Remember am
Speaker 1: three odorone to help you remember it's a class three
Speaker 1: anti arrhythmic and to remember these super highyield adrast drug reactions.
Speaker 1: Remember taking amyodoron is a bitch. Blue skin, interstitial lung disease, thyrotoxicity,
Speaker 1: coronial deposits of patotoxicity, and finally, remember sotolol is a
Speaker 1: beta blocker as well as a class three potassium channel blocker.
Speaker 1: Remember it as soapotolol pot to help you remember it
Speaker 1: also blocks potassium. Finally, our class fours. Remember the meds
Speaker 1: in this class by remembering fornication leads to venereal disease
Speaker 1: formication Class four veneal disease, verapamel and deltizem. Remember these
Speaker 1: are non dihydropurity in agents. They decrease calcium entering during
Speaker 1: phase four and zero in notal cells, prolonging phase four
Speaker 1: and zero indications, rate control in a FIB and a
Speaker 1: flutter SVT. Remember your adverse drug reactions by remembering CCB constipation,
Speaker 1: cardiac block, bradycardia. That's your anti rhythmics. Let's do five
Speaker 1: quick questions to test your knowledge. Question one, Which of
Speaker 1: the following anti rhythmic drugs has the most potent impact
Speaker 1: on blocking sodium channels in the myocardium leading to the
Speaker 1: greatest reduction in the slope of phase zero depolarization. Again,
Speaker 1: which of the following anti rhythmic drugs has the most
Speaker 1: potent impact on blocking sodium channels in the myocardium leading
Speaker 1: to the greatest reduction in the slope of phase zero depolarization.
Speaker 1: Choice A Lytokane B maxilatine, C flecanide, D disopyramid e
Speaker 1: verrapimil Again A Lytokane B maxilatine, C flecanide, D disopyramid
Speaker 1: e verrapim il. So that is going to be answer
Speaker 1: C flecanide. So which of these meds has the most
Speaker 1: potent sodium channel blocking activity. We have five choices, and
Speaker 1: one of them we can knock out right away answer
Speaker 1: ever rapimil. It is a class four calcium channel blocker,
Speaker 1: so let's eliminate that option. So then we're left with
Speaker 1: four choices Lytokane, maxilotine, flecanide, disopyramid, which are all sodium
Speaker 1: channel blockers. And if we remember the demonic all we
Speaker 1: have to do at this point is find the saltiest food.
Speaker 1: So let's think about the foods and how salty they are,
Speaker 1: which sounds ridiculous, but it works. So let us mayo
Speaker 1: we know has the least amount of salt, which has
Speaker 1: the weakest sodium channel blockade. That's our Class one B
Speaker 1: drugs double quarter pounder, moderate amount of salt, moderate sodium
Speaker 1: channel blockade which are Class one A drugs, and then
Speaker 1: finally the meds we should be looking for fries Please,
Speaker 1: which are the saltiest and have the strongest sodium channel blockade,
Speaker 1: are our class one C and since fries Please represents
Speaker 1: propaphenone and fleckanide, we have to look for these meds
Speaker 1: and luckily Flecaninde is present in the answer choices, so
Speaker 1: we know that answer C Flecanide is the correct choice,
Speaker 1: which is a Class one C agent exerting the most
Speaker 1: potent sodium channel blockade and has the greatest impact on
Speaker 1: reducing the slope Phase zero. Question two, a fifty eight
Speaker 1: year old man who has recently started on a new
Speaker 1: medication by his cardiologists presents to the emergency department. After
Speaker 1: beginning therapy, he reports episodes of dizziness and near syncopede.
Speaker 1: An ECG obtained in the emergency department shows a markedly
Speaker 1: prolonged qt interable followed by polymorphic ventricular tachycardia with a
Speaker 1: characteristic twisting of the QRS complexes around the isoelectric baseline.
Speaker 1: Which of the following medications is most likely responsible for
Speaker 1: this patient's presentation atacine B diltiaism C quinidine D maxilotine
Speaker 1: E metoprolol. Again a lytokine B DILTIAZM, c quinidine D,
Speaker 1: maxilotine E metoprolol. So that's going to be answer C quinidine.
Speaker 1: This question is describing a patient with prolonged QT and
Speaker 1: polymorphic ventricular tachycardia with twist and QRS complexes so torsa
Speaker 1: de point. So which medication class that we've covered today
Speaker 1: are most likely to cause prolonged QT and torsads And
Speaker 1: you've got to know this. That's your class three potassium
Speaker 1: channel blockers and your Class one A sodium channel blockers.
Speaker 1: So now that we know which drugs to look for
Speaker 1: in our answers, let's start with your potassium channel blockers.
Speaker 1: We remember those drugs with the mnemonic aids aids, amiodorone, beutilide, deftolide, dronetone,
Speaker 1: and sodolol. None of those meds are present in the
Speaker 1: answer choices. So next, let's search for our class one
Speaker 1: A drugs. Remember your double quarter pounder on a foot
Speaker 1: long hot dog on which represent disopyramid, prokanamide, and quinidine
Speaker 1: and quididine. We can see as answer ce A Class one,
Speaker 1: a drug that, as we discussed before, is notorious for
Speaker 1: prolonging the QT interble and causing torsades, is the most
Speaker 1: likely cause of this patient's presentation compared with the other
Speaker 1: medications and the correct answer for question two. Question three,
Speaker 1: a sixty four year old man was started on a
Speaker 1: new anti rhythmic medication several months ago. At a routine
Speaker 1: follow up, he reports new fatigue and notices bluish gray
Speaker 1: discoloration of the skin over his face. Laboratory studies reveal
Speaker 1: and elevated TSH, as well as an increase in serum
Speaker 1: aminotransphrase concentrations, AST and ALT. Which of the following medications
Speaker 1: was most likely initiated in this patient in the past
Speaker 1: few months. A dofetylide B sodolol, c amiodorone, D flecanide,
Speaker 1: e verapimil. Again, A dofetylide B sodolol, c amiodorone, D
Speaker 1: flecanide or e verapimil. So that's going to be answer
Speaker 1: c amioterone. So a correct answer is answer c amioterone.
Speaker 1: You better know this one. Remember, amiodorone messes with so
Speaker 1: many different organs in the body, and it's why there
Speaker 1: are so many monitoring parameters needed when initiating and continuing
Speaker 1: on this medication just X ray, thyroid function test, cerum,
Speaker 1: amino transferrase levels, et cetera. C Amiodone can cause a
Speaker 1: number of different adverse effects. The main ones though, are
Speaker 1: in the mnemonic b itch, because taking amiodon is a bitch.
Speaker 1: Blue skin which is seen in this patient, interstitial lung disease,
Speaker 1: thyrotoxicity which we see here as evident by the increase
Speaker 1: in TSHS, was the complaints of fatigue likely secondary to hypothidism,
Speaker 1: cornio deposit and then finally hepatotoxicity which we also see
Speaker 1: in this patient with the increase in ASD and AOT.
Speaker 1: So don't forget taking amiodone is a bitch. The other drugs,
Speaker 1: while they may have some adverse effects seen in this patient,
Speaker 1: like the hepatotoxicity, amiurone is the only one to potentially
Speaker 1: have all of these clinical manifestations. Question four. A seventy
Speaker 1: year old man with a history of hypertension and HR
Speaker 1: fibrillation presents to the clinic complaining of recurrent palpitations. His
Speaker 1: hemodynamically stable and his ECG confirms atrial fibrillation after failing
Speaker 1: other therapies, the patient is started on an oral medication
Speaker 1: that primarily prolongs phase three repolarization of the ventricular cardiac
Speaker 1: action potential, increasing the action potential duration and effective refractory period.
Speaker 1: Which of the following medications was most likely initiated in
Speaker 1: this patient? A Lytokane B metopol law, C do fetylide,
Speaker 1: D verapimil E maxilotine. Again A Lytokane B metopo law,
Speaker 1: C do fetolide, D verapimil or E maxilotine. So that's
Speaker 1: going to be answered, C do fetolide. So this is
Speaker 1: not an easy question, but let's break it down. So first,
Speaker 1: avoid all of the noise. The only part of this
Speaker 1: vignette that matters is the statement which drug in this
Speaker 1: list prolongs phase three repolarization, increasing action potential, duration, and
Speaker 1: effective refractory period, and by definition that is a potassium
Speaker 1: channel blocker, which in this case the only potassium channel
Speaker 1: blocker listed is de fedolided the d and aids the
Speaker 1: other meds. B. Motopol Law is a class two beta
Speaker 1: blocker which mainly affects phase four of pacemaker cells lytoicanum,
Speaker 1: oxilotine or lettuce and maomeds are Class one B sodium
Speaker 1: channel blockers which act on phase zero and Finally, d
Speaker 1: Verapamil is a class four calcium channel blocker which affects
Speaker 1: primarily phase four and zero of nodal cells. Question five,
Speaker 1: A sixty four year old man with a history of
Speaker 1: atrial fibrillation is being managed for rate control. He was
Speaker 1: previously prescribed a calcium channel blocker, which was discontinued due
Speaker 1: to intolerance. The treatment plan now shifts to a beta blocker.
Speaker 1: His medical history includes mild, well controlled asthma managed with
Speaker 1: occasional albuterol and hailer use. Which of the following beta
Speaker 1: blockers is the most suitable option for rate control in
Speaker 1: this patient? A proprano law B natlol C pindlelal D
Speaker 1: metopo law E timil again, A propranolol B naanilol C pindlelol,
Speaker 1: D metoprolol or E timilol. So that is going to
Speaker 1: be answered D metoprolol. So we have a patient with
Speaker 1: a history of a fib and mild bronchospastic disease. He
Speaker 1: didn't tolerate calcium channel blockers. Who are going to start
Speaker 1: him on a beta blocker non selective beta blockers hit
Speaker 1: both the beta one receptors in the heart as well
Speaker 1: as beta two in the lungs, which can cause broncho constriction,
Speaker 1: so these are not recommended in patients with bronchospastic disease
Speaker 1: like asthma. A selective agent, on the other hand, at
Speaker 1: lower doses will hit primarily beta one receptors and can
Speaker 1: be used with caution in this patient population. So the
Speaker 1: only question you need to ask yourself at this point
Speaker 1: is which is a cardio selective beta blockers in the answers,
Speaker 1: And the easy way to know is just to remember
Speaker 1: that a beam of light is direct and find a
Speaker 1: beta blocker that starts with B, E, A, or M.
Speaker 1: In this case, that would be metoprolol, which is a
Speaker 1: cardioselective agent, and the correct answer for this patient. All right,
Speaker 1: that was your anti rhythmics. Try not to be too overwhelmed.
Speaker 1: It is a lot, but try to just focus on
Speaker 1: the highest yield stuff and try to focus on the demonics.
Speaker 1: If you can try to remember those, you'll get through
Speaker 1: the exam and you'll be fine. Thank you so much
Speaker 1: for listening to the podcast, and thank you so much
Speaker 1: for the support