DIP Episode 346 - Cardiovascular Pharmacology for The USMLE Step 2CK/3 Exams Part 1 (+ 11/1-5 Step 2CK/3 Course Reminder)

Okay, welcome. My name is Divine. This is episode 346 of the Divine Intervention Podcast. And to this podcast, I'll be going over something that is very high of step 2, CK step 3. And that is cardiovascular pharmacology. So the thing is, the USML step 2, CK and step 3 exams both test cardiovascular pharmacology. But they have a somewhat different focus compared to step 1. So that's step 2, CK step 3 focus is what I'm going to be detailing in this podcast. And that's very likely what I'm going to be doing as well in the next podcast. It's not something I can cover in one podcast. So this is definitely going to be a tour of three podcast series. But if you listen to these podcasts, you'll feel very comfortable with this material and pretty much at least that's what I'm trying to achieve to the best of my abilities. If you know and understand what is in this podcast and the next podcast, then any cardio pharmacology question you get on your exam with very high degree of certainty, you will get it right. Again, I'm not going to say 100 percent, but I'm going to get you pretty close to 100 percent. And the thing is, this podcast, the goal is not going to be to give you a bunch of stuff to memorize. Again, don't get me wrong. There's going to be information to memorize for sure. But I'm going to make a very strong attempt to explain pathophysiology so that you actually really understand why certain things are a certain way. So encourage you to just come on this journey with me.

And I think you're going to have a very fun ride. I really like a cardio farm. So if cardio farm has been something that she I really struggled with this thing, I am really praying that your troubles will be over after this podcast. Now, before I get into it, just a quick housekeeping thing. If you're taking the USMLE step 2 CK or step 3 exams, any time within on November, December, our strongly encourage you to attend the course I offer, it's a step 2 CK step 3 review course. It starts off with a test taking strategies course on the first of November. That's from 2 to 4 30 PM, Pacific Standard Time. And then it continues as a 24-hour review course. It's 24 hours total. It begins on the second of November and runs to the fifth of November. It's from 10 a.m. to 4 p.m. Pacific Standard Time. In the course, we go over about, it's now actually more than 2000 scenarios roughly across an internal medicine, psychiatry, surgery, pediatrics, OB-GYN, neurology, biostatistics, ethics, communications, healthcare systems. We go over some key screening guidelines, go over some key vaccines, go over infectious diseases. We go over multi-system processes and disorders. And then we also have like a triggers section where we go over a host of things that are just very high-year-old associations to know for the exam. Again, I've had many people like get emails every week. I've had many people attend these courses and they've done really well on their exams.

I don't know if I'm going to be able to hold a course in December, but for sure God willing, I'm going to be holding a course in November. So if you're taking your exam in November or December and it doesn't matter where you are, begin of your dedicated period, middle of your dedicated period, end of your dedicated period. I've even had people take these courses two days before the exam and they found you to be very beneficial. So again, that's something you're interested in. I'll shoot me an email through the website and I'll give you some more information and details. But again, I promise you it will be definitely worth your while. It's a course that's held over Zoom. Again, I've had many people take it and do really well. It will absolutely, absolutely be worth your while. The testing and strategy scores will teach you about testing in processes. But the review course will teach you content and it's going to teach you that content in context. At least you've listened to my podcasts. You know that I'm not very big on just again giving you information to memorize. You'll understand why things are a certain way. But I will highlight it to you. The way the MV is going to test it on an exam. Okay, so let's get right into this podcast. So what did they give you a question about a young guy? And they tell you that for the last two hours he has been having very severe parpetitions. And then he comes to the emergency room and they tell you that it's hard.

It is like 210 bits per minute. Right. And then they don't even give you many clues beyond that. So this is just some guy that's like 25 years old. And then they say what's your next best step in management? Well, I'll really hope that you're saying to go ahead and give this guy Prokena might. Right. Go ahead and give this guy Prokena might. This guy has Wolf Parkinson white. Right. Wolf Parkinson white is not going to be an old person's problem on your exam. It's going to be a young person's problem. For instance, like 50 something years old or whatever. You need some very strong reasons to say, Oh, I think this person has WPW on the test. And the thing is sometimes our friends at the MV is instead of putting the term WPW. Here's what they will do. They'll call it a super ventricular tachycardia. Because WPW is in fact a super ventricular tachycardia. Right. And remember on an e-key, she are going to find that classically described Delta wave. Right. But again, what you do are smart friends at the MV is do these gigs instead of calling to Delta wave. They'll tell you that, Oh, EKG shows a short PR interval plus a wide QRS complex. I'll say that again, a short PR interval plus a wide QRS complex. If you see that, you absolutely want to think about WPW. That is just them describing the Delta wave to you.

And newsflash for those of you that are taking the USM Ls, I will encourage you, especially step two, see case step three, you know, more or sometimes don't expect you should pretty much not expect any buzzwords. That is something that is becoming more and more extinct on the exam. These days, the MV is a very big on descriptions. That's why sometimes I almost feel like again, no one can say this for sure. But I most feel like they do this because of the renewed push towards using Anki in medical education. Anki is amazing. But again, I feel like many people use Anki wrongly. They just blindly memorize facts. They can blindly do closed deletions. But the actual understanding they don't have. Right? So the thing is, I'm telling you, if you're studying for these exams, as you're memorizing those buzzwords, make sure you understand like, what in the world do do these buzzwords mean? Because you can get in hot water very quickly. I'm telling you this, the MDM Es are almost like a descriptive buzzword test. They just describe everything. Even in the answer choices, right? Again, instead of putting Kawasaki's disease, just putting new co-cutaneous lymph nodes syndrome. Right? So again, those are things you just have to get used to. I'm telling you this, not as, oh, wow, Devine took his USML years ago. No, no, no, no, no. I do know many people that take these exams every single week. Right?

So again, I will encourage you, make sure you're not just memorizing or you actually understand them, what you're trying to memorize. Okay. Right? So this guy has WPW. Right? So WPW, again, is shredded with a perqueteamite. Right? So what's the big thing to know about perqueteamite for step 2, see, step 3? Remember, perqueteamite is an anti-rhythmic. It's a sodium channel blocker. Right? It's a class 1 A anti-rhythmic. Very high-yield. It is a class 1 A anti-rhythmic. Right? So perqueteamite is the drug of choice for WPW. And the thing is, if a person has a fib with WPW, because many of us are used to, oh, if a person has a fib, put them on a bit of blocker or non-dihydroperidine calcium channel blocker, like verapamilotele tyazine, you cannot do that if they have a fib with WPW. The drug of choice for e-fim with WPW is going to be perqueteamite. And remember, perqueteamite is a drug that you're just giving the acute phase of WPW. It's not a drug that you place people on long term, right? In general, if you want good long-term treatment of WPW, the smart thing you're supposed to do on an in-bim exam is to oblige those pathways, right? This is something that's usually done by an electrophysiologist. They're going to go ahead and oblique those pathways. And that's how you're going to go ahead and treat Wolf Parkinson's white syndrome.

Now remember, what if they tell you that, okay, this person is studying Wolf Parkinson's white, I mean, sorry, on a perqueteamite, whoops, person is studying on perqueteamite. And then they tell you that, oh, the notice that after a few days, he starts completing a joint beam. He has like a rash on his face. He starts having like, you know, like, pain whenever it takes a deep breath, like signs of serocides. If you see all these things, I want you to think of drug-induced lupus, right? I want you to absolutely think of drug-induced lupus. Remember, drug-induced lupus is associated with anti-histonantibodies, right? And perqueteamite is one of those drugs that can cause drug-induced lupus. What are the other drugs that can cause drug-induced lupus you need to know for your exams? Remember things like sulfonamides, remember hydralazine, remember isomiasid, right? Remember phanytoine, remember perqueteamite, remember the TNF inhibitor, etan receptor, remember etan receptor is not a monoclonal antibody. It's actually like a decoy receptor for turmeric versus a factor, right? So again, don't forget the drugs that cause drug-induced lupus. So phanyamides, hydralazine, isomiasid, perqueteamite, phenetoin, and etan receptor, right? Those are high old ones to know for exams. And it's also very high old to know that this drug-induced lupus is something that we find in people that are slow-acetylators, right? Let me tell you this.

I mean, obviously you can find in people that are not slow-acetylators, but it's very common on nbim exams in people that are slow-acetylators, right? Again, I know you may say like divine, no one really cares about this fact. Trust me, you should really care about this fact. There's one of these bizarre questions, pop up on the exam, everybody will get it wrong. You don't have to be one of those people because you're paying attention, right? So remember, slow-acetylators, because the thing is these drugs, especially like perqueteamite, they are metabolized, right, by acidylation, right? So the thing is if a person is a slow-acetylator, right, they can begin to have problems with metabolizing perqueteamite, properly, right? So that slow versus faster sedalator paradigm. It's one of these things that, biostatistically, it shows up in a bimodo distribution, right? Bimodo distribution, right? Obviously on one end of the distribution, I'm going to be the slow-acetylators. On the other end of the distribution, I'm going to be the fastest sedalators. Remember, that kind of same concept of people that have Hodgkin's lymphoma, right? Hodgkin's lymphoma shows up in like young, very young people and also shows up in adults, right? People around the age of 50s, right? Those things that illustrate the biostatistical concept of bimodality in general end up being pretty high-yodon on the exam.

Now, what if they give you a question about a patient and they tell you that all the patient is hemodynamically unstable, right? And they tell you that, oh, they see an EKG, you notice they have a white complex regular tacky arrhythmia, right? So the person is hemodynamically, oh, sorry, the person is hemodynamically stable, let me not say unstable. Let me see, hemodynamically stable and then you get an EKG, you see a white complex regular tacky arrhythmia, right? Again, what arrhythmia does this person have to start? I really hope you're saying all the violence, that this person has a v-tack, right? This person has a v-truckler tacky cardia, right? So what's the big thing to know about this person? Well, let me, let me break some things down for you. We see it's a white complex, when something's a white complex arrhythmia, it's a ventricular arrhythmia, that's setting stone. And then when you see the term that, oh, this thing is a regular tacky arrhythmia, then that should pretty much go ahead and tell you that, oh, the spaces between the QRS complexes are completely equal, right? The spaces between the QRS complexes are equal, right? So that's one good thing to know there. So white complex regular tacky arrhythmia, right? This person has v-tack. Now, this person has v-tack and they are hemodynamically stable. The reason is v-tack and they are hemodynamically stable.

I really hope you're saying, okay, divine, looks like the next drug we're going to be giving these people is a muterone, right? A muterone, a muterone is the drug of choice for treating hemodynamically stable v-tack, right? Immuterone is the drug of choice for treating hemodynamically stable v-tack on NV Me exams. Again, the thing is, there's some exceptions to this rule, absolutely. But those exceptions, the NV Me largely does not care about those, right? So v-tack, hemodynamically, hemodynamically stable. You're going to do a muterone. Remember, if you're on stable with v-tack, you're going to be getting synchronized cardioversion. And then if you have no pulse and you have v-tack, you're going to be getting on synchronized cardioversion. That's essentially another term for different relation. If you want to learn more about all these ACLS algorithms, check out episode 104. I mean, it's basically an ECLS podcast. If you listen to that podcast, pretty much everything you need to know about ACLS for your USMD exams, you're going to find in that podcast. So how does a muterone work? So the thing is a muterone. Primarily, it's a potassium channel blocker. It's a class three anti-rhythmic, right? So potassium channel blocker, it's a class three anti-rhythmic. But to be honest with you, a muterone does many other things. It's also a also block sodium channels. It also has some bit of blocking activity. It's just a very ubiquitous drug.

It's a pretty awesome drug, but it has a lot of side effects, right? It has a lot of side effects. And remember, besides v-tack, in a person that is hemodynamically stable, and the thing we can use a muterone for is we can use it in a feb. We can use it as part of a rhythm control strategy in the management of a feb, right? The chronic management of a feb. Because remember, people that have a feb, they can pursue one of two treatment strategies. They can have a read control strategy where you can use a bit of blocker or you can use a non-dihydroperidine calcium channel blocker, like verapameil or deltaiazine. But alternatively, you can also use a rhythm control strategy where you're actually trying to avoid the readme, chemically, with a muterone, right? A muterone can be used in those circumstances, right? Although rate control, I'll say this, rate control is more often used on imbim exams than rhythm control, right? Rate control is more often used on imbim exams than rhythm control. Now, the thing is, a muterone, look at the name, amyudu aron, right? Ayudu, it has Ayudu in the knee, right? That's iodine, right? You probably remember this from, I don't know, high school, college. I know certainly used to do some of these experiments back in the day in Nigeria with starch. We will add iodine and then it will change the starch, turning blue, right? The thingy is starch obviously is a carbohydrate. There's lots of carbs in your skin.

So the thingy is, amyudu aron likes to do the scholar thing, just because of the iodine contains, right? So you can just call all your cornea, right? People, they can have like, almost like this whisker like physical exam finding with your cornea. Again, it's just from discoloration, right? Amyudu aron can also cause like, discoloration of the skin, right? Can cause blue skin a discoloration. Now, remember, amyudu aron is metabolized in the lever, right? So if your lever doesn't work, it should not be on amyudu aron, right? That's just a simple thing to know for your exams. And then remember, what if the tell you that a person has been on amyudu aron, right? And then the person starts having, you know, over a six-month period, they start having like, you know, progressively worse than inshotness or breath, exercise intolerance. And they tell you that, oh, you're listening to these people's lungs and you're hearing crackles. If you think about that, I want you to think of pulmonary fibrosis, right? Pulmonary fibrosis. Remember, amyudu aron, absolutely can cause pulmonary fibrosis, right? That's one of the big things you want to keep in mind on the exams, right? So it's going to cause pulmonary fibrosis. That's going to show up as a restrictive lung disease. If you want to every serious show in normal or slightly increased, right? And in those cases, the DLCO will be decreased, right?

Because again, you're making the ability of oxygen to diffuse across the amyudu aron membrane, a lot more difficult, right? A lot more difficult. And remember, amyudu aron can cause both hypo or hyperthyroidism, right? Because again, it contains iodine, right? So you can take advantage of either the wolf chikof effect or the iodine-based alphenomenon, right? In causing a hypo or hyperthyroidism. That is definitely a very high yield thing to know for the purposes of the of the USMELI exams, right? You need to definitely know that amyudu aron can cause both hypo or hyperthyroidism, right? Now, some of you may be like, okay, define like which one goes with which one. The thing is, the iodine-based alphenomenon is when a person gets hyperthyroidism, right? After getting iodine or some kind of iodide, iodine, right? So it's almost like an iodine-induced hyperthyroidism. That's the Yodbist alphenomenon. On the flip side of things, the wolf chikof phenomenon is an iodine-induced hypothyroidism, right? It's an iodine-induced hypothyroidism, right? So Yodbist al goes with hyperthyroidism, wolf chikof goes with hypothyroidism, right? Hypothyroidism. Basically, just think of them as opposites of each other. Yodbist al is the opposite of wolf chikof, right? Yodbist al is the opposite of wolf chikof. And just let me just take one small quick detour here.

One very nice with the contested thing is they can give you a question about a person that becomes like tachycardic, tachypnic, has increased diptendon reflexes after they just got like some kind of CT study, like some CT scan with contrast. The thing that's causing that problem is essentially the iodine, because remember contrast contains iodine, right? So that iodine-induced contrast by well-due, Yodbist al phenomenon is causing hyperthyroidism in those people, right? Again, that's very, very high-yod to know. That is very, very, very, very high-yod to know, right? So Yodbist al hyperthyroidism, wolf chikof, hypothyroidism, right? Those are very high-yod things to know for the exam. I promise you they're very important to know for your test, right? So they can cause both hypo or hyperthyroidism, right? Hyperthyroidism, Yodbist al hypothyroidism, wolf chikof, hypothyroidism wolf chikof. Okay, right? So there's probably like the big things to know about a mutant room for the USMA Ds. Now what if they give you a question about a patient? They tell you that a patient is studying an anti-hypertensive, and they tell you that, oh, you know, you know, three weeks later, the patient has been noticing like swelling of their legs, that you know, kind of gets better a little bit at night and stuff like that. Whenever you see stuff like this, I really want you to think of calcium channel blocker, the dihydroperidine calcium channel blockers, right?

So it draws like, I'm low-dipine, I'm low-dipine, my cardipine, my fatty-pin. Those are things you definitely want to make sure you know. So the thing is, these calcium channel blockers, right? If you, of all the anti-hypertensives, they're like the big, big, big ones that tend to cause peripheral adema. That's a classic thing they love to test on, on exams, right? So how exactly do these drugs work? Well, these drugs are visual dilators, right? Because if you remember, they are, they, if you look at the vascular tree, you know, from these big arteries and all that stuff, you form arterials, and then after you form arterials, you form capillaries, after you form capillaries, you form venials, right? Now, here's the thing. The thing is, for the arterials, right? They are the primary sites that controls your systemic vascular resistance, right? Your arterials are where you have primary control of your systemic vascular resistance. So the thing is, these arterials are dilated, right? Because again, these are calcium channel blockers, you need calcium for smooth muscle contraction, right? So if you block these calcium channels with, again, again, a drug like I'm low-dipine, that's gonna cause them to not contract, they're gonna relax, and if they relax, they're gonna dilate, if they dilate, that's gonna reduce systemic vascular resistance, that's gonna reduce after load, right? If you reduce after load in those circumstances, that's obviously gonna be a good thing, right?

That's definitely gonna be a good thing, right? Because that's gonna lower the person's blood pressure, right? But the thing with that is, because you're dilating those arterials, you're sending more blood to the capillaries. If you send more blood to the capillaries, you're gonna jack up the hydrostatic pressures in those capillaries, and when you jack up those hydrostatic pressures, you're gonna have increased fluid extrovasation. And when you extrovasate that fluid, then that's gonna cause peripheral adema, right? So in general, the way we're gonna treat those problems with calcium channel blockers is we can actually dilate those venials, because again, remember I said you have arterials first, and then arterials feed the capillary, and then the capillary is drained by the venial, right? So the thing is that venial that drains these capillaries, those postcapillary venials, they're dilated by ACE inhibitors, obviously if you dilate those venials, then that's gonna draw the blood away from the capillaries, that's gonna reduce the hydrostatic pressures, and the capillaries, and that's gonna decrease fluid extrovasation, and that's gonna fix the peripheral adema. So that's actually a very high-yield thing to know for exams. Whenever a person has peripheral adema, that's associated with the use of the dihydroperidine calcium channel blockers, the drugs of choice for treating that are your ACE inhibitors, right?

Your ACE inhibitors, arps, they're perfectly fine for those purposes, right? Now it's also very high yield to remember what's gonna happen to a person's heart rate if they are pleased on a dihydroperidine calcium channel blocker. Well I would really hope you're saying, oh divine, these people are gonna have a reflex tacky cardio, that's very high yield to know, they're gonna have a reflex tacky cardio. Well what's the deal with this reflex tacky cardio? Well if you think about it, you take a dihydroperidine calcium channel blocker, that's gonna lower your systemic vascular resistance, right? So if you lower your SVR, you're gonna have less pressure on your borer receptors. So your borer receptor is gonna be like, where's my blood pressure this low? So you're gonna speak to the brain and then your brain is gonna be like, okay, we're gonna send the sympathetic discharge. So that sympathetic discharge is gonna increase the speed of conduction down your AV node. So the person's heart rate is gonna go up, you're gonna get a reflex tacky cardio when you take a dihydroperidine calcium channel blocker. Now it's also very high yield to know for NV Me exams, that these dihydroperidine calcium channel blockers, you generally want to be very smart. I mean, you want to be careful and essentially try to avoid combining them with drugs like cell identifyl, right? Remember that's a viso-dialiter or drugs like nitrate, remember those are viso-dialaters, right?

Or drugs like alpha one blockers like Prasocene or Terasocene or Doxazocene, you want to avoid combining them. Again, whenever you combine two viso-dialaters together, that can massively increase the presence risk of orthostatic hypertension, right? Orthostatic hypertension. So that's one thing you want to avoid if you can, right? So what are some of the things you may see? What are some other things you may see for this dihydroperidine calcium channel blockers on NV Me exams? Well remember you can use these drugs for variant angina, right? Prins-metal angina is gonna be a young female that very likely smokes and has chest pain that is worse at night, right? That's a coronary visospastic problem, right? A coronary vessels they're not occluded, they're just visospastic, right? So you're gonna give those dihydroperidine calcium channel blockers to help induce circumstances, right? And remember, these dihydroperidine calcium channel blockers can also be used in hypertensive emergency. Remember hypertensive emergency is when a person has very high blood pressure. Again, the number doesn't matter. I know that people, again, that's why I feel like some people their brains are full of things for step two, CK step three. That's not very necessary, right? Like you see people nourish all these blood pressure cutoffs. So you're gonna just refuel. You probably don't need to know those blood pressure cutoffs for your exam.

The key thing to know is if a presence block pressure is crazy high and they have signs of an organ dysfunction, then in those circumstances you won't think about hypertensive emergency, right? So one of the drugs you can use in hypertensive emergency, you can use labeta law, you can use my cardiopine, you can use clevidipine, you can use sodium nitroperocyte. One that you may consider is a femtolamine, right? But that's really used on the USML exams. So I'll say, like cardiopine, clevidipine, labeta law, and nitroperocyte. Don't use hydrolyzing for the management of hypertensive emergency. You'll get it wrong when you're exam, right? So you see these cause functional blockers I mentioned, these dihydropyredients, clevidipine, like cardiopine, those are perfectly acceptable drugs for the management of hypertensive emergency. And then remember, if a person is pregnant, right? Remember there, you cannot give most of the anti-hypertensives you'd classically use in pregnancy, right? Because there are many of them are terrarrogens, right? But remember, an eye fatty pain is a calcium channel blocker that is safe in pregnancy. Remember there's this numonic that hypertensive moms love my fatty pain. I'll say that again, hypertensive moms love my fatty pain. For the anti-hypertensives that are safe in pregnancy, right? The hitch is for hydrolyzing, the M is for methyl dopuh, the L is for labeta law, and then the N is for my fatty pain, right? Hypertensive moms love my fatty pain.

My fatty pain is a drug that can be used, is a drug that can be used in pregnancy. In fact, it can be used in OB-GYN in two different scenarios. One scenario is used for hypertension in pregnancy, but another scenario is that you can actually use it as a topolytic, right? You can actually use it as a topolytic. You can actually use it as a topolytic, right? So what is a topolytic? Well, the topolytic is something that you can use, right? It's something that you can use to delete labor. It's something you can use to delete labor, right? So when you want to delete labor? Well, you may want to delete labor in a situation where a person has, you know, let's say if they've gone into labor, right? And you're like, wow, this person is at like 28 weeks, 29 weeks. Obviously, that's a premature baby, right? In those circumstances, the thing you want to do on an MBB exam is you want to want to give a topolytic to slow down that pregnancy. And then, too, you want to give like beta metasome to promote fetal long maturity, right? Especially if you're at less than 34 weeks. And then you also want to give magnesium for neuro protection, right? You're basically trying to cut down on the child's risk of, of a, what do I think? You want to cut down on the child's risk of cerebral palsy, right? That's if they are less than 32 weeks, right? So that topolytic is going to basically stop the uterus from contracting. Well, there are two topolytics you're supposed to use on MBB exams.

And you know which one to use by where you are in pregnancy, right? So if you're 30 weeks or less, you can use endomethacin. Endomethacin is the first line to a coletic in people that are 30 weeks or less on MBB exams. But if you're over 30 weeks, you obviously cannot give endomethacin. Endomethacin is a cycloxygenase inhibitor. It's going to reduce the synthesis of firstaglandins. Well, if you give that, then it sounds like you're trying to close the child's doctor's arteriosus, and then the child will die, right? We don't want that, right? So in those circumstances, you're going to use Niphety Pin. Niphety Pin is actually a first line to coletic that is used after 30 weeks on MBB exams. That is a very high-yield little piece of information to know for exams, right? So again, these calcium channel blockers, right? You can use them in two front in OB guy. Niphety Pin can be used as a tocoletic. And Niphety Pin is also an anti-hypertensive that is very safe in pregnancy. And then remember that these drugs, these dehydroperating calcium channel blockers can also cause constipation. Again, you need calcium for smooth muscle contraction, right? So the thing is, remember, your GI tract is lined by smooth muscle. So if you give a calcium channel blocker, then you're not going to be able to have adequate contraction of your GI tract, right? And that will obviously not be a good thing for these people. It can cause constipation, right? It can cause constipation.

And remember, if they give you a question, let's say they give you a question about a person, and they tell you that, oh, this patient came in with a worst headache of their lives, really, really bad headache. And then they tell you that, you know, you get a non-contrast CT scan of the head and it's negative. Obviously, you're going to proceed after that to a lumber puncture because you're looking for Zanthochromia. And then you notice, wow, that this person's CSA has like 5,000 rib blood cells per millimeter cube. Obviously, that's a ton of blood. This person has a sub-racidoid hemorrhage. Remember, a sub-racidoid hemorrhage, is an example of a hemorrhagic stroke. Now, the thingy's blood is very irritating to the brain. So the thingy's blood can cause viso spasim of cerebral vessels after a patient has a hemorrhagic stroke. Well, if you have viso spasim of cerebral vessels, that's obviously not going to be a good thing, right? Because if you have viso spastic, it's almost like you have imprints made of laryngina in the brain. That's not good. If pre-spedal laryngina can cause an MI, well, viso spasim of your cerebral vessels can certainly cause like an ischemic stroke, superimposed on a hemorrhagic stroke, so it's almost like you have the hemorrhagic stroke first. And in that hemorrhagic stroke, can serve as a midest for you to have an ischemic stroke because of the blood that's irritating the cerebral vessels, right?

So what is a drug you can give to present that post-hemorrhagic stroke, viso spasim? That's going to be a calcium channel blocker known as Nymodipin, right? That's a calcium channel blocker known as Nymodipin. Nymodipin is an excellent drug on endemic exams to reduce the risk of a person having post stroke viso spasim, right? Because you don't want them again to have an ischemic stroke, superimposed upon the hemorrhagic stroke that he started off with. Now remember, these calcium channel blockers, right? There's the dihydroperidine flavor, right? These ones all end in dipin, dipin, dipin, dipin, dipin, dipin, dipin, right? But there's also the non-dihydroperidine calcium channel blockers, right? So the thing is the dihydroperidine calcium channel blockers, they are more specific for blood vessels, right? But the non-dihydroperidine calcium channel blockers, like Vera Pamel or Deltaia Zem, these are more cardio selective. These ones go after the person's heart more, right? So these non-dihydroperidine calcium channel blockers, what are some key things you can see them being used for an exams? They can be used for angina, right? They are one of the first line agents you can use for angina, right? Angina, you know, chest pain, the worst is with exertion, it gets better with the rest, right? Again, usually for people that have angina, you're probably going to do some kind of stress test on them. And by the way, I've made a stress test podcast back in the day, right?

But you're going to do a stress test on these people. Then after they're going to put them in either on a nitrate or a bit of blocker, or a non-dihydroperidine calcium channel blocker, like Vera Pamel or Deltaia Zem, right? And remember, these drugs, because they are cardio depressive, you also want to avoid them in a person that has acuity compensated CHF, right? For patients that could decompensate it, congestive or failure. You don't want to give a Vera Pamel or Deltaia Zem, that will be a good thing for those people. Now remember, Vera Pamel or Deltaia Zem, they can also be used for A-Fave, right? Again, in a rate control strategy, remember rate control for A-Fave can involve either the use of a bit of blocker, or you can use a non-dihydroperidine calcium channel blocker, like Vera Pamel or Deltaia Zem. And then it's very high you to know, right? That these non-dihydroperidine calcium channel blockers can also be used for SVT, right? For supraventricular tachycardia, remember, it's going to be a narrow complex regular tachyorydmia. It's narrow complex because it's from above the ventricle, right? It's from above the ventricle. So that's why it's a narrow complex regular, regular species between the curious complexes, equal. It's a narrow complex regular tachyorydmia, right?

So the thing is, if a person has an SVT, obviously you're going to try the vagal maneuvers first, you know, massage your carotids, put your head in cold water, tell them to blow into a straw, you know, stuff like that, right? Because again, think about it, if you're blowing to a straw, right? You're going to be increasing in trathoracic pressure, going to be banging on your bar receptors, so your bar is going to be like, whoa, my blood pressure is too high, right? So they're going to speak to the brain, and then the brain is going to send a path to the fatigue discharge, when you send a path to the fatigue discharge, that's going to slow down the rate of conduction down your EV node. That's going to lower the presence blood pressure on heart rate, right? So that's a good thing, that circumstance, but if that doesn't work, obviously you're going to proceed to a denocene, we're going to talk about that a denocene in a different podcast, but, you know, you're going to proceed to a denocene, but after you put it, you'll give them a denocene, usually that's going to abort the arrhythmia. You can't say, okay, giving a denocene problem solved, deuces, bine, no, you can't do that. The person is just going to flip right back into a high heart rate. So usually after that, you've given a denocene, you're going to give it a bit of blocker to bring down your heart rates, or keep it low, or you can put them on a non-dihydroperidine concentrated blocker, like verapet meal, or deltaism.

And then don't forget that verapet meal actually increases the secretion of prolactin in the central nervous system, right? So the thing is, if a person is on verapet meal, or they tell you that the person was recently started on a drug for angina, right? Or for SVT, and then you notice that this person is having like an acomastia, having gallactorea, right? If you see things like that, or they are becoming infertile, or they're having like lullabido, problems like that, you want to think about verapet meal induced hyper-productinemia, right? You want to think about verapet meal induced hyper-productinemia. So I think I'm going to go ahead and stop here. I'm almost certain this cardiovascular pharmacology series is going to be, like actually the my think about it, I'm like, it's probably going to be a three or four-part case series. Well, let me tell you this. The reason that it's this long is because cardio is something that integrates well with many different disciplines, right? So the thing is, this may be a podcast about cardio from ecology, but it may be just many other things you're learning, right? Like literally it's already, we've talked about thyroid, talked about pulmonary fibrosis, we've talked about peripheral edema, we've just talked about like lupus, like just different things, right?

So the thing is, as I'm going over this, because again, I know some of you may be like, this method is a little disorganized, but to be honest with you is actually one of the better methods to teach and explain this material, because one, you're learning in context. Two, you're going to be able to see it in an exam mode, because the thing is, that's one thing many people don't realize is, it doesn't really make sense to learn USMD material in a linear fashion, right? Where it's like, okay, oh, divine, organize it for me, talk about all the bit of blockers, mechanism of action, uses, side effects, no, that's why you see I love to use scenarios, scenarios, scenarios, and to be honest with you, that's how I teach my course, right? And again, it's just something that's more helpful, because on your exam, they're not going to have a physiology section, internal medicine section, no, that's ridiculous, right? In your first thing, questions, they may be an ubigan question throwing there somewhere, a farm question throwing there somewhere, a search question throwing there somewhere, right? So, the thing is knowing those things is just going to help you out a lot more on your exam. So that's why again, I love to use these scenarios, I just feel like that's the thing that kind of differentiates me from many of the other people you see out there on the market.

So, hopefully you found this podcast to be helpful, but again, I promise you, if you listen to like the three or four podcasts in this series, going to integrate things for you really nicely, and you're going to know them really well for you exam, right? And the thing is you're going to learn a lot more than just cardiac from a ecology. Again, as I do at the end of every podcast, I do offer one on one tutoring for all the US Meli exams, step one, step two, CK, step three, preclinical medical exams, third year clerkship shelf exams, and you know, if you're a medicine resident, I need tutoring for the medicine training exam of the medicine boards, I do offer tutoring for those. And then again, obviously, I have this step two, CK step three course. I'm going to have some step one course offerings, it's probably going to be coming later this year. I'm going to hopefully announce it pretty soon once I get the details and kinks worked out. And then I also help with ERAS applications, right? I do a lot of mock interviews, again, I've started interviewing a lot of people, again, you know, also an admissions committee for a year. So, I know a lot of these processes pretty well. You know, many people have worked with her now in residency. In many different specialties, Durham and Esthesia, Surgery, many different disciplines. So, if you need help with those, just shoot me again and email through the website and I'll be more than happy to guide you in the right direction.

And then I have a podcast, a new website actually, Skull Divine Intervention, Life Lessons.com. Actually, there's a podcast attached to that, it's called the Divine Intervention Life Lessons podcast. Yeah, you can look for it on Apple podcasts, but many people have said, oh, divine, you know, I love the life lessons you put at the end of your podcasts. I'm still going to be putting some at the end of these podcasts, but I decided to just start a dedicated website. You know, where it's just short podcasts, you know, like 10, 15-ish minutes long, just a lot of Bible-based teaching, you know, just something that released to a common problem that we face as human beings. You know, let me not say a common problem, common problems we face as human beings. So, if you're listening to those podcasts, again, I think that's going to help you. I think I'm on episode 29 of 30 right now. So, I'm going to be adding more and more every week. So, you know, just Divine Intervention Life Lessons podcast. And then, you know, I do have a You Tube channel. Actually, I have this thing that's going to be coming out soon. I'm going to be making a ton of videos and I'm going to be putting on You Tube. So, I'll encourage you actually sign up for my You Tube channel, subscribe to it is called Divine Intervention, USMLE Podcasts and Videos. And in that, so I'll see it again, Divine Intervention, USMLE Podcasts and Videos. Thank you for those that have subscribed.

If you subscribe to it, that's where I'm going to be putting and pasting all my videos. And then the other thing I'm going to say is, you know, I have this podcast on Apple Podcasts on Google Podcasts and on Spotify. Right. So, if that's something you're looking for again, find the podcast there. You'll find the most recent 150 podcasts. If you're looking for the earlier podcasts, then go to the website of any intervention podcasts with an S dot com. Right. Are you able to see all the podcasts all the way from episode one? You can download them there because if you don't, I think I'm also pretty sure you can speed them up on the website as well. And, you know, any slides I have for some of my podcasts, you can download them through that medium as well. And then the last thing I will say is if you need longitudinal tutoring, right. So, there's this thing I do with people, when I tear them longitudinally all through their, you know, preclinical years of med school, all through their shelf exams. Again, if that's something you're looking for, shoot me an email through the website and I'll give you some more information. So, thank you for listening to me. I'll see you in the next podcast. Have a wonderful rest of your day. God bless you. Thank you.

It is a Class 1 A antiarrhythmic that blocks sodium channels.

The drugs Labetalol (L), Nifedipine (N), and Metoprolol (M) are often remembered by the mnemonic "Hypertensive Moms Love My Fatty Pain."

Cerebral vasospasm, which can lead to delayed ischemic stroke.

Drug-Induced Lupus (DIL) associated with drugs like amiodarone and hydralazine.

Dilation of arterioles increases capillary hydrostatic pressure, leading to fluid extravasation into the interstitial space.

Jod-Based phenomenon (iodide $\rightarrow$ hyperthyroidism) and Wolff-Chaikoff effect (iodine excess $\rightarrow$ hypothyroidism).

Procainamide or Amiodarone (Class 1 A antiarrhythmic).

Non-dihydropyridine CC Bs (Verapamil, Diltiazem); they can cause bradycardia or AV block.

Preventing cerebral vasospasm following subarachnoid hemorrhage (SAH).

Endomethacin ($\le 30$ weeks) and Nifepipine ($> 30$ weeks).

Jod-Based (iodide excess $\rightarrow$ Hyper); Wolff-Chaikoff (excess iodine $\rightarrow$ Hypo).

Amiodarone; restrictive pattern with decreased DLCO.

Procainamide or Amiodarone (Class 1 A antiarrhythmic).

Non-dihydropyridine CC Bs (Verapamil, Diltiazem); they can cause bradycardia or AV block.

Preventing cerebral vasospasm following subarachnoid hemorrhage (SAH).

Endomethacin ($\le 30$ weeks) and Nifepipine ($> 30$ weeks).

Jod-Based (iodide excess $\rightarrow$ Hyper); Wolff-Chaikoff (excess iodine $\rightarrow$ Hypo).

Amiodarone; restrictive pattern with decreased DLCO.