DIP Episode 347 - Cardiovascular Pharmacology for The USMLE Step 2CK/3 Exams Part 2

Okay, welcome. My name is Divine. This is episode 347 of the Divine Intervention Podcasts. And in this podcast, we're going to be continuing that series on cardiac pharmacology for the USMD Step 2, CK Step 3 exams. I'm going to be going into Part 2, right? And just as a reminder, again, for taking Step 2, CK Step 3 or Complex Level 2 or 3 within the next month, I will encourage you to sign up for the course I have starting next week. It starts with the MBME Testicking Strategies course on the 1st of November, that's Monday. It's on 2 to 4 30 PM Pacific Standard Time. That's three hours behind the Eastern Time. So that's like 5 to 7 30 Eastern. And we'll be going over a testicking processes. It's a process course. You'll learn how to take MBME exams. Again, I've had more than 500 people take the scores, probably more than 1000 actually. Again, that I found really good benefit from it. I've seen people that literally after attending the Testicking course, they jumped up 20, 30 points, right? Just from that alone. And then I have the review course that's taking place from Tuesday to Friday next week. It's from 10 PM to 4 PM Pacific Standard Time. So essentially, that's going to be from 1 PM to 7 PM, Eastern Standard Time. And again, in that 24-hour period, that's six hours every day.

We will be reviewing internal medicine, surgery, paediatrics, OB-GYN, psych, neurology, multi-system persists and disorders, biostatistics, effects, healthcare systems, professionalism, communications, all those weird things. We're going to review them. And then we're going to have a trigger section, kind of spread out across the course, where we just rapidly review a ton of material in a short time frame. And obviously, there's time to answer questions. But again, you're going to learn a ton from the course. Again, I've had many people that have been very successful doing that. So if you're interested, just shoot me an email through the website, and I'll give you some more details on the cost and registration. Okay, so let's jump right into it. So I know the last time we talked, we always stopped. We talked about the calcium channel blockers, or talked about the non-dihydroperiodine calcium channel blockers. So now, let me just go straight to my next video. So what if they give you a question about a patient? And the theory that this patient, again, is a 24-year-old guy, comes in for the past 30 minutes, he's been having like severe politicians. And in detail, you'll see a narrow complex, regular, tacky rate near. Well, if you see that, really, the first thing I'm thinking about is an SVT. It's a narrow complex, so you cannot be from the ventricle. You've got to be from above the ventricle. So it's a superventricular tacky cardio.

So now, with this superventricular tacky cardio, well, what's going to be your first step? Or your first initial step is going to be to perform some kind of vagal maneuver. Well, if that vagal maneuver doesn't work, then you're going to proceed to Adenosine. Adenosine is actually the next drug I want to talk about. Adenosine, they love to test it in many different contexts, one in being an example. So the thing is, Adenosine, the big thing you want to know is that it's the drug of choice to abort an SVT. It's a very rapid way to abort an SVT. So remember, you don't give Adenosine to people that have WPW. If you give a person that has WPW, Adenosine, and those people are going to be in some very deep troubles. Adenosine is not given in WPW. That's one of the SV Ts for which Adenosine is not ideal. Adenosine, in general, you can give it for pretty much every SVT, but WPW. Now you can give three doses. But again, remember, as we said in the last podcast, before you can't just stop the Adenosine, abort the Aridmi and say, okay, done. No, you're going to put them on either a bit of blocker or a non-dihydroperidine consumption blocker. Like, if you're up in Melodil, tires them to keep them at a good heart rate. So what are some other key things you want to know about Adenosine? Well, remember, Adenosine can be used in pharmacological stress tests.

So remember, many people that make this mistake on exams that, oh, the try to merge stress tests, like the method of stress and the method of imaging together. In fact, I talked about this. I believe in a podcast on stress tests. So that's something you may want to consult if you care. But the thing is, if a person cannot exercise for any reason, right? Let's say they've been amputated, they have peripheral arterial disease, they have really baddles to arthritis, right? Or they have a histrovalidic stenosis, then in those circumstances, you cannot do an exercise stress test for those people. You're going to do for those people. You're going to do for pharmacological stress test. One of the ways you can perform a pharmacological stress test is with Adenosine, right? It's with Adenosine. Adenosine essentially is a very powerful visual dileter, right? So the thing is, let's say they have three coronary vessels, you have one of them is a schemic, but the other two are fine. If you give Adenosine, Adenosine is going to be able to dilute those other two that are fine, right? But the thing is that third one that is not fine, it cannot dilute, because many times, whenever you have a schemic coronary vessels, on their own, they dilute to their maximum value, they cannot dilute any more, right? So basically, is that differential in dilation that forms the basis of something called the coronary steel principle, right?

So essentially, those two vessels that are fine are going to dilute really well. And because they dilute really well, obviously there's going to be more blood flow through them. Well, a fixed amount of blood is getting to the heart. So if there is more blood flowing through those two fine coronary vessels, then there'll be less blood flowing through that one bad coronary vessel. So because there is less blood flowing through that one bad coronary vessel, that can begin to trigger schemic symptoms, right? And when you trigger those schemic symptoms, right? That basically gives you a positive test result. Either you notice that, wow, we're seeing like EKG changes, or we're seeing that the person is having like a warm ocean abnormalities, or things like that. Whenever you see stuff like that, then that tells you, okay, that's a positive stress test, right? So that's actually the whole basis of the coronary steel principle, right? So that's essentially how adenosine works in the pharmacological stress test. Another drug that they could use along those lines, that's kind of similar to adenosine, right? It's a drug called regadenosine, regadenosine, R-E-G-A-D regadenosine, R-E-G-A-D-E-N-O-S-O-N, right? And also you can also use a dipyredomol, dipyredomol, believe it or not, can be used for this pharmacological stress test. On NV Me exams, the way it works is that it's an inhibitor of adenosine deaminis.

So because it inhibits adenosine deaminis, it's going to build up your levels of adenosine, right? And essentially you're getting adenosine-ergic effect if there's a word like that. You heard it here first. So you have that kind of effect, and again, you basically get the same thing happening with the coronary steel principle. And then it's also high to remember that adenosine and dipyredomol, right, as from the pharmacological agents, they are contraindicated in people that have bronchospastic disease, right? So people that have like really bad asthma, really bad COPD, right? If your airways are not good, it's not a good idea to get adenosine or dipyredomol, because those agents are very powerful bronchoconstrictors. But if you give those agents to people that have reactive airway disease, then they can go into respiratory failure and die. And obviously that's not something that we want, right? And remember when people take adenosine, they're going to have this sense of impending doom, because it literally stops the person's heart, right? It literally stops the person's heart transiently. Okay, now what if they give you a question about a patient, they tell you that this is like a 75-year-old guy, right? And they tell you that he has a history of angina that's been treated well with the Deltias M, right? And then it was also recently standing on a bit of blocker, right?

But then they tell you that, man, for the past like two days, he has been out of it, he has been very somnolent, and then they give you an EKG, or they give you his heart rate, and you notice like it's 35, right? And then you see all these prolonged PR intervals, so an EKG. If you see that obviously this person has a heart block. Well, the thing is if a person has a heart block, or you know, they have like some kind of a brady arrhythmia. One thing you can actually do to speed up those people's hearts transiently, you can either do a pacemaker, we can also actually give them an atropping, right? Remember, atropping is a most grainy receptor antagonist, right? So that's the mixture that we're going to talk about. Atropping. It's a very classic cardio-drug that you love to test on exams, right? But what are some of the other things we can use atropping for besides the tridium-brady arrhythmias? Well, remember, we can use atropping for a gun of phosphate poisoning, right? Remember, a gun of phosphate, the way they work is that they inhibit acetylcholine esterides. When you inhibit acetylcholine esterides, you're going to bump up a presence levels of acetylcholine, so the presence is going to get a cholinergic toxic syndrome. So one way you can forestall that cholinergic toxic syndrome is by giving a most grainy receptor antagonist, like atropping.

Remember, gun of atropping first, and then after that you're going to give pre-dedoxic to help your regenerates, that bad destroyed acetylcholine esterides. And don't forget, we can also use atropping to treat calcium-channel blocker toxicity, right? Many times, if a person has toxicity from a calcium-channel blocker, you're going to give calcium-gluconins. Again, if you're overdose on a calcium-channel blocker, it will make sense that calcium-gluconin will help. But in addition to doing that, you're also going to give atropping, right? Because calcium-channel blockers, they slow down the speed of conduction down the EV node. So if you give a most grainy antagonist, remember, your parasympathetic system also slows down the speed of conduction. So if you give a most grainy antagonist, you'll increase the speed of conduction down the EV node, so they are very helpful in those circumstances. Now, what if they give you a question about a patient? They tell you that this patient, you know, has a history of like decompensated CHF, and you know, this patient was recently placed on a drug. And then, they tell you that, oh, this patient has been completely no blurry vision, that everything kind of looks yellow in his visual field, since this drug was started. And if you see this, what should you be thinking about? What are you thinking about? The juxtaposition, right? Dig, dig, juxtaposition, right? So how does digoxin work?

Well, the big thing you know about digoxin is that it's an inhibitor of the sodium potassium ATP spot. I'm telling you this, many people domestic stuff up on exams. And to be honest with you, believe it or not, I've seen people explain this thing just flat out wrong, right? Again, everyone makes mistakes, even I make mistakes, right?

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Okay, now one of the things that's kind of high you to know about the job sentence, how it modulates potassium and how it is affected by potassium levels. Notice what I said, how it modulates potassium, that's one concept. And then the second concept is how is affected by potassium level. So the job sentence, kind of adjust your potassium levels in the body. But on the flip side, your potassium levels in the body also affect the way the juxtap works. Let me explain. Let's start with the first construct. Right? So the thing is if a person is on the juxtap again, the juxtap we said inhibits the sodium potassium ATP is pump. That pump we said takes three sodium out of cells and puts two potassium into cells. So if you think about it, if you give a person the juxtap and you inhibit that and you're not going to be able to put potassium into cells. So since you're going to put potassium into cells, it's going to hang out on the outside of a cell. If you hands out on the outside of a cell in the bloodstream, you're going to have hyperkalemia. So the potassium side effect of the juxtap is hyperkalemia. The juxtap can cause hyperkalemia. I'll say that again, the juxtap can cause hyperkalemia. So if a person has an internal disease, we're pretty supposed to have a hyperkalemia in the first place giving those people the juxtap does not appear to be the smartest idea in the world. Right? So that's something we want to definitely keep keep in mind.

Now with the second construct, how potassium levels affect the juxtap? The thing I want to say is again, I said already, I've said this and I'm not. The juxtap inhibits the sodium potassium ATP is pump. Okay. That's true. But if you keep this in mind for the juxtap to actually inhibit that sodium potassium ATP is pump, it actually sets on the potassium site in that pump. Right? So the thing is if a person is high pokey limit. Right? So I'll say again, the juxtap sits on the potassium site sits on the potassium site to inhibit that pump. Right? So if a person is high pokey limit, well, there's more open spots on the sodium potassium ATP is pump for the juxtap to bind to. If the juxtap binds there, then it can accumulate on cost toxicity. Right? So whenever your high pokey limit, you're actually pretty supposed to have in ditched toxicity. Why? Because there are more binding sites for the juxtap on the sodium potassium ATP is pumps that exist in your body. Right? So say for it, because think about it, what is one common pill that's taken by people that have a heart failure? They take water pills like ferozamide. Well, what is ferozamide cause? It causes hypokelimia. Because it causes hypokelimia, right? That can predispose you to ditch toxicity. Now, remember if a person has dejuxting toxicity, right? You can give those people the anti-dage fab fragments. Right? I think they call this deji bind in the hospital, right?

But those anti-dage fab fragments, they are like monoclonal antibodies against the juxtap right? You can use that to reverse a dejuxting toxicity. Now, what if they give you a question about a patient, you know, the tell you that this patient is getting a, you know, getting a blood transfusion. And within like two minutes of the transfusion starting, the patient starts complaining of like profan�s shortness or breath. Right? And in the question, they're wise enough, and they tell you, or the patient has no flunk being has no hematuria. Right? If you see this, right? I would really hope you're thinking of some kind of an aphylactic transfusion reaction. Right? Remember, these are a phylactic transfusion reactions actually type one high-press sensitivity reactions, right? And don't forget they are classically associated with people that have IGA deficiency, right? If you have a deficiency of IGA, then I, IGA becomes foreign to you. So since it becomes foreign to you, you're going to make antibodies against it, especially IGE antibodies. So if you take a blood, if you get some kind of blood transfusion, and that blood transfusion contains IGA, right? You know, it's going to cause cross link in of those IGA fibers when you buy, I mean, IGA antibodies when he binds to them, then you have degranulation of your muscles and stuff, you know, the person is going to end up in a hot water, right? So essentially this person has an anaphylactic transfusion reaction.

But what is the drug of choice for treating an aphylaxis? Would all be a pinneferin, right? A pinneferin. A pinneferin is the next cardiac drug I want to talk about. Right? So when he uses a pinneferin in those circumstances, remember a pinneferin is a pro-adrenergic agent, right? But it's a very powerful bit of to agonist, right? So he's going to open up your earring. That's why it's the primary treatment and anaphylaxis. And the thing is, if a person has anaphylaxis and give the first dose of a pinneferin, it doesn't work. It doesn't help. Give more a pinneferin, right? Give more a pinneferin. Those things actually motivate it. That's something that actually love to test quite a bit on the USML Es, right? You've given one a pinneferin dose and you're like, oh, let's stop. No, no, no, don't stop. Give another dose of a pinneferin, right? Now, what are some other things that a pinneferin can be useful for on NBME exams? Remember, a pinneferin is also a second line pressure for the moneyment of septic shock. Remember septic shock, the first line pressure is going to be neuropinneferin, right? But, after neuropinneferin, the second thing you're going to try is a pinneferin. A pinneferin is a second line agent. That's very high autonome. It's a second line agent for the moneyment of septic shock on NBME exams. Then a pinneferin can also be used in many of the ACLS algorithms, VTAC, you know, ACES to lay all those things. I'll encourage you to, again, check out episode 104.

Literally, that episode is on ACLS. It's a very high value episode to know for you exams. Okay, now, what if they give you a question about a patient? They tell you that this patient, you know, she's at 34 with gestation and she's been having like a very severe headache and blood pressure is like one-line, you have a 120. And the CEO was the next best step in management and he tried to get you to pick a drug. I really hope you're saying, hmm, this is going to give this person magnesium sulfate, right? This person has preeclamsia. The essentially beginning to inch towards the clamsia, then you're going to start seizing very soon. Well, in those circumstances, you're also going to give magnesium. You're going to give magnesium. So, one of the big things to know about magnesium, we're remembering magnesium is the drug of choice for a clamsia, right? Or if you're even trying to prevent, let's say a person has severe preeclamsia or whatever, you're trying to prevent them from flipping all the way to seizures. I want to go ahead and give those people magnesium sulfate. And the thing is sometimes, the thing is dejuoxin, right? I mean, many times we know that dejuoxin is classified as an anti-rhythmic drug. But the problem with dejuoxin is sometimes it can actually cause people to have like de-indrops or ribbons. The way we treat those ribbons, associated with dejuoxin toxicity, is actually by giving magnesium.

Magnesium is very useful for ribbons that are raised from dejuoxicity, right? And then don't forget that obviously a person's, a person has a polymorphic V-tack, right? Which we call torsad, the point, right? To set the point, twisted of the point, right? The drug of choice is going to be magnesium in those circumstances. And again, remember, if your magnesium is out of whack, and I'm giving you, I'm less than trying to fix your hypo calciumia or your hypochylemia, the hypochylemia and hypochylemia will not fix if your hypochylmysemic, right? So many times you want to correct people's magnesium first, before you start correcting their calcium and potassium. So that they can actually respond to the replicium of calcium and potassium. And then, what if they give you a question about a patient and they tell you that, oh, this is a patient, you know? So if I have your old guy as a history of morphine, it comes in past 30 minutes, he has been having like very severe chest pain, right? And that's all they give you. And maybe you see his blood pressure is like 1.8, over 150, right? And you see, what's your next best step in management? Well, I really hope you're like, oh, sounds like this guy has a yoddy dissection. But if a person has a yoddy dissection, your first step is you're going to give them a beta blocker, right? I mean, you know, there's diagnostic testing and all those things, right? But the primary thing I want to talk about here is the pharmacotherapy, right?

Remember, for every kind of yoddy dissection type B, type B literally doesn't matter. You're going to start off giving a beta blocker, right? You're going to start off giving a beta blocker, right? One common mistake mentioned is, oh, let's give hydrozene because the blood pressure is high in yoddy dissection. Don't do that, right? Basically, given hydrozene, actually, I think if I'm pretty sure about this, it worsens outcomes in yoddy dissection. And maybe like divine, why does that make sense? Well, think about it. Hydrogen is a very powerful visual dialyde. If you dialyde your blood vessels, your bire receptors are going to be like, right? So you're going to send a big sympathetic discharge. If you send a big sympathetic discharge, well, guess what's going to happen? You're going to have increased heart rate, increased contractility, right? And if that happens, then you're ejecting blood from the heart with more force. If you eject blood from the heart with more force, going to be slapping on that, you know, that dissected in tema even more. Right? So you're going to worsen the dissection. Don't give hydrozene ever in yoddy dissection. So beta blockers are the drugs of choice, right? Because again, they essentially slow down the heart, decreased contractility, right? So you have, you just have less forceful blood coming out of the heart. So you're going to like not worsen the dissection as much.

Although remember, if you have a type A dissection, after that beta blocker, you're going to take this little surge and ready for it. If it's a type B dissection, you're just going to do a medical management only. You're just going to do a beta blocker and kind of leave it at that, right? So what are some key things to know about beta blockers, for example? Remember, beta blockers, you know, obviously, there's an emin convention that goes with them, right? So for those that go from E through M. So as an apple to M through mom, those ones are beta ones selective, right? They're beta ones selective. But anyone from the letter N as a Nancy, all the way down, those are beta one and beta two, right? They are non selective, they block both beta one and beta two receptors. Now what are some other key things to know about beta blockers? Remember, beta blockers, they're very powerful. Again, think about it. If a person has asthma, we give them our beautiful role. A beautiful role is a beta two agonist, right? So it wouldn't make sense to give like a beta blocker to a person that has bronchospastic disease like asthma, right? You're literally reversing the pathophysed of asthma. That's going to be, I mean, you're basically like encouraging the pathophysed of asthma. That'll be bad, right? So beta blockers, if you have a history of asthma or again, really bad reactivary disease, like even a beta blocker is not a smart idea at all, right?

And they remember, again, beta blockers, because many people think of beta two receptors just with an early. Then these beta two receptors, we also find them in the blood vessels, right? They have diluting receptors when you activate a beta two receptor, it dilates your early. When you give, when you activate a beta two receptor, it also dilates your blood vessels, right? It also dilates your blood vessels. So if you think about it, if a person has like visospastic disease, like renolds phenomenon, right? Or the visospastic disease, like, uh, come on, define things like prince metal, and these days, prince metal, and she's called a very intentional exams, right? For those people, you don't want to give them a beta blocker, right? You don't want to give them a beta blocker, right? Because the mbmi, you know, they're counting on the fact that, ooh, for pressing has angina when medicine say the word angina, like, ooh, beta blocker, constant channel blocker, beta blocker, constant channel blocker. He has that's true, but very anti-angina cannot be treated with a beta blocker. If not, you'll cause coronary visospasm and kill the patient. So you don't want that, right? So for pressing has a history of renolds phenomenon, for pressing has a history of prince metal angina, or if they have a history of like, I think it's called like, burger's disease, right?

That, um, vasculitis, I talk about it in my vasculitis podcast, where they're like big smokers and they have all these problems with their fingers, right? Giving these people beta blockers is not a great idea. Again, I know some of you may be like, wow, they find this a kind of weird association here. It's a weird association, but it's weirdly high yield for the USMLA exams. I definitely know the stuff if I read you, right? And then remember, beta blockers are also contraindicated in a presence that has cocaine or methamphetamine intoxication, right? They are contraindicated in a presence that has cocaine or methamphetamine intoxication, right? Cocaine or methamphetamine intoxication, no beta blockers, right? No beta blockers because again, when a person has cocaine or metham intoxication, they have like a sympathetic toxic drum, right? A pro sympathetic toxic drum, right? So the thing is, at least your beta to receptor is open. And as your sympathetic nervous system activates that beta to receptor, it's causing a viso dilation. So that's bringing out your blood pressure a bit, right? So if you give a beta blocker, the thing that's going to happen is that beta to viso dilating blood, reducing blood pressure, reducing effect is gone. So you're going to get on or post alpha one stimulation and you're going to get into trouble. Now, also remember beta blockers, you avoid them if a person has acute decompensated C H F, right?

Notice what I said, I said before I literally said that beta blockers, the improved survival in congestive heart failure, that is true. But on the flip side, it's particularly important to understand to be aware of the fact that you don't give beta blockers in a person that has acute decompensated C H F. I mean, the heart is already not working really great. Well, you shouldn't be giving something that's going to cut you, depress them some more, right? So I could decompensated C H F, don't give a beta blocker, don't give a non-dihydroperidine calcantial blocker, right? Now remember beta blockers are also used for A-fap, right? Again, they slow down the speed of conduction through the AV node. So they are really good management for A-fap, right? They have something that can be used in a read control strategy for A-fap. And as I've talked about before, right after you give a denocent for a super ventricular tachycardia, you can give it a beta blocker of your upper middle of the entire exam, right? To keep your heart rates down, right? And obviously for a person who has like heart block, given a beta blocker, right? It's not a good idea. I mean, if you look at the names block block, right? Block block given to block block, right? It's probably not a good idea. Beta blocker, heart block. No, those things don't mix very well, right? So if you have heart block, stuff is already not going through your AV node. You don't want to give a beta blocker down.

Oh, gee, let's maybe really, really stop those things going through the AV node, right? That'll be a terrible terrible terrible idea, right? So it's actually very high to know this again. The drugs that are contrary to getting in heart block beta blockers are going to be one of them. The non-dihydroperidine consumption of basically anything that slows conduction down the AV node is not good. Beta blockers, non-dihydroperidine consumption of blockers, like if you're up and able to retire them, not a good idea, right? Or the juxtaposition is not good in heart block. If you give the juxtaposition, again, remember I said it, the juxtaposition is a muscronic receptor agonist, some muscronic receptor agonist. You'll slow down the speed of conduction through the AV node. That is not a good idea. And the person that has a heart block, right? And then again, remember beta blockers, the improved survival in CHF, right? So these are going to be drugs like metoprolol, carvidiol, and besoprolol, right? I remember it as like, you know, MCB, right? Metoprolol is the M carvidiol, that's what it's called, coreg in hospital. That's the C, the besoprolol. Those are the three beta blockers that are being shown to improve survival in congestive heart failure. And remember, if a person, now this beta blocker of proprenolol is actually kind of high yield, right? People, they love to test proprenolol on MBM exams a lot, right? For many different reasons, what are these many different reasons?

And also, maybe like, wow, divine. I thought this is a cardio farm podcast. Yes, it is, right? But again, the thing is the USML Es, that's why, again, if you're just memorizing things in a linear fashion, you're not really helping yourself with the exam. The way you should be studying is one, understanding the concepts and then two making integrations, which is what I try to do with many of my podcasts, right? But if you look at this, proprenolol, they love to test proprenolol in many different contexts. Well, I mean, one context they love to use proprenolol for an exam is thyroid storm, right? Thyroid storm. Remember the first drug when a person is going through a thyroid storm, the first drug you always give is proprenolol. Why is that? Well, the reason you give proprenolol is that it's a very powerful inhibitor of the five prime diodinies. The five prime diodinies converts T4 to T3, right? Which is very active and that helps, right? And it also helps with the hypoagenergic symptoms in thyroid storm. Because remember, one of the things that thyroid hormone does is that it places more, it increases the number of beta-wond receptors, you have in your myocardial cells, right? So that prosynpathetic effect of thyroid hormone is shut it down by giving a proprenolol. Now remember, if a person has portal hypertension or divided solar cells, then you can use it as a solution.

Now remember, if a person has portal hypertension or divided solar cell viruses, if you want to give a solar cell viruses per relaxes, beta blockers are actually pretty good for those circumstances. If a person has stage fright, right? Stage fright, you know, it's a kind of performance anxiety where they are very afraid of giving public speeches. Proprenolol is great for those people, right? Or if you see a person that was just placed on an antidecotic, right? Remember, and you know, they are placing all over the place, they can't seem to stay in one place. That's acathesia, right? Proprenolol is one of the drugs of choice for the management of acathesia, right? And also if a person has essential tremors, proprenolol is great. And also, maybe like, wow, proprenolol is very high yield. Yes, trust me, it is very, very high yield, right? Proprenolol is one of these drugs that pretty much almost always shows up on USMD exams, right? Proprenolol is also useful for essential tremors, right? If a person is having like eight or more migraines every month, right? Those people are kind of these for migraine prophylaxis. Believe it or not, beta blockers like proprenolol are amazing for migraine prophylaxis, right? And then continue on this beta blocker theme. Don't forget, you can use your beta blockers for glaucoma, right? Because remember, your sympathetic system actually promotes the production of acosumer, right?

So if you give something that is anti-sympathetic, like a beta blocker, like Timolol or Nidolol, I'll say that again, Timolol or Nidolol, right? Then those things will prevent acosumer production and that can decrease the introcular pressures in a pressing with glaucoma, right? And then another beta blocker that is very high yield to know, then we'll wrap up here today is labidolol. The love, love, love, love, love to test labidolol on MBME exams. Remember, labidolol is an alpha beta blocker. It blocks alpha-1 receptors and beta-1 receptors, right? So what can we use labidolol for? Well, remember, labidolol is actually the drug of choice for lowering blood pressure in patients that have a stroke, right? So remember, if a person has a stroke, you know, you want to keep the systolic blood pressure less than 220, you want to keep the systolic blood pressure less than 120, right? The way you keep the blood pressure below those thresholds is with labidolol, right? Labidolol is actually one of those drugs that are actually pretty safe in the management of hypertensive emergencies. Remember, I've said this admonism on this podcast. The drugs used for hypertensive emergencies, fall into one of four categories, either labidolol or clevidipine or nicardipine or nitropercyte. That's it. Maybe a distant fifth can be phantolamine, right? You should not use any other drug outside of the five of mentioned for the management of hypertensive emergency, right?

And remember, labidolol is one of these anti-hypertensives that's also pretty safe in pregnancy, right? Labidolol is very safe in pregnancy, right? And again, labidolol is actually one of these beta blockers you can use to manage erotic dissection, right? Again, it's an alpha beta blocker, right? It's an alpha beta blocker because it's, I mean, it's amazing, right? Like labidolol is like the ideal drug. First thing is first, it reduces your afterload, right? Because it's a viso that, you know, reduce your afterload by blocking alpha one receptors. But then it also lowers your heart rate by blocking beta one receptors, right? So by blocking beta one receptors, it's actually reducing your myocardial oxygen demand, right? So labidolol is an amazing, amazing, amazing, amazing drug. So I think I'm going to go ahead and pause here. Listen to me this too long. I feel like I've talked about quite a lot of details today, right? But again, as I do at the end of every podcast, I don't for one or one tutoring for many exams, you know, step one, step two, see key, step three, preclinical medical exams, 30-year shelf exams. Actually, do this thing called a longitudinal tutoring, where let's say you're studying of med school and you need someone to like tutor you for pretty much all the med school subjects. I'd be happy to do that.

Or if you, you're studying of your 30-year of med school and you need someone to tutor for every shelf exam, you know, most times I meet people for about like four or five hours per shelf exam. And again, those people that do this longitudinal tutoring, they essentially set themselves up to do really well on the US ML exams because you're essentially like learning how to take these tests like from a very early stage, you're getting the understanding down and everything, right? And then by the time your US ML is come along, you're like very, prepared, very ready for it from the get go. And you know, I mixed study plans with people as well. And you know, again, I offer these US ML courses, you know, for step two, see key, step three, complex two, and three, the MBME Tested Instrategist course. Again, I have some next week if you're interested, shoot me an email. I'll be bringing up some step one course offerings very soon as well. But other things, I guess I want you to keep in mind, these podcasts are on Apple podcasts, you know, Google podcasts and they're on Spotify, right? So if you just look for divine intervention podcasts, you can find them, find them over there. And then, you know, many people have told me, have gone in countless emails, wow, divine, I love your life lessons. I love your life lessons. Don't get me wrong. I'm going to be talking about life lessons on this podcast, but I decided to literally start a whole different website.

It's called divine intervention, life lessons.com. I'll say that again, divine intervention, life lessons.com. If you go on that website, I've made about actually more than 30, I think life lessons and I add every week, every week, every week, right? So they're like podcasts, you know, most of them are like on the 30 minutes alone, most of them are like 10 minutes actually, right? But basically in those podcasts, I take like a, you know, it's Bible based teaching, I take a life lesson that is common to many people that think it's like a problem that exists in the world and talk about it, give practical tips and practical strategies. And then, and actually this podcast is an Apple podcast. If you just look for divine intervention, life lessons, you'll see that there's actually, it's actually on an Apple podcast. And then I have a website, right, divineinterventionpodcast.com. If you subscribe, you'll get an email notification whenever I make a new podcast.

And then I have a You Tube channel, divine intervention, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a You Tube channel, you have a

Adenosine.

Wolff-Parkinson-White (WPW) syndrome, due to the risk of profound and dangerous conduction changes.

Magnesium Sulfate ($\text{MgSO}_4$).

Beta-blockers (e.g., Labetalol, Esmolol).

Inhibition of the $\text{Na}^+/\text{K}^+$-AT Pase pump; visual changes like xanthopsia (yellow halos).

Phenylephrine or Epinephrine.

The coronary steal principle; it causes generalized vasodilation, making stenotic vessels appear ischemic by reducing flow through them.

1) Bradyarrhythmias (e.g., heart block); 2) Organophosphate poisoning; 3) Calcium-channel blocker toxicity.

Anti-digoxin Fab fragments (or specific antidotes, depending on institutional protocol).

Labetalol. It blocks both $\alpha_1$ receptors (reducing afterload) and $\beta_1$ receptors (lowering heart rate/demand), making it safe for hypertensive emergencies.

Worsening cardiac function, as the heart is already struggling and needs maximal output.

Adenosine and Dipyridamole, because they are powerful bronchoconstrictors.

The coronary steal principle; it causes generalized vasodilation, making stenotic vessels appear ischemic by reducing flow through them.

1) Bradyarrhythmias (e.g., heart block); 2) Organophosphate poisoning; 3) Calcium-channel blocker toxicity.

Anti-digoxin Fab fragments (or specific antidotes, depending on institutional protocol).

Labetalol. It blocks both $\alpha_1$ receptors (reducing afterload) and $\beta_1$ receptors (lowering heart rate/demand), making it safe for hypertensive emergencies.

Worsening cardiac function, as the heart is already struggling and needs maximal output.

Adenosine and Dipyridamole, because they are powerful bronchoconstrictors.