DIP Episode 333 - The Clutch Pressor and Inotrope Podcast for Step 2CK/3

Okay, welcome. This is episode 333 of the Divine Intervention Podcast. In this short podcast, I'm going to be talking about pressers for the USML East Step 2 CK and Step 3 exams. Pressers are just things that people kind of heat study in and thankfully the information you need to know for Step 2 CK is Step 3 from a press service practice is pretty minimal. So I just want to basically cut local of that here, but again, as you know, I'm not going to be giving you just straight up information with zero context now. If I do that, that would not be very helpful, obviously. Right. So what are going to be doing today is we're going to be talking about pathophysiology. We're going to be talking about clinical scenarios where you would employ those things on on MBM exams as I do. For those of you that are taking Step 2 CK Step 3 anytime soon, because I know a lot of people are going to be taking the exams within the next month. So your scores can be out in time for years. I do have a course coming up like a Step 2 CK Step 3 review course coming up next week. It's Thursday Friday and Saturday and have an MBM testing strategy scores coming up on Wednesday next week. Again, tons of people have taken these courses and they've done extremely well on the exams. So if that's something you're interested in, just shoot me an email through the website. Again, I've had many people that have taken the exams very recently as recently as like today, even. Right.

And again, I've been getting very good reports, very good feedback on the course. So if you're interested in the course, just shoot me an email through the website and I'll give you some more information on cost and things like that. Okay, so let's just jump right into it. So I think the best way to describe the topic today is to just break things up by I know tropes versus visa pressers. Right. So let me talk about I know tropes first. I know tropes by definition. They work almost exclusively on the heart. Right. Because if you think about it, you use a pressure when you're in a state of hypertension or when your blood pressure is really low. And you want to try to maintain profusion to your body's organs and tissues. So you can raise your blood pressure in one of two major ways. Right. One is you can make the heart beat stronger and faster. Right. That'll be positive I know tropy. Right. And I know tropy is an agent that by definition works on the heart alternatively. Another way you can make this happen is by giving a visual active agent a visual pressure. Right. So this is something that is more like a systemic vascular resistance increasing agent. Right. Because if you increase systemic vascular resistance, that will increase up that will be a good climb down on your blood vessels. And that's going over all cause an increase in blood pressure. So let's go ahead and talk about these basically today.

I'm going to be talking about about like seven drugs and that will be pretty much it. So in terms of the high note tropes, right. So what if they give you a question about a person and the person started taking an I know trop and few days later, the person developed like yellow vision abdominal pain hyperculemia. If you see this, I really hope you're thinking about the Jackson, right. The Jackson remember the Jackson on MDM exams the way it works is that it inhibits the sodium potassium ATP. So the thing is if you inhibited the sodium potassium ATP, then there'll be less sodium coming out of your myocardial cells. If there's less sodium coming out of your myocardial cells, then there'll be more sodium intracellularly in your myocardial cells. If there is more sodium intracellularly, then the sodium calcium exchanger will stop working. Because remember that exchanger is job is to get calcium out of the myocardial cell and bring sodium in. But if there's so much sodium inside the cell, the gradient for sodium to rush into the cell for calcium to be pumped out goes away. So ultimately when you take the juxtaposition, the amount of intracellular calcium you have is going to go up and that's going to cause more I know tropy. So that's how the juxtaposition is a positive I know trop. But there's a few key things your friends at the MBME need to know about the juxtaposition one is for president has the juxtaposition toxicity.

It's very high you to remember that if you give anti-dage fab fragments, right? So I'll say that again. Anti-dage fab fragments you can reverse a diger toxicity. It's basically like a monoclonal antibody against the juxtaposition. And then the juxtaposition there is this potassium conundrum that many people tend to screw up on exams. I believe it or not, they test this stuff like all the time, right? People just mess it up all the time, right? So the thing is I'll say the statement and then I'll explain the pathophysic because it makes perfect sense if you just reason through it. The first thing is the juxtaposition causes hyper-kilemia as a side effect. But on the flip side, if you are hyper-kilemic, you're pretty supposed to dig juxtaposition toxicity. So let me explain what I mean, right? So the thing is we know that normally the sodium potassium ATP is pumped. The first thing that we know about the juxtaposition is to get three sodiums out of the cell and two potassiums into the cell. So it gets potassiums literally into cells. So if for some bizarre reason, you inhibit that sodium potassium ATP is pumped with the juxtaposition, then you're not going to be able to get potassium into cells. If you can get potassium into cells, then you hang out in your bloodstream. If you hang out in your bloodstream, you're going to have hyper-kilemia, right? You're going to have hyper-kilemia. That's a very high-yield thing to keep at the back of your mind for exams.

But so some of you may be like, okay, divine, that makes sense. I understand why it did causes hyper-kilemia. Well, how does hypo-kilemia predispose you to dig juxtaposition? Well, let me explain. The thing is again, we just said that the juxtaposition works by inhibiting the sodium potassium ATP is pumped. If inhibiting the sodium potassium ATP is pumped, that's how the drug as we know it works. But the thing is, for you to inhibit that pump, it needs to bind to the potassium binding site. So the thing is, if you're a hypo-kilemic, let's say for example, you're digging diuretics at the same time as the juxtaposition, which is not an uncommon practice, that's going to lower your potassium. That's going to create more binding sites on sodium potassium ATP is pumped for the juxtaposition. And if you create more binding sites, then the juxtaposition can accumulate and can start getting toxicity, right? And getting like very mature ventricular contractions, you can get quite a number of different problems. Okay, so those are kind of like the big things I want to mention with the juxtaposition. Now, the next inotropa will go to, what is that inotropa that can be used for chemical stress tests? I would really hope you're saying, oh, the vine is dubular mean, right? So dubular mean is a simple molecule to work with, right? So dubular mean is beta one agonist. Remember, we have beta one adrenergic receptors on our blood.

We find that the afrin material, but we also primarily find it in the heart. And when you activate that receptor, remember, it's a G-pertine coupled receptor. It's a stimulatory G-pertine coupled receptor that's going to cause you to have an increased heart rate and increased contractivity, right? So in people that cannot exercise, for example, you can do chemical stress test by basically stressing out the heart, by giving a beta one agonist like dubular mean. Another thing you can also do is, you know, there is also the coronary steel principle, have described in many different podcasts that you can use for chemical stress tests, which like diperidomal and adenosine. But we're not going to go into that today because we're focusing primarily on pressers, have described that in other podcasts in the past. So that's kind of like a big thing there. So what do we use dubular mean for? Again, like I said, we use for chemical stress tests. And we also use for people in cardiogenic shock, right? We use for cardiogenic shock. Now, one thing I will just say is, one of our friends at the MBM, every now and then, the right these bizarre questions, where they ask you what will happen to the renal and genome-dosterone system. If a person is placed on dubular mean, well, it's kind of high you to know that, remember, beta one receptors are also found at the afren material of the nephron, right? And when you stimulate beta one receptors, that increases renal production.

So when you give a beta one agonist like dubular mean, your renal goes up, your angiotensia one and two both go up and your adenosine will go up as well. That's a high you thing to keep in mind for exams. And one thing I just want to say, these anal tropes, none of them have any mortality benefits, like heart failure and anything like that. Okay, now the final pre- anal trop I'm going to talk about is merino. So merino and the good thing about merino is it's a pretty awesome drop for many reasons. So merino is a force for diastries in habiter. So maybe like divine. I know force for diastries in habiter is a very good at decreases systemic vascular resistance. How can a force for diastries in habiter be a positive anal trop well the thing is remember force for diastries is an enzyme that breaks down cyclic AMP. Well, the thing is cyclic AMP is kind of like a guy that kind of acts different ways based on where he is, right? When you have increased cyclic AMP in your heart, it's actually going to make your cardiac muscles contract better. But when you have an increase in cyclic AMP in your blood vessels, it is smoke muscle, you're going to have a relaxation. Right? So the thing is merino is actually pretty great because when it makes your heart work better, but two, it reduces the amount of work your heart has to do. Because think about it. If you're basically AMP in smoke muscle in blood vessels, you get visual dilation, you're decreasing after load. Right?

So that's making it easier for blood to be ejected out of the heart. So the thing is merino is good in the sense that it increases your cardiac output. But at the same time, it decreases after load. Right? So it increases that cardiac output again by increasing cardiac contractility. Right? So it raises your systolic blood pressure. But at the same time, it's bringing down your dastolic blood pressure because your after load is going down. So if you look at the spread between the systolic and dastolic blood pressures, that's your pulse pressure. Right? So merino widen your pulse pressure. That's very important and very high to know for purposes of exams. Okay. So now let's jump into the visual pressures. Right? So again, these are agents that work primarily by constricting blood vessels as a means of proping up blood pressures. Right? So the first one I'm going to talk about. Right? So what if they give you a question about a patient and this patient is in septic shock? And then this patient starts, you know, you've given Norepinephrine and the Norepinephrine, you've got into like the maximum tolerithy therapy and then the ask for your next best step in management. Are your next best step in management is to add visual pressing. I'll talk about Norepinephrine in a bit. Norepinephrine is the first line pressure in septic shock. Right? But visual pressing, right? It's a drug that is basically second line in the surviving sepsis algorithm.

If you in terms of adding pressures for septic shock, basically for septic shock, first line is Norepinephrine. Second line is visual pressing. Third line is epinephrine. Right? So visual pressing, how does visual pressing work? Well, visual pressing is actually a derivative of anti-diarreratic hormone. Right? So the thing is, if you really think about it, it does many things to maintain your blood pressures. Right? So visual pressing again by acting on the visual pressing V1 receptor. Right? Remember that visual pressing V1 receptor is a GQ coupled receptor. Right? So it does all those protein kinasey businesses. Right? And by doing that, it causes a visual constriction and that increases your blood pressure. Remember, visual pressing, that's not only its useful in exams. Right? Remember, if you have like a six-year-old boy that is bed wetting, right? Remember, you need to be over the age of five to bed wet. Those kids can be treated actually with visual pressing. Right? We can treat them with visual pressing. Again, the thing you're more like, decimal pressing. Remember, decimal pressing again is very, very similar to visual pressing. Right? So because basically we know that visual pressing, decimal pressing there, kind of like A, B, each analogs. So the business will suck up free water from your urine. So you don't lose volume. Right? That's going to obviously raise your blood pressure and that's going to prevent the child from peeing in the first place.

So do remember, in general, if we're treating a person that has no channel linear recess, we're usually going to do fluid restriction at night as a first line measure. Second line measures could be things like decimal pressing or any recess a lot. And then another thing you may see visual pressing used for an in-beam exam. Right? Again, in the decimal pressing form is they can give you a question about a person that has this bleeding disorder and they tell you that the PTT, the bleeding time are both elevated. And the person has an abnormal restocity and co-factor assay. Right? In those situations, I hope you're thinking about the willy-brand disease. In the willy-brand disease, remember the way you treat it because remember it's obviously the efficiency of a willy-brand factor. The way you're going to treat that is by giving a decimal pressing. The decimal pressing is going to increase the release of a willy-brand factor from your WIBO-PALADY-BODY. If you release more of a willy-brand factor from your WIBO-PALADY-BODY, that will help a person that has a willy-brand disease. Remember the PTT goes up in the willy-brand disease because those people, the A-Factor 8 now has a decreased half life. Because the willy-brand factor is like a protecting group for factor 8. Another use, when MBM exams for visual pressing again in the decimal pressing form, is in a pressing that has bleeding in the setting of nst-degener disease.

Because remember when you have nst-degener disease, you have uremia, when you have high levels of urea, then your platelets don't work well. You can improve platelet function by giving decimal pressing. That's why it's actually very helpful in treating the coagulopathy as a social-st-degener disease. The next person I'm going to talk about is phenyl-effren. The good thing about phenyl-effren is it's a pure alpha-1 agonist. It's a pure alpha-1 agonist. Remember, we primarily have alpha-1 receptors on our blood vessels. When you activate them, when you agonize them, that's going to cause a visual constriction. Usually they like to bring in phenyl-effren, and it's close cause in effedering, e-p-h-e-d-r-i-n-e. They are both alpha-1 agonists. When you activate those receptors, that's going to climb down on your blood vessels. When you climb down on the blood vessels, that's going to ultimately cause you to increase your systemic vassal resistance, and that's going to raise your blood pressures. Remember, when you raise your blood pressures like that by alpha-1 agonism, that's going to increase pressure of blood, just banging on your bar receptors in your blood vessels. When that happens, your heart is going to be like, whoa, what is my blood pressure too high? You're going to get a very powerful parasympathetic discharge. When you get an alpha-1 agonist, you're going to have a reflex-breedy cardia. You're going to have a reflex-breedy cardia.

Usually, where do they use effedering or phenyl-effren on in-bini exams? They use them primarily for a pressing that just gets an aesthetic. Remember, an aesthetic can really drop a presence of blood pressures. If you get an aesthetic and your blood pressures drop, they can just give you an alpha-1 agonist. That thing will just very rapidly raise your blood pressures. Finally, the last person I'm going to talk about is Noripineffren. For the most part, we use it as the first-line pressure in septic shock. It has both alpha-1 and beta-1 effects, but the predominant effect is alpha-1. This is blood pressure in that way. Remember, for septic shock, first-line is Noripineffren, second-line is viso-pressant, third-line is epineffren. The last person I'll just say about epineffren. We use it a lot for ECLS algorisms. When a press-e has like a cardiac arrest, has many of those ventricular arrhythmias. We tend to interchange epineffren and amylo-ron. Remember, we use epineffren because of its beta-2 agonist effect in a person that has an aphelactic shock. In fact, if a person has an aphelactic transfusion reaction, it will be a very good situation to use epineffren. I just intended this to be a very short podcast, but if you know all these things I talked about, I'll be really shocked if you've got any press or I know a troprolated question wrong on your septic-2-c case-tept trick exams.

As I do at the end of every podcast, I offer pretty comprehensive review courses for the USML's Step 2-C-C-Cance Step 3 exams. These are group courses that I held over Zoom. Many people have attended these courses and found it to be helpful. I also do want to want to learn for Step 1, Step 2-C-C-C-Step 3, pre-clean, cool medical exams, 30-ish-off exams. I know many people are preparing the IRS applications now, so I help with that process, reviewing personal statements, recommendation letters, IRS applications, and more interviews. I do all those things. If you're interested in any of those things, just shoot me an email and I'll be happy to point you in the right direction. I also have this podcast on Google Podcast, Apple Podcasts and Spotify, and then I also have a You Tube channel right, Divine Intervention USML Podcasts and videos. So thank you for listening. Have a wonderful rest of your day. God bless you. Thank you.

Norepinephrine.

Administration of anti-digoxin Fab fragments (monoclonal antibody).

It increases contractility (inotropy) via PDE3 inhibition while simultaneously decreasing afterload by causing systemic vasodilation.

Norepinephrine has both alpha-1 and beta-1 effects, whereas Phenylephrine is a pure alpha-1 agonist.

The Renin-Angiotensin-Aldosterone System (RAAS). Beta-1 stimulation on the afferent arteriole increases renin release.

Anaphylactic shock or ECLS algorithms, due to its potent beta-2 agonist effects.

Milrinone.

Hypokalemia (low potassium).

Vasopressin.

Norepinephrine.

It widens the pulse pressure (increased systolic BP due to contractility + decreased diastolic BP due to afterload reduction).

Because it is a pure alpha-1 agonist, causing immediate and potent vasoconstriction.

Milrinone.

Hypokalemia (low potassium).

Vasopressin.

Norepinephrine.

It widens the pulse pressure (increased systolic BP due to contractility + decreased diastolic BP due to afterload reduction).

Because it is a pure alpha-1 agonist, causing immediate and potent vasoconstriction.