DIP Episode 264 - The Clutch Comprehensive USMLE Heart Failure Podcast

Okay, welcome. My name is Devine. This is a piece of 264 of the Divine Intervention Podcast. And into this podcast, I'll be talking about a topic that is floorily high yield for all the USMEL exams. Step 1, step 2, CK, step 3. It's a topic where you can pretty much guarantee you're going to see a few questions on these on a test. And this topic is also like super clinically relevant because I'll see almost all disciplines. In some way shape of form have to manage this condition at some point in the patient's care. So today we're going to be talking about heart failure. And again, I'm going to be very thorough. There's going to be a very complete street ties on heart failure. So if heart failure is something you're struggling with, it won't be a problem after this basically. And again, as a reminder, if you're interested in setting up for any of the courses I have coming up the next three days. So tomorrow, the 21st, right from 2 to 4 30 PM Pacific time. I have a Testikin Strategy course. And then on Tuesday and Wednesday, the 22nd and 23rd, I have a comprehensive step to CK course. Again, that covers internal medicine, PEAD, surgery, OB-GYN, Neuron, psych. It's known to 5 PM, Pacific Standard time on both days. So if you're interested in setting up, there's still very few sports left. You're welcome to send me an email through the contact feature on the website. And then we'll go from there. Okay, so let's jump straight into heart failure.

Right, so the thing is heart failure, you can look at it from many different perspectives. Right? But the thing is ultimately you want to understand it in the context. I mean, really, my goal with this podcast is for you to understand, but also to cover pretty much any base that is reasonably possible on an in-beam exam, O-D-B-M exam, new in-beam exam doesn't matter. Right? So let's talk about some dichotomies with regards to heart failure. Right? So let's talk pathophysiology first. So remember, you don't look at heart failure in many different ways. Right? Like for example, what, or maybe let's say one star here, what causes heart failure? Right? So the thing is, you can get heart failure in one of two ways. Right? You can get a systolic heart failure. Right? Or you can get some kind of dastolic heart failure. Well, how do systolic heart failure arise? Right? Usually there will usually be some kind of thing that injures the myocardium. Right? It can either be like like a schemia, like a person getting an MI, right? Or you know, just some kind of like physical damage to the myocardium. Right? And then the myocardium will infarct. When the myocardium infarcts, all these inflammatory cells, right? Again, remember what you learned from the performance back in the day. All these inflammatory cells will show up, right? And when they show up, right? They release all these pretty easiest and all these things that ultimately would like, you know, destroy the car- the myocardium.

And those things will make the myocardial cells weak. If you're weak, right? Think about it. Let's see if you've not eaten for 20 days. And I tell you, oh, please carry this 100 pound wheat. You'll see it divine. I'm sorry. I can't help. Right? So if those myocardial cells are weak, right? Then they won't be able to work effectively. They won't be able to contract effectively, right? So just something to keep at the back of your mind, for example. That's how people get systolic heart failure, right? That stolic heart failure usually that reaches from some kind of infiltrative disease or some kind of fibertic disease, right? Again, remember, I've compared in a prior podcast, that stolic heart failure to like almost like restrictive lung disease, right? And then I've compared systolic heart failure to almost like emphysema. It's almost like obstructive disease of the heart, right? So it's just a nice construct to kind of parallel between both. So, you know, if you have some kind of infiltrative disease, some kind of fibrocess of the heart, right? That makes the myocardium very stiff. If you become stiff, then you're not very compliant. And if you're not very compliant, right? Then you will not be able to feel appropriately, right? Like if you adjust the little blood to the heart, the heart pressures go up like significantly, right? So ultimately, when a person gets in these kinds of troubles, right?

Like, you know, beats a stolic, beat that stolic heart failure, doesn't matter. Ultimately, if the heart is not working well, right? Then you begin to have blood backing up in the lungs, in the extremities, just, you know, depending on the kind of heart failure a person has, right? And the thing that happens is ultimately in a person that has heart failure, the cardiac output is going to be low, right? And if your cardiac output goes down, guess what? That is going to increase the activity of the reneal and jetons in an adostroenterosis step, right? Because you'll be hypoperfusing the afraid material. If you hypoperfusing the afraid material, right? When you're reneal and jetent, your, your GG cells will start freaking out. You'll be like, raise the blood, where my blood go, right? They'll start freaking out and we'll be free-cowls, right? You'll begin to release a ton of renein. And as your renein goes up, right? That will increase your angiotensin one. Ultimately, right? That angiotensin won't go to the endothelial cells, right? That line the pulmonary capillaries, you make angiotensin two. And then that angiotensin two, right? Would ultimately go to the zonal glomerulosa of the adrenal cortex, amicure, elisa, adostro, right? So all those things, you know, will make you, your heart and your sympathetic nervous system will also be very nervous as well, right? Because if you think about it, right? When your cardiac output goes down, right?

Your bar receptor sends that, ooh, blood pressure is low, right? So they will signal your medulla, right? And that will ultimately cause you to have this big sympathetic discharge, right? And when you have that sympathetic discharge, that will also feed off of this renein and your tensin activity, right? Because remember, beta one receptors also found on the GG cells, right? So when you have more sympathetic activity, you stimulate those beta one receptors, you stimulate those GG cells, right? And you make a ton of renein, right? So ultimately, your heart is trying to compensate for all these things going on, right? So, you know, with this sympathetic overdrive, with this renein and your tensin adostro and system of regulation, right? Your heart rate is going to go up, right? Your cardiac contractivity is going to go up. That's great, right? And your blood volume is going to go up. That's great as well. The only problem is all these compensatory mechanisms, right? Because think about it, let's say again, I'm just giving an analogy, right? So let's say I see that you've not eaten for 10 days, right? And let's say normally you work at a job where you carry, you live 50 pounds, right? And then I see you've not eaten for 10 days, but I'm like, dude, I'm really sorry, right? Like the economy is not great, so you need to work a little harder, right?

So instead of lifting 50 pounds, you're not lifting 100 pounds, even if you've, you're lifting 100 pounds on not eating for 10 days, right? So, you're trying to compensate, well, you're already compensating on very limited resources, right? So that extra compensation is going to enjoy the percent more, it's going to put more wear and tear on that person, right? So it's like, oh, before the person was handling 50 pounds. Now, the person has less energy because they've not eaten for a long time, but you're putting even more work on them, right? So the heart is trying to compensate, the body is trying to compensate, but that extra compensation will ultimately accelerate the injury on the heart, right? So the heart function will begin to deteriorate some more, right? And then after a while, the heart will completely crap out, right? And one thing I think I should also mention is this whole concept of high output heart failure, it's actually a kind of heart failure that exists. I'll talk about that some more in a bit, right? But let's keep going, right? So what are some things that can happen in a person that has heart failure? And remember, you can have heart failure, like that is limited to the right side. When a person just has right-sided heart failure, right? Basically, like, again, everything will just backup, right? So, those people have like congestion of their like SVC and the IVC, right?

They can even have like, you know, fluid accumulating like their lower extremities and all that stuff, right? So they'll have like, sacred edema, lower extremity edema and all that stuff, right? But usually those people will not have any pulmonary complications. You won't have like fluid in the lungs, but if a person has left-sided heart failure, right? Again, the only thing they can do is they can't output. So again, fluid will backup, right? Again, just always drop block diagrams for these things, you know, make most of it clicking your brain, right? So, you know, again, the ventrulla pressures will be elevated, right? But now you begin to congest the pulmonary vessels, right? So those people have like crackles in the lungs because all that fluid congestion, right? All those pulmonary vessels that are congested, right? That will cause an increase in the hydrostatic pressures in those vessels, right? And when you have an increase in hydrostatic pressures, you'll have fluid extra versition into the into the lung parankham, right? That's what ultimately lead to the pulmonary vascular congestion that will cause the wet lungs, right? So a person will have pulmonary edema, right? And remember that ultimately, again, if those pulmonary vessels are chronically congested, right? Then over over time, right? That pulmonary congestion will lead to pulmonary hypertension, right? And then that pulmonary hypertension will then give rise to a right heart failure, right?

In fact, the most common cause of right heart failure is left heart failure, right? Just one of those quips you here on embankment exams, you hear clinically on the wards and stuff like that, right? So, so usually again, people that will, you know, start off with left heart, left side of your heart failure, they didn't ultimately have right side of heart failure, right? At that point, they are safe to have biventricular heart failure, right? So again, just all things you want to keep at the back of your mind on exams, right? So again, and don't forget that heart failure is graded, right? So remember heart failure is in grades, right? So people can have like grade one heart failure, usually for the most part, these people's injection fractions like more than 60% is like roughly normal, right? And then just go down by 20s after that, right? So if your EF is from 40 to 59%, that's great to heart failure, right? If the EF is from 21 to like 39%, that's great. If you're less than 20% or you know, you're right, at that 20% mark, right? That's great for heart failure, right? And again, pathophys wise, again, as I've described, right? Again, many, many things can cause heart failure, right? Again, for pressing has an EMI, right? A myocardial infraction. That's going to, again, cause infraction of those myocardial cells, those inflammatory cells will come to fix the damage, right?

But as they are fixing, they are weakening those myocardial cells because of all those produces and all that badness they release, right? And also people having hypertension, people having valvular disease, right? People that have like erotic stenosis, for example, or mitra regurg, or eodic regurg, or whatever, those things can ultimately lead to heart failure, right? And the thing is usually, when a person has heart failure, right? Especially again, the one that, let's say it's coming from erotic stenosis where like the left ventricle has to like keep contracting against like really, really high pressures, right? That will ultimately give rise to a pressure overload, right? So again, like erotic stenosis, hypertension, those are probably like the two most common causes of pressure overload on in-beaming exams, right? Also, you can also find out with hypertrophic cardiomyopathy, so the way that the body, the right heart to respond, right? The heart to be like, okay, I got it, working against increased pressures, right? So let me get bigger and bifier, right? So it will limer your cardiomyopathyum down in parallel, right? So those people have like concentric hypertrophy, basically the heart will remodel, right? Whenever the heart is injured, it always remodels, right? I just kind of think of it this way, right? If you have a room, right? And you know, let's leave lived in this room for like 70 years, right? Over time, you'll be like, yeah, this please looks terrible.

I'm going to go ahead and remodel it, right? Because the police has been injured consistently over time, right? So you're like, let me remodel this room and or tear this room down and build something new, right? I guess in the case of the heart, tear me down and building something is a heart transplant, right? But you know, I can try to remodel, right? So whenever your heart is subjected to like elevated pressures, right? As the mechanism behind the heart failure, right? Again, from like erotic stenosis or from hypertension, right? Because remember, when a person is hypertensive, that increases after load, right? Remember, if you kind of think of it this way, if you're trying to run into a bedside, right? You can run into on a regular day of the week, you can run into a bedside easily, no big deal. But on Black Friday, that's a different story, right? There's a ton of people in the way, right? That's the kind of same thing that happens when a person has hypertension. There's like a ton of blood in the way, right? And there's all these turbulence and all that badness, right? So like, it's harder for blood that's coming out of the heart to run through those doors of the yard of the yard, like run through the walls of the heart and all that stuff, right? So that causes an increase in after load. Whenever you have a chronic increase in after load, right, that's again, going to make the living sugar have to work really hard to get blood out, right?

That's ultimately going to cost again the heart to remodel in a concentric fashion. It will lay down saccharomeres in parallel, right? Just to make the heart bigger and be fear to deal with that problem, right? But the thing is over time, as that heart gets bigger and be fear is like you're laying all this myocardium, myocardium, myocardium, myocardium, myocardium in parallel, right? These saccharomeres in parallel. All those myocardium, your laying in parallel, those will begin to take up lumen space in the heart, right? So the heart will not be able to feel appropriate, right? And again, those people's hearts get very stiff, right? Because many times when you have concentric hypertrophy, it's also accompanied by like fibrosis, right? Your heart begins to lay down on this fibros tissue. So that makes the heart very stiff, very non-compliant, right? So it makes it very hard to feel, right? That's ultimately only to a best, stomach heart failure. And remember, that's associated with an S4 heart cell, right? But if a person is subjected to like chronic volume overload, right? So let's say a person has like eotic regert, for example, right? Or a person has myocarditis, right? The heart will say, okay, wow, I'm dealing with all this increased volume. So let me try to get a bigger cavity size, right? Bigger cavity size. So instead of like stacking people on top of each other, right? Or stacking saccharomeres on top of each other.

Your body will stack up saccharomeres from end to end to end to end to end to deal with that increased volume, right? That's eccentric remodeling. That eccentric remodeling again is not ideal, right? Because yes, you can go from, because think about it, right? It's like, let's say you're trying to, I think something that will really make this really obvious is, let's say you as one human being, you're trying to hold one human being. It's very easy, right? You can literally squish that human being big time hulk, right? But if you're like, oh, you know, let myself and 10 friends go hands to hand, hands to hand, and we're trying to hold one person. Yes, encircle that person. We'll have so much space surrounding that person, right? But the problem is, we can give a nice big squeeze, right? Because it's almost like the squeeze is ineffective, because there's just too many people, right? Holding hands to hand, like ends to end, right? So that's what happens in systolic heart failure, right? That's why those people tend to have reduced the ejection fractions. And usually when a person has systolic heart failure, eccentric remodeling, eccentric hypertrophy, that's going to be associated with an S3 heart sound on an ambient exam, right? And again, as you're, as you're, as you're pressing heart failure, right? Again, the running and retention adduction system, getting into high gear, right? So, remember, an retention, it's a powerful visual constructor, right?

So that visual construction, again, will increase after load. So the heart will have to work even harder, right? Or if you're thinking about it, fence from the outdo-stron perspective, outdo-stron, Mickey Raps, or most sodium, at the level of the principle set of the collecting duct, water is going to follow alongside, that will increase blood volume, that will increase preload, right? That will increase your end systolic volume, right? So again, that will increase the myocardial work, right? So again, you are overworking and already depleted myocardial, right? That's why those compensatory mechanisms they help, transiently, but over time, they will cause the hearts to fail even more on an at an accelerated rate, right? So again, I know you may be like, wow, divine, you're spending like 15 minutes just on battlefields, but again, I'm telling you, if you understand what I'm talking about, if you're understanding these reigning changes and all that stuff, then a lot of what I'm going to try to explain to you, as time goes on in terms of treatment and all that stuff will make perfect sense in your head. And again, heart failure, again, it's just one of these things, there's almost no discipline that you're getting to where you will not deal with heart failure, right? And there's almost no endemic exam, like step one or step two, see, step three, that you'll take where you would not have to understand heart failure, right?

So you might as well just go ahead and learn, learn these things right away, right? So again, systolic heart failure, again, is what people call heifer if, right? Heart failure will reduce ejection fraction, right? Typically you see these are people that have ejection fractions, less than 40 percent, right? For presents, EF is less than 40 percent, right? Those people are said to have heart failure with reduced ejection fraction, right? Again, the heart is not contracting, right? So because you're not contracting well, right? Your stroke volume goes down, so your credit couple goes down. Remember, your credit output is your heart rate times your stroke volume, right? Your heart rate times your stroke volume, right? And again, typically these people, they'll tell you that, oh, they have like a displaced PMI, a displaced point of maximal impulse. Remember, your point of maximal impulse is in the fifth intercostal space in the mechlavicular line, right? But when a person has like dilution of the heart, remember, this heifer causes a diluted cardiomyopathy, right? Now, move the person's PMI, the point of maximal impulse to like, your movie lateral, you'll take it more towards the axel, right? And these people already, if you haven't, again, like I said, you'll have an history heart sound. One other thing you may see here is that these people may also have like this thing called like an increased cardiothoracic ratio, right?

So remember, normally if you're looking at a chest x-ray, the ratio of the size of the heart to the size of the entire thoracic cavity, right? It should be about 50 percent, like the width, width of the heart, right? Like if you're looking at a like a PA radiograph, right? The width of the heart to the width of the entire thoracic cavity, the ratio should be like 50 percent or less, right? But again, if a person has diluted cardiomyopathy of more than 50 percent, right? More than 50 percent. And again, what are the things that cause this heart failure reduction fraction? Many things, right? For a person who has like a skinny heart failure, right? Like from an MI, right? Chronoid artery disease, they're like that again, we give rise to here for it, right? And also remember, for a person who has alcohol, it's a big time chronic alcoholic rate. There's such a thing as alcoholic cardiomyopathy, right? For a person who has myocarditis, remember myocarditis can, because by infectious causes like the coxache B virus, right? Remember, that's the most common cause of viral myocarditis, but it can also be caused by non-infectious causes, really, especially drugs, right? Like doxorobecin, donor-rebecin, those things can cause myocarditis, which can give us a diluted cardiomyopathy. Just doziuma, right? It can cause a reversible diluted cardiomyopathy, right? Unlike doxorobecin that causes an irreversible cardiomyopathy, right?

Remember, clasapin, clasapin is also one of those nasty drugs, right? Remember, use it as an anti-psychotic, it's the most powerful anti-psychotic, it's the one that has the most effectiveness, actually decreases the presence of suicide risk and schizophrenia, right? But again, don't forget, right? It's associated with myocarditis, which can ultimately give us a diluted cardiomyopathy, right? So again, just things to keep in mind, right? For example, right? And then there is also heart failure preserved ejection fraction. Again, this is the dastolic heart failure, right? That I've talked about again, these people who have like a very stiff leventricle, right? And the thing is the prognosis, right? For people that have here free for here's a fifth, if the one is pretty much the same, right? But again, don't forget, these people have an increased, they'll have an S-for-heart sound, right? And you'll have a normal heart size on a chest X-ray, right? That's a key unique difference, right? So they will maintain that 50% or less cardiothoracic ratio, right? And again, the things that cause this, again, for the most part, right? Again, hypertension, really by the orthostinosis, hypertrophy cardiomyopathy, right? When a person has like some kind of restrictive cardiomyopathy from like, I'm a lawyer or whatever, right? Those things all give rise to, those things all give rise to a hip hip, right? Again, dastolic heart failure, heart failure preserved ejection fraction, right?

And then one thing I also want to mention here is a high-opored heart failure, right? So high-opored heart failure, remember, basically, let me set up a construct for this, right? Let me set up a construct for this, right? So let's say, I'm telling you this, let's say you're working, you know, let's say, initially you're working eight hours a day, right? You know, great life, eight hours a day, five days a week, not a big deal, right? And then, let's say you then, you know, go up in medicine, right? Let's even come like a resident, for example, right? And let's see, start working 12-hour a day, 60s a week, right? That's 72 hours a week. Raise you out, you're really tired, right? I mean, like, I feel like most times when residents sleep, the asleep is almost always great. They fall asleep easily, right? I don't know if there's a scientific proof behind this. I'm just making this up so this is a joke, right? But I imagine that it's probably like decreased REM sleep lead, and see when the president becomes a resident, right? This goes straight to like sleep, and they're gone, right? But then let's assume, you know, you're a kind of resident that is in a kind of residency where you work really, really hard, right? Again, I'm not going to mention any specifics here. I don't want to get in trouble. But let's say you're working 15-hour days, six days a week, or seven days a week, right? You're putting in 100 hours, right? Again, that's causing injury to your body, right?

That's causing injury to your body. Those people have no reserve, right? Those people have no reserve. And again, you can maintain such elevated hours for prolonged periods of time, but one time the president will get sick, the president's body will crap out, and they won't be able to give anything anymore, right? That's pretty much the kind of thing. If you notice, you are getting more and more injury to your life, right? As you work longer and longer and longer and longer hours with no breaks in between, right? You begin to make mistakes and all that badness, right? That's the same thing with the heart, right? That's the same thing with the heart. The heart, if you keep putting a person under increased load, increased load, like the president's heart on the increased load, right? So say, for example, like people, let me say, I tell you, oh, you know, let's say, say, oh, I'm going to make sure you work out 22 hours every day, right? If a person is working out like an hour every day, that helps your cardiac function. That's good. You know, your cardiac output has to go up, you know, for a short period of time, like a one-up period during the day, right? But, for example, right? A person is working out 22 hours every single day, right? That chronically increased cardiac output, again, the heart is a muscle. After a while, the heart will get tired, the heart will crap out, and the heart will feel, right? The heart will feel.

Again, you cannot maintain peak performance, like that for your heart for a prolonged period of time, right? That's why when people leave on the conditions of like stress, right? The heart is always high, right? And they always have this fight-of-flight response all the time, right? That causes a chronicly elevated cardiac output, right? Again, those people can ultimately down the line after many, many years, they can develop heart failure, right? So the thing that causes high-up or heart failure, right? Again, basically, this person has chronically increased cardiac output, right? That is the common final pathway, right? So you may ask yourself, okay, define what are the things that cause a chronically cardiac output? Well, many things, right? For a person has anemia, right? For a person's hemoglobin is really low, right? The body is like, I need oxygen, I need oxygen, right? So your heart is like, okay, okay, okay. I will increase my heart rate so that the blood can make more rounds through the body again. That will chronically stress out the heart and that overtime the heart will fail, right? Or if a person, I mean, that's really high-up or heart failure is literally the mechanism behind Hydro-Sphytalis. When a person has like, breakdown of the heart, say for example, like, I mean, like a hemoglobin apathy, right? Like if a person has like, or maybe wouldn't bring it closer to home like a parable-be-nineteen infection, right? In uterus, right?

Or like an autoimmune hemolysis from like, arachink compatibility, those kids have profound anemia, right? Ultimately, that will give rise to high-up or heart failure. When the person's heart goes into failure, right? Then, fluid will back up all around the body, right? That's why it's called Hydro-Sphytalis, right? It's happening to the fetus and the fetus is hydropic, right? Because of fluid collection around the body, right? If a person has like a thymine deficiency, right? Like a vitamin B1 deficiency, right? That's what's called like berry berry. Remember, this is something that I'm finding in a person that has a wernicic or soca of syndrome, right? If you have a thymine deficiency, again, think about it, many pathways in your body do not work, right? Like your pyruvate, your hydrogen is complex, it's not going to work, right? Remember that requires thymine, right? Or your pentoschol-sphyt pathway, especially the nonoxidative phase with transkylolids, that's not going to work, right? So basically, people that have these problems, right? People that have a thymine deficiency, they have like impaired ATP generation, right? If a person has impaired ATP generation, right? Then the heart is not having enough ATP to work with, right? So it's almost like the heart is running on reserve all the time. Again, that's going to stress out the heart. If the heart is subjected to that chronic stress, again, the heart is a muscle after a while, it'll be like, okay, I'm done, right?

And again, the person going to have a poor heart failure, right? Or if a person has like hyperthyroidism, remember thyroid hormone increases the production of beta one receptor, I mean the insertion of beta one receptors, right? When the surface of a myocardial cells, right? If you put more beta one receptors, you'll be more responsive to your sympathetic nervous system, right? So your heart will go up, your strobe will go up, your cardiac output will go up, right? Again, that chronicly elevated cardiac output right again will lead to again, higher-putter heart failure, right? If a person has a patched disease, right? Again, remember when people have patched disease, their bone marrow becomes super vascular, right? So let's say again, normally the heart is supposed to pump up to like a million blood vessels, I'm just making numbers up here, but because a person has patched disease, their bone marrow becomes hypervascular, right? And now the heart needs to support 5 million blood vessels, right? Again, that obviously is increased workload on the heart. If there is increased workload on the heart, right? Again, the heart will try, try, try, try, try, try, try, put over time, right? The heart yes is working at higher output, at higher output, at higher output, at higher output, but again, the heart is a muscle over time, that heart will crop out and fail, right? Or if a person has a fisture or a fistula creating disease, right? So for example, right?

Like if you notice, people that are placed on dialysis newly, right? Those people need to watch them initially, right? Because again, they can go into higher, they can go into higher output heart failure, because again, remember the normal order of event in the body is that an arterial leads to a capillary, blood slows down in that capillary so they can have gas and nitrate exchange and then it will go to a venue. But if that capillary is scrubbed out of the equation, right? Because you have a direct conduit between an artery and a vein, right? Like an avi fistula, right? Then that slow down mechanism in the capillaries is gone. So blood is just zipping from battery to vein. The heart will be like, wait, I thought I sent this blood out like a second ago, how does blood get back here so quickly, right? Again, the heart will be chronically stressed, and when the heart is chronically stressed, that will ultimately again give rise to a higher output heart failure, right? So what are some other things that create a vifistula? The person has trauma, right? For person he's stabbed or something, right? Again, if a person has like an arterial puncture procedure, let's say a person gets like a has an MRI and you're trying to do like a cardiac cathode, whatever, right? You're going to puncture the femoral arteries in that patient, right? Again, sometimes that can ultimately give rise to the formation of an avi fistula, right?

Or if for some reason a person has like a oslaway boron to disease, right? Again, remember that disease is called a hereditary hemorrhagic telogenjectasia, right? Those people form a lot of avi-malfornations, right? I mean, what do you think those telogenjectages are? Those are examples of avi-malfornations, and those people have big enough av Ms. Again, that can give rise to a higher output heart failure, right? Or remember, people that have like kidney disease, people that have liver disease, whenever people have these organ diseases, the body responds by forming all these avi-fistula, right? Forming all these avi-fistula to do with all those increased pressures, because fluid is not being dealt with appropriately in the body, right? Again, all those avi-fistula can ultimately give rise to a higher output heart failure, right? So again, just again, all big things you want to keep at the back of your mind on examples, right? Now, in terms of heart failure, right? So again, the MBMID allows some of these epidemiological questions, right? Like, what's the most common cause of heart failure? It's actually coronary artery disease, right? The biggest risk factor for heart failure, I'll tell you right now, right? The biggest risk factor for heart failure is coronary artery disease, right? It is the most common cause of heart failure, right? It is the most common cause of heart failure, right? The second most common cause is hypertension, right?

And again, I've talked about many of the things that can cause heart failure, right? Now, remember earlier, I talked about how you can grade heart failure by ejection fraction, right? But there is this thing called the New York Heart Association like classification for heart failure. It's more of a classification based on function of the patient, right? So say, for example, like this person, you know, can undergo like no physical activity, doesn't bog them at all, right? That's class one heart failure. That's my heart class one heart failure, right? Class two heart failure is a person that is completely fine at rest, but you know, when you do like just a little physical activity or you begin to have symptoms, right? That's class two. That's my heart class two heart failure. That's New York Heart Association, right? I'll call it my heart from now, right? And then if a person has like, if a person like requires just very tiny physical activity, boom, and they start having symptoms, right? And you know, they're basically not able to do most physical activities. Think about a class three heart failure, right? So usually this is one people struggle with, right? So class two versus class three again, people that have class two or class three heart failure, they're going to have problems with physical activity at rest. They are completely fine, right? But roughly, at least I'll say for purposes of NV Me exams, right?

But the thing is, the thing that triggers the symptoms is different. People that have class two, uh, nine heart class two heart failure, right? Regular physical activity will precipitate symptoms, right? But people that have nine heart class three heart failure, just a major of activity, right? Almost think of it as you sneeze and boom, you start having heart failure symptoms, just very minimal activity, very minimal activity causes symptoms, right? And then class people that have nine heart class four, these people do have like anything, anything, they basically cannot carry out any physical activity without, you know, feeling uncomfortable. And also when they are at rest, they have heart failure symptoms, that's nine heart class four, right? That's nine heart class four heart failure, right? Now, remember, uh, when a person has heart failure, right? Like, again, like if you're trying to let's say a person comes in for the first time and they've never been diagnosed with heart failure before and they have in symptoms, right? You know, you can check the BMP. And again, where does this whole BMP business come from again? My goal with this podcast is after you listen to this, you feel like, wow, I really understand heart failure. Like, I really, really understand heart failure, right? So, um, uh, so what, what would, what would, what would those this elevated BMP business come from? Well, the elevated BMP business believe it or not, right?

Think about when a person's heart fails, right? Fluid is going to back up in the person's ventricle, so in the person's etra. So the body will be like, okay, um, I gotta find a way to get rid of this extra volume, right? So the body actually produces some natural diuretics, right? It so happens that they are called it and they are produced by the ventricles. So ventricles and the etra will make sense, right? That the etra and the ventricle should be used by the body as a sensor, right? Of a person's fluid status, right? So if the person has heart failure and the ventricles are dilated, the etra dilated will flow it because of the fluid backup, right? It would make sense that the etra and ventricles should be able to produce hormones, right? Like AMP and BMP, right? That cause you to essentially peel out more, right? That causes a, they have a natural redic effect, right? So remember, AMP stands for etra and natural redic peptide and BMP stands for brain derived natural redic peptide, but again, it's from the ventricles basically, right? So these peptides, right? They cause a person, they have a natural redic effect, they basically try to get rid of volume from your body, especially through the kidneys, right? And one tip bit I'll throw in here is that these things, AMP, BMP, right? Obviously for a person is having like heart failure exacerbation, a ton of like fluid on board, you want these things to be around, right?

Because again, they essentially like the body is, is almost like human leasex, right? Naturally, they're like leasex, it's made in the body, right? So you want these things to persist and guess what? There is an enzyme known as neprilysin, neprilysin actually breaks down this etra and natural redic peptide and BMP, right? So obviously for a person who has heart failure, you don't want neprilysin to be working because if neprilysin is not working, then AMP and BMP will persist, that will help you get rid of fluid and that will improve your symptoms, right? Again, I'm setting you up for the pharmacological therapies we're going to be going into in a bit, right? So that again, you can truly understand the heart failure, right? Again, I know this podcast will be on the long range of things and again, I apologize, but again, just really try to follow along, really, really try to follow along. If you follow along and you understand what I'm talking about, right? You'll be in a, you'll be in a really, really good shape, you'll be in a really good shape, you'll be in a really good shape after all, after all is a set and a, okay? So how do we treat a person that has a CHF exacerbation, right? Especially when they have like really bad point of redeem, right? The first thing you want to do, there's a nice to money you can remember, right? LMNOP, right? LMNOP. So what does the ELSTAN for, right? The ELSTAN for leasex, right? That's pure summary. If those people are diuretic, right?

If these people are diuretic, you give an IV diuretic, right? Again, remember diuretic, especially if you're a summary, those are loop diuretics. Remember, those things can trigger them through the thiocese, right? Because remember, loops lose calcium, right? Remember, loop diuretics can also cause a sensory neuro here in loss, an MDM exam, right? And they can trigger it down attack, right? So remember, these loop diuretics, right? Again, they work at the level of the thickest sendent lamp of the loop of hell, right? That's what they call loop diuretics, right? They inhibit that sodium potassium-tucloride-symporter, right? That brings in sodium-tucloride ions into the thickest sendent lamp of the loop of hell, right? Remember, when a person is taking a loop diuretic, it's almost like a person essentially having a batter syndrome, right? Having like batter syndrome, remember, batter syndrome is an autosomal recessive disease, right? And then the M stands for morphine, right? The M stands for morphine. Remember, morphine, you know, make those people less anxious because it's a little short of breath, right? So, you know, they're kind of anxious, right? But the thing is, morphine can help, right? It can help with that anxiety. And again, morphine also has some vino-dialidin activity, right? It can actually dilute venus, right? So that would decrease preload somewhat, right? And then the N stands for nitroglycerin, right?

You can give the nitroglycerin in many different formulations, right? But again, you want to be careful, though, the person that has a preload dependence, right? So like, if a person has like right heart failure, as the cause of their heart failure, right? Don't give those people a nitrate, right? Again, those people need their preload like nothing, right? So if you really crush those people's preload, those people can get in big trouble really fast, right? They can get in big trouble really, really fast, big trouble really, really fast, right? So, if a person has like a right-sided M, I remember those people have like an ST elevation, like it's two, three, an AVF, right? Again, those people don't give them a nitrate, right? Again, nitrates, many people erroneously think on MBM exams that those things cause coronary viso-dilation and that's how they help. No, no, no, that's not how they help. The way they help is that the cause of inodilation, so that would decrease preload. If you decrease preload, then the heart will not need to work as much. It's almost like you're offloading some weight from the heart, right? And the thing is these nitrates, they also pretty awesome in the sense that they essentially help you pull the fluid in the legs and not in the lungs, right? Fluid when you pull in the lungs, that's going to kill the person. When you pull in the legs, it's not going to kill the person. It's just more of a cosmetic issue.

It's just more of a minor annoyance kind of deal. And one thing I guess I want to highlight here is that whenever a person has pulmonary demon, right? In the setting of heart failure, that'll be associated with an elevated pulmonary capillary wedge pressure, right? That'll be associated with an elevated PCWP. Remember, PCWP is a sore gate for the left-eatural pressure, right? So those people's pulmonary capillary wedge pressures will be more than 18. That's the magic number you want to remember in exams. It'll be more than 18. That's how you differentiate a cardiogenic cause of pulmonary demonetema, like heart failure, from a non-cardiogenic cause of pulmonary demonetema, like ARDS, right? In the case of ARDS, the pulmonary capillary wedge pressure will be less than 18, right? It'll be less than 18, right? Okay, so LNOP, right? So set L is L6, M is morphine, N is nitrates, right? Nitrogen is serene, O is oxygen, right? If a person's O2 sets her low, right? Go ahead and give them a weight and give them oxygen, right? And then P stands for positive early pressure, right? Positive early pressure, right? So you can use C-PAPO-BIPAP, right? So you need to be like divine. Now, those C-PAPO-BIPAP help in heart failure. Believe it or not, it actually helps. I have absolutely used it a couple of times in heart failure patients have treated. Basically, the thing that happens with C-PAPAP-BIPAP is that essentially in the sense make intra-thoracic pressures really high.

If you're making intra-thoracic pressures really high, that's going to kill preload, right? And if your preload goes down, then the heart does not need to work as hard, right? So those C-PAP-BIPAP, the primary mechanism behind the utility in the treatment of an acute C-HF exacerbation is because they crush preload, right? They crush preload, right? That's why it's called C-PAP, continuous positive early pressure or BIPAP, something positive early pressure, right? So those things again, ultimately crush a preload, that would decrease the myocardial oxygen demand, that would decrease the myocardial workload and that would help. In fact, many times when people go on C-PAP-BIPAP, that actually prevents you from having to inter-beat those people, right? But obviously, if you try those things and it's not working, you're going to tube those people, right? And then remember the P, right? Let's say P means two things, also means positioning, right? Obviously, that patient is not going to be sitting back, right? That's kind of asking for that at that point, right? So you're going to see that patient upwards, right? So that they don't get in trouble, right? Okay. And what are some things we can use again, acutely? Notice I'm not seeing chronic management, I'll talk about chronic management of heart failure in a bit, right? But in terms of acute management of heart failure, right? So again, what are some things you can use from Acrologic to treat these people?

Well, don't forget your simple mathematics, right? You can use a debitamin, remember, debitamin is a beta one agonist, right? So because it's a beta one agonist, right? You'll act on the beta one receptors, right? And that will ultimately cause your heart failure to increase, right? Because there's more, there's increased speed of conduction down your EV node, right? And then that will also cause your cardiac output to increase, because again, you are contracting better, right? So it's a positive vinyl drop, right? It's a positive vinyl drop, it's a positive vinyl drop. And then don't forget, you can also use dopamine as well, right? Remember, dopamine works at different doses, right? So when the patient has like low dose dopamine, right? That'll activate those D1 receptors, right? That's the thing that causes like the dilation of the renal vessels, right? And then at medium dose, this is the dose you essentially want to target, right? That's why you don't give unlimited doses of dopamine when the patient has heart failure, right? You give the medium dose, the medium dose dopamine acts on beta one receptors, right? So that'll give you that positive nitropeca support, right? High dose is not what you want, right? Because remember, high doses, right? Dopamine is an alpha one again is that high doses, right? And at those high doses, that will increase your system evascular resistance. That's going to make your heart work even harder, right?

Because it's having to contract against the increased resistance, right? That's why really if you're the kind of person that likes physiology, you really should consider specialties like ICU, right? For example, right? Consider being an intensivist, right? Because like there are many times people just do things in medicine, they don't think about it. They're like, oh, this algorithm says do X, Y, Z, right? But don't think about it. There are sometimes when a person is hypoxic and giving an oxygen is not the right thing to do is not every time that you treat hypoxia with oxygen, right? Especially in pediatrics is not every cause of hypoxia that's treated with oxygen, right? But that's beyond the scope of what I want to discuss today. So let me go ahead and get back on topic, right? So, you know, you can use that obviously, right? And then don't forget you can also use merino, right? Merino is a phosphodacere is inhibitor, right? So phosphodacere is inhibitor, right? So remember, phosphodistory is, right? It inhibits the breakdown of cyclic AMP, right? And also, if a person takes merino, the cyclic AMP will go up. And maybe if I could define how those this help? Well, the thing is when cyclic AMP is elevated in myocardial cells, that actually causes an increasing contractility, right? It mixes myocardial cells contract better, right? But when cyclic AMP is elevated in smoke muscle, it actually makes those smoke muscle cells relax. So guess what? Merino is amazing, right?

Because merino increases your cardiac contractility, right? But in your blood vessels, it actually causes those smoke muscles to relax. It actually causes visual dilation. So guess what? It actually decreases your systemic vascular resistance, right? So if you really want to take this to a logical end, which again, occasionally we see a new world, we see an MDM exams, merino by being a positive vinyl trope, right? It increases your cardiac output, right? So that's going to increase your systole blood pressure, right? But by being something that causes a decrease in your systemic vascular resistance, right? It's causing a visual dilation, right? So that's actually decreasing your systole blood pressure, right? So your SDP is going up and your DPP is going down on merino, right? So ultimately, merino widen your pulse pressure, right? Merino widen your pulse pressure. Just one again, one of those weird, bizarre things that you see tested on an MDM exam. And hopefully you won't get it wrong because you've, you know, listened to those podcasts, right? And then what are some other things that you can use for pressing the heart failure, right? Again, especially at QT where you've tried all this medical therapies, nothing is working, right? You can use something called an intra-yodic balloon pump, right? An intra-yodic balloon pump, right? An intra-yodic balloon pump. So how does an intra-yodic balloon pump work?

Well, if you think about it, basically the way this pump works is, so how do you, how does this work? Right? Again, it sounds like a big word, but it's very easy to understand. Just follow me here. It's so, and again, on these newer MDM exams, these are not things that will be surprised, if you, you know, pop up on the test, right? And again, it's also useful to know clinically, right? Especially if you're doing an ICU rotation, even as a resident in the future, you absolutely need to know how intra-yodic balloon pumps work. Again, I've worked with patients that have needed intra-yodic balloon pumps. I don't know, even during my cardiac surgery rotation at Hopkins, right? We absolutely have to use a balloon pumps and a few folks. Okay, so how does this work? So basically, you know, you puncture the femoral artery, you insert into the femoral artery, you thread it all the way through the femoral artery, right? So the descending ear, right? It's a balloon, right? So the thing is the balloon works in a weird way, right? The thing is the balloon inflates when the heart is undergoing the astral. Remember, during the astral, the primary priority of your heart is to feel with blood, but also to produce the coronary arteries. Remember, the coronary arteries are profused in the astral. Right? So the thing is the intra-yodic balloon pump actually inflates in the descending ear during the astral. So think about that. How will that help? If it inflates during the astral, right?

That will almost create like pressures, that will, because it's inflating, right? So it's literally occluding the lumen of the ear of the descending ear that will cause blood to back up into the ascending ear, right? And remember that the coronary arteries come up, come up, uh, like, uh, an annulus, right? In the ascending ear order, right? So those coronary arteries, right? Like because there's this backup of blood, because the balloon pump is descended, right? That will actually force more blood through the coronary arteries, right? So industrially, that will actually help the coronary vessels to be better profused. But guess what? Incistally, that balloon, that balloon deflates. So when it deflates, it almost creates like almost like a negative pressure in the descending ear order, right? So that will actually make it easier for blood to leave the heart, right? Because it's almost like you've created this pent-up suction effect, right? It's almost like you then pop up the balloon. When you pop up the balloon, right? It's like, everything just peters out, right? So that makes it easier for blood to leave the heart, right? So that actually increases the presence of cardiac output, right? So intralerial balloon pumps ultimately, right? They help with reducing afternoon insulin, right? An increasing coronary profusion, industrially, right? Again, it's kind of high up to now. Again, you don't need to know it in like crazy amounts of detail, right?

But if you kind of understand these basics I've explained, if you see a balloon pump question on your test, you're going to get it right. I'm telling you that right now, right? And then obviously you can also use like assist devices like an L-vat or an R-vat or a By-vat or whatever, right? Basically, those ventricular assist devices, essentially what they help you do is that they they take blood from the ventricle, right? So it's almost like you're taking over the function. That's why they are called ventricular assist devices. They take over the function of the ventricle, right? So the thing that happens is they essentially are things that sit in the ventricle and they suck the blood that's coming from the atrium, right? They suck the blood coming from the atrium, they pump those things, right? And there's tubing that connects it to outside the heart. So you're essentially taking over the function of the ventricle, right? Those things again can be inserted in a QT and a person that has like really bad heart failure, you've tried all the medical therapies you know and they're not doing very well, right? Although there's also used other uses for R-vats or L-vats or whatever, and we can always talk about that in a different podcast. Let's keep going here, right? So this is how you manage heart failure QT, right? This is how you manage heart failure a QT, right? So now, how do we manage heart failure chronicly, right? How do we manage heart failure a chronicly, right?

Now one thing you may see on MBME exams, especially with these again newer exams that have these health systems questions, right? One thing that actually really does help in a person that has heart failure is cardiac rehab, right? Cardiac rehab. Cardiac rehab is almost like a structured SSI program, right? When a person is like part of a heart failure clinic, right? And you know, they just undergo like different physical activities that you know, kind of helps them adapt to their reduced heart function. Again, it doesn't improve survival, but it absolutely helps, right? It absolutely helps. It increases the patient's quality of life. Again, those weird bizarre things, you may see, let me see on MBME exams, right? So let's see a person has heart failure right? Chronicly, you want to manage these people, chronically, you want to manage these people. Well, what are some things you want to do? Right? So what are the initial drugs that a person that has heart failure needs to be started on? What are some things they need to be started on? One thing I'll say is these drugs are things that are used to treat people that have hay frif. Heart failure reduce the ejection fraction, right? So whenever you hear the term, oh, this drug improves survival, bloody, bloody, bloody blood in a person that has heart failure, it's for hay frif. It's not for hay frif, right? People that have that study card failure or heart failure will preserve the ejection fraction.

There are no pharmacologic therapies that are being shown to improve survival at all or reduce mortality to anything, right? So all these drugs I'm talking about are for hay frif. People that have hay frif, you just basically control their risk factors, right? So say, for example, if they have hypertension as the thing that precipitated their hay frif, give them an anti-hypertensive, right? But again, these drugs that I'm going to talk about are for hay frif. They would have heart failure. We reduced ejection fraction, right? We reduced ejection fraction, right? So how do we manage heart failure, right? So again, what are the drugs you absolutely need to put these people on first, right? These are drugs that if they've been diagnosed with heart failure, right? You want to put them on these drugs first and foremost, above all else, right? The first thing, and again, if you understand the pathophys that I spend like 15, 20 minutes describing in the beginning, then all these drugs will make perfect sense to you. We don't have to think too hard about these things, right? And what is the first group of drugs you want to study people on usually? You want to study them on an EC inhibitor on ARB, right? You want to study them on an EC inhibitor on ARB, right? Again, why would these things work? Remember, I said when a person goes into heart failure, the arena and your tensile industrial system is kicked into high gear, right?

And again, you know, those things try to compensate, but that compensation will actually accelerate the failure of the person's heart. And also, and you're tensing too, and our dose theorem, those things actually cause remodeling of the heart. You actually need to be a big, big role in the remodeling of the heart, right? So you're trying to basically block all those mechanisms by giving a person an EC inhibitor on ARB, right? So every patient that has heart failure needs to be on an EC inhibitor, right? But if an EC inhibitor for some reason, we can't take it because they have like hereditia, and geridima, or they have like some big time contraindication to an EC inhibitor, like, you know, like really, really bad cough or whatever, right? They can put those people on an ARB, right? You can put those people on an ARB. Now, one key classic thing, one of the memories that these ACE inhibitors, these AR Bs, they can cause an increasing creatinine, right? They can cause hyperchalemia. Those are the classic side effects that you tend to throw an MBIM exams, like you want to be aware, right? You want to be aware of those things on MBIM exams, right? And these ACE inhibitors, AR Bs, they actually improve survival. This is Florida, Ohio, to know. They actually improve survival in heart failure. Now, there is a drug class that looks just like these ACE inhibitors, AR Bs, and they actually improve survival in heart failure. They are known as ARNI, right? They are known as ARN Is.

Basically, it's a combination of an ARB of an anandotensing to receptor blocker with an neprilizing inhibitor, right? Again, I've explained what neprilizing does. Neprilizing brings down AMPMBMP. So if you inhibit neprilizing, your AMPMBMP will go up, right? And that will cause a dyritic effect, right? It's almost like, again, like, you're trying to increase the amount of dyritic in your body, right? That's what neprilizing does, right? So you give a neprilizing inhibitor, right? So this combination of drugs, like I'm sure you've probably heard of this drug, a known as Intresto, right? Intresto. That's the treatment. The drug is known as a combination of our Sartan. That's an ARB, right? Remember those AR Bs ending Sartan, right? So it's a combination of our Sartan and Sakubi trail. Sakubi trail is a neprilizing inhibitor. These drugs, these fluoridly hyalutrono, especially for the newer AMPM exams, these ARN Is have actually been shown to improve survival in heart failure. There's deep don't tons and tons and tons of trials that are shown these drugs to actually improve survival in heart failure, right? So we've talked about ACE inhibitors, AR Bs. We've talked about the ARN Is, right? Although those ARN Is, you only use them when people have tried ACE inhibitors or whatever they've tried, whatever and it's not working, right? So, but just remember that the actually improved survival, you need to know that for your USML exams are sure, 100%.

Now your beta blockers, beta blockers are the next group, beta blockers, again, remember if you give a beta blocker, especially like the Tuper Law or Carvelli Law, or the Super Law, these drugs, again, they'll decrease that sympathetic overdrive that is observed as a compensatory mechanism in the pressing that has heart failure. That will decrease that remodeling of the heart and again, that will ultimately help the person, right? So, although one thing I'll say with these beta blockers, again, don't give them to a person that has like an acute decomposition of heart failure, right? But again, you use them as chronic management, as chronic therapy, right? As chronic therapy, as chronic therapy. And then in heart failure, you can also use diuretics, right? I mean, usually people that have heart failure, they're going to be giving diuretics to take home with them, but these diuretics actually do not increase survival, they do not improve survival, they just make a pressing symptoms feel better, right? But they do not improve survival, right? And one of the reasons that people get these diuretics is that these diuretics actually help, right? Because they cause hypochylemia as a side effect, right? So, that almost counterbalances the hyperchylemia that you find with many of these heart failure drugs, right? Like your ACE inhibitors cause hyperchylemia, your AR Bs cause hyperchylemia, beta blockers, right? They also cause hyperchylemia, right?

The aldosterone antagonists I'll talk about in a bit, they cause hyperchylemia. The joxin causes hyperchylemia, right? So all these drugs, they cause hyperchylemia as a side effect, right? So, diuretics almost try to counterbalance that with the hyperchylemia that they cause. Again, maybe like divine, why do you keep emphasizing this potassium? You think I'll be emphasizing it if it's not something that your friends at the MBM love to test. Think again, I promise you, these things are like most of the things I'm seeing in this podcast, they are floridly high, you know, for example, I'm sure. If you've done enough MBM exams, if you've treated enough people like I have, you'll know that these things are things that show up time and time again on MBM exams. So again, I absolutely encourage you, make sure you know this stuff and know it pretty well for exams, right? So these diuretics, right? Again, usually if you're somebody that's like the go-to drug, right? You know, sometimes they use me tola zone, right? But again, these things, they help pretty well in a person that has heart failure, but again, remember, they do not improve survival at all. They just help with symptomatic management, right? And then the next set of drugs I'll talk about, right? Again, don't forget you are a dose-term receptor antagonist, right? These things block the mineralocodicoida receptor, the out dose-term receptor, right? So these are drugs like Spirino lactone, right? And a Plierino, right?

Remember, the big defense is transparent lactone and a Plierino is, yes, they both block out dose-term receptors, but Spirino lactone also blocks Androgen receptors, right? So Spirino lactone can cause gynecomastia, a Plierino does not block Androgen receptors, so it does not cause gynecomastia, right? But again, before a person is placed on these out dose-term receptor antagonists, make sure you read the question carefully. They must have already been placed on an isine inhibitor, on ERB plus a beta blocker, plus a diuretic. Before you start them on these out dose-term antagonists, you basically must have taken all those other drugs before you are then placed on an out dose-term antagonist. That's again, super high up to no, for example, right? And again, remember, these drugs, they can cause renal failure, right? They can cause hyperchilemia, right? And again, they do improve survival in a person that has a heart failure, right? They do improve survival in a person that has heart failure, right? Another drug that's classically used in heart failure on the example, right, is the juxtaposition, right? The juxtaposition is used in a heart failure. Again, it improves symptoms, but it does not improve mortality at all. It literally does not improve mortality at all, right? It improves your symptoms, it makes you get hospitalized less, but it does no effect on mortality in a person that has a heart failure, right? And how does the juxtaposition work?

Remember the juxtaposition, right? It inhibits the sodium potassium ATP is pump, right? It inhibits the sodium potassium ATP is pump. Now, let me tell you something about the juxtaposition. For the juxtaposition to inhibit the sodium potassium ATP is pump, it actually binds to a potassium site on that pump, right? I'll say that again, it binds to a potassium site on that pump, right? It binds to a potassium site on that pump. This is why when people have, when people have hypochylemia, they are pretty exposed to getting more ditch toxicity because the juxtaposition combines to more sodium potassium ATP is pumped, right? So hypochylemia predisposes a person to the juxtaposition toxicity, right? From again, the juxtaposition juxtaposition is accumulated, right? But and make sure, pay attention here. Again, I know, I promise this podcast is going to be ending very soon, right? But if you don't understand this, there are some NV Me questions you will get wrong. The NV Me recognizes that people don't think this deep on this stuff, right? So the occasion is throwing all these like, V questions you try to mess with your head, right? When you're hypochylemic, the juxtaposition will binds to more sodium potassium ATP is pumps. Now, we're seeing a risk of ditch toxicity, right? So think about it, right? What are the people that get hypochylemic? People that take diuretics, I don't know like people that guess what?

That are treated for heart failure because diuretics cause hypochylemia, right? So you can imagine that again, you may see a person having like mental status changes, abdominal problems, right? Changes in the vision, right? Taki, they're having like all these heart problems, all these arrhythmias, right? And you notice that, this person is being treated for heart failure. Again, check the potassium levels, right? That hypochylemia may be predisposing them to be coming in a ditch toxic and remember, Dage, right? Again, works by inhibiting that sodium potassium ATP is pump, right? So hypochylemia predisposes you to ditch toxicity. But one thing that happens with ditch as a side effect of ditch itself, of dejuoxing itself is hyperchylemia. Dejuoxing can cause hyperchylemia. How does that happen? Remember, dejuoxing inhibits the sodium potassium ATP is pump. If you block that pump, remember what does that pump do normally? That pump brings three sodiums out of the cell and takes two potassiums into the cell. When you block that pump, you will not be bringing potassiums into the cell, okay? And if you do not bring potassium into the cell, it will hang out outside the cell. So the person will have hyperchylemia, right? So again, gets these two potassium facts concerning dejuoxing straight, for ending exams. I've literally seen these tested on exams before. Again, this stuff is super high, you know. When you're a hypochylemic, you are pretty exposed to getting ditch toxicity.

When you are taking dejuoxing, you can get hypochylemia as a side effect, right? So dejuoxing can cause hyperchylemia as a side effect. And don't forget that ditch toxicity, right? You can treat it with those, it's called Digibind in the hospital, right? You can give those anti-gauge fib fragments, right? To treat dejuoxing toxicity, right? To treat dejuoxing toxicity. And one thing you should also know is that dejuoxing is actually a most chronic receptor agonist. So it actually slows conduction down the EV node. So usually when people have a taking gauge, they can get pretty cardio from the ditch, right? But one of the reasons I'm saying this, you may be like, okay, if I was the M&E association, I'd get a note here. If a person has WPW, you cannot give them dejuoxing. Do not pick dejuoxing as an answer, because it will slow conduction down the EV node. And guess what? They'll make those people symptoms even worse, right? They'll make the asymptoms even worse, right? Because it's almost like you're blocking the EV node because you're taking a most chronic receptor agonist, like dejuoxing. And you encourage them more flow of a current through the bundle of chemt, right? And again, that can make the person essentially get V-fib and that. You don't want that, right? That's not ideal, right? So any kind of WPW, you almost, you always, not almost always, you always treat WPW of any sort with any comorbidity. Even if they have a, a-fib, right?

We WPW on exam with Prokina Mide, right? And we're Prokina Mide is one of those class 1a and teridmix, right? It's a sodium channel blocker, right? It's a sodium channel blocker, right? And then one of the drugs you can use to treat heart failure. This is something that you especially see on step one, but again, if they want it to be mean and not very nice to people, they can throw this on step 2, see this step 3, right? It's definitely a drug that has popped up on exams, right? It's in first seed, right? Iverbrading, right? So Iverbrading is one of these drugs you can give to people, right? That have taken pretty much every drug you can use for heart failure and they're not getting better, right? You can give Iverbrading, right? You can give Iverbrading, right? So Iverbrading, basically what it does is that it inhibits those phony sodium channels, right? So if you remember, I brought from step 1, right? There's this thing called the piece-maker potential that happens in the heart, right? So there's a phase 4, there's a phase 0 and a phase 3. The phase 4 of that piece-maker potential, one of the things that causes those piece-makers, right? Like your essay, nodio, AV node, right? To start firing, right? It's an influx of sodium ions, right? So those sodium ions, right? Again, they can ultimately cause, you know, the heart to fire and all that stuff, right? Those essay notes to fire, right?

So the thing is those channels that make those those phony channels that bring in those sodium ions, you can plug them with Iverbrading. Iverbrading is spelled as IVA, B-R-A-D-I-N-E, right? Iverbrading, Iverbrading, right? So it blocks those phony channels, when you block those phony channels, right? Then you'll bring down the slope, you'll read, basically, right? You essentially like bring the persons, you slow down the rate of depolarization in phase 4 of the piece-maker of the piece-maker potential, right? So that's how Iverbrading, that's how Iverbrading works, right? And then one thing you want to remember is also like in African-Americans, right? So like isosobite nitrate and hydrolyzing, right? It's actually something that's been shown to improve survival in a patient that has an African-American, right? That have a heart failure, right? So hydrolyzing, right? Remember, it's a natural dilator, right? And then isosobite nitrate again, right? It's a good viso-dilator, especially like veins. It's very good at dilating veins, right? So again, in pro-survival, right? Now one weird, bizarre way, they may give you isosobite nitrate and hydrolyzing as an answer on a test. In a non-African-American, we'll be a person where the cannot tolerate is inhibitors or AR Bs for some reason as heart failure management. You can put those people on bideal. Again, bideal is the combination of hydrolyzing and isosobite nitrate, right?

And then one other thing that actually has been shown to, actually like these are non-medical therapies that have been shown to improve survival in heart failure, right? Remember, one key one is cardiac recircination therapy, right? So cardiac recircination therapy, right? So usually this is something you're using people that have like a reduced level of drug ejection fraction like less than 35 percent, right? But also one high-yield thing you want to know for pro-survival in the MBM exam is the ejection fraction, right? I mean the QRS, people that are giving cardiac recircination therapy essentially these people must have a QRS complex that is white. It must be more than 150 milliseconds, right? It must be more than 150 milliseconds, right? Those are the people that classically get cardiac recircination therapy on exams. Usually you do this in conjunction like a biventric lipis maker. Again, this absolutely improves survival in heart failure, right? And again, I'm going to summarize all the things that improve survival in heart failure like right after this, right? And then one other thing that also improves survival in heart failure right that has a mortality benefit is placing an ICD, right? Like like an implantable cardiac adfibrillator, right? And again, usually you're placing people that have like A Fs that are very low, like in the 30 percent, for example, or lower on an MBM exam.

And then obviously if you've tried all the medical therapies known to man, you've tried all these fancy devices, right? And none of it is working. And that person is going to need a cardiac transplant, right? That person is going to need a cardiac transplant. Again, I want to be thorough again. My apologies, those listening to this podcast sound like super super super sorry, right? But I don't know, I just want to be complete here because this stuff I want to talk about is actually kind of high yield to an overexample. So, I'm actually going to talk about our heart transplant, right? I'm going to talk about heart transplant. I'm going to talk about heart transplant, right? So this should not take too much time, right? But basically again, if you've tried everything, tried every device, it's no working, right? You're going to go ahead and transplant this transplant this individual, right? And the reason I want to talk about heart transplant is I feel like I can talk about some other transplant-related things that if you wonder that basically we would want to answer more questions, that are related to other kinds of transplants that are not even cardiac transplants. Although my goal, hopefully in the very near future is to make a podcast just on transplants, right? Just on transplants, just on transplants, right? So, you know, heart transplants again, if tried every therapy is no working, right?

Then, you know, those people need to, those people need to be giving heart transplants, right? Now, the thing with heart transplants is that what are some things that are contraindications for these transplants, right? And contraindications just to transplants in general of any type, right? For a person who has like a stage 4 cancer, right? Like a cancer that is incurable, you're not going to be transplanting those people, right? Or if those people have like a really bad systemic illness, right? Again, you're not going to be transplanting those people, right? Or if they have like an organ in the body that has failed, that is like not the organ that is being transplanted. That's also less it like they have like really, really bad kidney disease or like an stage liver disease, right? Those people cannot get heart transplants, right? And if a person also has like really bad pulmonary hypertension, again, they cannot get a heart transplant, right? If a person has really bad COPD, right? Let's say that the FIV one is like less than like a liter, right? Those people again cannot get heart transplants. And also if a person is like an addict, right? Like a big time drug addict or a big time alcoholic, right? You don't want to damage the heart rate giving those people, right? Those people are not going to be getting any kind of heart transplants, right? They're not going to be getting any kinds of heart transplants, right? So what are some bad things, right?

That can happen in a person that has a, they can have a heart transplant, right? Obviously you can you can reject the heart, right? You can reject the heart. The thing is whenever you see any signs of dysfunction of the heart after transplant and they're asking what is your next best-ipping diagnosis? You want to go ahead and perform something called an endomaiocardial biopsy, right? You want to go ahead and biopsy that heart. If you biopsy that heart, right? You can find out what kind of rejection they have so that you can basically treat it and treat it, treat it correctly, right? I want to go ahead and make sure you treat it correctly, right? And then, so you know, I remember, right? If they have rejection while you're transplanting the heart, right? That's hyperacute rejection, right? When you're printing out a hyperacute rejection, that's bad. You need to take out the organ, you just you've just tried to transplant, right? And look for a new organ, right? Acute rejection is any rejection that can happen like up until a year after you're going into transplanted organ. And then after a year of transplant, right? That's going to be a chronic, that's going to be chronic rejection, right? And if they give you a question and they say, oh, what's the most common cause of death, right? You know, like in the in the first year, right? After transplant, right?

Like, or in the first few weeks after transplant again, all these prognosis, risk factor, morbidity, mortality questions, those are things that they throw aggressively on these new hearing being exams, right? If you see stuff like that, right? You want to think about infection. Infection is actually the leading cause of morbidity, mortality, right? Just after a person gets a cardiac transplant, right? Because again, these people are profoundly immunosuppressed, right? But if they're asking you about like late, let's say like years after a transplant, like at least a year or more after a transplant, right? Especially a heart transplant. The most common cause of death, right? It's actually going to be from the aloe graph, right? Like the transplanted heart, having like vessel problems, right? Like vascular problems. Sometimes you may see it referred to as as a vasculopathy of the aloe graph, right? That's the most common cause of death years after a person gets a transplant, right? And then the second most common cause of death, again, pay attention to this. This is Florida, high or two. The second most common cause of death years after a person gets a transplant, especially a heart transplant is actually cancer, right? Because the thing is, remember, your immune system helps you deal with malignancy, right? So if whatever bizarre reason, right? The presence is on immunosuppression, right? Then you're basically wiping out those people's immune systems.

Those people tend to get a ton of cancers, right? In fact, the most common cancer that people that have like transplants, really heart transplants get is they tend to get like skin, like skin cancers, right? But you can also get like long cancer, they can get like non-hot skin, lymphoma and all that stuff, right? So these are just basically all side effects of the immunosuppressive therapy that these people are on, right? So let me see, is there any other thing I really want to talk about? No, I think pretty much I've talked about everything I want to talk about, right? So again, I'll talk about a quick life lesson at the end. It should be very quick and quick and dirty, right? So I'm not dirty. I hope you're helpful for your life. Let's put it that way. But thank you for listening. Please subscribe to the You Tube channel. Again, remember, it's God of any intervention, USMV podcast and videos. I hope to start making videos again. Very soon that I'll be posting on that. And then, although also post the audio versions on the website. And then, you know, please subscribe to the podcast. It's on Apple podcasts. It's on Spotify, it's on Google Play. Again, any feedback or whatever, right? Any routines or rankings, right? Those absolutely help, right? And then, if you want to get a notification whenever I make a podcast, I mean, if you're also, you know, if you have one of these podcast apps, you'll get a notification, like whenever I make a new podcast, you'll be updated, right?

But also, you can get an email notification if you subscribe to the Word Press website, divining intervention podcast.com. And you get a notification whenever I make a new podcast, right? And then, so what's my life lesson for today, right? So my life lesson for today is working selflessly, working selflessly, right? This is something that's especially important for people that work in teams, you know, like medical students, physicians, stuff like that, right? Or even many in activity and life, right? So you think I would say is whenever you're doing work, don't try to do bad work. Try to do good work. Try to do excellent work, right? Because if you think about it, right? There's a part of the Bible that says whatever your hand finds to do, right? Do it as on to God. It's your reasonable service. Don't try to do it as a man pleaser, right? Because you're trying to forgive me for lack of a better term, kiss someone's, you know, what I'm talking about, right? So always do good work because you're just like, you almost think of it as like your service to God, right? You're not doing it because you want to impress your attending or you want to impress your resident. You're just doing good work because that's your standard, right? So like, and the thing is if you're consistently produce good work, people will always look for you. That's the truth, right? You'll be recognized, right? Again, whatever you saw, you reap.

If you saw good work, you'll get, if you saw excellent work, you'll get excellent result from it. That's just the truth of life, right? That's just the truth of life, right? And again, people recognize those that do excellent work, right? Because they'll know that me and this person has standards, right? So like the way you write your notes as a medical student, showing up on time as a medical student, rounding on your patients, doing things in a timely fashion, right? These are all excellent things, right? Even as a resident, right? Don't just do the minimal needed to get by. Do solid work, right? Do it like, do it like you're working for someone that is almost like a mindset kind of thing to be honest with you, right? Like when you're doing like, oh, I'm doing this work because I want to honor God, I want to serve God as a game's doing it because I want to please my attendant or please the resident that I'm working on there. If you have that perspective when you're working, then you're very likely to do good work, right? You're very likely to do selfless work, right? So even if you're not being thanked, even if you're not being rewarded by your resident, even if they're not recognizing it, even if they're not saying, oh, great job. That shouldn't be the reason why you should do good work. Doing good excellent work should be your standard, right? Again, as a human being, many people say, oh, half standards, half standards, half standards, right?

Half your own personal standards, half your own personal standards of of excellence. When people almost let excellence almost be like a trademark for you, hopefully, those of you listening to what a trademark is, right? It's almost like something that, you know, like the Coca-Cola company, they have like a trademark, right? You see, like, the puts Coca-Cola, it's like a specific sign, like you can't go and just slap it on any product, right? And then you see TM by it, TM means trademark, right? So let excellence be your trademark. When people see the kind of work you do, let them be like, oh, yeah, this is this is the work that divined it. Oh, no, no, no, no, this is the work this person did because they just know that, oh, if you're seeing something that needs gold and it's excellence, they know where it's coming from, they know the source, right? So let not your words be the thing doing the talking for you, let your actions, let the results you produce, be the things that are that are speaking on your behalf, right? Again, remember the Bible says that let your light so shine before men, right? That it may see a good work time glorify your father, right? So if people are seeing, man, this person has great works, they want to find out what is your secret, right? And it can almost inspire other people to start doing that kind of work, right? For example, I'll give you a classy example, the Miami Heat, right? Look at Miami Heat, right?

These people did even qualify for the playoff's last year. I don't think they did, right? But this year, these people are in the Eastern Conference Finals and with the way things that shape you know, it sounds like they're going to win the Eastern Conference Finals, right? But what was one of the things that changed, right? Jimmy Butler went to that team. It's not like, and you know, they also drafted really well, right? But I'll say Jimmy Butler was like the big, big, big, big fridge and design. Jimmy Butler has like an insane work ethic, like this guy works out at like 3 a.m. in the morning, right? The thing is, people saw that attitude in him. He's teammates, saw that attitude in him. He's a hard worker. He doesn't care about how many points he scores. All he cares about is just working hard and putting his team in a position to succeed. He's very selfless. He doesn't because you see some of these major stars in basketball, they're like, I got to get my 30 points, my 10 rebounds, my triple double. No, no, no, no. And there are some players like that. Again, I'm not going to mention anything, right? But I'm recognizing Jimmy Butler because he doesn't, you may see in a game, he may score only 10 points, but he's team wins. That's what he cares about. Points doesn't care about nothing, but he gives maximum effort every single time. Those are the kinds of people you absolutely want to have on your team, right? They don't care. They are not looking for their own glory.

They are looking for the team's glory, right? So Jimmy Butler is selfless in that regard, right? He's the superstar, right? But he doesn't load money. Nothing. He's always putting in maximum effort. And the thing is that maximum effort he puts in just inspires every other person on the team, right? Even people that, oh, before this to work out at 70, he's the commoner 3 M to work out. And it's no surprise. He has essentially changed the culture of that organization. That's why they are succeeding on such a high level, right? Even as a dad, right? Again, children are great copycats, right? If you are modeling maximum effort, if you are working selflessly showing like good works as a dad, then your kids, your wife, your spouse, they want to copy what you're doing, right? Again, people do not run away from good things. I'll tell you this right now. Good things, excellence attracts, like if a person is excellent, you will attract excellence, right? Again, like like like birds of the same feathers, this classic scene in Africa, that birds of the same feather flock together, right? Again, if you want to attract good people to your life, if you want to change culture, right? If you want to change culture for the good, begin to model that culture yourself. And then you begin to attract people, right? So hopefully you found this podcast to be helpful. Sorry again, this is a little longer, right? But again, it's a cardiology podcast. It's just one of those things I do.

Whenever something is a cardiac-based podcast, I try to not rush through it because cardiology is one of those things where you cannot just memorize your window of success. You actually got to understand what's going on. So thank you for listening. Again, if you want to sign up for any of those courses starting to more in these still a few spaces, send me an email through the contact me button on the, I mean, tab on the websites, divineinterventionpodcast.com and then we'll go from there. So thank you for listening. God bless you. Until next time, see you.

Systolic heart failure (reduced ejection fraction) or diastolic heart failure (preserved ejection fraction).

The Renin-Angiotensin-Aldosterone System (RAAS) and the Sympathetic Nervous System (SNS).

A displaced Point of Maximal Impulse (PMI) laterally, an S3 gallop, and potentially increased cardiothoracic ratio (>50%).

Cardiogenic edema has a PCWP > 18 mm Hg; ARDS has a PCWP < 18 mm Hg.

ACE inhibitors/AR Bs are the classes; ARN Is (Angiotensin Receptor-Neprilysin Inhibitors) represent the most advanced form shown to improve survival.

It causes venodilation, decreasing preload and reducing myocardial workload/oxygen demand.

Heart Failure with Preserved Ejection Fraction (H FpEF), which results from pressure overload (e.g., hypertension, aortic stenosis).

ACE Inhibitor/ARB/ARNI, Beta-blocker, and Mineralocorticoid Receptor Antagonist (MRA).

Anemia (low hemoglobin) or arteriovenous fistula formation.

Increased risk of digitalis toxicity, as both conditions can affect potassium handling and cardiac rhythm.

ARNI (Angiotensin Receptor-Neprilysin Inhibitor).

Allo graph vasculopathy (vascular problems with the transplanted organ).

Heart Failure with Preserved Ejection Fraction (H FpEF), which results from pressure overload (e.g., hypertension, aortic stenosis).

ACE Inhibitor/ARB/ARNI, Beta-blocker, and Mineralocorticoid Receptor Antagonist (MRA).

Anemia (low hemoglobin) or arteriovenous fistula formation.

Increased risk of digitalis toxicity, as both conditions can affect potassium handling and cardiac rhythm.

ARNI (Angiotensin Receptor-Neprilysin Inhibitor).

Allo graph vasculopathy (vascular problems with the transplanted organ).