DIP Episode 445 - The Clutch MI Complications Podcast (Step 1-3)

Okay, welcome. When is the vine? This is episode 445 of the Divine Intervention Podcast. In today's podcast we're going to be talking about MI complications. MI complications. This podcast is super high yield. Simple as that. It is super super super high yield and it's for step one or step three. It test the stuff on step one, on step two, on step three. Show of exams. It won't make school exams test the stuff. So let's talk about it. So what if they give you a question about a patient? They tell you that he's a 55-year-old male. He comes into the emergency room. 30-minute history of severe chest pain and they tell you that his proponents are markedly elevated and you know they tell you that he you know while he's been evaluated in triage he dies immediately and then the ass was the most likely cause of death. Well if you see something like this I'll really hope you're saying oh divine this is probably some kind of ventricular arrhythmia. This is some kind of ventricular arrhythmia. So this person clearly has an MI. Your tropes are elevated. Right, remember when you have an MI you're gonna see certain things on an EKG. You're gonna see the STL innovations or you're gonna see a new left bundle branch block. Remember you don't always have to see STL innovations to say oh wow this person has an MI. You may not see the elevations but you may see a new left bundle branch block. It's gonna tell you percent and the tropon is elevated that person's got an MI.

So this person has an MI and they see the die immediately very quickly first 24 hours. The most one cause of death in the first 24 hours after an MI is an arrhythmia. It's almost always on your exams going to be a ventricular arrhythmia. If you're trying to go for one specifically go after V-Fib but if you don't see V-Fib you can pick V-Tec as well. V-Tec also happens in the setting of an MI. But just again thinking in general ventricular arrhythmia is the most common cause of death that's very high up to no in the first 24 hours after an MI. Then our friends at the USME Lies especially for people taking step one. They love to ask that you know within the first you know few hours or day like first few hours or like the first day or day or about. What kind of gross changes are you gonna see on the heart? They can even put pictures. So for some of these things just look at gross images slash histological images so they kind of sticks in your mind. One thing they love to do is they can essentially throw an image and the heart to look dark. The heart that is infarcted is gonna have a dark discoloration. So what kind of necrosis typically happens in people that have had an MI? It's gonna be coagulation necrosis. Coagulation necrosis. And if you're asking what's the most common kind of MI? Well, most common kind is is an LED infarct. I believe it's responsible for about three quarters of MI is about 75%. Remember with that one you're gonna see ST elevations in V1, V2, V3 and V4.

I remember if you're gonna have to an R-C infarct then you're gonna be seeing ST elevations in 2, 3 and EVF. Remember those people are pretty independent. So giving them nitrates is maybe another good idea because nitrates are very powerful with no dilators. It's gonna kill their preload. Those people are gonna get regular MI treatment minus nitrates plus fluids. They're gonna get fluids because some gentle amount of fluids because it's gonna help with giving them preload. And remember V5, V6, 1, and EVL is a circumflexing part. That's a lateral infarction. But again, that's not the main focus of today. So let's kind of walk through like the progression of things that can happen after a person has an MI. So what if they give you a question they say, oh, you know, this person had an MI 48 hours ago. The person got a coronary of hospitalization. But now this person has been completely no worse than just being the details of the presence of a fever. The tell you that you see ST elevations in multiple leads beyond the original leads that had ST elevations. And then the tell you that the person's ESR CRP is markedly elevated. The person has a local cytosis. And it tells you that whenever the person leans forward, the chest pain is gets better. When a person leases back, chest pain is worse. Then what's going on here? Again, notice is like the first, it's like two days, like first three days after the MI, you know, just literally first few days.

I want you to think about something on us, February, not Sparic or Ditis. February, not Sparic, Ditis. Right. So what's what's going on here? Well, if you think about it, roughly after 24 hours after you have an MI, inflammation is going to set it because your body is like, wow, there's that tissue here. I got to deal with this dead tissue. So they want to three after an MI, you're going to have acute inflammation. Acute inflammation is heralded by neutrophils. Neutrophils are kind of like the big, big things. Remember, another thing for neutrophils, PM Ns. And you see neutrophils on exams referred to as polymorphal nuclear leukocytes, polymorphal nuclear leukocytes. That's another thing for neutrophils on exams. So think about it. What are some of the hallmarks of acute inflammation? Well, you know, there's color, there's rubber, there's, you know, color means things kind of get hot, right? When a police is in flim, it kind of gets hot. There's rubber, right? It kind of gets red. And the thing you may see is a tumor, right? Remember, edema is a hallmark of inflammation. We know that things like, you know, your, your, when you have inflammation, you know, that we released things like histamine and bradykine, those things increase vasculoprimability, right? So that's going to cause a deem. Fluid is going to see part of blood vessels into the interstitial. That's going to cause a deem. We know that when cells die, the sodium potassium ATP is pump doesn't work.

So sodium is going to rush down its gradient into the cell. But water is going to follow. That's going to cause cell swelling. So these are all hallmarks of acute inflammation. So if you think about it, if your cardiac myocytes are going through this problem, then they're going to start swelling. And as they swell, the heart is going to be rubbing that swollen heart, those swollen myocardial cells, going to be rubbing against the pericardium. As the rub against the pericardium, they're going to irritate the pericardium. That's the pathophysiology behind fibrenospereic raditis. Okay? That's the pathophysed behind fibrenospereic raditis. And in general, when people have pericarditis from an MI, your treatment is aspirate. I'll say that again. Whenever a person has pericarditis from an MI, your treatment is what? Aspirate. Very good. So please don't give these people insets. Some insets like Indomethacin, the inhibit collagen deposition. And the thing is those dead myocytes, your body is going to replace them with collagen, with fibrosis. So if you give insets or give steroids, those things can impair the lean down of that collagen, that fibrosis. So the injury is not going to heal properly. If it doesn't heal properly, the person's heart is going to rupture. And that's not a good thing. We're actually going to talk about those ruptures here in a bit. Okay? So again, fibrenospereic raditis, we've talked about the pathophysed, aspirate, aspirate, aspirate, aspirate, aspirate.

Okay. But so we said that kidney inflammation is sitting with neutrophils. Well, what happens if photo 7? Well, this photo 7, we go from acute to chronic inflammation. And we know who are the big boys of chronic inflammation. It's going to be macrophages. Macrophages, macrophages, macrophages. Because macrophages, some cardiac myocytes have literally died. So they need to take away these dead myocytes. Well, the thing is my, macrophages do an awesome job. You know, they're very good at, you know, killing, they're very good at removing the chronic cells. But the thing is when they're there, when they're around in the area, they release some things, right? I just kind of think of it as like a cleaner. Let's say a person really cleans things really, really well. But you know, when you're coming, you're like, wow, there's no bacteria here. They've cleaned up this whole area. It looks so good, smelling good. But in that cleaning, maybe they use like very toxic chemicals. So they can kill off all those bacteria. So those toxic chemicals can cause like some long term problems. Kind of think of it as a similar macrophages. They're very, very good. Wendy's shopping a place, you know, they clean up the badness. But the stuff they release is kind of toxic. It's kind of nasty. It can weaken walls of things, right? They have all these produces and things like that that kind of weaken walls.

I mean, think of a person that has COPD, you know, from smoking, you know, you smoke, smoke, smoke a lot. Macrophages are going to come and clean up the nasty particles from the cigarette smoke. But as they're there, they're going to release all these produces. All those produces, they weaken the walls of things. Like for example, they literally will weaken slash chop the walls of your poor pulmonary pyrochemical. That's how people have that pretty bad old and then they get into trouble with infezema. So that's something that happens in the long, clear happens in the heart. But in the heart, the things that they're cleaning up are the necrotic cardiomyocytes. As they clean up these necrotic cardiomyocytes, yes, they're going to do a good job of cleaning it up. But they're going to release things that's going to weaken the walls of tissue. So if you weaken the walls of tissue, many bad things can happen. Like for example, they can see, oh, wow, this person had an MRI a few days ago. And then now they have this, so they don't say, you know, bad shortness or breath, crazy pulmonary edema. And they tell you that you hear a holosis stomach murmur at the left-low external border. Well, that's the murmur of a VSD. So I really have a VSD that just develops out of the blue. Well, it's because your interventricular septum has literally ruptured. Interventricular septum has literally ruptured. And again, just think about it.

I've kind of given one pathophase that, oh, macrophages, they make the walls of the tissues weaken. But again, think about it. When you have inflammation, again, you're going to get a lot of swelling. If things swell, swell, swell, swell, they can swell to the point of a rupture. So you can get an interventricular septum rupture. It's going to present as a VSD murmur. Another classic rupture pattern that happens is a papillary muscle rupture, right? Or sometimes the ocolary rupture of the quartetendony. They want to mess with your head on exam. So it's pretty much the same thing. Papillary muscle rupture, rupture of the quartetendony. If that happens, you're going to get the murmur of mitral regurgers. So again, a lot of pulmonary edema, swelling decomposition. And you see this holosis stomach murmur at the apex. Well, that's going to tell you that's a mitral regurgurge murmur. And again, left-low external border is VSD murmur. That's an interventricular septum murmur. Holosis stomach murmur, apex, that's the mitral area. That's going to be the murmur of mitral regurgitation. Mitral regurgitation. Mitral regurgitation. That's a papillary muscle rupture. Again, you can see it referred to as rupture of the quartetendony. And they remember your ventricular friwals can also rupture. Usually those people, they're not going to do well. They're going to go into a postless electrical arrest because again, the ventricular wall is ruptured.

I don't know how that ventricular is going to be contracting very well at all. So you may be seeing a signal in the heart. You may be seeing electrical activity, but there's no pulse. That's P, postless electrical arrest. And you're also going to notice that this probably have like the development of like sodium tamponat. The development of sodium tamponat. Sodium cardiac tamponat. The kind of tamponat that wow, the heart is like just shuts down very quickly. Again, when you see those things, think of the ventricular friwals rupture. Now, one thing I want to keep in mind is again, what will the tissue look like grossly? Again, this, I'm seeing this a lot for the step one force that I listen to this podcast. Well, the tissue look like grossly around like these four through seven of an MI. It's going to look yellow. It's going to look yellow from that inflammation. I remember I say the first few hours, like first two to four hours of their mouths, first day of their mouths. It's going to look more black from the coagulation and the process. But from around these four thereabouts, the tissue is going to look yellow. It's going to look yellow from the inflammation, right? From the macrophages kind of doing their, doing their deeds. So now we've kind of talked about the first seven days. So let's talk about what happens from weeks one to three. Which one to three? So you know, I get inflammation has happened. Creating inflammation has happened. Now we bring in a fibroblast.

Fibroblast is that collagen break layers. So the ones that are going to come down and make that collagen. So what kind of collagen are they going to lay down? So it'll be type one collagen. Again, I know so I'll be like, divine, who cares about these details? I'm telling you, you should better care. They love to test these things on exams, right? So you're going to lay down type one collagen, right? So the first thing you're going to see from these fibroblasts doing their job is granulation tissue. You're going to see granulation tissue. It is weeks later, they're going to start seeing fibrosis and deposition of of collagen. Now the thing is this collagen is like your body's best efforts to fix the problem. Obviously it's not going to be as good as your original. That's just a truth. I just kind of think of it as like an original and a fake counterfeit. Counterfeit is never as good as your original. It doesn't matter how great a counterfeit is. It's usually pretty rare for a counterfeit to be as good or better than your original, right? So the thing is this fibrosis and collagen, yeah, it's good. Is the body's next best measure, but it's not as good as the original myocardial cells that we're there. Because the thing is collagen is not as strong as myocardial. So the collagen that is replacing the myocardium that died is not very stable.

So as the heart is contracting, contracting, contracting, collagen is not built to handle pressures like myocardial cells are built to handle pressure. So the thing that's going to happen is the instability of those walls can lead to the formation of ventricular aneurysm. So it's pretty high yield to know that typically when people have an MI and the develop of ventricular aneurysm, it's going to be more than a week after a set MI happens. So if they give you a question and you know, you see that well, it's the first 70s after an MI. I will encourage you, please don't think of ventricular aneurysm. You want to think about it and coloneurysm after a week. Because again, it's that collagen that's deposited. Collagen has to deposit for you to form a ventricular aneurysm for the most part, not always, but for the most part, not always, but for the most part. So, you know, and obviously that aneurysm is a poly contracting segment of the heart. It's something you can see very well on echocardiography, but the big, big, big fear of complications since collagen does not contract like regular myocardial. The thing that can happen is you can basically have a myrothromus. When a myrothromus forms, it can cause a stroke because the thrombus can flick off and then go to the brain, go to one of your several vessels and cause an embolic stroke, cause an ischemic stroke from embolism. So, that's one of the things we worry about. So, again, that's the way of ventricular aneurysm presents.

You see a person basically like a few, you know, a week, more than a week after an MI, they develop like a stroke. And then the Italian echocardiography, the Italian that is the same one of the hard-ass econtractor or is not contracting as well, think of ventricular aneurysm. And let me see you see a balloon of the wall of one of the ventricles, again, think of ventricular aneurysm. That's the way it's going to present what it exempts. And then what if they give you a question and they say like, you know, like, a person had a name like five weeks ago or a month ago, whatever. And all the person is having like this very bad chest pain, you know, fever, glucose, itoces, gets worse when the person leans back, gets better when he leans forward. When you see that, I really hope you're seeing, and you know, you're going to see an invalid ESR CRP. If you see this, I really hope you're seeing, oh, divine. This sounds a lot full of like dressless syndrome. And again, our friends at the NB needs that they're very good with not giving you the terms you're familiar with. So instead of calling dressless syndrome on your exams, believe it or not, they may call it autoimmune pericarditis. Or believe it or not, they may call it a post-biocardial infarction syndrome. So again, please expect any of these three terms on exams. Please, please, please, don't be caught on our wares. Don't be caught on our wares. Expect any of these three terms on exams for dressless syndrome.

They may literally call it dressless syndrome. They may literally call it autoimmune pericarditis. They may literally call it a post-biocardial infarction syndrome. If you see any of these things, think of dressless syndrome. And because it's an inflammatory issue, your ESR is going to be up. And again, like I said, how are you going to treat it? High, see it after me. High dose aspirin again. High dose aspirin again. High dose aspirin. You're going to give high dose aspirin. Please, please, please. On your exams, they'll show not give NSAI Ds. Again, I've already said NSAI Ds and he'd be collagen deposition. Persons, my cardio wall's going to rupture. That's what's going to happen. So you don't want to do that. So you don't want to give NSAI Ds. You don't want to give steroids. Indomethicine, especially, is a horrible, horrible, horrible NSAID for presenting the sudden M.I. Honestly, for the first six months after you have an M.I., you really shouldn't be taking a regular NSAID. It's not a smart idea. Remember, NSAID and aspirin, they're kind of very different in the way they work. NSAI Ds, being a hip-hip cox, one on two, reversibly, aspirin, inhibits cox, one on two, E-reversibly, very, very big, big difference there. Very, very big, big difference there. So again, those are all the names you would see. Again, no NSAI Ds, no steroids. High dose aspirin is where it's at. So again, what's some potential pathophys behind a dressless syndrome? Because think about it.

Why is it that you have an M.I.? And then boom, your immune system starts attacking your heart. It kind of seems bizarre. Why did that happen? Well, there isn't why that happened. Again, potentially, the thing that makes a lot of sense to me is that, again, think about it. When a person has an M.I., you know, sodium potassium, you know, there's not much ATPB released to the heart. So your myocardial cells, sodium potassium ATP is pumped, which, you know, is responsible for about 70% of the energies of the cell doesn't work. That doesn't work. Then, you know, sodium flow down is good into the cell. The cell will swell and rupture. As the myocardial cells rupture, they're going to start releasing antigens into the bloodstream that are ordinarily not in the blood stream. Remember, literally when a cell ruptures, the stuff inside is going to be open-failed into the rest of the body. So your body is going to start seeing this, myocardial cells are seeing man. These are not antigens I'm used to seeing. This is kind of weird. I don't see these antigens. These antigens are usually walled off, you know, by intact, well-functioning myocardial cells. But cell ruptures, boom, you don't see staccinal these stains. Well, as you see these stains, well, that's going to cause a problem here. But it's going to be like, this thing is not a potential of the time. So you're going to start making antibodies against it. Start attacking your heart. So this is why this process takes weeks.

It takes weeks. It doesn't happen immediately. Because, you know, when you make antibodies, you need to generate the right, you know, hypervariable region. You've got to have all this class switching, all those things. Those processes take time. It's not something that happens immediately. So that's how you can get dresslers syndrome. And again, we've going to talk about how you treat it. Okay. And again, as I wrap up, a few more things I want to talk about here. But if I do that, again, if you're studying for a step tour, step three, I have a review class taking place next month in the month of March. It's going to be a 20 hour class. Many people have taken in front of you to be extremely helpful. If you're taking step one to step three, also have a few classes you may find to be helpful. Have an MBA me test taking strategies class. There's one taking place on the 17th of March. Again, it's for step one, all the way to step three. If you want to, because again, many times on examples, it's not about being good at just the knowledge. It also have to be good at taking tests, picking the right answer, reading exam questions carefully. Even picking answers where you don't even know what the question is talking about. All these things are possible, not falling for MBA me traps. These are things I go over in my two and a half hour MBA me test taking strategies class. Tons of people have taken the class funded to be tremendously helpful.

And then, I mean, even the, even the 20 hour review class for step two, step three, I've had people that within the course of the week of the class, they are scores that have improved almost 40 points literally just within the course of the week of the class. You see this, but they're like, wow, I'm on my final day of the class, well, the vine I took an exam just before this final day of the review. My scores are bumped up like 30 points. I've actually seen this is not an all common occurrence during the class. And then also for step one to step three, you know, I have a biostatistics bootcamp is a four hour class. I have one happening in the month of March. I will just have one yesterday. I'm going to be advertising the one in the month of March very soon here. And then I have a social sciences and ethics class. Again, also for step one to step three, as we know, 10 to 15% of the USMEL exams, these these cover social sciences, ethics, quality improvement, healthcare systems, communications, many of those, you know, just weird, wonky things. You may not see many resources. It's about 10 to 15% of the exam these days. And again, you know, many resources just give definitions of things. They don't show you how these things will be applied on the exam.

So if you want to get very good at learning these concepts in the context of clinical presentations in the context of healthcare systems problems, just like you'll see on your exam, then you want to consider the five hour social sciences and ethics review. I actually have one taking place today from 49pm mountain time. But if you can't make the one today, then just be on the lookout for the ones I have in the future. And then for step one, I have a 25 hour class. Again, I have one taking place. I believe from the 20 to the 24th of April. So again, if you're interested in any of these classes, just look at the announcement podcasts I meet on them or just shoot me an email through the website. And I'll be mother happy to give you some more information. All of them are held over zoom. So it should be able to attend them pretty easily. Okay. So let's go ahead and continue. So what kind of heart failure will a pressing develop after they have an MI? Well, obviously my cardiovascular cells have died. If they've died, they're not going to contract very well. So you're going to develop a systolic heart failure. Remember when your heart muscle doesn't work great, then they're not going to be able to pump blood for very well. So over time, that blood is just going to be collecting in the heart, collecting in the heart. So you're going to be doing volume overload. How do you respond to volume overload?

Well, you're going to lead down your cardiac sacrameres in series, going to lead him down in series. So you're going to have an eccentric hypertrophy. That's going to lead to dilether cardiomyopathy. Right. So when a person has a skin of the heart from an MI, they're going to develop a dilether cardiomyopathy. They're going to develop a systolic heart failure. They're going to develop a heart failure to reduce the ejection fraction. That's why many people over time, after a NMI, they're ultimately going to develop a heart failure unfortunately. Although one of the best ways to kind of reverse that is your exercise and a healthy diet. There are some people that have actually recovered by your cardio function, believe it or not. I mean, you're going to take the drugs on whatever that they prescribe to you. But you can actually recover a good amount of cardiac function by just exercising and you have pretty, like a very strict, healthy diet. It's just something, but that's, again, please, none of this broadcast is healthcare advice. You might leave me very, but again, I think many of these things are pretty high yield, for example. Literally, these broadcasts are just, for example, not for clinical decision-making. Again, I got to throw that disclaimer. Okay. And then, again, I want to maybe go over a few more things that you'll be seeing on exams. I mean, seem a little, little weird to you if you were to see them.

So what kind of shock will a person develop in the setting of an MMI? Well, they're going to develop a generic shock. So what kinds of things should you see? Well, think about it. If your heart doesn't work, your cardiac output is going to drop. So in cardiac shock, your cardiac output should go down. So if your cardiac output goes down, well, your heart is not going to be empty and it'll blow very well. So what should you show of your cardiac pressures? Well, I would really hope you're saying, oh, divine, my left-age pressure, which is the, which we call the PCWP, the Pomonaic Appelerial Wage Pressure. Or the CVP, which is the central veneous pressure, that's the right-age pressure. Both of those should be elevated. Both of those should be elevated. Both of those should be elevated. And if you think about it, again, why would a person have Pomonaire Dima after an MMI? Again, if your heart doesn't work, then three is going to back up into your Pomonaire tree, to your Pomonaire vessels. That's going to raise the hydrostatic pressures on your Pomonaire capillaries. And increasing those hydrostatic pressures is going to cause fluidization. So that's going to cause Pomonaire Dima. That's going to be a cardiogenic Pomonaire Dima. So in that case, your PCWP is going to be more than 18. Contrast that with a person that has a non-cardiogenic Pomonaire Dima from ARDS, because of increased blood slurper mobility.

There, you're going to have Pomonaire Dima, but it's going to be non-cardiogenic. Your PCWP is going to be less than 18. It's going to be less than 18. But if you have cardiogenic Pomonaire Dima, your PCWP is going to be 18 or greater. There's something you want to keep in mind for, for example. So you want to keep in mind for, for example. And again, the one thing I would say, the one thing I would say is maybe like in summary, in summary. I think the one thing I want to say, I think there's some things I just want to put together at the end here. So they really get this stuff. Because I mean, people get these things wrong. For this podcast, if you're like, oh, divine, I want to quiz myself. Let me tell you some things you should do. One, ask yourself. Can you recognize an interventricular septal rupture? Two, can you recognize a ventricular free war rupture? Three, can you recognize a papillary muscle rupture or rupture of the cardiotendomy? Four, can you register what the lab value should be in cardiogenic shock? These are almost like questions I'm telling you to answer for yourself. Five, what is the biggest risk factor for myocardial rupture? You should kind of get that point based on the whole topic of this podcast, which is an MI, right? Six, what are, when those, what kind of necrosis do you see in the cardiac myocyte? When a person has an MI? Seven, what's the most common cause of death in the first 24 hours after an MI?

Eight, what will you see grossly on the heart within the first day? What do you see by D4? Nine, how does a favorite North American ID present? Is he treated? What's the pathophys? Ten, dressless syndrome. What are the odds? What are its alternate names? How does he present? When does he present? How do we treat it? You got to know these things. Eleven, what is the pathophys behind rupture? What's the pathophys behind free-brained oscaricoditis? What's the pathophys behind dressless syndrome? I talked about all these things. Twelve, what's going to be trouble the pressures in the heart during the acute phase of an MI? Thirteen, what are some classic signs and symptoms on an e-keyg of an MI? Versus what are the classic signs and symptoms on an e-keyg of paracoditis? You should be able to answer all these questions. I think 14 or 15, how those of the chocolate and yours in present? Can you label out stroke patterns that could present from a person having an MI? For a person who has a stroke from an MI, what kind of drugs should you get us prevention? Should we get in anti-placid agent? Should we get in anti-coagulants? It's going to be anti-coagulants because it's a cardiogenic source of stroke. So these are all questions you want to make sure you can answer. If I want to question, it can throw an example. Which of the following interventions is best at reducing the risk of myocardial rupture after an MI? The answer you want to be picking is early re-vascularization.

If you re-vascularize early, if your cardio cells are going to die, you're not going to run into any many troubles. I'm also just adhering to the pharmacotherapy. There's a very strict drug regimen. There's supposed to be an after an MI. These are all things they can test on exam. These are things you want to make sure that you know. These are all things you want to make sure that you know. These are all things you want to make sure that you know. And again, one thing I'm just going to say is in general, these ruptures tend to occur at the interface between where you have healthy myocardium and dead myocardium. Why is that? Because it's almost like you have too many forces and shear stress at that region. The dead myocardium, because the sodium potassium ATP foam does not work, it's going to swell. Then the living myocardium because they're trying to compensate. They're going to be contracting like crazy. They're going to be contracting very hard. They're going to be in a hypercontractile state. So most of these bad complications and whatnot, they tend to happen at the edge of a healthy MI and you know, dying, dying. I mean, sorry, healthy myocardial cells and dying myocardial cells. So I think I'm going to go ahead and stop here. But again, all the stuff I've said I promise you, none of this stuff is low yield. A lot of this stuff is extremely high yield for all the USMD exams.

Again, as I do, at the end of every podcast I offer one on one tutoring for all the USMD exams, step one to step three, preclinical medical exams, 30-ish-elf exams. Then I have review courses for step one, for step two, for step three. And I have some courses that are for step one, all the way to step three, like the NV Me testing and strategy scores for two and a half hours, the biostatistics bootcamp for four hours, and the social sizes and ethics review for five hours. And then I have a You Tube channel, the one intervention, USMD podcasts and videos. That's where I put the videos that I make and some audio versions of these podcasts. And then I have these podcasts on the major apps, Apple Podcasts, Google Podcasts, Spotify. And then I also have with ER As applications, mock interviews, rec letters, personal statement, editing, all those things. Even discussing around clizzies are things I've done with many people. And many people have found it to be extremely helpful. And then I have another website called divineinterventionlifelessens.com. There's actually an Apple Podcast associated with it called the divine intervention life lessons podcast. You know, many people said, oh, divine, I love the life lessons you put at the end of a podcast. So I was like, okay, fine, I'm going to make many of you down a question. I made a separate website. In fact, we have more than 160 podcasts right now on there. And every week I post two podcasts, usually about 10 to 20 minutes long.

And using the Bible, I discuss approaches to solving certain life problems. So again, just go ahead and check that out. Again, I think it's something I'm going to be fine to be very helpful. So thank you for listening to me today. Again, I promise you this stuff that I discussed in this podcast. It's a 30 minute podcast, but this podcast is extremely high yield. So listen to it, understand it. And I trust that things will go well for you on your exam. Well, until episode 446. Bye for now. God bless you. Thank you.

Ventricular arrhythmia (specifically V-Fib or V-Tach).

Coagulation necrosis.

VSD is holosystolic at the LLSB/apex; Papillary muscle rupture causes mitral regurgitation (holosystolic murmur at the apex).

Heat, redness, swelling (edema), and pain.

Type I collagen.

Ventricular aneurysm.

PCWP will be $\ge 18$ mm Hg.

Neutrophils (Polymorphonuclear leukocytes/PM Ns).

High-dose Aspirin (NSAI Ds are generally contraindicated due to rupture risk).

Macrophages release toxic substances that weaken tissue walls; the Interventricular Septum ruptures.

Necrotic myocardial cells rupture, releasing antigens into the bloodstream, which triggers an autoimmune attack weeks later.

First few hours: Dark/Black (coagulation necrosis). Day 4-7: Yellow (due to acute inflammation and macrophage activity).

They inhibit collagen deposition, impairing the body's natural healing process and increasing the risk of cardiac rupture.

Dilated cardiomyopathy (Systolic Heart Failure).

Neutrophils (Polymorphonuclear leukocytes/PM Ns).

High-dose Aspirin (NSAI Ds are generally contraindicated due to rupture risk).

Macrophages release toxic substances that weaken tissue walls; the Interventricular Septum ruptures.

Necrotic myocardial cells rupture, releasing antigens into the bloodstream, which triggers an autoimmune attack weeks later.

First few hours: Dark/Black (coagulation necrosis). Day 4-7: Yellow (due to acute inflammation and macrophage activity).

They inhibit collagen deposition, impairing the body's natural healing process and increasing the risk of cardiac rupture.

Dilated cardiomyopathy (Systolic Heart Failure).