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heard about and see. Okay, Cool. Got it. Eso The other couple of members on the team is Robert Beach and Kristen Beach. They are very significant members of the team they help to rob primarily works to allow is involved in the filming process. So he films all of the things that you guys see on YouTube. He also is responsible for editing them. Publishing them here also helps with a lot of the social media stuff. And then we have Kristen. Kristen also helps me drawing on the white board. She's also doing a lot of her own nursing videos, which is really cool. She also helps out with a lot of the social media. And then another 30 member that we have is Meena Rogie. He is awesome. He is the chief of a lot of our actual like medical writers and an illustrator. So he has been working really hard to see a lot of these notes that you guys, if you guys have checked out our website, we have a lot of amazing notes and illustrations, and he's helped to really kind of lead that off, and also he's kind of starting this whole process of the ah, step to course, we're hopefully going to try to start making So that's our team. Um, we kind of really enjoy being able to have these opportunities. This is Ah, the third opportunity that we've had to kind of meet with some students across the world in different areas. And, uh, you know, just be able to have a good time, talk about science, medicine and hopefully learn a lot. So I'm really excited. So today we're going to do a case study. I'm with you guys, and one of the things that that was brought up to me is that you guys really like some cardiology stuff. So I had a patient who had some cardiology related problems, and, um, I thought I'd be really cool to talk about this one. So we'll go ahead and get started. Hope it's really cool. If you guys have any questions, something doesn't make sense. I'm completely off. Put it down the comment section, let me know, and we'll talk about it. But first off, um, this is so often I don't really do these cases where they are really most time. They're fictitious on our YouTube channel. They're made up. Um, I kind of just try to make it seem like a really case. This is a really case. This is actually one of the patients that I saw in my hospital. Um, and I had to manage. And so I thought this would be really cool to see what it could look like. And how sometimes it's never really like straightforward. It's never really clear cut. It's not super obvious, and often times you want to rip your hair out because you're really struggling to figure out how to manage the super complicated patients. And if some of you guys are looking into managing patients and your emergency departments hospital medicine or you're looking to work and I see you, you'll deal with a lot of these very complicated patients. So right, here we go. Uh huh. All right, so we'll start off with kind of just a brief part of the patients. HPI. So it was a 72 year old male had a past medical history of a transient ischemic attack. Um, he has a history of COPD, tobacco abuse, hypertension hyperlipidemia and Type two diabetes myelitis as well a CKD stage two, and he came into the emergency department with complaints of chest pain. And then if we obviously with every piece of chest pain, we should go pick your ST the living crap out of her, right? And so when he described it, it was an acute onset. It was a constant, heavy, kind of squeezing type of pain. He described it as that radiated to the area of his left shoulder, and he admits that the pain that he had in his chest that was substernally was constant was heavy. It was squeezing, radiant. If the left shoulder it occurred primarily when he was sitting down at rest. But whenever he got up to go and walk around, it got much, much worse. Okay, Patient also admits that whenever he was kind of walking outside because he wanted to go and walk it off, thinking that maybe that would help this pain, chest pain, he actually started to kind of get a little lightheaded and fell. And when he fell, he hit his shoulder on the ground really, really hard. And he was also complaining of a 10 out of 10 right shoulder pain. So the wife called M s, brought the patient into the emergency department to be examined when the patient got to the emergency department. We obviously want to do a pretty good history. Look at his past medical history, asking these questions, and he was able to verbalize these things that he did have a history of a T i A. A couple years ago. He has some pretty significant cardiovascular disease risk factors. He takes aspirin, though, for his cardiovascular disease. He takes 81 mg a day. You also has hypertension. He's supposed to be taking his labetalol 200 mg every 12 hours, twice a day. Sometimes he's compliant with it, though he also has Type two diabetes, and he's supposed to be taking metformin. A grand a gram twice a day has last a one C Whoa. 11% and that was about two months ago. So he's not been compliant with his metformin, his diet and exercise as well. He also has hyperlipidimi a all right, So his last LDL that was actually record about two months ago from his primary care physician was about 200 and his each Dale was a little on the lower end, and he's supposed to be taking atorvastatin 40 mg qd. But as some of you guys know, one of the common chief complaints of being on a statin is you could get myopathies. He was complaining of some actual muscle pain, so he decided to stop taking it. Yeah, and he also has COPD from his tobacco abuse. He's supposed to be using albuterol inhalers, just prn whenever he has some wheezing or shortness of breath. And he's also supposed to use an inhaled cortical steroid budesonide twice a day. Um, it needs to propose to stop smoking, but he continues to smoke. So we got a kind of a little, um, resistant patient here, kind of a bear in that way. It doesn't really want to make a lot of changes past surgical history again. Have that t I A. But there was no particular intervention. He didn't get any kind of tea pee A. He had a cold a cystectomy for some colecystitis that he had in the past. And allergies. No known drug allergies or food allergies. So my question to you is this is something that you guys were going to get. Honestly, if you're in the emergency department, if you're in a hospital medicine setting. And I see you or you're even a family medicine practitioner. A lot of patients will present with chest pain, But for those of you were working in the emergency department, this will be a very regular complaint. You have to be able to differentiate. What are the types of chest pain that you are not really concerned with? Aren't life threatening that they can potentially go home? They're not going to die versus the types of chest pain that are scary. Will make your butthole pucker and make you really, really nervous and say I am not sending this patient home. I'm admitting them to the floor or I'm admitting them into the ice. You I'm not, by any chance, sending them home. So my question to you is if If we do this whether it be in the chat whether this be, um, someone's already starting it, uh, whether being the chatter, whether it be yes, commenting, um, eating yourself. Ah, what are the six most common concerning types of differentials for a patient with chest pain. So someone already had mild cardio infarction. Aortic dissection. Oh, they're flowing in. Holy crap, P e tension. New mown aortic dissection. Cardiac tamponade. God, there's just one more. You guys hit pretty much all of them, except for one last one. So you guys hit pretty much all of them you guys had. Let's see if Okay, everybody got it. Okay, you guys got it. All right, so I'll click it. You guys hit it right on the head. So the most fatal cause you can remember them by the pneumonic pet back. So, pet, Mac is pulmonary embolism. You guys said that one. You guys are awesome. A soft gel rupture tear. That was the one that took a little bit. But you guys eventually got to it. Tension pneumothorax, mild cardio infarction. And this could be an end Stand me, It could be stemming. And also within that grill, move myocardial infarction. You even have under that umbrella. The acute coronary syndrome is obviously unstable. Angina and stemi stemi All of those can present with chest pains and could potentially, uh, definitely have a fatal thing. Fatal type of event that can happen here. Aortic dissection in cardiac tamponade. So you guys get the nail on the head. These air Definitely the ones that you want to remember here. So with that being said, there might be one of those particular differentials that are popping up that are a little bit like, Oh, which one could this be? I imagine that you guys were very, very smart. Already have an idea of which one this could be. Um, but again, we're going to go through those and say, What kind of test would I particularly order in this case? But those are the six. Once I'm concerned about, I don't want to miss. Okay. The other complaint, the associate ID symptom that this patient complained off was that traumatic shoulder pain. They fell down, hit their shoulder. What are some potential, like? Ones that could be like, It's not severe, but it's something that could be very painful. I don't really want to send them home without giving them an intervention. What are some potential types of problematic issues that are acute traumatic shoulder problems that could be causing this pain? Yep. So you hit the big ones. Dislocation, fracture? Yeah. And then there might even be something else. This one's the most minor one, but there may be some type of tendon or ligament. Like rupture or avulsion? Yep. And then absolutely some of you guys even said, like a trap. Nerves? Definitely. There could be some nerve compression if there is a good fracture. If there's some type of dislocation, they're definitely could be some nerve entrapment. They're absolutely So you guys are really, really smart. All right, so right away, we kind of have our differential in our head. Right? Person came in with chest pain. I got it. Least the six most worrisome types of chest pain in my head right off the get go. Second thing is, I have at least three differentials for this really bad shoulder pain that he has and at least the three most significant ones that I don't want to miss. I'm gonna go in. I'm gonna do my physical exam. Now, when I do my physical exam on the patient, these are the things that I see. So I look in the first thing that you should do that's a part of your physical exam, is looking their vital still in there and take a look on the screen on the monitor. What is their heart rate? Okay, he's tachycardia at 1 30. His respiratory worry is 22 breaths per minute, so he's a little too Kipp. Nick, Are you that BP? What the heck? BP is 88/62. It's not too great, right? So he's definitely a lot lower than 100 millimeters of mercury. So his systolic pressures a little low, and his diastolic pressure is 62. It's It's a little low, too, but I'm a little bit more concerned about that systolic pressure. Okay, temp, 98.6 degrees Fahrenheit. So he's not febrile. Um, s P 02 is 88% on room air. Oh, sorry, guys. I'm not very good with the Celsius. I should be better with that son of a gun that is 37 degrees Celsius. You guys probably use that over there. Well, there is a complete difference in the guidelines conversion factors. All right, but yet 98.6 or 37 degrees Celsius. So he is a febrile in this scenario, and it's s p 02 is 88% on room air. That's that's not great. But that's not terrible, considering that this patient also does have COPD so a COPD, especially if they're a very chronic stage type of COPD. 88% might be where they live on their own, so I wouldn't be like right away. Oh, shoot. This person is 88% to kidney. They may be naturally to keep Nick, but you can't also rule out that they could be having some other type of process going on here. So definitely 88% doesn't scare me right off the get go, knowing that he has an extensive COPD history. But the fact that is to keep Nick and a little bit on that lower and on his 02 saturation makes me just a little bit more quick to say Could be something else that's actually exacerbating their issue or something else going on. Okay, cool. So tachycardia it to Kipnis. Hypotensive and maybe a little high pox seeming, But that could be chronic. We look at him, he does appear like he's in distress. He's in pain. He's a little too Kipp Nick. He's a little short of breath. Cardiovascular wise. We go, we stick our staff, the scope on the chest. We definitely hear his rate being a little bit faster than we would like since tachycardia. His rhythm, though, is regular, and he's got a normal s one s two. But you hear this additional. And if you're you're able to hear this, you're you should be a cardiologists. I've only heard this once, and that is they heard additional s four heart sound. So an additional s four hearts on, I guess. Let me ask you guys, What could unedited s four heart sound, uh, be potentially concerning for if you guys are preparing for, like your step two? Yeah, aortic stenosis. Definitely. Hypertrophic cardiomyopathy. It also could be concerning for just, like, hypertensive types of diseases. Right. So you get that left ventricular hypertrophy from, ah, high after load. So hypertension. But it also could be like, you know, patients who get, like, an acute myocardial infarction. They can also sometimes get it s for heart sounds so all right, so he's got this s for We don't know if it's chronic. We don't know if it's, you know, a cute thing. Um, but we go to next thing we listen to his lungs, we listen to the lungs, he's got some rails or crackles bilaterally. and they seem a little bit more course rather than fine his abdomen up son of a gun, his abdomen appears nondistended, so it's not protruding. Um, it's also not really tender when we're palpating all across the abdomen, all four quadrants and his bowel sounds. When we're listening, they sound normal. Active. I don't hear any hyperactive bowel sounds. I don't say here in the absence of bowel sounds, either. So that's good. And then musculoskeletal wise, he's got an obvious deformity of his like right shoulder. It's like squared off. And then when his arm, it's kind of like Stuck, it's like stuck in this external rotation type of position and slightly abducted. It is very tender to touch around that area of the shoulder joint, and he's not really able to do any kind of like active range of motion or passive range of motion. It hurts too bad to do that, so we have the patient with chest pain, shoulder pain. We have our differentials, most scary ones for chest pain, most scary ones for the shoulder pain. We got our actual vitals and the things that may be a raking us a little bit more quick to say this patient is really sick. They're somewhere in the middle or they're they're stable at this point time, right? I guess my question is, would you guys be a little bit more nervous about this patient is saying that they're stable there somewhere in the middle or their unstable? What would you guys say if you went into this room? You saw all of this. Would you bleed more to stable? Unstable, or they're like they're somewhere in between the middle. And that might be dependent upon your sense of hum. For maybe you're used to seeing patients who are super sick, and this isn't bad for you, but I guess in the grand scheme of things, this should always should be something that you're going to look at. If the patient looks really, really bad, I think about that. So, what do you guys think? Do you guys think they're kind of stable? Unstable? Yeah. I would go with them. Kind of being a little bit more unstable at the point time. They're in a lot of pain. They They're a little hypotensive there. Tachycardia there too. Kipp. Nick, I think they're a little unstable. Okay, Ah, let's see. Here. Let's go to the next thing that you guys are great. Okay. Okay. So we go back then, cause if we had to determine which one do I need to focus on first? Going to focus on the chest pain of the shoulder pain. I'm going focus on the chest pain because that chest pain stuff is likely to kill the person before a shoulder pain issue, right? I mean, there's obviously certain extensions, but, you know, I would say I would be leaning more to most of the time. The chest pain has got anything I got to focus on a lot more quickly. So with all of these late forth, But, you know, in front of you, which one of these? Maybe it's maybe like, I don't know. Still, which one of these do you have? A little bit more of? Ah, high suspicion for I guess, is a good question. Right. So which one do you guys think Maybe I'm just a little bit more concerned about? Okay. A year? Um, I am. I am. I am. I am I I Attention with her. Yes. So here's the thing. It's kind of tough to say. Still, I would definitely think about this. Think about the patient's risk factors, right? So this is where you got to go back. And you gotta remember all these things that you're learning like Think about risk factors. So think about risk factors for someone having a pulmonary embolism. You got to go back to that stuff for Virgos. Try that. Do they have anything that makes them hyper coag? It'll do they have anything where that would induce any type of endothelial injury? Do they have anything that's going to cause a Stasis of blood flow? And in these situations, there could be some factors that definitely increases the patients risk of indoor feel injury. The fact that he is a smoker, but he seems like a relatively kind of mobile guy. He hasn't had any kind of surgical procedures lately. Yes, have been immobile or had anything that's required him to be bedbound, and he doesn't have any underlying hypergly. I get a bill condition that's been listed here, such as, like a factor five leiden of protein, C s deficiency nephronic syndrome. You know, the whole whole gambit of super kind of rare causes, but it's still a possibility, right? It's not something that I can completely rule out. He also what's the most common cause of the corner, And it is, um, would be a DVT. It's not always the most common, but it's definitely is gonna be like, you know, upon that list. So I'll be looking. Do they have any issues with calf pain? Do they have any swelling? A symmetrical swelling of one side of the leg? Do they have any calf pain in the past couple of days? So I take a look at that as well. Those are also things to be thinking about since DVTs air likely the most common cause of someone developing a piece. So think about the risk factors right now. A lot of the risk factors don't really point me to a pulmonary embolism. So my suspicion based upon the patient's oh, here, this is a good one. What's the criteria that determines my pretest probability for a P E? I remember every single factor that's in it, but I would say that his is relatively low. What is that criteria call that determines your pre test? Yeah, his well score. So we could calculate it if we wanted to, and you can also use are perfect score to of perks was really good. One is well, perks scores is very good. I like that one was. Well, those are more likely to be easy. People who use that perks score. Yeah, but for your like exams, your boards and stuff, I tell you, I think the Wells might be a little bit more commonly referred to, but I say his pretest probability is relatively low. This office, you'll rupture tear. That's usually gonna be someone who, like, had some type of serious, like a vomiting episode or had a lot of trauma to this area, some type of surgical procedure near that area. I wouldn't say that there's anything that really pops out that to me, tension with or ACS. I think that's not a bad thing to say. However, one of the things I think is super obvious about attention pneumothorax that wasn't on this person's physical exam is that when you go on auscultate the lungs, what would be one of the obvious things that you would you know here or not here? Yeah, Gordon said. Nothing. The absent breast sounds so his lungs were more rails. E. There was no absence of breath sounds. So with that being said, I don't really think it's attention New move or ACS as well. Myocardial infarction. We got to think about the risk factors and then oh, yeah, Laurent said. Asymmetrical chest infection definitely could be. Also, sometimes the trick. It can be deviated a zoo. Well, that's a possibility. Usually that's easier seeing on a chest X ray, though. But easiest thing is just go, go Listen, right, go listen to the lungs. That's kind of the best thing to do. But my cardio infarction wise think about risk factors for this patient. He's cut the worse one diabetes. He's got the second most common one. Hypertension. He's a smoker. He also has hyperlipidimi. A. He's greater than 65. Oh, man, this guy has got a lot of the gambit of things that puts him at very high risk for ah que coronary syndrome or some type of a scheme of heart disease category, Right? So that being said, he has a lot of the risk factors. Also, think about the the classics findings on the physical exam they present with this type of pain that's usually squeezing. It's substernally. It radiates to the left side. So I'm definitely leaning to that one aortic dissection. He also has a lot of risk factors for that. Right? So he has hyperlipidemia. He is a smoker. He has hypertension. We don't know if he has any order can do. Here is, um maybe hasn't been tested for them, but he's definitely at risk. EKG can help for diagnosing in mind. Yeah, absolutely. Yeah. And that's what we're going to get to. I'd say he's lower on the end for aortic dissection Just because, you know, that causes that tearing type of chest pain that radiates into, like, the scapular area and then cardiac tamponade again. If I was listening to his his heart, I would hear decreased heart sounds. He is hypertensive, but I would also potentially cease um, JVD a zoo. Well, right now, these are the part of the backs tried, so usually try. It is pretty much you don't really see it in the the medical field. It's good for exams, but it's not too common. But nonetheless, I would say I'm leaning more to, um I and I think most of you guys are a swell. So, labs, they can potentially help you here to discern which one of these you're concerned about. But you often times if you guys had to pick them again, these are going to be the most distant, important ones. I'd say a CBC. You can't ever go wrong with getting one of those. They just help me to look for anything that could be an incidental. So are they bleeding is really something I'd be concerned about. So if they are bleeding having aortic dissection and they're sanguine ating, they're having going into hemorrhagic shock of some kind, I would want to make sure that they're not acutely anemic. I would also want to make sure that their platelets aren't super low, a swell that they have like a thrombocytopenia as well. CMP is you can't go wrong with these. Well, they just give you a good idea the renal function, liver function, any kind of complications as well. And, uh, the other thing is proponents and you guys so someone already set it here. Gourmet said troponin and d dimer So a d dimer. I wouldn't I wouldn't be opposed to that because I'd say that patient that low pretest probability. I think I'm just a little bit more bias. And also the e d didn't order one for this patient just because often times a lot of things that patient have. If they have a lot of things going on, a lot of things can elevate your d dimer. So it's just so non specific and it doesn't really lead me down the the way of staying on That's definitely rules out Peek, because if you get the d dimer, it is elevated because they have something else going on that's elevated that D dimer not the p e. Unfortunately, that may lead you to go order an unnecessary CT pa. So I'm not always a big fan of ordering a d dimer. But for your for your exams. Yes, you should consider a d dimer as ah, since he has a low pretest probability. But just realize out there in that world, there's a lot of things that elevate the d dimer, and it may just cause you to go down the wrong path for ordering unnecessary tests. Here's a good question, though. This is what I made mistake of so many times I want to see what you guys think. Proponents. Is it better than EKG for determining of my cardio infarction, or is an e k g better of determining of myocardial infarction? Okay, kg EKG, EKG, GI proponents. Yeah, not wrong to pose distinguish instantly. And Angela, definitely opponent would tell us more about some type of, you know, infarct. In that case, yeah, rather than, like, you know, esquina. Definitely. I would definitely take that into consideration. So here's the thing for troponin they take a couple hours. Um, toe actually start kind of rising and peeking. And so if the patient is having a stemi, they actually will show more hyper A Q T waves and ST segment elevation before they're have a troponin. And so I always say, you know, is it good for the best patient chest pain? Yes, but again, get your EKG first. That is the gold standard. Because if you go and get the troponin is and they're elevated that what does that tell you? What Proponents can be elevated in a lot of different conditions. It doesn't have to just be in an m I and so that's something to think about because there is things like what's called demand ischemia, where there's a lot of other factors going on in the patients. You know their their body at this point time that could be causing the myocardium to work harder and caused that your opponent lead to occur, sometimes called demand ischemia. And so I think it's better to get the EKG. And if the EKG shows ST Elevation, get those proponents. If they show some ST Depression T wave inversions, it also is in a bad idea to get proponents because, as someone already said, little distinguish instead me from a stable angina. So yeah, okay, so did I miss anything there? Okay, so if we got this person's labs, he had a CBC was normal. His creatinine is 1.21. His bun was 33 sodium was 1 28. Potassium 5.6 chloride, 77 bicarb 11 glucose. Oh, my gosh, 5. 30 and troponin was point oh five. And normal for our Japonese is like less than 50.2. So when you're looking at this, there's definitely some things like pop out at you, right? But before we go over those things. My question for you is we didn't get an EKG just yet. We're going to get one we're gonna look at when we did order EKG. I'm not going to tell you what it found, but we got the troponin was point Oh, five just a little bit over the normal level. You're likely going to get cereal proponents if you find something on that kg. So keep that in the back of your mind. Should I get cereal proponents? We didn't get the EKG yet, so I can't say yes yet. The hold off. Okay. I want to see what you guys think of these labs, though, because they're all wonky on this patient here. So what do you guys make of his renal function? If his baseline creatinine is 1.2 of? Is that an acute kidney kidney injury? Or is that just a CKD um two in this case? Well, you guys think Think it's an a k I or do you think it's just his chronic kidney disease? So his baseline's 1.2 and his new creatinine 1.21. So I would say ckd Stephan Stephan said ckd I would agree with that. And the reason why is is you have to understand the definition of an acute kidney injury, right? So acute kidney injury. There's what's called the K diet go criteria and the K Daigo criteria, which is used. There's also the rifle criteria. Maybe that's come across for acute kidney injuries. There's the rifle and the diet. The Kate I goes a little bit more preferred in stent in certain scenarios, but either way, they both agree on the fact that in order to have an acute kidney injury on top of your chronic kidney disease, you have to have an increasing your creatinine and 48 hours That's greater than 480.3, so greater than or equal to a 0.3 above your baseline. Creatinine within 48 hour period is defined as an a k I. And if it's within a seven day period, you can also say if it's greater than or equal to 1.5 times. Whatever their baseline creatinine is is also considered an a k I. And the higher you go beyond 1.5 times that baseline. The worst. The acute kidney injury is so in this case, it's 1.2021 point 21. That's not greater than 210.3 increase right. That would be at least like 1.51 in that case. So I would say there's no acute kidney injuries. That's a good thing to think about, because that determines our management of the patient. What do you guys make of? Ah, son of a gun. What do you make of that low sodium? Do you guys think it's a really That's my question. Is it really? And what I mean? And I realize that is his actual true serum. Sodium. 1 28 There. Is it something else? It's not. It's not really yes, you ever iPhone is. It's It's pseudo Ah, hypo pseudo hyponatremia Due to hyperglycemia, right in that hypoglycemic events, it's going to just it's gonna increase the osmolarity right, and that's going to definitely help Yank. A lot of the water out of the blood stream is, well, Yanga. Lot of the sodium out of the bloodstream and into the kidney to bills, and so you're peeing a lot of that out. If you fix their glucose, their sodium will most likely normalized, and there's actually a formula and we'll show you that can actually correct for this. Okay, so yeah, Why is it not true? Yeah, again, it goes back to the to. The whole concept is that whenever you have this high glucose level, right, you're getting into the whenever you have the glucose filtering across the, um never have the glucose that's filtering across the blue Maryland basement bring into the proximal convoluted tubule cells. Right. You have all these glucose molecules. Glucose is going to bind with those sodium glucose co transporters and bring sodium with it into the proximal convoluted tubular cells to get re absorbed. But in this case, there's too much glucose that those receptors get saturated. They read that reach that transport maximum. They're not able to bring the sodium with them. And so because of that, it changes that whole process where some of the sodium and water can get lost. But again it goes back to the osmolarity of the blood stream. It gets a gets significantly changed in this situation. Okay, so if we go back, definitely is not a real sodium, and then the other thing is is an eye and gap. So if I actually, we'll do it here in a second. But if we correct the sodium, you'll get a different number and I'll show you how to do that in a second. But his and I and Gap is and I and get something to consider, right? So if I were to actually, there's a calculation in here that you can utilize. It's on M D cow and on MD. Calculate can actually put in a patient's like corrected glucose. And whenever you go through that and you actually account for his corrected glucose, you'll actually get something really interesting. So let's actually see what that is. Me. Go through these. Oops, I went to quick How I give you doesn't the answer there? Sorry. So if we look here and we actually take into consideration with the patients, true sodium is if you actually do the sodium correction for hyperglycemia. Sodium is 1. 28 is glucose is 5 30 is true. Blue is true. Sodium is 1 35 so that is actually true sodium. If you guys going to mg count, there's this formula. It's called sodium correction for hyperglycemia, and if you plug all of these numbers into that. It'll give you his true serum sodium, which is 1 35. So then, if I go through and calculate this patient's and I and Gap, it's actually 1 35 minus 77 minus 11, which gives me an an eye and gap off 47. Oh my gosh! And and I and Gap, that is pretty significantly high. What happened there? Um, and and I and Gap, that is greater than 12 is definitely considered to be a high. And I got and I got metabolic acidosis, Right? So that's something very interesting as well that we see here. So we doesn't have an acute kidney injury. It's just this CKD. He has pseudo hyponatremia due to his hyperglycemia, his and I and Gap is elevated 47 and his glucose is Gargantua. Sleep high at 5. 30. So my question for you is is what do you make of that? If a person has a high and I and Gap, their glucose is through the roof, what kind of additional tests would you want to order to consider that yet even said it iPhones at it? Yeah, James said it DKA definitely got to be thinking about that right? And the reason why is he has a history of diabetes. And so so someone said, Why don't you account for the potassium and the and I got Oh, and that's a good question. So the reason why we don't really account for potassium potassium, it's so so small and your extra Siler fluid that it's pretty much know, like if you actually think about ourselves pretty much are inside of the self interest. Cellular early is where most of our potassium is when you're considering the and I got you're considering the serum, the extra sailor and I and Gap. So you're taking the extra sailor sodium minus the extra sailor chloride, minus the extra cellular bicarb. If you take in a consideration the amount of potassium in there, it's so small and so insignificant that it doesn't even. It's not even worth putting it into. The calculation is the basis of that process. But that's a great, great question. Yeah, I'd be concerned about diabetic ketoacidosis in in this patient, so right away I would be considering ordering what other thing? So he said he's on metformin, doesn't have diabetes. Type two ruling out ticket, so you can still have DKA a in type two diabetes. It's more common in type one diabetes, but you definitely can't. And if you guys remember also said he was not compliant with his metformin. He hasn't been taking his metformin like he should. He should be. He's also not eating properly. He's also not exercising again. Do keep in mind. DKA is not as common in a patient with diabetes type two, but it is a possibility. Yeah. So you guys were saying a BG key Tones? Yeah. Baby elected. Great. I love it. Why would you order lactate just out of curiosity? Why? Why would you would relax? Think that's a great one. I agree with it. But tell me why you order a lactate lactate acidosis. Okay, Definitely. And metformin can lead to it. The only thing is, he hasn't been taking his metformin right, so you can get a metformin related lactic acidosis. He hasn't really been taking it, though, but it's possible, especially since he has chronic kidney disease. So since he has renal failure, and if he was taking his metformin, it's a possibility you could have a metformin related lactic acidosis but he's also hypotensive. He's too Kipp neck. He's tack a card. Ick. I gotta be careful. Make sure I don't miss any kind of, like shock or hypovolemia and bang. And then he said, It's absence. I don't want to miss anything like that. So lactate. Sometimes a good idea. Plus, I don't know if you guys know the pneumonic for what I think is the easiest one to remember for lactic acidosis. Armour for the most common things I don't like to remember things that I'm not really ever going to see. S Oh, I remember cult K u L t k for ketoacidosis. You for your Remicade AssiDomaen this l for lactic acidosis and tea for toxins. All those super kind of rare ones that I probably won't see too often, but I'll keep it in the back of my mind. Okay, So with that being said, if I see an an eye and got metabolic acidosis, I should always check ketone is check lactate and look at their creatinine and urea your bun. And that could already give me an idea of the most common causes of someone having it. And I gap metabolic acidosis, right so right away. I agree with you guys. I would get a lactate, I would get key tones. And if I truly wanted to determine if they truly were acidotic or acid Demick, I would get an ABG because they could have this and I and got metabolic acidosis and their Ph could be normal. So if I wanted to turn on how bad their asked doses Oh, my gosh, they're, like 7.0 on their pH. That would be a good thing, because that can alter the activity of certain pressors. So yeah, I would I would definitely get a BG key tones lactate. And again, I already have my bun and creatinine to take a look at it. If I really wanted to, you can add on something called Osmolarity dap I I think that's past the school. This lecture, though, but that would help you with the toxin mediated things. Okay, I hope that made sense and helped let me go to the next thing now. So you guys pretty much hit the nail on the head. Definitely does have doesn't have, like a true AKI CKD. His high point of treatment isn't really it's pseudo because of his hyperglycemia. You guys are on the ball. His Trucility was 1 35. If you correct his sodium, then do the and I and got calculation his and I gap is a whopping 47. So because of that, I want to rule out the cause is of an anti and got metabolic acidosis. Get an ABG to look at the degree of acidosis. Also, what else were the ABG help me with? So it's gonna give me pH. It's gonna give me bicarb is also gonna give me oh two in the 02 with an arterial blood. His 02 sat was like 88. He was a little too Kipp Nick. Yes, COPD so he could have some alterations or fluctuations. And it's 02 and the 02. So what? Tell me if he has any hypoc senior or hyper Cap me is, that's also another benefit. Get the key tones for the ketoacidosis. Get Thesiger Um Osmolarity because that's where you can calculate the asthma would happen was telling you guys about a lactate and then we already have his urea from his Ah, cmp. So with that being said is this was his ABG. What do you guys make of that? What you guys make of that? Definitely. Um What? What do you So 7.21 pretty acidotic, right? Uh, 80 82. That's his 02 saturation. That's his 02 saturation. Uh, not all of our apologist. Partial pressure of arterial oxygen within the blood. What do you make of that? 82. Is that low? Is that high? Is that normal? I said lower. Normal. Is it lower normal 82 millimeters mercury. What do you think it's on the lower end of normal? Yep. Yeah, it's on the lower end of normal. So it usually the lower end is like 80 80 to 100 is considered to be like a normal partial pressure of arterial Oxford. So he's He's technically not super hypoxic. Really? He's right in that lower end of normal. Yeah. So not too bad. 30 that is, is CEO, too. So, normally, our CEO of the two is anywhere from like 35 to 45 so it's a little low. And that should make sense. Right? Because if he's breathing faster, if he's too kipp Nick, he's blowing off his 0202 would be a little bit lowers. That makes sense. And his bicarb is a whopping 11 and Bi Carbon, usually like 20 to 26. So that's way, way lower. He's definitely tanking his bicarb. And so let's see why his key tones were positive. You guys are on the ball, so he's definitely got a DKA. He's got a d k because the sugar super high. He has an acidosis. He's got a bicarb drop, and he's got key tones within his blood and urine. His serum osmolarity was normal, so that also rules out like an h a jasa hyperglycemia hyperosmotic syndrome. His lactate was 4.1. Oh, shit. What's a normal lactate? Less than and it's converted from Institution Institution, but approximately less than what would be normal. Active. Yeah, and then he said to that's, that's That's I say that pretty, pretty common average is less than two is pretty much normal active. So he's a he's. He's way above that. Um, he's at 4.1 that's a little high. It's a little high. So he's got a what? This is why you guys are so darn good. He's got a lactic acidosis and he's got a cumulus of those is Oh, shoot is your is 33 a little bit high? Not too bad, though. So unlikely your remake acidosis because your Remicade, as it does, is when someone has a really bad acute kidney injury on top of their CKD or they're a complete end stage renal failure there at CKD five and they need to be on dialysis and they aren't getting their dialysis. So I would I would argue that his urea is not high. It's unlikely causing his acidosis. You have be be a support. We're not even close to it. This is This is an unfortunate case. Okay, here we go. So I think you guys did a pretty good job with that. He's got a small troponin anemia. We get his EKG, okay, and just just keep in mind. I didn't get to the EKG yet, but keep in mind, you get serious opponents. There must have been a reason I got a troponin right When we when we do that, we we want to make sure that we don't blindly order them again because a lot of things can cause a proponent elevation. But when we did it and there was a reason the second one was 15 and it started almost 30. Holy crap. That's really high. So if something had to happen okay. Is this EKG? What? What do you think was going on here? So we always do rate rhythm, right? You can go through the whole process rate rhythm. You can do the axis. I just like to go right. Rhythm right to ST segments. So, weight, I'd say he's not going to fast on this case. Um, which is obviously this is the EKG we found online. This isn't the real patients EKG. And if you remember from his physical exam, he was actually going fast. So again, right? Not too bad. But in real life, he's going fast. Rhythm is regular. And then when you look at his ST segments throughout it, You guys already heading it. You guys are too darn good. Yeah, he's got an ear. Stamey. Yeah. So I'd say he's got a little bit of ST Elevation. I think there's even a teensy bit in the V one, but definitely v two v three, v four. And look over here. He's even hitting one in a V L1 in a V l. A. What part of the wall of the left ventricle. So what part of the wall of the left ventricle are you heading when you get one and a VLDL elevated? You guys already said V two V three before is like anterior septal and anterior apical wall. But, yeah, he's getting like that higher lateral wall. So this dude's got his anterior septal anterior apical a little bit, and he's even getting a little bit of anterior and, like, lateral portion of his his left ventricle. And then you can see here. He's got reciprocal changes in his Ah, insulin. Lead three here. Okay? With his ST segment depressions so pretty significant. And then what are these called? Here's another good thing Or what are these things called? You see, we definitely have ST segment elevation, but you see this part here from as we're going up, Yeah, yeah, can't get anything past you. Hyper a Q T waves Hyper Q T waves are actually the first sign of, uh, of a standing. So this would be a very early sign. And that's what happened is that this guy had, Ah, in real life he had hyper Q T waves, and that came up first. And then he had some ST segment elevation and then some reciprocal changes over there. So reciprocal changes. That's a good idea. That's a good question. So the whole purpose of reciprocal changes that really helps us to differentiate between someone having a true, like myocardial infarction versus something else called benign early repolarization so benign early repolarization You can get like these ST segment elevations, and it's usually benign finding, Um, and this can happen where, when you're looking at them and you're seeing ST Elevations like this, if they had no reciprocal changes, that would automatically think about benign early reports. And the second thing is that usually there's a very odd morphology of benign early reports where it kind of sometimes takes a little fish hook type appearance at the ST Segment junction before it goes into the T wave. Those air the significance of it. So I would say the main primary reason of the reciprocal changes is to help you have a higher pretest like ah, higher probability or suspicion of a schematic changes to the myocardium rather than benign early repolarization of the Myocardium. And those are two. Big difference is because one is worthy of going to the cath lab, and the other one is not worthy of going to the cath lab. Okay, here's his chest X ray. Are you guys making this not good? I'd say. Recall that like cotton balls in his lungs. Right. We call that. Yes, I'd say it's like pulmonary edema, right? So definitely looks pulmonary edema like Yeah, and so usually they get, like, plural effusions. It's hard to see here, but you might even have, like a little pleural effusion on this side here. It's tough to see, but there may be some pleural effusions because there's the blunting of that cost, a phrenic angle. And sometimes when there's a blunting of the cost of phrenic angle, sometimes you can get, um, definitely some pleural effusions there. And then, if you look, it's almost like impossible to make out his cardiac borders. And so usually here, that's kind of following the pattern of the pulmonary vasculature. There's a lot of interstitial fluid that's kind of lying in between the pulmonary vasculature, particularly around the Peri Hilar area, and as we work out you, even if we were to rarely zoom in here, you can see these horizontal lines. He's a call, curly, be line. So he's got a lot of pulmonary, a demon. It's bilateral. It's associate with pleural effusions. So with his likely him having an M. I, he did develop what's called flash pulmonary Edema is probably helping. Some complication of his M I of his left ventricle, which is the anterior septal apical and lateral wall, are all fract up. He's probably not contracting blood out of that left ventricle, and it's backing up into the left atrium, backing up into the pulmonary circulation and third, spacing into those interstitial spaces. Causing pulmonary edema is this is called cardio cardiogenic pulmonary edema and son of a gun. I got to fast cardio cardiogenic pulmonary edema, so he likely has some problematic issues there that we go and check his 02 sat up later. I bet it's going to be a little bit worse and eventually get an ABG that will come back and showing a little bit worse. Arterial oxygenation. So this happened a little bit later. He started about some shortness of breath and boom. We see this card a genetic pulmonary edema. So he's had a lot of problems already. We take a look at the shoulder X ray. What do you see? Anybody could pick this out, right? What did you guys make this shoulder X ray? Yeah. This located this located? Yeah. Ouch. Anything is a good way of thinking. Yeah. So this is an anterior shoulder dislocation. Um, so yeah, Tasha, Boom. It's technically, you need a lateral view to really, really specifically diagnosis, but and your shoulder dislocations, the more common type of shoulder dislocation. Um, so yeah, and his situation. It's anterior shoulder dislocation that was in this patient. So it was one of those ones that we picked. So so far, this guy's got an M I He's got lactic acidosis. He's got ketoacidosis. He also has a, uh your shoulder dislocation and cardiogenic pulmonary edema. Things get worse. Maybe so. Answer. Ladder Stamey. Cardiogenic shock. So cardio cardiogenic shock. Because think back he has his left ventricle. Is infarcted super bad right now. The anterior. If you get if you hit your anterior portion of your left ventricle, say goodbye to your ejection fraction because it's gone. And so because of that, he's gonna be hypotensive member. He was hypertensive when he came in. He's going to get even more hypertensive. Potentially, he wasn't able to push blood out of his left ventricle is backing up into the pulmonary circulation getting cardiogenic pulmonary edema. So that day and he was tachycardia. And so when you get hypotensive, it creates a reflex tachycardia to try to increase your cardiac output. So he was tachycardia, hypotensive and cardiogenic pulmonary edema. And if you actually went and felt his extremities, they were kind of cold and pale, period. So he's definitely within that cardiogenic shock category. He's also within that area, potentially. We didn't know when we first got his 02 sat. It wasn't bad. And we got that ABG. It wasn't bad. Later on, he had a repeat a BG because his 02 saturation actually dropped down to like, 75%. When he was actually a nasal cannula. They sent another a BG, and his 02 was much, much lower. So he did go into acute hypoc stomach respiratory failure because off that cardiogenic pulmonary edema, it was just altering his gas exchange process. Get diabetic ketoacidosis. Just like the gas a dose, it's and a right anterior shoulder dislocation. Go. So my question for you is that we're treating the anterior lateral stemi. What was his 02 on the auction? Yeah, it was 75% later. So originally it was he was 88% on room air. And then they got the ABG when he first came in. And it wasn't too bad. His po two is ah, was 80 82. I think it was on the ABG. Later he started to have some difficulty breathing, and his 02 sat dropped to 75%. I think he was on six liters of oxygen at that point time. So with that being said, he's definitely going into slowly that hypoxemia range. So and your bladder stem? What's the what's the treatment that we should do for this patient? What's what should we do? What? What? What do I got to give this patient? He's already had pox six. So I'm gonna give him oxygen. Yeah, You remember Mona, right? So we got the oxygen on board nitro. Not a bad idea, since it's not the right side of the heart. Aspirin definitely. Give him 3. 25 of aspirin and then jeweler anti platelet therapy. So we got the aspirin, and then we got to give something else a pizza White 12 receptor inhibitor. So again, depending upon your institution, I would consider maybe something like clopidogrel versus ah, take a girl or Oh, iPhone. Good point. Yes, he was hypotensive. Yes. So we would not give him nitro know he was hypertensive. So if we did do that, we gave him nitro. We would drop his pre load, dropped the ravine. It's return to the right side of the heart, dropped the venous return eventually to the left side of the heart. And then worse in his injections. Action outwards. So, yeah, he would become more hypertensive. So good call iPhone. Do not give this guy nitro. So yeah, I would definitely keep him on auction. Give him aspirin. I would avoid morphine, but if you have to, because they're still having a refractory chest pain. Give him the morphine. Give him the dual antiplatelet therapy, which includes aspirin and clopidogrel. Or two category. But it depends upon the institution. And then after that, we could do something else. So someone said with his coat to what would be the oh to target. That's good question. So for COPD patients, I prefer 88 to 92%. Um, for patients with a ski MC like an event, I would probably a melittin. But higher, even though they have a COPD underlying like their disease process, we want to get a much oxygen to the myocardium is possible. So if it wasn't having any kind of a scheme it event, I would aim for 88 to 92%. But now that he's having this active, am I I'm gonna infergen than 94% is what usually the guidelines would say is try to aim for greater than 94%. So that's what I would aim for. I would go for greater than 94% and I was just up my oxygen whether I had to go from the nasal cannula, it's a high flow to Optifoam. I would go up until I reached the oxygen goal in this patient. Okay? Yeah, oxygen. Do not do nitro bid cool iPhone. And then I would also give him aspirin clopidogrel. What else would I want to give him those because he's going to the cath lab. I'm gonna use the anti platelets to kind of reduce the thrombosis, but I want to prevent the propagation of the thrombosis by giving happen. Matilda beast. Yep. So I would give him happen. So I would you aspirin clopidogrel, bulls him with heparin, put him on a drip or an infusion of that brain given auction to titrate to greater than 94%. Avoid nitros. Try to avoid morphine, cause usually we have to give it. It's a worse prognosis, but give it if they need it. And also, more thinking dilate your vessels so it can also cause hypertension. So I want to stay away from morphine as well in that scenario. So these are things I would do right away after I've done that. Then I would send him to where PCI. Yeah, and some of the cath lab baby. So I reduced the thrombosis with aspirin clopidogrel. I reduced the propagation of it with heparin Bullis. An infusion increases. Oh, to supply. I would like to use a nasal cannula if necessary, but if I have to upgrade to a nonrebreather if I have to upgrade to a high flow nasal cannula Opti flow. I will to meet that goal. And then the ultimate goal is to revascularize go to the cardiac cath lab. That is the desired treatment process. We would rather do that than new Thrombolysis. And then after that post Emmy care, you add on the other things that you would like beta blockers, ace inhibitor statins, all of those fun things as well. And then continue if they get a stent. Uh, it's called a drug alluding stent. Usually we want to prevent any stent thrombosis for at least the first year. So we'll continue that dual antiplatelet therapy for about a year and then stop, and just to aspirin and four hours and 120 minute distance. Oh, yeah, yeah. And so again, this may be another thing to consider. Uh, I don't know if there is a difference across the different areas of the world, but preferably here. We try to reduce the, uh, the utilization of thrombolysis just because it's inferior into consideration to the cath lab. So, for us here, let's say that we had an institution that didn't have a cath lab and you went there and you had a stent. Me, you would get thrombolysis. And if you were at least within a product, you know, a certain proximity to a nearby cath lab, you would get transported that cath lab as long as you met that time frame and window to go to get the cardiac catheterization. So yeah, we just They're just a superiority of cath lab in comparison to thrombolysis. Okay, what would you do for the cardiogenic shock? So he is hypertensive. So his left ventricular stroke volume and cardiac output, or worse. And at this point, time so I can give drugs that can help, Hopefully augment that decreased contractivity of the left ventricle if the MYOCARDIUM. Responds to it. What kind of drugs? What I want to give in this scenario. Um, that could potentially increase my stroke volume. My cardiac output, my BP. What I give? Well, you guys think I know troops. Alpha receptor agonists, a vasopressin path. A medic. Okay, so you guys were hitting it on the head, so Yeah, Dopamine s Oh, someone said dopamine are dressed. I'm not the biggest fan of dopamine. And I think it's the devil's drug. But if it's all you have, you use it so I don't. Troops is a great one, and I prefer the term I know Presser. So there is no troops and then there's I know pressors. So I'm the troops pure. I know troops would be something like dobutamine our Miller known. That's not a bad idea in this patient. I could consider dobutamine or milrinone just taking a consideration. You put someone on dobutamine, it's gonna increase their heart rate. He's already around one. I think he was like 1 20 something 1 22. So it might up his heart rate a little bit. And if you're okay with that now, at least not popping them over like 1 50. Sustained. I'd say that's not a bad drug milrinone a little bit better, but it's also a renally excreted. So if he's got really bad kidneys at this point, which is not his kidneys are working appropriately, it's that's a good drug as well. So milrinone is something to consider. Here's the thing that you got to realize when you put someone on Dobutamine are milrinone. It squeezes the heart but dilates the vessels. So what could that due to their BP, If I only put them on dobutamine or Milrinone, I give him dobutamine or give him a million. And I check his BP a little bit later after I put him on it. What'd you expect happen to the BP? Yeah, it'll drop. So that's not something that we want. So we want to avoid giving it by itself. And if you do, just keep an eye on that BP so it doesn't drop. So sometimes what the best thing to do is is do a little dobutamine to give a little bit of squeezed to the ventricles. But give something else that will clamp down on the vessels a little bit so that you don't drop their pressure. And so I prefer to do something like dobutamine or milrinone, plus something like norepinephrine, because that gives you a little bit of squeeze. And guess what else norepinephrine does. It squeezes the ventricles to epinephrine. Is another drug to consider as well, because epinephrine will squeeze the ventricles and squeeze the vessels. So these are drugs that I would consider. So I would consider something like that. You always have to defend the map. The mean arterial pressure defendant like it's going out of style. So generally, depending upon your institution, some lame for like greater than 65 is enough to perfused your organs. And so one of the things that you can consider I'm not the biggest fan off, but I'd be very careful because he's already got cardiogenic pulmonary edema. You can give fluid and it helps the increase the blood volume in the BP. But don't give them tons because you're just gonna push it into the lungs and make their breathing even worse. So I give small bolus. Is I? Honestly, I'll do like 2. 50 bolus is every now and then to see how they respond to that and then you do a nine oppressor. So start this up first to get their BP up a little bit like norepinephrine norepinephrine then followed up with the dobutamine or milrinone because that will increase their cardiac output. Okay. And when you do this, used to sometimes want to really get a factor, it measurement of their BP. So sometimes you put in, we'll put an arterial lines that gives you a continuous accurate measurement of their BP and also tells me if they decide to go a systolic for some reason, and that gives you continuous monitoring. Here's another thing. If you're running some of these, like really highly concentrated drugs through of prefer live E, you might want to consider a certain type of line that goes into a large vein that can really deliver these really caustic and concentrated medications. What kind of ah catheter would you want to put in if you're putting in these large amounts of fluids are not large, large amounts of concentrated drugs that can potentially be caustic in nature. Concordes a lot of like extravasated in and necrotic risk. If it does, and filtrate into the the subcutaneous tissue, what kind of line would you want to put in maybe a year here? Yeah, central line. So central lines are great in these situations of when you're running in these high doses of pressors or running a lot off. So like an internal jugular vein catheterization, a subclavian being catheterization and if you're in a code of femoral vein catheterization and so that's what we did. We I put an arterial line into this patient so that we could get continuous BP monitoring. And since he was hypoxic, another thing about the arterial line is I could pull off a BGs pretty frequently. I also put in a central line into this patient, and that was gonna be because they were getting a lot of pressors. And then the next thing I want to do is I'm a big fan, and I highly suggest you guys to please get good at doing this. If you're gonna be working in a hospital is I'm a huge fan of bedside like informal echoes. And so I would perform a bad side echo on this patient. And when I did, I saw some not really great things, and I I I saw the patient had a significant wall motion abnormalities of his entire interior wall and, um, just a very low ejection fraction. His ejection fraction was around like 25%. And so because of that, I like to take a look with my my echo and take a look at the heart. So you had a low e f I started them. Actually, this patient, I started him on dobutamine. I put him on Levophed. I put an arterial line in them and I put a central line in them to run these pressors and then did a formal informal echo on him just at the bedside, just to look at his ejection fraction to look at his wall motion abnormalities. So this was his bedside echo. So do you guys see this here? Do you see if you're taking a look here? I don't know if you guys can see this. This is actually on this one here. This is a parent sternal long axis view. And when you look at this parasternal on access view on this patient, here's his left ventricle. That's his right ventricle. You see his right ventricles moving really nice. It's moving really, really nice. But his left ventricle look at it. You see, here is lateral wall. You see the septum. They're barely even moving into the Lumen you see here his mitral valve. It's barely touching a septum. Usually whenever a good contraction occurs, that valve will touch the septum. And so his ejection fraction. When you calculated using what's called M mode, his was around 25% So he had some really significant. We called a kindness ist of his left lateral ventricle of the lateral wall in the septal wall. And his ejection fraction was really low. And then this is another view of that patients heart. So again, you can see that. Right? Ventricle. Look at the comparison. This is what I like to see when we start this over here. Look at the right ventricle compared to the left. See how that thing is just clanging a banging. And on this side, that lateral wall isn't really moving very much. And that septum just isn't moving very much. I didn't get a good look at his his eight packs, unfortunately, but you can also see his mitral valve. Look how little that thing is moving getting nowhere near the septum. So for this, this person had a really low. You have about 25% and global April kinesis of his septum and lateral wall. I wasn't able to get a picture of his apex, though, okay? What? You guys think of that pretty cool, right? What's unfortunate for this guy? But it was I thought it was a pretty interesting thing that you guys could see here. Okay, Next thing for this patient. He's acutely hypoxic, right? So with that being said him being this acutely hypoxic state, I didn't give you his repeat. But in this case, well, that actually is a type of it should be 94%. I apologize. It should be 94% on this patient, since he is having this a scheme make event. I like the same for greater than 94%. That's what the guidelines actually suggest. Yes, So I would actually change that there is a greater than 94% is what my goal is. And that's what I'm titrating my oxygen against. So right now he's on six liters of nasal cannula. He decided a little bit and then we put him up and we got him eventually to around 89% on six liters of nasal cannula. But that pulmonary edema that he has is what's definitely causing his hypoc senior. That's becoming the issue here. So the next thing is I want you guys to think about here is I am a big fan of bi pap. Bi Pap is great because by pap actually have something called peep positive. End expiratory pressure and that positive and expiratory pressure that you exert within the alveoli keeps those alveolar open distended and pushes the fluid out of those interstitial spaces. And that really helps and being able to mitigate this process of pulmonary edema. Also great thing about bi pap is that you control the F I 02. The percentage of oxygen should give this patient. And so I condone that, up from 21% which is room air all the way to 100% off of concentrated inspired oxygen. And so that's what we ended up doing for this patient is to push that fluid out of the interstitial spaces and to give them if i 02, we put them on by pap. And then since we put them on that presser to squeeze the vessels to increase the BP in the in a troop to squeeze the left ventricle, we gave them some Lasix or furosemide to pull some of that fluid out of the interstitial spaces as well. Okay, And then again, if your squeeze it in that left ventricle, you'll be able to get blood out of the left ventricle. So it's not backing up into the left atrium backing up into the lungs and again precipitating that pulmonary edema. So these are your this year. Best friends I love by PAP for these patients were cardiogenic pulmonary edema. Diaries them to get some of that fluid out of those interstitial spaces. And then I know Tropic agents to get that heart to squeeze and get the blood out of left ventricle. And again, those were dobutamine in your Miller. Now, the other thing is, I like a BG is to really tell me if I'm making any improvement in their oxygenation. And so usually I'll do to someone that Rachel had that is, by half the same, a CPAP. That's a great question. So by pap is, by level positive airway pressure. So what you're the difference is this. CPAP is that's primarily for, like obstructive sleep apnea patient. Since I I used that like a fat neck. So when I sleep, I clued my airway. So what happens is with CPAP, it's the same pressure, so it's like it's like sticking her head out the window. When you're going like 90 miles an hour on the highway, it's just hitting you with the same velocity of air. So you pick a pressure on CPAP. Let's say you pick 10 centimeters of water that you're gonna push into their lungs whenever they take a breath in, and you're going to continue to push that same 10 centimeters of water and during expiration. And so because of that, that's usually good for someone with who has the upper airway obstruction, especially someone like, you know, obstructive sleep apnea patients where obesity hypoventilation syndrome. But I pap is a little bit more comfortable, and it's actually more effective because with bi Pap, you pick what's called an inspired Torrey Airway. Pressure usually start with, like 15 centimeters of water. That's the pressure that I'm pushing in the lungs during the inspired to reprocess does really stent them open and open up the airway and push air in, give good title volumes to get yanked in and then, during the expired tray freeze. When I'm breathing out, it only pushes in a little bit of pressure, and that's going to be somewhere. I usually start 50 and five, so 15 of inspired Torrey positive, very pressure and five of expiratory positive airway pressure. It's a little bit more comfortable to breathe with because it's like you're getting hit with a little bit less air during when you're expiring after bull. And then also again, I can control their f i 02. But I can control fo to a CPAP, so they're really the difference is is with bi pap. You're giving them two types of pressure's. One is the high pressure during inspiration. Ah, low pressuring. Expiration with CPAP you're giving them the same pressure during inspiration expiration. So it's really more of a comfort. And then, also again in the hospital by pap is superior for a lot of these kinds of cases. In comparison, the CPAP, which is primarily outpatient sleep apnea. Thank you, Legend. You're a legend. Okay. So again, I like to look at the ABG every six hours if I have an arterial line. Okay. I hope that made sense. Diabetic ketoacidosis. I'm gonna ask you what I got to get this patient. They got a glucose of, like, 5. 30 man. Well, I gotta get there, but also a little, you know, with that sense, I got to give him some kind of medication. What I give him What? What kind of drug. Would I give him that would help get the push. Those? Ah, yes, Insulin. My next question is what kind of insulin When I give them rapid acting when I give him, you know, you're short acting like humor, you know, uh, Humulin or ah, oregano, insulin. Or they give him long acting like Lantis or large enough something of that nature. Yes. You guys are saying insulin. Um and then I've you fluids. I would get my fluids, But again, don't give him too much. Little bit to 50 cc. Bolus is because of his cardiogenic shock. And ah, some potassium grade greater. Get a lot of it, Greg. Yeah, here's the thing. So when a patient has a glucose like this, I am not going to try to attempt to manage that extremely high because of because pregnancy is very resistant to ah basal bolus scheme where you use like rapid acting insulin, long acting insulin. I would probably start them on an insulin infusion. So that's a regular insulin. Um, and so you would start them off on a particular like rate. Sometimes it can be depending upon your ah institution. They may have it may differ sometimes, like 0.1 units per kilogram is what you'll start off with, but again put him on an insulin fusion and target. Like a glucose of, like 90. The 1 40 is kind of the ideal range and so, usually starting insulin. If you that's the best and that's Humulin or regular insulin, that would be the first thing, and I would titrate that to a particular goal. 90 to 1 40 is the Common Institutional guidelines, according to the Sugar Trial and the The Shine Trial. So those are what I would start with, um, and then once you get a little bit more stable on that insulin infusion, they've been on, like the same rate for about like 24 hours. Then I would transfer them over to, like, a sliding scale or a basal bolus scheme of insulin. But I would not start them on either of those two, right off the get go with the sugar that high. Okay, I would give him fluids you guys were killing. Look, you guys all set the right answers here it, so I give him fluids, but I give him a little bit. Not too much and then I would check the potassium. My question is, why am I checking the potassium? What the heck does that have to do with anything? Why is it the potassium an issue? What's what's What's the diabetic ketoacidosis got to do with the potassium once I got to do it? Yeah. Yeah. Yep, yep. Sounds, sounds study. Potassium into pas is so where it's gonna push the potassium right into into the cells. And so because of that, it could potentially change your your potassium level. So, yeah, you guys are awesome. And then just mind and I and got make sure eventually just closes. It normalizes. That's one thing that we're doing. Okay, you guys are on the ball. Next thing, lactic acidosis. What am I doing for the lactic acidosis? Well, you gotta think about what's the cause of this person's lactic acidosis? What is the cause of the persons? Lactic acidosis shock. What kind of shock typically me into getting more likely from lack of insulin are from, um, acute kidney injury. So hyperkalemic a and DKA can happen, and it's usually because of the hyper osmolarity, um, of the bloodstream. Because whenever you kind of yank off of the, um what happens is when you yank off some of the water, you can look dehydrated when you had DKA. So you yank out water out of your actual blood stream. And so it makes some of the plasma osmolarity maybe a little bit higher than usual. And so because of that, it what happens is the water gets pulled from your interest sailor fluid into the extra Siler fluid. And when that happens, it concentrates the potassium inside of the cells to where now they want to start exiting out of the cells. And so it leads to hyperkalemic. Uh, and when you have a d k A. But in reality and patients who have DKA their total body potassium is actually low because you're yanking potassium out of the cells during that DKA event. Okay, also, if a person is insulin deficient, those sodium potassium, the D pieces aren't working as well, so you're not pumping the potassium back into the cells, and so that's another reason that potassium can stay elevated. So it's kind of two. Thoughts behind that one is the potential insulin deficiency or insulin resistance. Either way, same concept potassium is getting pushed into the cell. Potassium goes up. Or if you're getting rid of tons of fluid into becoming a little bit more hyper as more within the bloodstream, it can yank fluid out of the cells and then subsequently pull potassium out of the cells. All right, cardio cardiogenic shock. So in this case, patients Kate, we have cardiogenic shock. So in cardiogenic shock, they're They're mean, arterial pressure is low. Mean arterial pressure is unidentified, are perfusion, right? So we're not perfusing the tissues? Well, we're not giving them auction for not giving them oxygen. They're not going to be able to go through their wholesaler respiration cycle and produce a TB. So what happens is pyruvate instead of getting covered and surgical A, it gets shunted into making lactate. And so this conclude to this lactic acidosis, and that's whenever the lactic gets too high. It's releasing protons that it drops the pH. Great. So cardiogenic shock is the cause of lactic acidosis. So how do I treat lactic acidosis? If cardio cardiogenic shock is the cause? This is a great question, right? Treat the got. Yeah. Whatever I did for cardiogenic shock is what I'm going to do for lactose acidosis. So it's a cardiogenic related hyperperfusion. I have a said it. She not He hit the nail on the head, fixed the cardiogenic problem. So his problem was a stemi cath him that you could open up that vessel reperfus the parts of the myocardium that have not completely infarcted yet. I know pressors, right. So leave a fed our sorry norepinephrine, epinephrine. And then I know tropes as well. Like your w demeanor, Myleran and small IV fluid Bolus is and generally what you try to do is you keep trending the lactate every six hours until it completely normalizes. But you know the cause. You fix the cause of it that fixes the lactic acidosis. Yes, sir. Beast. Okay, right into your shoulder dislocation. This one's easy. You just reduce it right? So I would just This one's not too bad. I thought it was just interesting because this patient had swimming the other things going on, which is terrible. I shouldn't laugh at it, but he got so much stuff happening that this is like the least significant out of everything has got got going on. But it's causing a lot of pain. And so to reduce these we're gonna do is to a close reduction technique. And the way that we did this was a traction counter traction method. But that's all it is. Put him on an immobilization sling and give him some pain medication again. That's the simple concept with this one. Okay, so now that we covered that, let's go to the next thing here. Complications. So we did all of these things for this patient. Help them out. Got these things fixed. They're in the, uh there in the corner. I see you right there trying to get recovery. And after they had the successful cath there, Shaq started to improve with the oppressors. They got their cath. The hypoxemia respiratory failure improved when we put them on by pap. And I know troops and furosemide their glucose eventually normalize their lactate normalized there, and I got normalized. Their shoulder pain started getting better. And then three days later, they started to exhibit left side of weakness. Stop responding to stimuli on the left side, on the left side. Oh, my gosh. What? What's what's happening here? What would what would you guys think of right away in this patient. Stroke is a good thought. Yeah, it could be a scheming stroke. Could be a hemorrhagic stroke. Definitely. I definitely agree. So, gourmet hit it right on the head. I definitely would be concerned about some type of stroke. Did he have? Ah, Dang. And I gave you guys the answers. All right, well, you guys already saw it. So we're going to send him for a CT. My about I click the button a little too fast, so he's exhibiting weakness on his left side. What the heck is this thing here? It was this big goombah he's got in his brain, so he has a huge, huge right frontal. I chh, um, so a huge right frontal interest, cerebral hemorrhage. Um, and that is a problematic issue there for him. So that's likely if since it was within its right frontal lobe, it probably was hitting all of the different parts of his. Um, uncle is leading to his weakness on the left side. Right. So he had left sided weakness of his upper extremity left side of weakness off his lower extremity, and he was likely they're not responding to a lot of this painful stimuli because it was actually causing a lot of mediastinal shift and probably compressing on his brain stem and giving him some decreased level of consciousness. So pretty significant bleed there. So that's something to definitely think about. So he's got a right frontal. I chh my question to you is what do you think caused this, right? Frontal? I see a change. What are the particular things here? Wasn't any kind of trauma, I don't think because this developed three days later. So it's unlikely that an acute onset Yeah, yeah, yeah, yeah. Yep. So happen Heparin was the cost for this one. He got too much happening. Yes. Stupid therapy to capturing levels. So when they bolus the happier and they put him on the drip, the infusion of happier and you measure the p t. T. His was greater than 200. It was just too high. Um, and this is a problematic issue of put him into this super therapeutic range, which a lot for it to really cause his his levels to get too high and increase the risk of bleeding. What's the treatment? So if he was still on the heparin infusion right, he was still on the heparin infusion. What could you give him to reverse the effect of heparin protamine soul fates? So someone's that be be said, How did you get a stroke again? So he had that right intracerebral hemorrhage. And again, that was because of the heparin that he was on because he had to be anticoagulated for the cardiac catheterization lab. And usually they keep them on anticoagulation a little bit after they've been catheterized. So he was just super therapeutic on that heparin. It was too high, caused some leaking with in some of the vessels. And then eventually he stroked out. That's right, he bled. So protamine sulfate in this case would be the treatment. But his his GCS is really, really low. He's not responding to painful stimuli. He's really not opening his eyes, too. Painful stimuli. He's not following any commands, and so his GCS is declining pretty rapidly that he would not be able to protect his airway. If you've Amit it, he wouldn't have a proper cough or gag reflex that he would be able to cough and prevent that from moving right down to his airway and causing aspiration pneumonia. So because of that, he was intubated. So I intubated this patient because his GCS just drop down too low. He was not responding, and I was concerned from not being able to protect his airway reverse that happen with the protamine soul fate and then had to call in neurosurgery because what can neurosurgery do to relieve that pressure? Decompressive? Yes, we could pop the top right so we could do something called a decompressive him a craniectomy. You could trephinating usually in this in a situation. I would probably go straight to popping that top off doing a decompressive hemicraniectomy where you remove part of the skull to allow for the brain to swell outwards. Maybe try and evacuate some of the blood if it's close to the cortex and put a drain into his ventricles to drain some of the blood because there was a little bit of blood. If you guys look here, there's a little bit of blood in his right ventricle and in his lateral ventricles here. So there's a little bit of blood in the lateral ventricles that's gonna eventually obstruct cerebrospinal fluid. And if you're gonna structural spinal fluid, you're getting up with hydrocephalus, so we'll put in a drain as well on TVD. So he got a decompressive hemicraniectomy before that happened. He had a central line. And so whenever they have this really big bleed, I want to give them a particular medication to reduce a lot of the swelling within the brain and quickly reduced danger cranial pressure before they go to surgery to get the hemicrania and the E v d. What are those drugs I can give to reduce the swelling? Yeah, he's like a man I hate, man. It's all but it is a good one to use if you're in a pinch. But 23.4% hypertonics sailing is a little bit more superior in these situations, but yeah, that's what ended up happening. So when this happened, I tube him, gave him the heparin I'm saying gave him the protamine sulfate, squeezed 23.4% into a central line caused called nurse surgery. They came bedside, put an e v d in and took him to the O. R. And pop the top off to relieve the pressure so that he did not hurt. He ate. You guys are on the ball. Unfortunately, this isn't all that happened to this guy. He came back after his decompression. So what's wrong with man? It's also the mannitol, sometimes, because that excessive amount of diaries is and one of the things with mannitol is with that excessive amounts of diary cysts. It can really like cause some significant dehydration to the patient. And so sometimes I'm not a big fan of that 23.4% Is that going to cause a significant of a diuretic effect in comparison to mannitol? Mannitol does cause some pretty significant diuresis. So I'm not a big fan of that excessive amounts of diuresis for these patients, especially if they're on the verge of hypertension. And I don't want to want to increase the risk of causing it to become more intravascularly dehydrated, worsening a particular kidney function, dropping their BP, altering a lot of their electrolytes shifts. But if you don't have a central line, mannitol is a great drug to get. If you don't have any other central access, I will give man, it's off. I don't have anything else that you know, accessible to me like a like a central line but complications for this guy. So he stayed intimated. He came back to the I see you. Um, here's the problem. He had a fever. IPAQ the fever, like a couple days later. Um, and he had the secretions coming from the Bentyl. Later, it was just nasty. It was cream me. It was thick. It was copious. He was constantly triggering the ventilator, too. Kipp Nick, constantly trying to fight and breathe over the ventilator rate. And then he constantly whenever he would fight and try to breathe over the Mandalay to rate he had these episodes where his oxygen saturation would drop. What do you concerned about? She's been antibiotic for a couple of days. At least more than 48 hours. Yeah, yeah. You know the hospital acquired pneumonia? Yeah, so he's been in the hospital for well over 48 hours. He's been intubated for more than 48 hours at this point. Time in the I see you now he's got fevers. He's got pearl and see Creation's. He's got hypoxia, and he's got to keep me as evidence of been breathing over the ventilator rate. What should I potentially do? What should I send off the test. I got direct sac direct access, baby. I could just stick it down there and suck it out. What could I grab? Yeah, I'm gonna send a sputum culture because I can start him on broad spectrum antibiotics. But I want the sputum so I can really tell what the bacteria is that I'm treating. And then he's also starting to get a little hypotensive. Maybe I'm going to get concerned about that. Ah, shoot. Maybe it you know, it's spread somewhere. What else would I want to get now that he's got this, like, really bad fever blood cultures to make sure that he hasn't been coming back to Remicade, increasing his risk of developing sepsis. So I'm going to get blood cultures, and I'm going to get sputum cultures on this guy. Okay, so we'll start him. We got we're obviously concerned for hospital acquired pneumonia. You guys were just too darn good. I'm gonna start him on broad spectrum antibiotics, usually to cover any kind of grand positive bacteria, especially Mersa into cover any gram negative bacteria in the hospital. Acquired pneumonia is especially pseudomonas that usually in our institutions, most commonly is vancomycin and piperacillin to go back to more vancomycin and cefepime. So we are kind of already hit that for you. So we're going to cover vancomycin in case of words. Case scenarios. Got mercy and pseudomonas. I want to cover that as the nastygram negative bacteria with any piperacillin taste of active. Okay. Okay. Yeah, this poor guy, man. All right, so we're treating him for his hospital, acquired pneumonia a couple days later, he stops making urine. The urine outputs significantly decreasing. Like he's making, like, very little. You're like 10 cc's of urine, like every every two hours. And so his urine outputs less than 20.5 sees per tape. Five ccs per kg, his body weight over the past 24 hours. And then we check his BNP. We're getting daily BMPs daily. CBC's on this guy, and Vancouver levels for him because he's on vancomycin. Yeah, it was creating bump to 2.42. You remember what his original baseline creatinine was? It was 1.20. So remember what the definition is for. Well, here. My next question is 1.20 to 2.4 to creatinine in a decreasing earn out. But what are you concerned about is just a CKD or acute kidney injury. Yes. So acute kidney injury on top of this guy's already present chronic kidney disease because it jumped greater than 0.3 with a 40 hour period and probably to the 1.5 times is based line, at least. So I'm definitely concerned about this guy having an acute kidney injury on top of his already present chronic kidney disease. So acute kidney injury. What's the likely cause? There's a lot of things that could be due to, but what's his most likely cause of this? Sepsis is definitely a possibility. You could have an acute to build a crosis vancomycin and so antibiotics. Yeah, it could be both. Honestly, it could be both. He could have some degree of decreased profusion to his kidneys, so that could definitely cause an acute bladder crosis, um, or could be vancomycin, which could cause acute to be the necrosis is Well, either way, we're concerned about it being one of these two things. When we checked his bank levels, his bank levels were super therapeutic. They check the trough level the next day, and his trough level was 30 which is usually 20 is about like you know where your upper limit upper him upper limit of normal is. So he's way beyond his normal level of therapeutic level of ankle mice. And so he's definitely in that range. Where bank, um, my son could cause never toxicity, so that was likely is cost and then already kind of gave you a little hand to this. It's damaging his kidney tubules. So is it prerenal are internal internal? Yep, All right, So this is something I like to do for my patients. This helps me out to determine like there's a lot of things that you can do checking like what's called the fena, like the fractional excretion of sodium check in the urine sodium checking the urine, creatinine, all that stuff that you guys learn in school. Those are good task for your exams, but I haven't found much clinical utility for them, and the I see you are in the hospital and what I've actually found more significance for and it's validated is what's called a frozen might stress test. And I heard you guys to try this. If you ever have a patient that you're trying to discern. So furosemide stresses, you actually give the patient a milligram per kilogram of body weight. Ah, bolus of furosemide and the whole thought behind that is, if they have a you know, good kidneys and their let's say that they have normally functioning kidney, you're getting enough profusion to the kidney. They're getting the actual furosemide into their kidney tubules. If it's getting into the kidney tube, it's it's gonna work on that thick limb of the ascending loop of Henle E and therefore block that transported to reduce the sodium and potassium chloride and water reabsorption. If your kidney tubes aren't working, it won't respond to that furosemide, and therefore it just won't even work. And so why I like to do this is I'll give a heavy bullets off rows. Um, I'd. And if they make more than 200 cc's within the first two hours, I know that the furosemide is getting to the kidney tubules. I know the kidney tubes are responding to the furosemide, and therefore it cannot be an intrarenal achy I if I give them the furosemide and their kidney tubes are not working. They're not responding to the furosemide. They will not actually have any benefit of it. And they won't make much urine because it's not gonna be able to respond to the first because the kidney to bills are damaged. In that sense, So what? I did this test he was. I gave him 100 mg of those movies 100 kg. I gave 100 mg of furosemide, and the only made about 100 CC's over the first two hours. So his kidney troubles are not working is therefore intrarenal. So he has to go on to the next step whenever the kidneys airway really, really bad and they don't even respond to a heavy bolus of furosemide. What's the next treatment that this patient is likely going to require? Because he's probably gonna progress where he's not making any urine? He's gonna give volume overload, is gonna get significant electrical abnormalities. He's going to end up with uremia. He's going to end up with a lot of problems. Dialysis. So shrimp J asked a great question, which is Kim? This worse in the eyes froze Might is also nephrotoxic. This is actually not necessarily true. Now here's your mom is it. Furosemide is not nephrotoxic unless the person is volume depleted. If the person is volume depleted, they're hypovolemia. That means that you're gonna have them go and get furosemide into the kidney tubules. And it's gonna work on the actual district. That loop of Henle e. It's gonna work on those cells and it's going to suck water into the kidney tube is suck sodium into the getting tubules, and you're gonna pee out larger amounts of volume. If you're peeing out larger amounts of volume and you're already hypovolemia, you're dropping their intravascular volume and therefore you're reducing their profusion to the kidneys. Over time, if you reduce their perfusion to the kidneys, you're going to reduce their glomerular filtration rate. You're going to reduce their excretion of creatinine. There were six creation of their be, um there are urea and that will bump their creatinine that will bump there bun. So if they're hypovolemia, then yes, you could be nephrotoxic giving them more frozen might. But if they have a normal volume or their volume overload it, which this patient probably to some degree is or their kidneys are just not working, the furosemide isn't going to do anything that's going to cause any more harm. They're eventually going to progress to full renal failure, which will require dialysis anyway, So that's a great question, because that was one of my concerns when I first started. This is like, man, if I give him the Lasix, would that make it worse? They could. But guess what? If you give him Lasix and they don't respond to it, it's likely they're going to progress to dialysis regardless. So unfortunately, with this patient, he had to get dialysis. His mental status never improved from his bleed his right side. And I see a gyn ever kind of like actually allowed for him to wake up more. His GCS remained poor. He never actually follow commands unable to be extubated. Because if I'm not being able to wake up follow commands, um, his respiratory failure was too bad. The family didn't even want him to get tricked because of him and not actually waking up on, and eventually the pneumonia just continue to get worse. And I told you the BP was on the softer side. Eventually, Then the moon you got so worse because we had to hold that vancomycin for a while because of his acute kidney injury, put him on CRT. He ended up eventually going into septic shock, and we put him on. I ended up having them on four pressors pushing fluid in to, um, eventually had code him and go through multiple rounds of CPR, and eventually he went a systolic and passed away. I mean, unfortunately, but this is the kind of patients you guys could get. And unfortunately, I think this is a good thing to remember is that not all patients are going to act the same way. Not all patients you can do every single thing that you possibly can for them, and sometimes it's not enough sometimes takes to come to their illness. I think that's a really important thing to realize a really, really important thing. Toe. Come aware of that, do the best that you can for your patients. Give them all you have, but don't hold yourself responsible. If you're not able to do everything that you can for them to save them. Um, sometimes you'll do absolutely everything and you feel like you failed. You feel like you didn't do the right thing or that you were really one responsible. Sometimes these patients will do everything they can, despite your efforts on gets just, unfortunately, the process of the disease. So I think that's also a big lesson. That's one of the things I've had a hard time with us. A new provider is getting used to some of these really, really sick patients doing everything I can for them. And after I do everything I can. I five for the my advocate for them Sometimes, unfortunately, Disease just takes that away from me. So I hope that this was pretty helpful. And I hope that you guys enjoyed it. I wasn't too depressing thio and on the bad note like that. But I just want you guys to understand this is really the sometimes the cold reality. Um, but I hope hope she has liked it. Good. I got a Robbie in here again. Um, he's going to present some stuff to you. I just wanted to say thank you guys. Seriously, thank you so much for the opportunity to, um, to be able to talk with you guys to have this opportunity to present this to you. This was surreal. And it was a great experience and you guys were super, super intelligent. And I truly can't wait to, ah, see the amazing things that you guys do in your future. So thank you guys so much. I'm gonna get out of the way, and I'm gonna let you go to step in here, okay? I kept the seat really warm. No, you're good. You're good. I won't take. I won't take much of your guy's time. I just want to thank you very much for allowing us to do this. This is awesome. Really quick. Could you guys I'll see this right here. The our website. Awesome. So just super quick, I think revamped already gave it to you. Um, but the coupon code, um, I just want to write it here. Super quick. Um, it's just medical high in ears. 40. Uh, go on our website, check it all out. But we have everything from our YouTube channel. Everything you could think of as far as extra resource is drawings, um, you know, before a lecture after a lecture notes everything you can think of. So if you come in here like, for instance, endocrinology, you could pull up a lecture. Um, and then you could literally just come down here. You know, notes and illustrations, whatever it might be, Grab what you want and then move right on. It's just everything you could think of. Um, we hope that it helps you, but, you know, also, if you do consider doing it, you'll be helping us out as well. So we just ask you, please check that out. Try and grab a membership either a six month or a year, and you'll save the most money on that. But thank you guys so much. Wonderful. Thank you. Thank you so much. Everyone's asking when is the next finals? Easy session. That's how our weekly stuff that we do, uh, I don't think it'll be the same. Uh huh. Yeah, but for those who want to know, it's next Tuesday. We're doing pediatrics. Um, thank you. Thank you so much. Uh, Zack and and Rob for helping organize this. It's been absolutely wonderful, uh, to have you guys on board on a live lecture that to go through a day session. If people have any questions regarding anything at all, please do a post in the chat, and we're more than happy to moderate and ask all of you guys sent. Sorry, a mist Christian. And so she does have some amazing videos, A nursing videos. It's well, so we are all huge fans, first and foremost. So you can You can imagine how all of us are absolutely trilled to have all of you guys here. Um, yeah. So if you guys have any questions regarding the YouTube channel in regarding anything that'll feel free to put on the chat And we, uh, more than happy to pose it to you guys, Uh, was it Zack? Kristen and robe. Question is, how do you balance everything? You still working as well? And still the, uh, time? Yeah. No sleep. Usually that's that. That's the answer. You don't sleep. Um, so, yeah, I I pretty much, um I work in the I see you on