Medical Lecture Notes on Fluid & Electrolytes (PDF)

GMT20240206-135231_Recording_1876x900 (1) Sat, 02/24 14:41PM · 191mins Thank you. Thank you. Good morning to those who are here so far. Good morning. How is everybody? Got some smiles. You guys survived last week and all the tests. So that's a good thing. Did you get your grade for. Yeah. We finally got it yesterday. I was with Dr. Owens and Dr. Talbot as the drama was unfolding last week. Quite, he had a quite an interesting week with tests, but. Well, that's good. Glad you got your grade. So got a few people trickling in, I think. I'll give them another minute or two. Thank you. Thank you. Okay. Well, I'm just going to go ahead and get started. I guess those individuals can catch up or re watch this on the video. So I gave you guys back if you missed it. You got credit for two questions on the exam. So I just wanted to kind of go through those two briefly. One was the dose response curve for agonist partial agonist. antagonist, inverse agonist. And I think the question asked, which one does not activate the receptor? The answer should have been antagonist. But I think a few of you put inverse agonist and I gave that back because I probably did not fully explain that the inverse agonist activates the receptor. It's just that the effect is a turning off of the cells activity. And the fact that an inverse agonist can antagonize the effects of an agonist. I can see where that could be confusing. So I gave points for that. The other question was, if you have a patient taking sodium bicarb and a drug that's a base, a weak base, how does that affect elimination? So the answer was prolonged half -life. And that's because you're expecting that bicarb to alkalinize the patient and putting that base in kind of a more basic environment. You expect it to be more so in that be non -ionized form. And that would promote reabsorption from the renal tubules as well. So you've got that drug kind of going back into circulation, recirculating, and theoretically extending its half -life. So I gave that one back. I did not give back credit for it, but I was kind of surprised that there were some of you that missed the question on up versus down regulation. And I think I had the question related to beta blockers, chronic beta blockade. So that's an important concept in pharmacology. We'll revisit that in future drug classes. So make sure you understand that in the presence of an antagonist, if you're constantly antagonizing that cell, the receptors on that cell, you know, that cell wants to do what it was made to do. So it's going to undergo genetic changes where it, you know, will tell itself or make itself form additional receptors in order to find agonists so it can perform the functions it wants to find. Additionally, and this is kind of beyond the scope of our class, and I don't fully understand it myself but it's probably going to undergo some sort of like plasticity or other types of changes in the receptors it already has where they are going to become more sensitive to any agonists that binds to them so they might hold on to it longer, or somehow exaggerate or enhance the effects of that receptor. So that would be except that would be expected in the situation of up regulation. Anybody have questions on any of those. Okay, so this week is like. completely review. It's probably going to feel a lot like nursing 101. But it is on the NBC RNA's content outline for your certification exam. So we do need to, you know, go through fluid and electrolytes, blood products. So I kind of termed it hematology part one. And we'll look at massive transfusion a little bit at the end. And then next week, we'll do part two of hematology, which is pro and anti -coagulants. The next module after next week, so in a couple weeks, is immune system. So you will notice on there, antibiotics, which of course is very key to what we do, antiretrovirals, which I am going to go ahead and keep that lecture on your, as far as us going through it, being tested on it, et cetera. The chemotherapeutics is in there as well. And I am not going to test you on chemotherapeutics. We are not going to go through it in class, but I'm giving you the information. The reason why I took this out, and I went back and forth on this, it's kind of a hard choice to make. Powered by Notta.ai But the NBC RNA's content outline is very vague. So I have to do my best to figure out exactly what they're asking us to do, as far as what to concentrate on and teach you in lecture. Starting February 1st, 24, so barely a week ago, anyone who takes a certifying exam after that, the content outline just changed recently. So chemotherapeutics used to be listed under pharmacology specifically. They took that out. So that is why I am not going to actually lecture on it. What is kind of vague and confusing is that when you get further down the content list and you see population specific. So the different populations are like obstetric, pediatrics. I think geriatric obesity, immunocompromised is one of those populations enlisted in that you'll see pharmacology. Well, that's very vague. I don't know what they mean by pharmacology related to an immunocompromised patient. So the fact that they kind of made that switch just makes me wonder if they're thinking more in generic terms of, you know, some considerations related to treating an immunocompromised patients with maybe anesthetics or maybe some of the drugs that they take. So I want you to have the information, but that is why we're not going to cover it specifically in class. It's just one, I don't have the time to cover everything. You guys know we have a thousand page textbook. And then NaGle House is another probably 1500 page textbook. It's very hard to comprehensively cover all of that information in two semesters. So I kind of have to figure out what to focus on for you guys, but I want you to have the information because there are some. There are some anesthetic considerations that are good to know for that patient population that's taking a chemotherapeutic drug or has maybe recently taken. Chemotherapeutics. So you should go through that lecture at some point, you know, even if maybe you're taking care of a patient in the clinical setting, you know, like your patient for the next day. Maybe it's on one of those drugs or when it's time for you to prepare a little more in depth for boards. Maybe look at it then or when you get to basic and advanced principles, which we're going to kind of change up that curriculum a little bit. But when you get to those courses. And they revisit that population of immunocompromised. Maybe go back and look at my lecture and notes on that then. So it's important information. I wanted you guys to have it. Last year was actually the first year I ever taught chemotherapeutics because back at my old university we had an oncology and P teach that lecture. So I actually personally had never taught it. But I taught it to the cohort of head of you. And I synchronously taught because I was actually in Cuba that week with the AA and a, but I put that recording in that module in the same PowerPoint slides and the worksheet that I kind of gave them. So again, I'm just reiterating when you get to that module in a couple of weeks. That information for chemotherapeutics is in there, but we're not going to specifically go through it in this class, but keep that information for yourself. Because. like Dr. Rubison and Bluemysin, really can affect cardiovascular respiratory system. So it's important to know those, just in case you encounter that on boards. Any questions on that? Or if you think of any, let me know. And then I am experimenting with Zoom. So I'm gonna attempt to administer a poll to you guys. It's not like a quiz, it's just a poll. So hopefully it pops up and you can see it. It's related to this lecture. It's just kind of for fun. And then we'll start the lecture. Thank you. Bye. And I'll try to figure out how to get the results to you. Thank you. Thank you. Thank you. Thank you. Bye. Yeah, a few more people that are going to finish. Thank you. Thank you. Okay, let's see, I don't know how to, I'm trying to figure out how to share it with you. I tried to read all kinds of frequently asked questions about this, but when you're in the moment, like none of those answers are helping me right now. Let's see. Maybe a 5A and the poll share the results. Can you guys, does it show you results? Okay. So, the first question was, do you understand respiratory variation? The overwhelming majority said somewhat, but could use a little more explanation. Maybe I should let the one person that knows it really well teach it for me. Number two, what is the preferred IV fluid in anesthesia? 69% said LR. We had a couple of votes for dextrose containing an albumin. Powered by Notta.ai And then a few people said normal saline. So we'll talk about that. To treat hypovilinea in adult undergoing anesthesia, I would probably start with how much fluid. Let me see if I can figure out how to get the answer for that. Which it's making me sign in. Probably able to get the answer for that one. Thank you. Moving on to the next one. Of course, I don't know my password. Zoom will not let me sign in. Which are blood type looks like a couple people forgot or don't know. I know I am B positive. I believe it looks like most people are a got some O's in there. Let's see what else. Number five and six. Are filling the blanks as well, which for whatever reason zoom is not letting me sign in. To get the answer. Hold on one second. I can't. I thought it was just going to give me the answer right away. Let's see. I'll come back to those. Seven, I'm taking care of a patient with taco or trolley. Most of you said no. I don't know that I ever have either, but I can't remember it was a while ago. Number three, as far as, if you have a patient with hypovolina and under anesthesia, how much would you give as a bolus to treat that? We had a lot of answers for 500, some for 250. Couple for a liter. And then some said PRBCs, some said isotonic, I guess fluid. I had a question on here. One unit of packed red cells increases hemoglobin by how much? Let's see, most people answered one. There's an answer for two, three, one for 0.5. Someone said 0.2, one to two. on hemoglobin and then increasing hematocrit looks like the answers. One percent, a lot of people said two percent, some three percent, five percent, half percent, four percent. I like that answer. That's a good answer. Sometimes that's why we're here is to try to, so we can learn these things because you guys all come from different educational backgrounds and things like that. Let me see if I can get rid of that. I got to stop here for just a second because I lost my window. I'm going to go back to the slide. Fluid electrolytes, blood products and transfusions. We'll start with physiology of your blood fluid compartments, which hopefully is reviewed for you guys. The majority of our compartments is in that fluid compartment and then that's divided into intracellular and extracellular space. Extracellular is divided further into interstitial fluid and about 20 percent is plasma. There are going to be some variations in these charts based on age, sex, body composition, things like that. This is for the most part what most people will be composed of. Body fluid compartments, intracellular is two thirds of your total body fluid. It is rich in potassium. Potassium is your major cation, intracellularly. That is why your serum level is so low around three and a half to five. Magnesium calcium, FOS is your major anion. intracellularly. And then there, of course, there are proteins as well. In the extracellular space, a third of your total body fluids, that's that we said that was divided between interstitial fluid at about 80% and plasma at about 20%. There are some other spaces like where you have your CSF fluid, GI fluids, things like that that are anatomically separate to call that transcellular. But it's part of the extracellular compartment. And those in that area is rich in sodium as the major cation and chloride as your major anion. So that's why in plasma, your plasma sodium level and chloride level are much higher, you know, 135 or so for sodium 100 roughly for chloride. So this just kind of shows it to you in a chart form. And we can look at our intracellular on the right side and then our extracellular on the left divided between plasma and interstitial and you can kind of see the distribution of your ions and which side they more so favor. Plasma is 90% water, of course that helps maintain volume within our vessels to transport molecules, about 7 to 8% of your plasma is consists of your protein so albumins we know are most prevalent we have globulins other types of proteins, they help maintain pressure volume. They're used for transportation just like they do bind our drugs, for example, they affect pH and coagulation, less than 1% or salts also contributing to pressure pH metabolism, and then we have gases so O2CO2, for example, which are involved in respiration and metabolism. Powered by Notta.ai Nutrients also in the plasma things like lipids glucose, which feed your cells and then from the cells will get waste like urea and uric acid for excretion. Other substances which don't particularly fit in some of those categories are things like hormones, which we know are involved in regulatory functions and then blood cells. So, of course, we know we all have different types of blood cells that we'll look at later and those help transport gases, fight infection, etc. So when we think about moving between compartments, you know, we talked a little bit about in pharmacokinetics some of the. structure of molecules that affects their ability to move through membranes. And we looked at kind of an example of a plasma membrane for a cell that might have different mechanisms for things to move across. Some things can freely diffuse, some things require active transport, require receptors or channels to move ions and things like that. So when we think about moving molecules or ions and things like that between compartments. So let's say between the plasma in your extracellular space into the interstitial fluid within that space, there's different things that are going to affect the ability to move between those two parts of the extracellular compartment or even between the extracellular space and the intracellular space. And so you can see an example on this slide of a vessel. And you know your blood vessels are aligned with endothelial cells, which have a variety of functions. We like our endothelial cells. But in this particular tissue, those endothelial cells have this junction in between them, a tight junction. And the tightness of that junction or the width of it varies depending on what tissue that vessel is in. You can also see there's this glycocalyx, this layer kind of sitting on top of the endothelial cell, which kind of will catch and trap molecules and ions and help prevent them from going outside of the vascular space. So this whole system being intact is very important to help regulate what should stay in the intravascular space and what's allowed to move out of it. So generally, small ions can freely move in most tissues. Proteins, larger molecules should not be freely moving. And that's because of those tight junctions and that glycocalyx layer. If you look at this slide, you can start to appreciate the differences between the vascular system and the extracellular space and different tissues. So the brain, for example, the blood brain barrier, the lung, the heart, these are tissues that really need a very tight connection between cells in order to help prevent too much movement of larger molecules out of the vascular space. Because of the threats of edema and things like that in an area like the brain. So you've got really tight junctions there. You can see these little mini- pores in this second cell in the middle. And that's to help facilitate transport of different molecules. If you go down the B, you can see there's these fenestrations, it's a little bit more open. So you can see those molecules are really starting to kind of flow in and out a little bit more easily. So if you remember in the renal lecture, when we looked at, we kind of went through the tubules and we were looking at all the different receptors and what diuretics affect what, in which molecules and ions are moving across. You know, we had our sodium potassium 2 chloride transporter, for example, on the apical membrane. But then you also saw some area in between those tubular cells that small ions could just freely move across. especially like in the proximal tubule, you could sodium and calcium and magnesium, you could just easily go right between the cells on their own. They didn't need a separate channel or pump or anything like that to necessarily move those. So that's an example of this right here in the center. So these types of vessels with these more greater fenestrations are found in the kidney and even some areas of the brain. Down here in C, you can see even larger gaps. You can see these bigger pores in the cell to allow certain molecules to flow across. So this is what it looks like in areas in the liver bone marrow. There's I think another example of differences here for the endocrine in the gut, the endocrine system and the gut which has additional fenestrations that allow movement of particles back and forth. So when you're absorbing, reabsorbing certain things from your diet out of the gut, it's because of these pores and open gaps in between those cells that line the intestines that are allowing reabsorption of vitamins and things like that. Powered by Notta.ai So in an inflammatory state, we know that our endothelial cells start to undergo changes. So we have a lot of times a breakdown in those tight junction gaps. We have breakdowns in our glyco -calix layer, and we allow unfortunately larger molecules, proteins, things like that to move through where they should move. So out of the vascular space into the interstitium. So normally, for example, albumin movement is about 5% out of the vascular space into the tissues. And the surgical patient who has now entered into an inflammatory state because of the trauma to the tissues and blood vessels and things in an area, that movement can double. If, for example, a patient in the ICU that is septic, because of the systemic inflammatory response, that movement of albumin can quadruple. So then that's when you're struggling with, the ability to maintain fluid in the vascular space. A lot of times it's because you're losing a lot of these proteins, macromolecules, solutes that would help hold that fluid into the space. It's starting to go out into the tissues because of that endothelial damage. So monitoring intravascular volume status. We have standard monitors. We have more invasive monitors. Blood pressure, noninvasive versus arterial line. A lot of those things will vary and are usually patient and surgery specific when it comes to anesthesia. Typically, I don't need an arterial line to do a lap coli in most patients, but if you had a patient with, you know, maybe heart failure and an ejection fraction of 25%, that patient may absolutely require an arterial line for a fairly benign and maybe even quick case, but just the fact that you maybe need to keep a better eye on their volume status. Interoperatively, or for example, let's say that laparoscopic coli cystectomy became an open belly procedure. Maybe they could not do everything they needed to do with the small portholes for laparoscopic case and you had to open that belly, then it becomes a whole different procedure, right? So there will be, you know, you will make those decisions kind of with your team. You'll learn how to make the decisions of how much we need to, I guess, monitor and have control over volume status during anesthesia. So we're going to look at now static versus dynamic parameters to measure and monitor volume status. Typically, we use static parameters. The problem with static parameters is that usually it's going to give you one measurement in time. So you take a blood pressure on a patient or you look at their current heart rate, you know, it's giving you a snapshot at that moment in time. It's hard to really assess the degree of changes in tissue perfusion that are kind of going on with one blood pressure. And it may, it just is not giving you a full picture. With blood pressure and heart rate, using those as a parameter to measure or to monitor volume status, the idea is that it can be very unpredictable. You may have a patient that, let's say they're hypotensive after you induce general anesthesia, because you've vasodilated and they've been in PO, they're maybe a little hypovolemic. Let's say they're really young and they can compensate with an increase in their sympathetic nervous system. You will find that pediatrics young adults have very overactive sympathetic nervous systems. When they compensate for that initial drop in blood pressure and heart rate, and they really ramp up the heart rate and get their blood pressure back up because they improved their cardiac output, then you may have a blood pressure that looks normal. or maybe just slightly below normal. And from that alone, it can be hard to determine the degree to which they are truly perfusing tissues or they're truly hypovolemic. So, you know, that's why we consider, you can look at blood pressure and heart rate and say that patient's hypotensive, I see the tachycardic response, you know, they must be hypovolemic, but it's still just not a great picture of overall volume status. If the patient's on a beta blocker, that can mask that tachycardic response. So that could affect your ability to assess it as well. CDP, we tend to not use CDP a lot, manastasia at all, unlike, you know, it's sometimes done in the unit for looking at trends over time, but it's just not always an adequate picture of preload volume responsiveness. And like pulmonary edema risks. Another static parameter is urine output. So, inhalation, anesthetics, surgical stress, and things like that can actually in and of themselves reduce urine output. It doesn't necessarily mean that your patient is hypovolemic, they can be uvolemic, but just from being in the state of stress with surgery and anesthesia, we often see a Powered by Notta.ai drop in urine output. Also, a lot of patients prior to surgery, you know, especially if they're, for example, childbearing age female, you know, they are typically going to, you know, maybe do a urine pregnancy test pre -op, so they've emptied their bladder. So to bring them into the OR, if it's a case where they have a fully catheter, you may notice they don't have a lot of urine output, does not necessarily mean they're... eulimic. So we consider urine output, again, a static parameter. And intra -oliguria, which is less than 0.5 ml per kilo per hour, is not a great predictor of acute kidney injury. If you have sustained oliguria kind of over days, then there's generally an acute, or sorry, generally an increased risk of kidney injury with that. But we have patients for such a short amount of time that if you're only judging intra -op urine output, it's still hard to tell if that patient is incurring or at risk for kidney injury. Mixed venous O2 saturation, which looks at global O2 delivery and tissue perfusion, is also considered a static parameter. So when you have changes in tissue perfusion or changes in O2 consumption, It's not a great way to assess overall volume status. Let's look at our dynamic parameters. Dynamic parameters are great to use if you want to know the degree to which your patient is fluid responsive. If you have a patient that is hypotensive, should you give them a fluid volus, or should you give them a vasopressor, should you give them both? That's kind of what we mean by fluid responsiveness. Also, if you are doing a surgical case where you are using maybe like an ERAS, enhanced recovery after surgery protocol, or something like that, a lot of times those protocols also use goal -directed fluid therapy. As part of the protocol, just to help minimize hyperbulemia and kind of giving too much fluid. So those again are, you would want to use a dynamic parameter if you're doing something like that, just to help guide that protocol. Dynamic parameters are beneficial if you have a major surgery where you're expecting a lot of blood loss or fluid shifts. So this might be like an open thoracic case, an open abdominal case, maybe an extensive spine surgery, things like that. So the first one we'll look at is respiratory variation in your arterial waveform. So there's different kind of data points you can look at to assess respiratory variation. So we can look at pulse pressure and you know difference between your systolic and diastolic. We can look at stroke volume. We can even just look at B2B. What's the change in systolic? blood pressure. And when you're assessing whichever data point you use, you know, just choose one or, you know, whatever your monitors, whatever information they're giving you, you would choose one of those parameters. And you're going to look at kind of that beat to beat difference as your mechanical ventilation as your ventilator delivers a breath. And, and allows that exhalation. So typically, you know, there's some things that you kind of have to, there's conditions I would say that you would have to maintain in order to use respiratory variation as a, you know, helpful assessment. One is that they should be on a controlled mode of mechanical ventilation. What we're doing is we're looking for that positive pressure breath that the vent is delivering When it does that it is increasing the pressure inside of the you know Chest wall inside the thoracic cavity. So when we increase that pressure We are to some degree you're going to cause vascular Collapse right so we're gonna kind of push against our vessels we're gonna start pushing against the chamber in the heart and We can determine from that the degree to which those vessels are Kind of resistant to that squeeze, you know, do they have a lot of volume inside and so they're not as collapsible Or you know the chambers of the heart, you know have a good amount of volume. They're not you know Kind of being pressed as much when you deliver a positive pressure Brats from your ventilator If you had a patient that was kind of spontaneously breathing with the ventilator, you know There's gonna be some differences in Inter thoracic pressure because when we Spontaneously ventilate and take in a breath, you know, our interest thoracic pressure is negative It's not positive as it is with a ventilator. So you really want to stick with the positive pressure Breath of the mechanical ventilator because that's going to give you Powered by Notta.ai that Very consistent state that you can assess those beat -to -beat differences and then the second condition I would say would be You want a patient that? Has good cardiac function And vasomotor tone so you don't want a patient that's for example in a fib where it's hard to kind of look at you know each subsequent beat When you're looking at maybe pulse pressure on your arterial line or something like that so those are kind of the conditions and then Next thing we're going to look for is is the degree of difference between that positive pressure breath. And once you've exhaled and you've lost that change or you've changed, I guess, the pressure in the enterothoracic cavity. So normal variation should be less than 10% to 12%. So from beat to beat, that stroke volume, if it varies between inhalation and exhalation, more than 10% to 12%, then we say that that patient is fluid responsive because that breath has collapsed your vessels and kind of pushed against your chamber so much that you know that they are not very full of fluid. So greater than 10% to 12% variation, fluid responsive, less than that, you would assume, or you're kind of assessing that that patient is tanked up enough, they have enough of a... of a fluid volume intravascularly that because there's less variation depending on your breath, be a better treatment for that patient as a vasopressor in the setting of hypotension. So here you can kind of see this in picture form. They're particularly looking at stroke volume, B2B. So with a lower preload, you can see the differences and they say you can really assess this just by observation and not even by having a specific number. And you guys have all probably done this in the unit where you've seen on pulse oxymetry or ALINE that you've got this nice variation. You've kind of got these waves that you can kind of plot out and see that that patient is quote unquote dry. So this is just kind of the more in -depth explanation for that. So you can see B2B stroke volume here is much different than that stroke volume after that breath changes after exhalation or inhalation. And then up here where preload is better, that patient is intravascularly more eubolimic. There's less of that variability. So that patient would not be responsive to volume so much. If anything, you're putting them at higher risk for hyperbolemia. So if you encounter a patient with hypotension, you would assess that, okay, their stroke volume is not varying very much or their pulse pressure or whatever you're using as your unit of measure. So that person is likely going to respond more so to a vasopressor. I'm sorry, my phone is going crazy. Okay. So, So this is again just looking at the same basic thing here, looking at pulse pressure and the variability with the respiratory variation. OK, so limitations to respiratory variation. Like I said, when you start to introduce those spontaneous breaths, you're kind of getting out of that nice consistent mode where you can really assess B2D differences. You just have too much change in the intratherastic pressures, too much variability that you could assess for respiratory variation. If you have tidal volumes that are too low or that is too high, that obviously could affect the degree to which you're collapsing vessels and such. Open thoracic surgery just because you've now open the chest. Elevated intra -abdominal pressure, tamponade, arrhythmias, I talked about, aphid, right heart failure. These are other conditions that can affect the ability to assess respiratory these variation. And some vasoactive infusions. Now, typically, you know, in intraop, we probably most likely are going to have a patient on a vasoactive infusion and can still. Assess the degree, some degree of respiratory variation. So it's not a complete contraindication, but it's just, it can affect the usefulness of it. As far as sensitivity and specificity, so sensitivity. Meaning it should, it measures what it should, and it measures it accurately. Sensitivity and specificity. It's important that you're looking at the entire picture. So it's dynamic parameters are still superior to using a static parameter, like. Noninvasive blood pressure, or you're an output. But you still want to look at the entire clinical picture. So you don't have to necessarily go just on one number. Alone, but looking at the entire picture of what's going on with the patient. Another dynamic parameter is the end, expiratory, occlusion tests. So this is helpful in the patient that does have some spontaneous. Powered by Notta.ai Venylation, or maybe they are in an arrhythmia, or you're using lower title volumes. So what you do for this is you would stop ventilation for 15 seconds. And then look for a greater than 5% increase in your pulse pressure pulse contour cardiac output is just a form of noninvasive. Cardiac output monitoring, so depending on what facility you're at. A lot of times if you have an arterial line, there's going to be some system that they have in place that you can also noninvasively assess cardiac output or there are sometimes just pads you can put on the chest or because I guess the arterial line is somewhat invasive, but there are other means for measuring cardiac output that you'll see in anesthesia that aren't a TE probe or some other more invasive system. This particular test has fairly high sensitivity and specificity, so that is another dynamic parameter. Ultrasound esophageal Doppler, echocardiography, of course you can assess chamber size, stroke volume, volume status with those, and then again the noninvasive technologies plus variability index. You can use basically put, it's like putting a pulse oximeter on and assessing the variability in that as a noninvasive technique for, and you would monitor their plus variability index and if it goes above 10 to 12% then they're fluid responsive. Pulse wave analysis, there's other different types and those can help measure cardiac output, assess fluid responsiveness, but they can have significant measurement errors just because a lot of times they are kind of very distal to the heart and kind of the activity of the heart. So it's not the best measurement obviously and ECHO would be more sensitive and specific. Lab values that we often look at would be lactate levels. So as that lactate level increases because your cells are typically, they have a hit in perfusion, they're putting out more acids as waste products and putting that patient at risk for lactic acidosis. So as you see your lactate levels increasing, in some cases we do serial blood gases, we're drawing those interop. That's usually something that we are monitoring for as a sign of overall tissue perfusion and volume status. With a most facilities, when we draw blood gas we kind of have our own special blood gas in anesthesia where we do also monitor like lactate, H &H, potassium, glucose, ionized calcium. So depending on the facility you're at, that would be the blood gas that you would wanna look for that gives you kind of that extra information when you're monitoring a patient. Let's take a 10 minute break or we'll come back at 10. We'll get started with IV fluids. Sorry guys, I had to take care of something. Okay, IV fluids. So, chrysaloids. Chrysaloids are fluids containing water soluble electrolytes and low molecular weight molecules. So, chrysaloids do not have proteins and they're classified by their tunicity. So, this is their effective osmolality and their ability to alter water movement across cell membranes. Isotonic, hypertonic, hypotonic. We'll look at those in detail. So, your isotonic and balanced chrysaloids. So, they have a composition similar to your extracellular fluid, the sodium concentration. Sometimes, the sodium is a little bit less, so they might be slightly hypotonic. If you're truly comparing it to our intravascular environment, they contain, or I'm sorry, their effective osmolality is about 270 to 310. For most of us, it's about 275 to 295 for us, our extracellular fluid. So, you can see it's very similar, just maybe slightly lower in some cases. They contain various levels of electrolytes, organic anions, and they contribute to strong ion difference, which I'll talk about on the next slide. So, we use isotonic and balanced chrysaloids to treat extracellular fluid deficits, administer drugs and blood products, and examples are normal saline, LR, plasma light, and normal saline. So, with an isotonic fluid, because it's very similar to our extracellular space generally, there's the osmolality is about the same. So, there's no movement between the cellular space. and the extracellular space. Strong ion difference. So I'm not going to spend a lot of time here because it can be a very complex topic, but some of the isotonic fluids can contribute to strong ion difference. And what we mean by that is it is the difference between the activity of your cations and the activity of your anions in plasma. So typically we're going to look at the cations and anions that are most abundant. So if you look at the first one, the parent strong ion difference, it's looking at sodium, potassium, calcium, magnesium, and Powered by Notta.ai it's subtracting out the anions of chloride and lactate. Typically, the most abundant ones or the ones we usually are looking at are going to be sodium and potassium on the cation side. and chloride on the anion side. So the true equation is what you see there, but usually when we calculate it, we're mostly looking at sodium and potassium. So we'll say sodium of 135 and a potassium of five, that's 140. And you minus your chloride of about 100, 140 minus 100 is 40. So that's how you get your normal approximate values about 40 milliclivalence per liter. And not all of your strong anions can be measured because a lot of them are going to dissociate completely. So this ion difference affects pH. So if you have an increase in your strong ion difference, there's an increase in your plasma pH. If there's a decrease, then there's a decrease in pH. So it kind of follows the same. This whole slide, even though it's a little more complex, some of the situation is basically describing how normal saline in excessive amounts can contribute to your strong ion difference to the point of decreasing your pH and leading to acidosis. So with the chloride levels in normal saline, we're adding kind of excess chloride. They're higher than our physiologic chloride levels. So when you give kind of excess normal saline, even though it's isotonic and it's very similar in osmolality to our physiologic extracellular space, because of those elevated chloride levels, we're increasing kind of that backend side of the equation. We're basically, if we're giving chloride of 154, or we're using chloride of 100, we're increasing our we're replacing this right side of the equation. So we're dropping our strong ion difference value if we're holding all other things almost equivalent, if that makes sense. So on this end, that increase in chloride, and maybe even that increase in other anions that can contribute to a decrease in the strong ion difference leads to a decrease in our pH. So it promotes an acidosis, and that's related to that higher chloride level. So anytime we have a decrease in SID, so for example, if you did have a patient with an increasing lactate level and decreased perfusion related to that, it's also... Contributing to acidosis causing an acidosis and that's. The reason why is that if all other ions are staying about the same. You're promoting an acidosis just because of that anion equivalent of lactate increasing. With saline, it's because of the increase in chloride. It's causing a metabolic acidosis. So, we try not to give excessive normal saline. To any of our patients because of that potential risk. Effective strong ion difference takes into account bicarb, albumin and phosphate. So, these calculations, there's other calculations you can subtract. Effective from a parent and all these things, you don't have to know. How to calculate that or anything like that. These are related to anion gap. If you maybe measured had that measured in previous patients or something like that. It just it takes into account different ions. But this is all this show you basically how excess isotonic fluids can actually contribute to. A change in your pH. Let's look at volume kinetics so. In actually, I'm sorry, I forgot to mention. On this page balanced, if you've ever seen the term balanced crystallite or physiologic crystalline. That just means that their composition is even more matched to, you know, our composition of physiologic. Extracellular space so a balanced crystallite would be lactated renewers. And plasma light compared to other isotonic crystallites like normal saline. So, if you answered which fluid do we tend to use the most in anesthesia it's LR it's lactated renewers. answer that you were right because it is balanced. It's just matches physiologic ion levels a little more closely. So looking at volume kinetics, there is variable distribution. So remember when we talked about drugs, we talked about pharmacokinetics and distribution, how do our drugs get from the area that you administer them to the plasma and from the plasma to the tissues and things like that. So this is looking at the kinetics of chrysaloids kind of similarly and that is influenced by physiologic status, dehydration, even factors, surgery and anesthesia can even be factors in distribution, changes in your vascular permeability, your Powered by Notta.ai extracellular matrix, things like that. So we know that if our cells, our endothelial cells that are lining our compartments. do have those inflammatory changes and they have those larger gaps and they have broken tight junctions and things like that and we're losing kind of our oncotic and osmotic influences and that fluid tends to follow those, that can affect the kinetics of your crystalloid volume. So it's just something to kind of keep in the back of your mind that just because you give a 250 milliliter bolus does not mean that that 250 milliliter bolus is staying in the intravascular space where you want it. So in healthy patients, the volume of distribution approximates the relative size of the compartment. So you remember we said that in the extracellular space when we have the interstitial only of the plasma and about 20% of that space is plasma, the volume of distribution of an isotonic crystalloid pretty much follows that. So 20% of what you give is gonna stay in that 20% of the, you know, 20% of that space is plasma. So that might be an easier way for you to remember that. So if you give, you know, a liter bolus, you only expect about 200 to 250 mls to remain in the intravascular space. The rest is gonna distribute out of that. And when you do infuse a volume, you know, nearly half of that effect can be lost in about 30 minutes. So even if you give a bolus to treat hypobolemia and let's say you see a change in blood pressure or heart rate or something like that, one of your parameters, static or dynamic, half of that volume can be lost within 30 minutes. So, you know, if you determine that a patient is fluid responsive and you're treating with fluid, you might kinda almost have to do that. titrate that fluid to the effect that you need, knowing that you're going to lose some of it to other compartments. So that these are numbers for approximate numbers for a healthy patient. If you think about a patient that has issues with, you know, like I said, inflammatory changes or sepsis or severe dehydration, hemorrhaging, something like that, then, you know, that distribution can change even more so. Hypotonic crystalloids have a lower effect of osmolality, and so therefore that fluid is going to want to enter into the cell. So it reduces the osmolality of your extracellular fluid. Hypotonic crystalloids are used as maintenance fluids treat solute free water deficits and to help give drugs. So examples of these are half normal saline 0.45%. 5% depturism water or plasma light 56. It's very, very, very rare to see a hypotonic crystallite use in anesthesia. Hypertonic crystallites have a greater osmolality than the patient so that fluid would then come out of a cell and into the extracellular space because we've increased the osmolality. These are used usually to target a desired solute concentration like sodium, for example, and basically to help support that fluid redistribution. So typically we're trying to pull fluid out of cells when we give a hypertonic crystallite. So examples are dexterous 5% in normal saline and there's varying concentrations of saline that can be given. So for example, like 3% saline, some of you may have used that in your patient populations in the ICU, which is designed to help maybe reduce the cellular edema. This chart from your text just kind of compares and contrasts different crystallite solutions. You can kind of look and see some of the differences of sodium and chloride levels in normal saline versus LR. And then there's a difference in isotonic fluid. Also you can see on here, for example, normal saline does not have potassium in it, which is why a lot of people advocate for using normal saline in a renal patient. But the increase sodium concentration can affect potassium movement. in the kidneys. So there have been reports that have shown patients receiving a lot of normal saline can become hyperkalemic even though normal saline doesn't have potassium in it. Calcium is in your LR where it's not in the other fluids. It also has lactate in it. So you can kind of compare and contrast the different types of IV fluids from that chart. A perioperative administration. So we give chrysalloids to help replace water losses, electrolyte losses, especially in our patients who have fasted for some amount of time. There are different arguments as far as how much fluid we should give. There's really no set protocol that we just kind of follow across the board. Historically, we've gone with a more liberal Powered by Notta.ai approach to giving IV fluids. And the ASA still kind of recommends a moderately liberal approach to infusing crystalloids. So their goal is to have a positive fluid balance of about a liter or so at the end of surgery. And with us now kind of shifting towards less preoperative fasting times, you know, we used to tell everybody nothing after midnight. It didn't matter if you had an 8 a.m. surgery or a 2 p.m. surgery. You know, we used to give those kind of blanket, you know, MPO guidelines to everybody. Well, now we're starting to kind of adjust that. Now patients are allowed to, a lot of times, drink carb -rich fluids up to a couple hours before surgery and things like that. So, you know, that's helping their overall fluid balance. So they're maybe not coming in as quite as hypovolemic as they used to. And of course, we want to use hemodynamic monitoring to guide fluid volume resuscitation. However, I have one here, liberal versus restrictive. So we are also starting to see more and more enhanced recovery protocols, ERAS protocols in surgery, which typically promote a restrictive approach to IV fluid administration. So some of those protocols, and it's highly dependent on the case that you do, facility you're at, things like that. But a lot of those protocols are saying, okay, you can give your patient a bolus if they're hypotensive, but otherwise you're, you know, starting to see more and more people put IV fluids on a pump at maybe 5 milliliters per kilogram per hour or something like that. So you're starting to see that more so with certain types of cases where you're getting into a restrictive approach because they've done studies and found that, you know, it might have help improve recovery to kind of minimalize how much crystallite a patient's getting. Now, usually they're looking at a whole kind of protocol of different interventions. So it's hard to know exactly the degree to which the fluid is affecting that alone, unless they're doing randomized trials with that. But, you know, they're also seeing that there's really no statistically significant difference between morbidity, renal injury, things like that. When they followed these patients, whether they got more of a liberal approach to fluids or a restrictive approach to fluids. So that's why we haven't like fully and completely changed practice. For the most part, you're just going to have IV fluids open to gravity and you control how much or how little you're gonna give. It's only gonna be in certain cases where you might start to see... Anesthesia, putting IV fluids on a pump, that's typically not, and historically has not been our practice. As far as normal saline versus the balanced crystalloid, there's mixed results on the effects on renal function. Balanced crystalloids, like I said, are generally favored in anesthesia. They're also often favored for resuscitation. Normal saline, we mentioned the hyperchloremic metabolic acidosis risk. And then with balanced salt solutions, even large volumes of those can risk in increasing your lactate levels, metabolic alkalosis and hypotenicity. Also solutions that contain calcium, there's a risk of micro thrombide that can form if they are also receiving citrate containing blood products. There are reports of patients doing just fine if they're given blood products with LR or another balanced solution that might have calcium in it. But typically, we try to use a solution that does not have calcium like normal saline. Colloids, so we're switching gears away from crystalloids. Colloids are fluid solutions that have large molecular weight particles suspended. So they're going to have macromolecules like some sort of plant or animal polypeptide or starch. They are natural or synthetic. Natural ones would be like your albumin solution. A synthetic or semi synthetic example would be gelatin and hydroxyethyl starch solutions. Albumin, there's lots of different concentrations of albumin. So I just want to remind you to definitely check the bottle that you are administering if you're giving albumin. Because obviously there's a big difference between 5% and albumin. and 25% albumin. And those are probably the two most common concentrations used in anesthesia. But 25% usually reserved for a case that really requires volume expansion and not giving too much. So maybe like a liver patient or trauma patient even maybe. Powered by Notta.ai But 5% albumin you'll see used maybe a little more frequently. Or some of the lower percentages. But of course it's produced from human blood. And the albumin is suspended in saline. It'll help increase serum albumin levels. So if you assess that you have a hypobolimic patient, hypotensive patient, and they also have a low serum albumin, that would be a great IV fluid to give them. More expensive compared to semi -synthetic. colloids and chrysalloids, it is pasteurized to reduce the risk of viral transmission. So a risk of reaction related to that is about 0.01%. So very, very rare, very rare anaphylactoid reactions can occur. And clinical trials show mixed results regarding morbidity and or mortality when comparing albumin to chrysalloids. So some people favor colloids if they find that they're having to just really struggling to treat hypotension. And instead of giving too much fluid, they'll give a colloid like albumin. There's really not a lot of evidence that suggests it's better for more, you know, less risk or more improvement in morbidity. So if you're looking at treating somebody kind of long term, probably more so in an ICU environment. There's really no added benefit. Like if you're correcting a low serum albumin, great. But otherwise if you're just trying to maintain someone with, you know, improve their volume status, chrysalloids going to be a lot cheaper. Hydroxyethylstarches, there's a variety of solutions in this category. They have different concentrations, different weights, different carriers. They do affect your osmotic pressure. Or I'm sorry, the differences in the solutions can affect the osmotic pressure, half life and collagulation effects. So basically, they to form these, they chemically alter starches like maize or potatoes. Hydroxyethylstarches, and I don't know if any of you guys have ever used these in the ICU or another setting, but they used to be very widely used in anesthesia until maybe, I would say six or so years ago, they really fell out of favor. And that's because of these black box warnings for certain populations. They were starting to see problems with excessive bleeding with PES -BAN and other types of PES solutions. And that's of course detrimental in the surgical patient. Renal injury was being, they were noticing a lot of that, especially if the patient already had some renal dysfunction to begin with. So these really fell out of favor. And in these particular populations, critically ill, renal dysfunction, open heart surgery, or if they've received an infusion before and then developed signs of coagulopathy, it's highly recommended you do not use one of these starches in those patient populations. The max dose, 20 to 50 ml per kilo per day, and that varied based on the solution and the ability to break down the starches. These solutions redistribute. So you give them, of course, you infuse them into the plasma, and then they enter into the tissues. So if you remember our basics of distribution, same thing. But the tissues, some of these tissues, the skin, the liver, the kidneys would actually hold on to these solutions, and then eventually they would redistribute and go back to the plasma later. So they were finding trace amounts of these fluids even up to six months after the fact. But when they're sitting in the liver and the kidneys and even the skin, they were causing issues in those tissues. So even for like in the skin, they were causing problems with itching. In the kidneys, they were causing dysfunction. As far as excretion of pest solutions, they are immediately filtered through the glomerulus, but the smaller molecules are in that solution were immediately filtered. But the larger molecules, unfortunately, were not filtered as quickly after metabolism. And so I think also that was for the reason why they could contribute to renal dysfunction. But these solutions are broken down in the plasma by hydrolysis. There are hydroxyethyl groups that could slow that process and then affect their circulation in the plasma. So they would unfortunately redistribute and continue to circulate. Adverse effects, decreasing factor eight and von Willenbrand factor, decreasing platelet function. impaired renal function. And then the anaphylactoid reactions for these are also just about as rare as albumin, maybe even more so. And the mechanism with how they affect kind of your platelets and your coagulation factors is also kind of unclear Powered by Notta.ai as far as how those are affected. But it could be related to these drugs kind of sitting in the liver over time or the solution. This is a chart to help, you know, if you just kind of want to look at it for your own information and compares some of the crystallites we talked about, but also, I'm sorry, the crystal Lloyds that we talked about, but also the colloids, if you wanted to kind of look at everything in comparison. So choosing a tropical fluids with crystallites. Usually, of course, that's our routine, fluid to use. We use it to replace those fluid losses that are sensible and insensible. I don't get into, basically, when you get to basics of anesthesia, I think that's the course you're learning in. You guys will learn how to calculate fluid losses for your patient. So you're gonna take into account the length of time they've been in PO, weight, the type of surgery they're having, and you'll be able to calculate losses and how much fluid you should administer hourly based on what you calculate to help promote more of a eulomic state. I'm not going into that here. I'm just more so concentrating on the pharmacology of the actual IV fluid. So you'll learn that later. But we do have ways that you can help calculate, and identify what's expected of your patient as far as losses that you might want to try to replace with IV fluids. And that's usually gonna be crystalline. We wanna optimize our intravascular volume. Again, we prefer balanced solutions. You might use normal saline and renal patient. If it's a patient that does not really produce urine or a patient heart failure, you might wanna consider administering that fluid with a micro drip IV set just so that you don't kind of fluid overload them if they're really sensitive to that. Another, if you don't wanna use a micro drip set because they can be annoying in anesthesia when you really wanna flush in a lot of drugs, one thing that I will do if I don't use the micro drip IV tubing is I will make sure that my IV fluids are clamped all the way off as much as possible. And I'll... just put like maybe a large syringe flush in line. And I'm just kind of flushing in my meds with that. But whatever you need to do to make sure you're not overloading those more sensitive populations. Of course, avoid large volumes of normal saline. And then we typically avoid dextrose containing solutions because of the risk of hyperglycemia. So that is one reason why we don't use D5 in whatever fluid. Unless you are using it as part of maybe if you have a patient on an insulin drip and maybe you're doing some protocol related to pancreatic surgery or something like that, you might use a dextrose containing fluid in that case. As far as colloids, we use these to expand microvascular volume with minimal capillary leak and the fluid responsive. So again, you want to make sure your patient to the best of your knowledge, does not have major vascular issues that would cause your colloid to be lost into the extracellular space or interstitial space. It can be used to replace blood loss until you reach a threshold to transuse a patient. So if you maybe have a blood loss of 500 ml, you could give 500 ml of a colloid. You can give it in a one -to -one ratio with your blood loss. It's preferable in patients with fluid restrictions. So again, if you have a heart failure, real failure, et cetera, and you know you need to give them fluid that they're responsive to that, but you want to restrict how much you give. That's a situation where you might choose to infuse a colloid. It helps reduce their risks of edema. But there is minimal evidence that colloids are superior to giving balance, crystalloid, and they're more expensive. Hypervolemia, there are preoperative factors that are going to increase your risk. We talked about fasting and MPO status. If you have a patient that is undergoing a GI procedure, they may have had to take a bowel prep preop. So they might be hypoglymic from that. If your patient's taken diuretics, of course, that's going to affect their volume status. If they have an inflammatory disorder, presence of interstitial edema or active hemorrhage. Surgical factors affecting hypoglymia, obviously bleeding. If there's a coagulopathy, and we'll talk a little bit about that at the end of this lecture, any sort of decreases in venous return so that could be related to the position the patient's in. abdominal insufflation with our laparoscopic surgeries. We're kind of blowing up that belly and that can decrease venous Powered by Notta.ai return a little bit or compression of the vena cava. Positive pressure mechanical ventilation, you wanna avoid high peep, avoid really large tidal volumes. Usually with lung recruitment, we're doing just lung recruitment maneuvers acutely. We might give a couple vital capacity breaths and maybe hold for a couple of moments to help recruit lungs in some situations where we're assuming that that patient's had alveolar collapse, but we don't use a lot of ventilation changes for lung recruitment in the OR just because of the short time that we have patients. We don't use it as like a long -term vent strategy usually. But of course, you know, those high tidal volumes and things like that can affect your blood vessels. Evaporative and insoluble fluid losses from a prolonged surgery. If your patient has a decrease in cardiac output or tissue perfusion, our anesthetics that we give, a lot of them are cardiovascular depressants. So you might have a decrease in cardiac output from that. And then there are risks of shock, organoskemia, and failure if you have prolonged hypovolimic states. So the question in the poll, what bolus dose might you start with to treat hypovolimia? For the most part, considering the patient and, you know, of course, you're going to treat your patient. You know, this is not for everybody necessarily, but most people are going to start with about 250 to 500 ml. As a bolus dose, see, you know, assess after that to see if you need to give. And then depending on your patient and the situation, of course, give more if you feel like you need to. Hyper, and that's for an adult. For peas, you know, it might be more like 10 milliliters per kilo. Hyper -volimia. So if we give too much volume, of course, it might be pushing that patient over into the realm of hyper -volimic. So you want to be careful when you're treating hemodynamic instability. It is very, very easy in anesthesia to kind of leave your fluids open and kind of forget about it while you're doing so many other things. And then some patient populations, they are going to be at higher risk for hyper -volimia. So you just want to keep an eye on how much fluid is kind of being infused in these cases. I can tell you most patients. do not get a fully catheter in surgery unless they maybe go, most people would agree the threshold is about four hours. If you give a surgery that's over four hours, you're anticipating giving likely about two liters or more of fluid over that time. Or you're expecting enough fluid shifting, maybe blood loss that you want a better eye on overall volume status. So that's typically when we put a fully catheter in. And I know that's kind of a tangent here, but usually when we're treating hemodynamic instability and we're giving IV fluids, for most cases we tend not to go over two liters of crystalloid in most kind of simple surgeries. Unless they have a fully catheter in place, and then people, I think, feel a little more free to get, give more fluid if they need to, but it's not very common to go over two leaders, I would say. And that's just to help prevent tipping that patient over into hyperbolemia. Other surgery factors when we're treating bleeding, you know, we tend to give a lot of fluid there, but you want to be careful because that can dilute out coagulation factors and exacerbate the bleeding. Other patient factors would be heart failure patient with compensatory fluid retention and the renal insufficiency patients that are at higher risk. Anesthesia factors, our anesthetics, whether general or anorexial, they do cause, like I said, my cardiodepressant and hypotension. So usually anesthesia responses to give fluids and a lot of times to give vasopressors, but you just again want to be careful with how much fluid you're giving. And if we fail to truly measure our surgical losses and how much our patients need to for maintenance from hour to hour, that can put that patient at risk for hyperbolemia. If we give more than we really need to give the patient. As far as fluid overload risks, the risk of reduction in tissue perfusion related to edema, imperidot 2 exchange, GI edema, decreased motility or Ilias, asides, and then coagulopathy. A goal directed fluid therapy is a fluid administration strategy that I already kind of mentioned before. Usually you're going to use a dynamic parameter to help guide that. the NERAS protocol and it's often used for major surgery where you're expecting a lot of blood loss, fluid shifting or things like that. Powered by Notta.ai And it just basically helps ensure that you've got adequate volume status before you give a lot of vasopressors. There's mixed results on using gold -directed fluid therapy. It may be beneficial compared to, again, that liberal approach or some other type of fixed volume approach. And an example of a gold -directed fluid therapy protocol might be three to five ml per kilo per hour putting the pump or the IV fluids on a pump and then giving a bolus of a crystalloid or colloid when your respiratory variation per unit goes over 10 to 12%. So that's one of the common protocols you might see. All right, let's move forward to electrolytes and minerals. Again, this is just a review and I am not very far in this lecture, so I'm going to kind of hustle here. Sodium, you guys all know, majority cation and ECF, lots of different functions, water balance and movement, osmolality, nerve impulse conduction and muscle contraction are key. So we definitely want our sodium in a normal range related to that. We take sodium in through the diet and IV fluids. And then the kidneys of course are the primary determinant of sodium homeostasis. So if you remember in your tubules, the vast majority that is secreted or filtered I should say is reabsorbed by the kidneys. So there it can be regulated also by your renin angiotensin aldosterone system, ADH and your sympathetic nervous system. And then excretion can also be stimulated by the parathyroid hormone and natriuretic peptides. So natri being sodium, uretic meaning you are going to secret or urinate those out. Hyponatrhenia, a variety of causes could be a hypervolemic cause like diluting out the sodium it could be a hypovolemic cause in that you are losing sodium with fluid. Salt wasting, and there's also some uvolemic causes and there's no real change in volume status. But you're maybe losing sodium related to adrenal insufficiency or something like that. Symptoms, surerilidema, confusion, coma, nausea, vomiting and muscle cramps. So treating it is going to depend on the underlying cause. Typically hyponatrhenia is not used. usually like a reason for us to delay surgery and anesthesia. If it's really, really low, that patient might be on some sort of hypertonic fluid, but it's not usually something we are trying to treat in anesthesia. Hypernatrenia, often from water loss, diabetes and sypidus are giving too much sodium in IV fluids or diet. So the problem with hypernatrenia is potential cellular death, altered mental status, seizures and coma. So again, treatment would depend on that underlying cause. Another electrolyte imbalance that typically we're not usually going to worry about treating in anesthesia and it usually does not delay surgery if it's not too severe. Potassium, we care about potassium. So we know it's majority intracellular as far as a cation. It is involved in membrane excitability, kidney function, it's a vasodilator and it inhibits thrombus, clot formation and platelet activation, and it influences osmotic pressure. Kidneys again primarily determine potassium homeostasis. So they're going to secrete potassium especially when you get further along in those two mules. There's lots of hormones that affect that, aldosterone, glucocorticoids, etc. We know that an acidotic state would decrease potassium secretion from the kidneys and that's because with acidosis, the kidneys are going to promote getting rid of those hydrogen ions. Some of those cells that have a hydrogen potassium exchange pump, it's going to promote bringing potassium back in, reabsorbing that in favor of getting rid of the hydrogen ions. So it can decrease potassium secretion and then the opposite with alkalosis. Hypokalemia, the primary cause is usually from a diuretic beta agonist, insulin, antibiotics, catecholamines can shift your potassium inside the cells and promote hypokalemia. GI losses is another mechanism. So symptoms we talked about briefly in another lecture, Skeletal Muscle Weakness. This could even progress to rhabdomyolysis, muscle cramps. Ilias, nausea, vomiting, abdominal distension, and dysrhythmias. Powered by Notta.ai So hyperpolarization, because of potassium wanting to leave the cell to help correct that hypokalemia in the plasma. When you have potassium leave the cell through potassium channels, you're causing hyperpolarization. This might seem a little contrary to that, but in the heart, your nodal cells, like your SA nodal cells and things like that, generally have an increase in their automaticity and excitability in a hypokalemic state. On EKG, you might see changes in the T -wave, U -wave, presence of a U -wave, tachyorythmia, and even other arrhythmias like torsades. Treatment usually depends on the cause. You can give potassium as a replacement, but if you expect a lot of intracellular shifting of potassium, then you wanna be careful to avoid hyperkalemia. PO is usually if it's kind of a milder case, a pypochillemia, if it's a life -threatening issue, or if the patient's exhibiting a lot of maybe EKG changes and weakness and things like that, then it might be given IV. 10 miliqlons per hour is kind of the max that they recommend going through peripheral line, 20 would be adequate for a central line. But since we tend to have peripheral IVs and anesthesia, just keep that in the back of your mind if you find that you are replacing potassium. And then the patient that has diminished ability to regulate their potassium, so patient with renal failure, diabetes, they are at higher risk of hyperchillemia when they're receiving treatment, potassium replacement, just because they have a harder time kind of regulating it as they should. Other side of the spectrum hyperchillemia, it can occur with potassium redistribution or when we inhibit secretion. So there's some certain drugs, for example, succinylcholine, SCH succinylcholine causes a lot of potassium shifting. So it can cause release of potassium from muscle cells and increase your serum potassium up to like a half miliqlons per liter. Aldosterone antagonist, beta antagonist, insides. I can see the other examples there, red blood cell transfusion, especially if these cells are aged, they are going to release potassium just from just what they've accumulated from being stored. Symptoms of hyperchillemia is a nice peaked T -wave. Your cures will kind of widen a little bit. Your PR will widen. With hyperchillemia, you tend to get a conduction block, decrease in automaticity and arrest. So that is why I'm happy to share this with you. potassium is used in like cardioplegia solutions and it's used for lethal injection because you get that conduction block. Parasigias and muscle weakness can also occur. So this is just showing the difference in the ECG changes, hypochillemia versus hyperchillemia. Usually when that potassium hits at least six, you're just gonna start seeing that T -wave peak. Treating hyperchillemia, we tend to give calcium and that's not because it really significantly affects your potassium level, but more so we're trying to help the heart. So calcium IV would help with that, those cardiac conduction blocks and the hit to contractility. Sonium bicarb, that alkalinization would help shift potassium into the cells and promote excretion or secretion. So the dose for that would be a half to one millilitre of lamprakelo IV. Many of you have probably done the treatment of insulin and glucose. It's usually recommended to give 10 units of insulin and 50 ml of D50. The D50 is just to avoid hypoglycemia from the insulin. And that can help drop your serum potassium by one and a half to two and a half. KXL8 helps with potassium excretion and the bile, beta agonist and lute diuretics also can help shift or eliminate potassium. Magnesium. Magnesium is often overlooked, but it is an important one. Major intracellular cation. It's usually, it comes as either an ionized form, protein bound or complex to an anion. Important in protein synthesis, neuromuscular function. It's an anti -arhythmic, it's a vasodilator, helps stabilize the blood -brain barrier and it can even decrease anesthetic requirements. If you had a patient on magnesium, for some reason, they would require less anesthesia. Typically, we get magnesium from dietary intake or supplemental administration. The kidneys regulate magnesium levels. Most of it's reabsorbed and then your bone can store magnesium and kind of affect plasma levels from storage and or release. Hypomagnosemia is from dietary deficiency, malabsorption or renal loss. Also from citrate binding in a patient that's Powered by Notta.ai receiving massive transfusion. So the symptoms of hypomagnosemia are usually high. Again, EKG changes prolonged PR and QT, diminished T -way, torsades, weakness, tetanine, fisculations, convulsions, nausea, and vomiting. Hypermagnosemia on the other end of that spectrum, excessive administration of supplemental magnesium. Symptoms, again, ECG changes, including conduction block and acystole. So a little more similar to the hyperkalemia in that aspect. Hypotension, respiratory depression, muscle paralysis, narcosis. So the treatment for this would be calcium, gluconate, 10 to 15 milligrams per kilogram, diuretics, or dialysis. It's rare unless you're actually supplementing magnesium. It's rare for a patient to just be hypermagnosemic. When we might give magnesium, so magnesium, I would say potassium actually, we don't give a lot of potassium in anesthesia unless you kind of have a patient that's really at risk or has issues with hypokalemia. But we do tend to tolerate some degree of hypokalemia in most anesthetic patients. So you don't see us really replace it a lot. Same with magnesium, we're not always replacing magnesium, but we do give magnesium for other indications other than increasing serum levels. So the patient with preeclampsia is a disorder in pregnancy with hypertension, protein in the urine and liver dysfunction. They will often administer magnesium to these patients for the vasodilation. And this is systemic as well as uterine. It can help increase the concentration of other vasodilators like calcitonin gene related PupTi and it can block the effects of some of our endogenous vasoconstrictors like endothelan 1. So magnesium is often given in a loading dose and then a prolonged infusion to these patients. It can cross the placenta and cause some of those same side effects that you saw on the hyperkalemia slide. Lethargy, hypotension and respiratory depression can occur in the neonate. Magnesium for dysrhythmias, it helps treat Y complex tachycardias, long QT syndrome, dejoxin induced tachyrythmias, and it might even be used for the heart surgery patient to decrease post op aphid. It can be used for analgesia. It has anti nociceptive effects. helps block your ability to sense noxious stimuli. And it has NMDA antagonist effects. So when we get to the second semester summer, we'll talk about other NMDA antagonists like ketamine, methadone, magnesium has that same mechanism of action. We don't routinely use it, but if you maybe had a chronic pain patient that is not responsive to normal opioids, it might be something that you use in your plan of care as a multimodal way to treat pain. Asthma, it can be used for bronchodilation. It's not gonna be first line for the asthma patient as a first line therapy, but if other therapies fail, it can help improve bronchodilation because it inhibits calcium and histamine. Pheochromocytoma, which is a tumor. That releases a lot of catecholamines on the adrenals. If that patient is undergoing surgical excision of that tumor, they're at risk for catecholamine crisis. So magnesium can be given to promote that vasodilation and help, you know, hopefully block those muscles from responding too much to the excess catecholamines. It can also reduce catecholamine release. With magnesium and all these other indications, you know, the text doesn't really go into specifics of dosing for each one. But generally it's going to be somewhere between one to four grams IV as far as dosing goes. Let me plow through calcium and I'll give you another or the rest of these electrolytes and I'll give you another break. Calcium, primarily in the skeleton over 99% is there. I and I is versus protein bound calcium. So when we talked about like pharmacology, the basics of drugs and pharmacologic effects and I told you that the ionized form of the drug is not the physiologic or pharmacologically active form. It's almost the opposite with calcium. It's the ionized calcium that produces physiologic effects. So this is usually the number we're more concerned about when we are looking at calcium levels, especially interoperatively. This is a typically a value we look at on serial blood gases and the OR is the ionized calcium. Normal is about two to two and a half. It is dependent on pH. So acidosis and alkalis is going to affect ionized calcium levels. Powered by Notta.ai Your protein bound calcium is about 40% of your total calcium serum calcium level and the albumin binds non ionized calcium. So even in when you're looking at a total calcium level, in the presence of nonalbumin, or sorry, low albumin, a low albumin state, liver patient, kidney patient, et cetera, it might show a decrease in your total plasma calcium level, just because you have that extra non -ionized calcium floating around, but it can shift to a storage site because it's non -ionized. It's not trapped on an albumin molecule. It's in a non -ionized form, so it can go into the tissues and that affects your serum calcium level. If that patient is asymptomatic, it could be because their ionized calcium is still normal, and so they're not really showing any, Physiologic changes, even though their overall calcium level that you would assess on a renal panel is low, if that makes sense. And that's even in a low -albumin state when you don't have a lot of calcium binding. Musculoskeletal, of course, contraction, neuromuscular transmission, contractility, vascular tone, coagulation, intracellular signaling. There's so much that calcium does. And then it's typically regulated through endocrine control, through hormonal control, vitamin D, pyrethyroid hormone, and calcitonin. So our bone acts as a reservoir, holds on to calcium, can release it and store it as needed to help minimize a lot of calcium alterations. Hypochalcemia in the presence of low -albumin and vitamin D, disorders of the pyrethyroid, pancreas, renal, citrate binding in a patient that's getting a lot of transfused blood products, symptoms they are neuromuscularly excitable. So peristegias, tetanine, twitching, spasms, risk of seizures, and dysrhythmias. And it tends to be rarely related to malabsorption, just because, like I said, the bone can release a lot of calcium when levels drop. Treatment, calcium chloride versus calcium gluconate. You guys probably already know, calcium chloride has three times the level of calcium in it than gluconate. There are some differences. Extravagation of calcium chloride is horrible to the tissues. I have actually seen this. I had a patient not that long ago. I refuse to get calcium chloride. in a small 20 gauge IV in the hand. And I had an anesthesiologist who said, it'll be fine, it'll be fine, slammed it in. That patient ended up with an extrovalization and sloughing in that hand. I mean, that hand went from normal looking to completely black by the time we hit Pachy. And this was at the end of the case. So, and that patient required a hand surgeon to come in and to breathe the tissue. It is a serious thing. Do not give calcium chloride in a hand or foot IV, please. Or, let someone else do it if they're telling you, it's fine, it's fine, you let them do it. Central line is preferred with calcium chloride. It's just detrimental to tissues. Calcium gluconate can be given in peripheral IV, less calcium than calcium chloride, but still effective. Either way, you wanna avoid rapid IV push. Just give it over a few minutes. and the dose is anywhere between half to two grams. If you're treating a low ionized calcium level with gluconate, you might want to give it one or two grams. If you're treating it with calcium chloride in the absence of an emergency situation, then you might want to start with a half to one gram of calcium chloride. Hypercalcemia, again related to parathyroid disorders, excess in the diet, could be induced by medications. And the symptoms of that GI smooth muscle relaxation, decreased neuromuscular transmission, polyuria, dehydration, renal stones, and shortened QT are all symptoms of hypercalcemia. The general goal for that would be to get rid of the calcium. So it's usually through loop diuretics. It's kind of the primary treatment for excess calcium. Corticosteroids can inhibit the effects of vitamin D, so that patient may be given hydroportyzone IV or pretentazone. And you can see some of the other drugs listed there, or hemodialysis, if it is acutely severe hypercalcemia. Phosphate, majority of that is intracellular functions, energy, signaling, cyclic AMP, it's got, of course, phosphate, immune system regulation, coagulation cascade. And we talked about phosphate as a buffer in the kidneys for acid -base balance. Homiostasis is similar to calcium because of that interplay. So vitamin D and parathyroid hormone affect phosphate, homeostasis as well. Powered by Notta.ai In the serant or in this situation of hypo, phosphatemia, it permits an increase of serum calcium because of their interplay, but it's usually related to or usually causes a decrease in your ATP and 23 dpg in your erythrocytes. 23 dpg stabilizes the conformation of hemoglobin and it affects its affinity for O2. So decrease D3 dpg, decrease release of O2 to the tissue, so it's a higher affinity to hold on to O2. So if you decrease that and transfuse, for example, blood in a cell that has less of that, it's less likely to give up oxygen to the tissues, which is usually what you need. Hi, high -pophosphatemia can also cause skeletal muscle weakness. type of inhalation, CNS dysfunction, and neuropathy. Having a high phosphate level is very, very rare, so I didn't even include a slide on that. Let's take a five -minute break. We'll do it a little bit quicker. So 11, we'll just say 11, 11 or 11, 12. We'll get started again. Okay, for the sake of time your mental break today, you could just put it in the chat If you could be an animal for a day, which animal would you be you don't have to put why you don't want to? and We won't go through everybody just because I'm running short on time, but What animal would you be? Yeah, I would be a golden retriever Oh specifically golden retriever. Yes, okay. I've done all day Dolphin oh giraffe to be tall Be a sloth just because I think it's to be lazy for it. Yes. I love sloths They're just so like chill I would love to fly so an eagle and the swim predators nobody attacks them Good answer. Oh Yes, pandas my absolute favorite animal in the whole wide world is the red panda I just think they're adorable and I really want to steal room from a zoo one day The red panda Anybody else if you could be an animal for a day Thank you. Is that everybody? I'm gonna have to go with maybe cat as well. They just really don't care. Lay around do nothing. I have one sitting right next to me right now. Okay, blood physiology and transfusion. So when we look at composition of the blood, about 45% is cells in your hematocrit. And then 55% is plasma and then the plasma has water, protein, nutrients, etc. So that is your basic composition function of the blood. We know homeostasis. It is a line of defense. Transports oxygen, nutrients, wastes and hormones and heat exchange. So from the core to the extremities. Blood cell sources, depending on when you may be accessed this PowerPoint, I changed this yesterday. So if you have the old version, this was kind of in there twice. So I just crossed that out. Well, if you have the new version and yours should look correct, but bone marrow obviously is our primary source of blood cells in 95% come from that and mostly in the pelvic breast spine areas. Femur and tibia are kind of secondary to bone marrow, but can be considered a primary source in pediatrics. The liver and spleen and lymph nodes also help regulate production and differentiation of stem cells into different types of blood cells. And then this, of course, stem cells proliferate and can differentiate as well. White blood cells, there's leukocytes, which are granulocytes or agranulocytes, which don't have little granules in them. They are defense, of course, against infection and foreign invaders. Bone marrow is the primary source for these, but you also have lymphocytes that come from lymphatic organs as a source as well, like your lymph nodes and your thymus. Red blood cells have a flexible shape. Hemoglobin is your oxygen -binding protein and determinant of your O2 carrying capacity. Erythropolepoetin, which stimulate red blood cell formation in the bone marrow. As far as destroying old blood cells, our liver macrophages will do that. So usually after about four months, those red blood cells entering into the liver are going to be destroyed and broken down. And it'll break it down into heme. And the heme is further broken down into iron and biliramin, which I think I have, yes, on the next slide here. So your aged red blood cells, rithercytes, will go into the liver broken down by these macrophage cup for cells. And it'll take that hemoglobin and further break that down into heme and globin. Globin is then its protein. So it's... broken down even further into the amino acids that make up that protein. Heating is broken down in iron and bilirubin. Bilirubin would then get excreted into bile and iron can be transported back to bone marrow to be used to form new red blood cells. Unemia, so we either have a reduction in red blood cells or hemoglobin related to, for example, hemorrhage, Powered by Notta.ai bone marrow failure, other causes of anemia. There are different types, dietary deficiency, kidney disease or nephrectomy, and then sickle cell disease, which can lead to hemolysis and destruction of red blood cells. Iron comes from your diet. Typically, if you are taking an iron supplement, you're going to take it with some form of vitamin C or vitamin C. might be added to that iron supplement to help increase absorption. It is bound to transferrin, which is just a glycoprotein that helps deliver the iron to cellular receptors. 80 percent of your iron goes into your bone marrow to form those new blood cells. It's also incorporated into reticulant endothelial cells and liver and spleen. Then as we synthesize new hemoglobin, that actually mobilizes the release of more iron from the tissues. It is a such a component of enzymes and plasma concentrations between 50 to 150. Iron deficiency has a very high incidence in menstruating females. It can be related to also inadequate dietary intake, increased requirements in the pregnant patient or due to blood loss, and interference with GI absorption. Iron deficiency anemia, those patients generally will take some supplementation to help with erythrocycine production and hemoglobin concentration, and usually can see a change in iron levels within days to weeks. Aglutination. Here we're looking at this glutinin antibody reaction. Aglutinogens are antigens, which stimulate the formation of agglutinin. Agglutinin is an antibody or other substance that would cause particles to aggregate. The problem with the process of agglutination is when we look at transfusion and the risks associated with transfusion. If we end up with this interaction in patients that have antibodies to certain antigens, we can end up with hemolytic transfusion reactions. There's type A and type B, your blood type is gonna have certain antigens. And then RH factor, depending on your RH factor, it's RH factor is an inherited protein on the surface of your cell, red blood cell. But if you have a negative recipient that gets exposed to an antigen from somebody you already positive, they can end up with an antiglute nation reaction. So this is just, I didn't type it all out for you, but of course you guys all know blood types and the antigens or lack thereof on the cells and then the risk for agglutination reactions. For example, type B donor with an anti -B type A recipient down here can have an agglutination reaction and homolysis. So let's look at red blood cell storage. Biochemical changes do occur as red blood cells sit in blood bank. So we start to deplete ATP and 2 ,3 -DPG. So I reminded you that that 2 ,3 -DPG, sometimes you'll see 2 ,3 -DPG, diphosphobiphospho, same thing. But it helps stabilize the hemoglobin in a shape or state that affects its ability to offload oxygen. So it stabilizes the deoxygenated form. So when we don't have that, then basically we're promoting the oxygenated form, but we're not allowing that hemoglobin to really offload that oxygen to the tissues. The shapes of the red blood cells, we know they're flexible, well that shape can change over time. And if the more red blood cells that you kind of have in this altered shape, once it starts to hit microcirculation like the capillaries and the smaller vessels, it can actually kind of clump together and potentially impair flow. It promotes an inflammatory response, so there's a risk for transfusion -related lung injury, decreases in O2 delivery, and increases in homolysis. Additional changes are looking at this further, I guess. The risk of adverse events is greater once you get two to three days out from donation. So you start having more red blood cell fragments in that solution. of packed red blood cells. They have impaired nitric oxide scavenging. So your endothelial cells release nitric oxide synthase. And we like nitric oxide because it is a nice vasodilator. It promotes an open patent vessel and promotes blood flow through that. And if we have impaired nitric oxide, reduced nitric oxide synthase, which helps form nitric oxide, then we're affecting even maybe some of the vessel dynamics when we transuse these RBCs. Plus nitric oxide can, the scavenging can actually help relieve or remove free oxygen radicals. So we take that benefit away Powered by Notta.ai as well. Let's. maybe put that patient at risk for inflammation, inflammatory processes. Sodium potassium ATPase failure occurs in older red blood cells, and that is what is contributing to that potassium leak, so we can no longer effectively pump potassium back into the cell. There is some mixed evidence as far as when all of these changes are occurring and kind of what is the, you know, the, I guess, time frame where we say red blood cells are too old, we should not trans -seize them. So we have the question of how does your HNH change when you administer one unit of packed red blood cells? I think the majority of you got the answer right, but one unit of packed red blood cells will increase your hemoglobin by about one gram per deciliter, and your hematocrit by about 3%. So one in 3%, if you guess those, you are on the right track, and most of you are close. So the minimum acceptable hemoglobin at which we tend to transfuse in the surgical patient population is highly patient -specific. You will see the literature kind of vary on this. There is not just one number we use across the board. So for example, the cardiac patient, we might use a hemoglobin threshold of 9 to 10 and prefer to trans -use them when they get to that number. Most surgical patients, it's usually going to be around 7 to 8. If they drop below 7 to 8, then we are probably going to trans use them, especially in the setting that they are still actively bleeding. If you have a young healthy patient, you know, younger adult, maybe even pediatric, most are recommending six, hemoglobin of six as your threshold. So more restrictive strategy for those patients. Of course, in the setting of acute anemia, you tend to see a compensatory increase in cardiac outlet and oxygen transport. When you start getting into that cardiac patient, heart failure patient, for example, or a patient with flow restrictions, they have less ability to compensate in the setting of acute anemia. So that's why we tend to use a higher threshold for those patients. This is usually an area of contention. If you are maybe doing a surgery, doing anesthesia for an inpatient, and you kind of have these serial, you know, H and H's that you looked at over time and they're sitting on a unit with an H, a hemoglobin of let's say like 7.5 and you're kind of like, well, do I transfuse them or not because they haven't been transfusing them on the floor or in the unit. But now they're about to go to surgery. So that's when you kind of take into account what surgery are they having? Are you expecting a lot of blood loss or is there a risk for a lot of blood loss? That's when you're having the discussion with surgery. And maybe even their primary care team to say whether or not you believe you need to prophylactically give transfuse hemoglobin that's in that kind of borderline range or do you wait until the bleeding actually occurs and you have those units nearby? You know, a lot of times we'll order blood on call to the unit or sorry on call to the OR and then have it kind of sitting and ready and waiting just in case you need to immediately give it. So those are considerations you'll kind of approach patient to patient case to case with your anesthesia team when you're trying to make those decisions. Considerations, of course we want to maintain intravascular volume like we talked about. Actively bleeding if we're controlling that, you know, and you're not expecting their hemoglobin and vaticra to drop too much more, you may or may not decide to transfuse. What are their oxygen carrying capacity needs? Do they have like low cardiorespiratory reserve or something like that? Do they have high O2 consumption because of a disease process? Like a systemic inflammatory response or something like that, then they may be more likely to need transfusion. And there's all kinds of different risk factors and then you got to consider that with the risks of transfusing a patient because it's not a benign. procedure. You want to make sure you have adequate IV access. If you can have a separate IV, that's great. In anesthesia, we often don't have central lines. We love large bore peripheral IVs. If you're doing a bigger case like a transplant cardiac case, then those patients tend to get a central line. But most of our patients, we would much rather have a 16 gauge or 18 gauge or even maybe bigger, large bore IV, depending on the case. Do your system checks, whatever your facility requires to help you avoid transfusion errors. Powered by Notta.ai Even in a setting of like a trauma case where it's just all hands on deck. And it's an emergency case or something like that. Usually, if you're in a big enough institution, you'll have kind of free hands available to help. Check blood as you're giving it and that kind of things to do your best to follow protocol there and then of course typically there's We like to use a filter for red blood cells transfusion to help remove any lingering clots or aggregates Or fragments that are sitting around and it might help also with leukoreduction if that was not performed by blood bank At the time of collection and that's just removing any white blood cells that might be mixed in Red blood cells are refrigerated. They're kept cold until you decide to transfuse So if you different facilities have this set up differently, but usually there is a cooler in your OR near your OR Or maybe even on a unit kind of adjacent to the OR that a lot of times we might keep red blood cells there Until you decide you need them actually brought into the OR And then sometimes facilities differ here. They may bring them to you on ice. They may bring them to you in some other way or if there's some external cooling place then the minute you want to transfuse them is when you should have them brought to the OR If it was previous any blood product that was previously thawed should be warmed So you want to use a blood warmer Ideally just to help reduce the risks of hypothermia and coagulopathy which is associated with giving cold blood products You never want to leave Pack red blood cells out of refrigeration for too long if you leave them out, you know, you kind of want to Try your best to keep track of the time when you receive them and they were no longer refrigerated And if you return those products the blood bank you want to write a time on there of how long they've been out of refrigeration Typically blood banks will not send those red blood cells blood cells back out for transfusion to another patient if they have not been refrigerated for greater than 30 to 60 minutes. That's a very short amount of time, especially in an anesthetic procedure where time gets lost, especially when you're getting blood products. So try your best to keep your eye on the clock if you have taken those out of a cooler. Normal saline is typically recommended. You can also co -administer red blood cells without buprenum plasma. Other isotonic crystallites have been used without adverse events. D5 or hypotonic solutions are avoided because they promote breakdown of that red blood cell. Red blood cells can take up glucose out of a glucose -containing solution and it can cause it to break apart. You want to administer other blood products? and separate tubing or a loan. So you want to give them either sequentially and flush in between or give them in a whole other IV. Plasma, so plasma is whole blood where we remove the red blood cells, platelets, coagulation factors, fibrinogen proteins. FFP, fresh frozen plasma is frozen within eight to 24 hours of collection. You can actually get cryo precipitate out of FFP and it can be transfused interchangeably with thawed plasma. It should be transfused within 24 hours once you thaw it. And as plasma is stored, you start to see less and less factors five and eight. It's usually solvent detergent treated to help kill viruses and remove debris. Usually we are replacing volume with plasma and coagulation factors with plasma. That's pretty much the only indication to give it. It can help with bleeding. So if you have an elevated PTT, PT9R, it can reverse warfarin, anti -coagulation. It's not the best choice, but it can be used, especially if you need to treat it a little more immediately. Like if you had a patient that did not stop their warfarin, but they need urgent surgery, you might give them plasma. And then it can treat coagulation factor abnormalities. Dose is usually about 10 to 15 mLs per kilo. If you're only giving it to reverse warfarin, the dose is about half that. So you may not need to give as much. But that dose 10 to 15 mLs per kilo, you would achieve about a 30% increase in your plasma factors. Thawed products should be refrigerated or kept cold. Again, you want to use a blood warmer to reduce hypothermia and quadulopathy. Cryo precipitate is formed from the slow thaw of frozen plasma and it can be stored up to three years. Cryo is very rich in factor one, fibrinogen, factor eight and factor 13. I would know those. Also, when we get next week, we'll look at the factors more closely. Some of them have different names, so I would know those names as well. And it does contain some other factors as well. So indications for giving cryo is usually hypofibrinogenemia, which is low levels of fibrinogen. Powered by Notta.ai And this can be from a variety of issues like massive hemorrhage or quadulopathy or dilutional. Cryo can also be given for hemophilia A and factor 13 deficiencies to factor 8 and factor 13. But it's usually not first line. It's after they have maybe not really responded to giving an isolated concentrate of that factor or they've been for Von Willebrands, for example, disease. We try to give Desma Presson. We'll talk about that later. But if that didn't work, Cryo is a potential option for that patient too. Cryo should be transfused within four hours. One unit per kilo weight can increase your fibrinogen in between 50 and 100. Sources kind of vary there, but that's about average. The minimum fibrinogen that we desire for hemostasis is about 100 milligrams per deciliter. So about half of your normal fibrinogen, normal fibrinogen is about 200, is enough for hemostasis. So we try to at least get that. Blood warmer is not necessary, but if the patient's hypothermic, it would be nice to use. And then you want to give platelets separately because they can interact with Cryo. Average lifespan of the platelet, 8 to 12 days, the spleen will ho

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