Lecture Module 4, Pharm PDF

: Okay, good morning. It looks like everyone is finished. : Does anyone have questions on the : Oh, gosh! I lost my train of thought anybody have questions on the contrast. Die lecture : from the previous module that we did not have time to discuss in class. : Yeah. A quick question. Are we resp...

: Okay, good morning. It looks like everyone is finished. : Does anyone have questions on the : Oh, gosh! I lost my train of thought anybody have questions on the contrast. Die lecture : from the previous module that we did not have time to discuss in class. : Yeah. A quick question. Are we responsible to know the dosing of those dyes? Is that something that should be incorporated in our study, or just kind of the indications and : concept. : Yeah, I mean, they are technically : drugs that you might give interops. So it\'s something you should be familiar with. Yeah. : Okay. Fair enough. : Anyone else. So far so good. : Or if you think of anything later, let me know. : Same with electrolytes. I mean, I know, most of this module should be reviewed for you guys. You know, you guys have all given fluids and given electrolytes. : This is a lot of this is just basic physiology, basic nursing, care and knowledge. So hopefully, we\'ll kinda breeze through a lot of it. But I will. : It is a lot. So we\'ll you know, we\'ve got a lot to cover here. : So we\'re gonna start up at the physiology of body body fluid compartments. : there we go. So we\'ve already kind of talked about total body water. : which is gonna vary in in different populations, right? Whether you are male female, depending on age, maybe depending on : whether or not your body composition has a lot of muscle, which is about 75% water versus a lot of adipose, which is only 10% water. So there are going to be some slight differences in that division of fluid and solid. And then, even in the division of the fluid space which is going to be intracellular and extracellular. But : you guys know, for the most part, the average 70 kilo person is about 42 liters, of total body water. : So in that extracellular space which is about a 3, rd we are dividing that between about 80% interstitial fluid, 20% in your plasma : so our intracellular space, very rich in potassium and phosphate potassium being the high highest : represented cation, phosphate being the major anion : intracellularly extracellularly we are rich in sodium and chloride sodium being the cation chloride being your major anion in the extracellular space, and of course, like, I said, divided between interstitial plasma. There are some transcellular spaces which are considered anatomically separate, like the Csf. And such, and that would be included in that extracellular compartment. : So you can see here. The distribution of our values. For, like the sodium chloride primarily in the Ecf versus potassium or yeah, potassium and phosphate in the Icf : and you can see that these should fairly well align, at least on the left side of this kind of dividing line : with your plasma levels, your serum levels of these particular electrolytes. So you know, sodium roughly, 141, 45. Because of this ability to kind of move in between these substances can move in between the plasma : in interstitial fluid fairly easily. So you\'ll see higher concentrations of these particular ions versus the substances and ions at the top are going to be primarily hanging out in the cells. : Now, the composition of our plasma primarily water. : We do have plasma proteins that we\'ve talked about in the past. Like albumins and globulins, they hold on to our drugs, they hold on to other substances. They create that oncotic pressure to help keep volume. Inside those spaces they participate in ph coagulation, etc. Less than 1% is salts, also contributing to osmotic pressure. Ph and metabolism. : We, of course, have O. 2 and Co. 2, that is being delivered to different tissues. We have metabolite, the waste products and metabolism coming back out of tissues. So all of those gases are going to be represented. : nutrients like lipids, glucose to feed ourselves, and then the waste products, like uric acid urea that comes out of those cells, hormones, vitamins, blood cells, etc. And you guys all know the composition : and the purposes of each of those different : substances. Now, if we look at the physiology of movement between compartments. Our small ions can move pretty freely. So I just mentioned that so between your extracellular space. : the in your extracellular overall compartment between the interstitial space : and the plasma. You know, those ions are moving very freely. So those levels are very similar : proteins macromolecules. Generally we don\'t allow that movement, and that\'s because of a couple different things. But your endothelial cells that line your vessels form kind of these tight junctions, and that : space between each cell is going to typically vary, depending on the tissues that : that these particular cells are in. So in some areas, they\'re going to be very tight in other areas. We\'re going to have larger pores that are represented in between those tissues that may allow different types of substances through. Additionally, we have this Glycocalyx layer on top. : You kind of see all the different hairs and things it kind of just catches things, so it does act as a barrier to prevent different substances from getting across this particular : a border. : So you can compare and contrast the movement between : different types of tissues or the different compartments, and how they\'re like basement membrane might look. So if you look at the extracellular space in, you know, for the blood brain barrier for the lungs for the heart. It\'s very tight. And so they consider that continuous endothelium. So it\'s almost as if there\'s really no : space between those cells that they\'re really just kind of sitting up against each other, and any kind of division in between is very, very tight, and is really intended to not let anything pass through out of the vasculature into that : interstitial space that could potentially move towards the cells so tight junctions there. When you move down to look at the kidney in a different area in the brain. So the choroid plexus : the glomeruli and those types of tissues have those fenestrations in between. So you can see where it\'s a little bit bigger of a gap. The pores they allow certain. : you know, types of substances and fluid and things like that to move through now they can still be highly selective, like we talked about with the kidney. It\'s not intended to necessarily let every large protein, red blood cell, etc, through. But there are some molecules that, based on : electrical charge based on size, can get through those particular pores down here, liver and bone marrow. You can see much bigger spaces in between these different gaps allows you to reabsorb different substances. And so we consider that a discontinuous : capillary endothelium, because you can see how you know kind of : jagged the basement membrane is on : in these particular tissues. There is a 4th type. So basically, these are phenotypes. And so these cells kind of have the genetic material that says, you need. You know, the vasculature in this area. The cells in this area are going to have this type of membrane. There\'s a 4th one that\'s not on this particular image, but it\'s what you would find in like the endocrine system and the gut : and it does have also these fenestrations which can be very selective as well, but they are. They can be induced to allow the absorption of different : molecules and substances. : So what happens when we have : a problem in that particular space with those membranes? So that is something we see in inflammation with inflammation. The endothelial cells are going to change the glycocalyx layer that\'s normally intact might become damaged. So that\'s allowing cell or substances to potentially move : transcellularly or paracellularly. We have a problem with that junction : opening up the size of those pores in some instances, and then that way we unfortunately allow larger molecules proteins to come through. : So normally, albumin movement. You know, kind of overall is about 5% : so it can, you can lose up to 5% or so of that albumin out of the vascular space into the interstitial space. : But when you have a process of inflammation which can double in surgery in quadruple, in a septic patient. : you can see how that could really affect the movement of those macromolecules drawing fluid out of the vascular space : and into the tissues. : So we will look at monitoring intravascular volume status, because this is really what helps to drive therapy. So I\'m trying to get you guys to the pharmacologic part of fluids, electrolytes, blood products. So that\'s why I\'m kind of starting with a little bit of physiology. And now we\'ll look at monitoring and give you just kind of an introduction of some of the things that : we use in the or you guys have probably used in the Icu maybe just a little bit of a little more information on that. Obviously, you\'re going to learn about monitors again. So this is not intended to be super thorough but basically. : you know, we typically use standard monitors : to help us give some kind of a basic assessment of volume status. The vast majority of surgical patients. We are just going to use a standard monitor, non-invasive blood pressure cuff and their heart rate. : If you\'re doing a more complex surgery, or you have a patient with a lot of comorbidities. Then you might advance your monitors so that patient might require an arterial line, a cardiac output monitor : central line with Cvp or something like that. So you\'re basically going to assess the risks : of large changes in volume status for your case and your patient, and then use that information to determine what level of monitors do I need? : So when we think about parameters to assess this, they\'re static and dynamic. Obviously static parameters. They\'re used more traditionally. They can be used with standard monitors. But they only represent usually like one moment in time. And so it\'s very hard, even when you\'re trending static parameters to get an idea of just kind of like : changes that are really occurring in the moment, because sometimes, you know, taking a blood pressure with a non-invasive cub. It can take : even a couple of minutes, really, for that to kind of go through a cycle if it\'s a hard if the the machines having a hard time measuring it, or whatever it is. So : you know, you\'re kind of waiting for that one single measurement. And it\'s hard to kind of get a beat to beat, you know, as the heart kind of pumps and pumps and pumps, getting a good picture of what? That those changes might, you know, look like with a static parameter, but we still do use them. So : we can get some information from our blood pressure or heart rate, and things like that, on whether or not our patient might be hypovolemic. Of course we don\'t really know about true tissue perfusion. So when we have a decrease in tissue perfusion that can go unrecognized, and a lot of that is because of compensatory mechanisms. So, for example, really, young patients, pediatric patients, young adults have. : very, you know, active and sometimes almost even overactive, sympathetic nervous systems. : So when there is a drop in volume, status hypovolemia. Your baroreceptors get involved. You have atrial receptors get involved, and all of these different things are going to trigger that sympathetic, nervous system trigger that Renin-angiotensin system to activate and compensate. : And so you may be able to maintain a normal appearing blood pressure. You may be able to maintain a high enough heart rate : to perfuse or to help, you know, improve cardiac output. But you still may not really be able to appreciate the underlying threats to perfusion that\'s going on. : If you have a patient on Beta Blocker, if it\'s working well enough, it can mask any sort of normal tachycardic response to hypovolemia. : and then, if you were to use Cvp, which Cvp is not really something we see in anesthesia, we don\'t tend to use Cvp like you may have seen in the Icus, but it can even be an inadequate measure : of preload and fluid responsiveness and things like that. I mean, it\'s reflecting somewhat what\'s in the right atrium but : it\'s not really even one of the better measures urine output. We expect : most anesthesia patients to have a decrease in their urine output. Additionally, we\'re giving drugs. We are putting them under surgical stress, which is going to affect that urine output. So even if they are euvolemic. : you are probably going to see a decrease in urine output. If your patient has a Foley catheter intra-OP, which we typically reserve for the patient that we are expecting a lot of fluid shifting, and we have to give a lot of fluid, or, if the case is long enough. : usually about 4 h or more we may put in a fully catheter : You could give that patient 2 liters of fluid over the K. Over the course of that procedure, and you may only see, like 150 come back : of urine. So something like that is kind of very normal, so that patient may be volemic because you replaced fluid deficits, but their urine output is low. So it\'s hard to really use that as a true parameter, because you may think urine output\'s low. They\'re hypovolemic. But they\'re actually okay. So it can be a little bit misleading : mixed, venous oxygen saturation which you know, is intended to reflect. Global O 2 delivery proportional to Co. 2 and tissue perfusion. But when you have changes in oxygen consumption, if you have someone with a, you know, severe systemic inflammatory response, or. : you know, infection fever, any of those kinds of conditions that really change. O 2 consumption : that can kind of change your ability to use mixed venous. O 2 sat : as a true reflection of how the tissues are being perfused, and volume status. : So if you\'re if you assess that your patient, you know : could be at risk for these large changes in volume status, and something that you feel like you will need to address : intra-OP. It\'s better to try to use a dynamic parameter. So these are used to assess fluid responsiveness, to direct or guide goal-directed fluid therapy : which we are starting to use more and more in the I not in the I see in the or : it\'s great for invasive surgeries, large expected blood losses, and a lot of fluid shifting so big cases. If you\'re doing a big thoracic case, if you\'re doing a large abdominal case, if you\'re doing a large spine case, if you are doing, maybe a revision of an orthopedic case, or something like that, where they\'re cutting into, you know. : large muscles, and it\'s expected to last for hours and expected to have a lot of blood loss. Those are the usually the types of surgeries and cases that I would highly recommend dynamic parameters and the advanced monitors that would go with that. : There can be some challenges with sensitivity and specificity, just basically meaning that the monitor is truly measuring what you think. It\'s measuring : and that it\'s giving you an accurate picture. So we don\'t, you know, really just rely only on a dynamic parameter. You kind of have to take the entire clinical picture into consideration. So. : but the good thing about these is that you can sometimes just look at a monitor : and determine. Yes, this patient is hypovolemic, or maybe even euvolemic, just by visualization. So that\'s the nice thing about them. : The 1st one is respiratory variation. There\'s many different ways. You can measure respiratory variation. You can use pulse pressure difference between systolic, diastolic. You can use stroke volume. You can use isolated just the systolic blood pressure, and you\'re looking at the : variation in your patterns with mechanical ventilation. The reason why we use : controlled mechanical ventilation for this is because you are delivering a positive pressure breath. : When you deliver that positive pressure breath, you are increasing intrathoracic pressure. So this is the opposite of you, and I spontaneously ventilating : and on inspiration. We have negative intrathoracic pressure. You now have positive. And because of that increase in pressure in the intrathoracic cavity, you are potentially, you know, compressing those vessels you\'re reducing venous return. You might be reducing the ability of the ventricles to fill and to pump. : So we look for the changes of that in our arterial blood pressure waveform, or you can use your pulse ox plus. And you can look at kind of those differences to see that when we increase that pressure, and we deliver that breath. Is there a drop? : Is there a lot of variation from inspiration to expiration? So meaning we have less volume in those vessels they\'re easily collapsible. : So : the couple kind of like considerations to assessing respiratory variation in the mechanical ventilation patient is that you want things to be fairly constant to have a good picture of this. You want their ventilation to be fairly constant. So you\'re delivering about the same tidal volumes and increasing that pressure about the same each breath. : You want vasomotor tone and cardiac function to be constant. So, for example, you don\'t want a patient with a fib where they\'re going to have these kind of irregularities beat to beat. : It\'s just going to make things a little bit harder to assess accurately. Now, normally, variation with respiration would be less than 10 to 12%. So if we have these larger variations. : of course, that suggests that there is a hypovolemic state, that patient is likely going to be responsive to fluid. So if we can : administer fluid, we should hopefully increase any changes in our parameters that we see like a drop in blood pressure. And things like that : lower than that, 10 to 12% level suggests that they are normal bulimic enough, and that if you are encountering hypotension, they\'re going to respond better to a vasopressor. : So hopefully, this curve looks very familiar. You know, it\'s a variation of a frank starling curve with the heart. So : this is basically showing. And I know you guys have all seen these waveforms of like : seeing that variability. And oh, they must be dry. But if you think about it from the frank, starling relationship that standpoint, the lower you are on this curve. : the more volume responsive they\'re going to be. : So if you look at this you know, if you increase their preload, you\'re giving them volume at these lower points on this curve. It\'s gonna have a pretty high or a greater increase in stroke volume. : So that is kind of characteristic of the volume. Responsive patient. So you\'re going to see your curves are going to kind of have that variation, that greater variation down here : as you progress up the curve, you guys all know. And I know you. You know this before you get to Dr. Owens\'s cardiac lectures that you know the stretch in the heart, you know. It only is going to take. : You know, you\'re only going to have the ability to improve cardiac output, improve stroke volume from stretch to a point. Right? So this is where we start to kind of plateau on that curve where, if we increase, preload, increase, stretch, you\'re not going to see the same jump in stroke volume. : because there\'s a point where we won\'t. You know, we can stretch too much, and it does not help our ejection. So this is going to be the patient that is not volume responsive. If they\'re kind of up here on this particular curve, you can give large volumes of preload or large volumes of fluid, I should say, to increase preload. And you can see you\'re gonna have very small changes in stroke volume : this is just an example of an arterial line waveform where you can see they\'re looking at pulse pressure. So you would take this Max : pulse pressure : value, subtract the minimum pulse pressure value. And then you\'re going to divide that number by the average of the 2. : And that\'s how you determine your pulse pressure variation. : So you would multiply that by 100%, and that should give you a percentage, you could do the same thing with. This is up here showing you just using the systolic pressure. So your Max systolic, and then take the lowest : oh, curve in the waveform at the bottom here : minimum systolic, and then divide that by the average of the 2 multiply by 100%. That would be your stroke, not your stroke, your systolic pressure variation. : Now, limitations to that. It\'s not as useful if that patient has some spontaneous ventilatory effort. : So if you think about the patient on the ventilator, you\'re trying to deliver tidal volumes of, let\'s say 500, but then they\'re starting to trigger, and maybe they\'re breathing, and their little tidal volumes of maybe 200. So you\'ve got this irregularity : in the pressure in that intrathoracic space. They\'re generating negative intrathoracic pressure on inspiration. You\'re generating positive. You may not be synced up well between your controlled ventilation and their spontaneous ventilation, or maybe you have them on an Simv mode, but : it\'s still variable, so that limits your ability to really use that : dynamic parameter more accurately low tidal volumes or high peep can affect the pressure in that area. Open thoracic surgery. Now you\'ve opened up that intrathoracic space. And so that\'s obviously going to affect your ability to accurately monitor, because there could be pressure changes : because of now open space. : If you have an increase in intra-abdominal pressure. : tamponade arrhythmias, right heart failure. Those are all : considerations, for you know, being able to use this particular parameter, and if they are on high enough doses of a vasoactive infusion. So if you go back to : the frank, starling curve and you get to that higher end of the curve : where we\'re really not able to improve our stroke volume, or cardiac output. : You will see that curve. Let me go back : to it. I don\'t have it written on here, but you will see this curve kind of drop down and flatten out in the patient that has a high afterload : so the patient that has poor cardiac function. : Lv. Dysfunction and high afterloads. Their curve is not going to look like this. It\'s going to be lower and a little bit of a lesser slope. So it\'s going to look a little bit more flat. It\'s going to plateau a little bit more quickly. : So when you have. : you know, a high dose phenylephrine drip that gives you a lot of alpha, one vasoconstriction. : you know. It really limits your ability to kind of use this particular parameter accurately, just because you increase that afterload you\'re affecting. Now your frank, starling curves. : Another type of test which I\'ve not personally seen, but in expiratory occlusion. Test. This test is very similar to our respiratory variation, but you can use it in the patient that has an arrhythmia, spontaneous ventilation, etc. So what they do is, they will stop ventilation : for about 15 seconds and then assess changes in preload. So they\'re looking for a greater than 5% increase in pulse pressure or pulse contour, cardiac output, which is : a non-invasive method for measuring cardiac output. And this particular test does have high sensitivity and specificity. So this is not something you would probably see in an operating room, but it\'s something that could possibly be done : in other units. : Ultrasound doing esophageal doppler using echo cardiography. Those are, of course, great tests to help : measure. You know the volume inside your chambers and their function : non-invasive. And sometimes we do. You know, bedside echoes in the or, if you are concerned about a particular, patient. : non-invasive technologies, you will see more often. So pleth variability index. So, using your pulse ox to get that same basic determination of variation pulse, wave analysis Co, 2 rebreathing. : I don\'t know how common it is to see that I\'ve never seen it myself. But basically : they\'re trying to like calculate a variation of fixed equation calculating Co 2, based on changes in end, tidal Co. 2 and Co. 2 excretion. So you don\'t have to know anything about Co 2 breathing. It\'s just I\'m just giving you different examples here. But these can measure cardiac output, help you assess fluid responsiveness. But they can have a lot of errors in their cardiac output measures : lab values are considered dynamic. So an increasing lactate level : or lactic acidosis. So you know that when you : do an interrupt abg and you get your lactate level, that\'s something that we\'re absolutely looking at to determine whether or not our cells have had, you know, decreased perfusion. They\'re starting to convert over to anaerobic metabolism. They\'re now producing extra lactate in response to that reduction in O 2 delivery. : And so that can help us kind of get some idea of global tissue perfusion. : However, you know, it\'s harder to, you know, really affect those acute changes because it you have to kind of keep drawing that particular lab. So it almost seems more like a static parameter in that sense. But you know it does change a little bit more quickly. And can be a little more reflective than like a blood pressure : questions on monitors or anything so far. : Okay, what is the total body? Water of 70 kilo, adult? : Good. : 42 liters. What percentage is extracellular. What percentage of your total body water is extracellular versus intracellular. : How much is extracellular? : Good. So 3, rd extracellular. Two-thirds were 67% intra : does anybody remember signs and symptoms of hyponatremia? : Mental says, changes, rebel edema, good : muscle cramps, weakness, hypotension, arrhythmias. You guys did good you got a lot of the neuro. : Parts of that. : Let\'s see. Treatment options for hyperkalemia. : popular, one insulin and glucose. : So insulin helps us shift potassium into our cells. : Yes, calcium calcium while not necessarily really having a huge effect on serum serum potassium levels. : Calcium is great to help stabilize the membranes : of our muscles and to : antagonize the effects of that increased potassium. Beta 2 agonists. Yes, bicarb : you guys got them calcium glucose insulin bicarb bicarb is going to help shift that potassium back into the cell, diuretics : helping us to excrete K-xalate, helping us to excrete : beta 2 agonists as well. Beta 2 agonists stimulate the sodium potassium pump : and if you guys remember the sodium potassium pump, we\'re going to push our potassium back into cells. : Hemodialysis to help us remove potassium and hyperventilation. : So we want to promote an alkalinizing state. : Because we tend to : exchange, you know, hydrogen for potassium. So the body would want to hold on to the hydrogen ions and get rid of potassium ions. : Which of those is the fastest way to correct hyperkalemia? : Take a guess fastest way to correct Hyperkalemia. : Everybody\'s all over the place with this : per valley and memory, master. It\'s actually sodium bicarb 5 min calcium, one to 2, although the calcium is again not correcting the hyperkalemia as much as it\'s really just helping the side effects. So it\'d be sodium bicarb : as taking 5 min hemodialysis is going to take a little while. They\'re going to be sitting there for a couple hours. Insulin works well, but still could take a little bit longer. : Then sodium bicarb. Why is dextrose given with insulin. : Before we move on. Can we talk about that a little bit. : Sure. : If sodium bicarb is the fastest way to correct Hyperkalemia, why did I never give that in the Icu it was always either insulin and glucose or dialysis. : K. Actually, I\'ve never, not a single time did anyone. : Because they didn\'t want to alkalinize. You know there could be other effects and side effects of sodium bicarb that they didn\'t necessarily want : where insulin and glucose, even though it acts a little bit more slowly. : May feel it may be a little bit more of a : a benign treatment if that makes sense, because you\'re giving the insulin. But you\'re also giving the glucose, which is your next answer. : Prevent hypoglycemia from that versus. Maybe any additional effects to : by car. So this is just specifically asking fastest way to correct it. You know, you have a patient of 6.5, and you\'ve got ekg changes. And you\'re like we need to do something. Now. : that\'s the patient. You might get bicarbon : but you might. You probably are going to do multiple. : you know, probably gonna give multiple different : drugs at the same time. : This is just kind of. : Interesting. : What memory master is saying, master is saying, based on probably : mechanism and onset, of how quickly can it move that potassium out of the serum into the cell. : and the answer is sodium bicarb. So don\'t you get to. And I just want to say this really quick,, and you can keep going, but when you get to boards you\'re going to have to sometimes totally forget about what you do. : Practice. : Yeah. : You have to kind of go with like a textbook answer. And this is kind of that same example of a textbook answer of you know which one is gonna kind of push things faster. : So. But I get what you\'re saying. So it\'s not even an argument of which one are we gonna typically do? : This is like, what\'s the textbook say, as the fastest one that makes sense. : No, absolutely. I, just yeah. It\'s curious. : Yeah, it is. That\'s the hard thing for you guys. For the next 2 and a half years. : It is too. : I\'m learning practice. : This is what we did in the or. : but when you take a C exam. : you know your, or might have done it different than this, or in this, or might have done it different than the textbooks, and we all know that our textbooks do not keep up with actual practice : as quickly as we would like. So sometimes you have to kind of go back words : when you\'re thinking about these things. : and we\'re going to talk about Hyperkalemia again when we get to endocrine. There was a little bit of it in your : electrolyte spotlight. But yes, so good. So dextrose, given to help prevent : the hypoglycemia. And we\'ll revisit this like, I said, when we get to : insulin therapy in the last lecture, how does serum potassium change in acute acidosis versus alkalosis. : Does it increase or decrease in acidosis : good, and then an alkalosis is going to be the opposite, so serum potassium would increase and acidoses. So : a lot of times you want to think of potassium, hydrogen as kind of this exchange? : So if we can push potassium into the plasma. Then we can maybe shift our hydrogen into cells and help relieve that acidotic state. : You can also think of the same kind of issue with excretion from the kidneys. : What are some of the physiologic functions of calcium calcium is involved in a lot of different things. : Why do we need calcium? : Yes, coagulation? Yes, nerves, yes, contractility. : So cardiac, skeletal, smooth muscle, coagulation, bone, membrane excitability. : neurotransmitter release. That\'s taking you back to the old neuron and action potentials and such presynaptic membranes. : Neuromuscular effects of hypocalcemia, lipo, calcinea. : neuromuscular in particular, good spasms, tetany twitching weakness and paresthesias : let\'s see one more of these what major side effects accompany a serum magnesium below 1.2 : you have a low serum level. : What are some of the major side effects? : Good seizures, arrhythmias? Yes, torsades tetany. : This is the other one like calcium. Magnesium is a membrane stabilizer. : What is magnesium used to treat : which you guys kind of had the answer in this 1st question : for the membrane stabilization. So I want you to think about that as kind of your clue for the answer for this particular question. But yes, magnesium is used for some of those other indications. You guys have : as a membrane stabilizer. We\'re particularly talking about the heart. : and it\'s the arrhythmias that can occur so : arrhythmias. How much dextrose is in a liter bag of d. 5 W. : What does d. 5 W. Stand for? : Good. So Dexter is 5%. : And you guys know what percent concentration is. So if we say 5%, you know how many : milligrams and milliliters that is equivalent to : or how to do that calculation. : So for those who may not know 5%, if you have a percent number, you take that decimal point. Move it one space to the right : that gives you milligrams per milliliter, 50 milligrams per milliliter so. : and a 1 liter bag of d. 5 W. That has 50 milligrams per milliliter. : We have 50,000 milligrams in that liter. : and for those of you who said 50 grand! : You are correct. : So that is how you determine : like a percent concentration. So we\'ll talk about these a little bit more in farm. I don\'t know if you guys maybe learned it in your chemistry physics when you had math there. But : you know, 2% propofol is 20 milligrams of propofol per ml. : half a percent of Bupivacaine : is 5 milligrams of pupivacaine per ml, so pretty simple way to figured out concentration using percents. : you guys ready for a break. : Yes, Jennifer said, there\'s really good anesthesia math videos. : Very nice. : All right, let\'s come back at 10 0, 5, and we\'ll start with fluids. : Okay, welcome back. : So let\'s talk about Iv fluids. You will actually learn about Iv fluids again when you get to basics of anesthesia later this year, and when you get to that course it\'ll be kind of a review of this, but also : more specifically how to develop a fluid plan : fluid management or volume management plan for interrupt. So I\'m not going to go into that in particular. I\'ll leave that for that particular course. But we\'ll look at just kind of the : pharmacology behind iv fluids and review that. : So we\'ll start with crystalloids. : So you guys all know crystalloids are going to contain electrolytes, low molecular weight molecules, but no proteins. : And then we classify them based on osmolality compared to plasma, so isotonic tend to be the solutions that we use in anesthesia because of that similar osmolality, and usually a similar profile altogether. As to the electrolytes you find in the plasma. : and then hypertonic. Greater osmolality, hypotonic lower osmolality. Those 2 types of fluids are typically used in medicine. So for different medical indications. : isotonic and balanced, we will start there first.st Balance just means physiologic. : So if you actually see the term balanced crystalloid. These particular crystalloids are going to mirror plasma serum levels of : you know, different electrolytes and osmolality a little more closely than some of the other isotonic fluids. So lr : plasma light are balanced. : So the isotonic fluids, because that osmolality is very similar : to physiologic, which physiologic is about on average 280 or so. You know, you\'re really not going to have much movement between outside the cell and inside cell extracellular versus intracellular. Hopefully, anything you give should stay in that extracellular space : does contain a variety of different electrolytes, some organic anions, sometimes like lactate, and it contributes to the strong ion difference which we\'ll talk about. : Usually it\'s used as volume replacement. We can use it to give drugs and blood products as well. But usually it\'s to to treat a deficit : in the extracellular space, so no movement should not have any movement of fluid in or out of a cell. : Now, strong ion difference. : This is the difference between those strong ions. So if you remember, when we talked about strong and weak acids and bases, and the strong ones will completely dissociate in solution. So : we\'re going to look at the difference between the cations and anions. Now, we tend to look at the ones that are most representative. So it\'s usually going to be out of this equation. Sodium and potassium : minus chloride. : So if you remember, sodium and chloride are kind of the main : electrolytes present in that extracellular space potassium being the main one present intracellular, but still the ones that we tend to use in this equation are sodium, potassium, and chloride. So if you take about a sodium of 1 35 plus a potassium of 5 that gives you 140 : subtract a chloride level of about 100 that would give you 40. So your normal, strong ion difference is about 40. : Not all of our strong ions can. Anions can be measured. So : the we have other anions. We have weak anions. Bicarb is one of the weak : anions in solution, and when we think about this difference in things that either promote an increase or a decrease, in that it can actually affect movement of bicarb : and that, therefore, can affect. Serum. Ph. So the general overarching idea here is that : physiologically, we are going to try to maintain electrical neutrality. : So if you have this group of cations that are present in the serum in a certain : distribution. So we have this high amount of sodium and a little amount of potassium, a little amount of calcium, etc. If we see shifts in the sodium level. : the other ones might adjust to help maintain neutrality on the positive side. Same thing with our anions. If you have an increase or a decrease in chloride, it can affect the potential plasma levels of the other anions to help maintain kind of a normal distribution of anions, and then together, the 2 are going to kind of affect each other, such that we try to maintain : your approximate difference of 40. : So when we increase our strong ion difference, meaning, we have maybe an increase in the number of cations. : It can lead to an increase in Ph, and the reason for that is that the idea is that we\'re going to help : maintain neutrality because we have. Now we have excess cations that\'s going to kind of signal the body to get rid of hydrogen : as a cation, and that\'s going to promote a increase in ph, because we\'re excreting acid. : If we have a decrease in our strong ion difference. : meaning we have excess anion so increase in chloride or an increase in lactate. : Then that\'s going to promote a decrease in Ph, because what is going to happen is we end up with lower levels of bicarb represented in that anion : kind of grouping, because we\'ve increased one of the strong anions like chloride. If we have less bicarb represented, or because of that decrease in Bicarb, we now have this excess in hydrogen floating around, which causes an acidosis. Bicarb is going to be used as a buffer, more so than it normally might be, especially in the : urine filtrate, but those kind of mechanisms together are going to contribute to acidosis. So when we decrease our Sid. : we\'re promoting acidosis. So that is why, when we have increases in : lactate that comes with low perfusion, or we have deep increases in chloride. : Like, if we\'re giving a lot of iv fluid that has a lot of chloride in it. : It promotes a metabolic acidosis. Because of this change in the handling of hydrogen and bicarb in relation to the levels of these other cations and anions and the goal to maintain neutrality. : The effective Sid : is also used, and it takes into account actually, the, you know, calculation of bicarb and the anion equivalent of albumin and phosphate that you don\'t normally see in the typical equation so you can calculate there\'s several different kind of : additional calculations, with strong ion difference that you can use to determine : the composition of, or the representation of, cations versus anions. : and how they can affect your ph. : let\'s look at kinetics. So think pharmacokinetics in the sense of giving a crystalloid. So distribution when you give, let\'s say, a liter of Iv fluid. How that distributes throughout the extracellular space, especially with it being isotonic. You don\'t expect really anything to go into the cell, but distribution is going to be influenced by a variety of different things. So physiologic status. : how dehydrated a patient was their surgical and anesthesia factors which could affect it? And then, if that patient had any changes in their vascular permeability or extracellular matrix, all of those things that we kind of talked about before with the different compartments, and what you expect in a normal state versus like an inflammatory state : for the healthy patient that has normal : fluid dynamics, normal like transcapillary movement. There\'s no hypotension. There\'s no changes in capillary permeability for that particular patient. About 20 to 25% of the Iv fluid you give : will stay in the intravascular space. : So that mirrors, if you think about our extracellular fluid and how it\'s divided between about 80% interstitial. : 20% plasma, it\'s the same idea. So about 20% of that liter and maybe a little bit more will stay intravascularly. : When you infuse a volume in that patient you can lose about half of that, and the effect of half of that. So if maybe it helped your blood pressure : or something like that, you can even lose that effect very quickly about 30 min. It does not stick around very long in the healthy patient, with normal kind of dynamics and movement. If you had a patient that was severely dehydrated or hemorrhaging. Vomiting has a lot of fluid loss. You may be able to hold that volume in those spaces a little bit longer, meaning that your : crystalloid is going to be more effective in those particular populations. If you and I, who have maybe been drinking water or tea or coffee all morning were to get a bolus of Iv fluid. Chances are it\'s probably going to be lost fairly quickly. : Hypotonic crystalloids, lower effective osmolality than the patient. So because of that, you would expect fluid to go inside of the cell where the Osmolality is going to be a little bit higher. : so water will redistribute into that intracellular compartment with hypotonic fluids. So these are used to treat usually to treat water deficits that are solute free can also be used for maintenance can be used to give drugs and examples are half normal saline. 5% dextrose in water plasma light 56, which has 5% dextrose. : Hypertonic solutions are the opposite greater osmolality. So water is going to shift out of cells into the extracellular space. So it\'s going to kind of contract down the cells and the tissues, so it might be used to help remove : excess water in those particular cells. So examples would be dexterous. 5% in normal saline, or these hypertonic saline : solutions. So 3% saline, etc. : crystalloid compositions. This is something you should know. These are almost always found in like board review. Prep : courses and questions, what is the sodium level in normal saline? What is the you know how much potassium is in? Lr, so that this is a chart that you should start to kind of become familiar with : especially with, you know which electrolytes are present which are not, and maybe even their values. So, comparing : the isotonic ones, you can see that sodium has a high sodium and a high chloride compared to physiologic. : And that\'s why, high levels are, you know, giving liters and liters of normal saline is not great because we start to increase that chloride, anion : contributing to that anion or that strong ion difference, so that would potentially decrease that number and put us in the realm of developing acidosis. : If you look at Lr and plasma, light. Their osmolarity is very similar to physiologic. Their sodium and chloride levels are very similar as well with the advantage going to plasma. Light : ph is very similar. These have potassium, also very similar to physiologic Ph or physiologic levels. : And then some other things as well. Lactated ringers obviously has lactate in it. So, you know, that\'s another anion. Acetate gluconate : are weaker anions as well. : So perioperatively so when we give Iv fluids, you know, for the vast majority of cases we are not necessarily putting that Iv fluid on a pump. : We are starting to see this more and more. As we start to embrace eras, protocols : and goal directed fluid therapy protocols. You may start to see Iv. Fluids administered via an Iv pump more often than before. Before. It was like almost unheard of to see crystalloid. : it, trans, you know, infused via pump in the or we would always do it to gravity, and we used to pretty much use a very liberal approach unless you had a contraindication to getting Iv fluid renal failure, heart failure. Whatever you were going to receive quite a bit of Iv fluid throughout the surgery. : usually promoting a positive fluid balance of one to 2 liters. By the time you get to the end of surgery, and that\'s because we are trying to replace : deficits from Npo time. We may be trying to replace deficits from blood loss. : We\'re trying to help augment volume status. When we give anesthetics which cause this widespread vasodilation and widespread decrease in heart function. : So there\'s a lot of reasons why we like to volume resuscitate. Additionally, if you have a long enough surgery. : and maybe it\'s an open chest, an open belly, and open back. : You know that patient is constantly losing : fluid to evaporation, or, you know, other types of mechanisms. So : we tended to do a more liberal approach to fluid administration. : We are now starting to kind of move towards restrictive approaches for a variety of reasons. You\'re going to see restrictive approaches : attached to enhanced recovery protocols, eras, protocols, and you\'re going to start to see it more because we we are starting to reduce Npo times : so patients, instead of saying everybody has to stop eating and drinking at midnight. : whether your surgery is at 8 Am. Or 2 Pm. : You know. Now we\'re promoting a lot of patients to continue to take in fluids, especially carbohydrate rich fluids : up to 2 h ahead of surgery. : So because of that, you know, we may not see quite the volume deficits, although there are some studies out there that even a longer Npf. Status doesn\'t necessarily mean you\'re going to have a much greater volume deficit. But in saying that even though there\'s you\'re starting to see more restricted : methods of giving fluids. There are some studies that are looking at long-term effects, and they\'re not really finding a difference between survival or morbidity, or things like that between the 2, : or I guess I should stick with just mortality between the 2. But they are possibly seeing increased rates of acute kidney issues in patients that have a restrictive : fluid regimen. Interrupt? : So I\'m sure that\'s dependent on a lot of factors. But that\'s something to kind of keep in mind. : Determine whether you\'re going to give a normal saline versus a balanced crystalloid like Lr or Normasol. : There\'s mixed results of whether or not one is preferable or better than the other. As far as kidney function or mortality. : You guys probably already know the vast majority of surgical patients are going to get a balanced crystalloid like Lr : overwhelmingly. That\'s what we\'re going to use for fluid volume deficits and resuscitation. : Normal saline large volume. We talked about the risk for hyperchloremic metabolic acidosis : and then balanced salt solutions. If you give large volumes of those especially Lr, you have a risk for hyper lactate, emia : metabolic alkalosis and hypotonicity : with those solutions, also, they tend to have calcium. So if you\'re actually giving a lot of blood products, you know your calcium can : bind the citrate or the citric combined the calcium from those particular solutions, the balanced solutions. : polloids? : and I should, and I guess I didn\'t mention before. With the crystalloid you will still see : providers give normal saline to the patient. That is renal patient : renal failure, renal insufficiency, because it doesn\'t have potassium. : There\'s a lot of kind of studies out there about that as well, because potassium excretion : can be affected with. The administration of Lr like it, you could potentially : decrease the ability to excrete potassium with Lr, and then there\'s also the issue of just because : Lr has. I\'m sorry you can affect excretion of potassium with saline. I\'m sorry I said that backwards, just because Lr. Has potassium in it, which it is a lower level than usually physiologic potassium : doesn\'t mean it\'s necessarily going to cause Hyperkalemia. So if you have a patient with Hyperkalemia. Maybe they haven\'t had dialysis or something like that. Generally you would avoid a potassium containing solution. But if they have a normal potassium, you may see people still give a balanced solution that contains potassium : because it\'s not expected to cause this huge increase in serum levels. : Colloids. So colloids have large molecular weight particles macromolecules, protein starches inside of that crystalloid solution. So if you think about the draw of fluid, it\'ll kind of help keep the fluid in that vascular space a little bit more effectively. : They can be naturally derived like albumin, or they can be synthetic or semi-synthetic, like your hydroxy ethyl starches. : So albumin there\'s a variety of different concentrations for albumin. The most common, you\'ll see, are probably 5% and 25% : albumin. : 5%. Albumin is the most commonly : infused colloid in the or 25%. You may see it used, especially if there\'s maybe like a shortage of 5% albumin, or if you\'re giving it to a patient that you really don\'t want to give fluid to. But you need the effects of : the colloid, so he might see 25% here and there, maybe given to like a liver transplant patient or something like that. : But 5% is gonna be more common. : So produced from human blood suspended in saline. If you have a patient, that\'s maybe Jehovah\'s witness, they may not accept albumin. So that\'s something. If you think you might need it, you might want to discuss that with them. : it does increase your serum albumin increases your colloidal osmotic pressure definitely more expensive than the synthetic colloids or crystalloids. It is pasteurized. So that way, we have less risk of viral transmission and infection. So reactions are very, very rare. : Point 0 1% so very rare : kind of like viral infections. Or you know, any kind of reactions related to organisms. Also, anaphylactoid reactions are quite rare : as well. : Now, clinical trials, looking at the superiority of giving albumin versus a crystalloid : for to treat a volume deficit really has found no difference in length of stay : time on the ventilator mortality, etc. So generally, we\'re going to reserve a colloid for the patient who needs resuscitation, but should not have large volumes of fluids : hydroxy ethyl starches. These are solutions which we used to use very regularly, but lately, because of black box warning, and I would say, probably within the last : 7 or 8 years or so. You rarely see hydroxy ethyl starches used in the or, I should say in particular. So these are basically chemical alterations of different types of starches, like maize or potatoes. And then they\'re in placed in solution. : The black box warning came because these starches : were associated with excess. Bleeding kidney injuries and other types of you know, major adverse events, especially in critically ill and septic patients that, you know need the functioning, you know, need things to function as well as possible. So it really led to this warning placed on hydroxy ethyl starches : to avoid their use, especially if you\'re concerned about renal function and coagulation. : so usually avoided in critically ill patients, open heart surgery, or if anyone has had previous signs of coagulopathy : after receiving one of these they really should not receive another dose : the max dose. I\'ve seen varying reports. So about 20 to 50 milliliters per kilo per day. If you are using : hydroxyethyl starch, and that can vary just because of the differences in each solution and your ability to metabolize and excrete the solution. : These particular colloids do have a lot of redistribution, so they\'ll leave the plasma, go into the tissues, and they may stay in the tissues for a while and then come back into the plasma. So they found, like trace amounts up to 6 months later. And so, as you can imagine, that could potentially cause issues in the kidneys like renal dysfunction in the skin. They were seeing, itching and pruritus : related to deposits of these starches that have kind of sat in the tissues. Unfortunately, before they\'ve moved back into the vasculature. : renal excretion can vary. So you have this immediate filtration of the smaller molecular weight polymers or parts of the solution. But you might have delayed filtration of the larger molecules. So you\'re waiting for different plasma enzymes to break down : these molecules, just like we talked about with different drugs, and then to be able to filter that through the kidneys and excrete it. So that\'s part of the problem with : hydroxyethyl starch is kind of sticking around in other tissues and having adverse effects. : Other potential effects decreasing factor 8. And Von Willebrand, which : the mechanisms at which these can really adversely affect coagulation are still a little bit unclear, but we do know that it can decrease these factors over time, decrease platelet function. : impair renal function and then potentially anaphylactoid reactions. But just like albumin had a low rate of reactions, as far as that goes, same with Hespan. Anaphylactoid reactions are still quite : rare. : This chart I got from a resource that gives you a comparison similar to the other chart, which was from, I think, your textbook. But this chart can compare the crystalloid and the colloid. So if you kind of wanted to know what\'s the difference between : osmolarity, what\'s the difference between sodium content. : etc. You can kind of I can\'t say. The 2 compare and contrast polloids and crystalloids, and how they work, and about how long they might stay in the body to volume, expand : so crystalloids, crystalloids by far are going to be the interrupt Iv fluid that you use for replacement. We can also use it to replace blood loss until we get to a threshold to transfuse. So you\'re typically going to start with crystalloid. And most people, this is kind of a loose. : you know value, but most people will replace about : one and a half crystalloid per, you know, amount of blood loss. : So one and a half to one : it can help optimize your volume. Status. Balance solutions are preferred for all the reasons that I mentioned. : saline like, I said, maybe use with renal patients, avoid large volumes of normal saline. : and then we do not usually administer dextrose containing solutions in anesthesia because we don\'t want to encounter hyperglycemia. We want to keep blood sugar controlled in the interrupt setting, so we usually do not give dextrose containing solutions. Now you may potentially see : a dextrose containing iv fluid : given in a very particular patient population, like I was trying to think back : in my own practice, and I think once upon a time. I think I gave : A. D 5 solution to a patient undergoing like islet cell transplant : of the pancreas. So usually it\'s gonna gonna it might be the patient, that is, you\'re really struggling with hypoglycemia. But : maybe you want kind of a stable : administration of glucose. Maybe you have them on an insulin drip for the surgery. : You may see something like that. In that case, instead of giving these large boluses of D 50 : you might prefer just kind of the slow infusion of A. D. 5 in a patient like that. : colloids used to. We will use a colloid to help expand volume. If there\'s minimal capillary leak, and if the patient is fluid, responsive, if you\'re using a colloid to replace blood, most people replace on a 1-to-one basis a little bit different than crystalloid, so crystalloid, a little bit more, 1.5 to one : versus a 1 to one replacement with colloid : again preferable and fluid restrictions. But consider, you know, in anesthesia, just like with any practice you want to be mindful of healthcare costs when you can. : So because there is minimal evidence that colloids are truly superior to giving balanced crystalloids to help, you know, expand vascular volume, to treat the fluid responsive to replace blood loss. You want to consider the : benefit of giving the colloid, which does cost more money versus just giving a little extra crystalloid. So if the patient can handle : crystalloid. It\'s better to use that. And you and reserve colloids for specific : specific indications when it\'s really necessary. : So for hypovolemia. : we have a lot of factors that contribute. I talked about fasting. If you have a patient that needed to do a bowel prep : that can, of course, promote Hypovolinia, there are newer bowel preps out there that\'s designed to help minimize total body water loss. But : you know there are some surgeries outside of the endoscopy suite that do require about bowel prep. So that\'s something you want to assess. Pre-OP : diuretics can, of course, contribute to hypovolemia, inflammatory disorders, active hemorrhage : etc. Bleeding coagulopathy during surgery, the patient\'s position during surgery, insufflation, use of positive pressure, ventilation. : etc. There\'s so many different potential factors that can contribute to hypovolemia. : So if you wanted to give a bolus of a crystalloid to treat hypogomia. : take a guess and tell me, how much would you give? : Take a guess in the adult patient, I should say : great, 2, 50 to 500. Exactly what I was thinking. So 2 50 to 500. It\'s a great starting point for a bolus and an adult : and then : assess after that, do you see the changes that you want to see in your dynamic parameters or static parameters. If not, maybe try another 2 52, 500 : hyperbolemia. So we have excess volume given. There are some factors that can contribute to hyperbolemia. Interop and some of these you\'ll have a better appreciation, for when you get into your anesthesia classes. But you know, if we\'re trying to : treat blood loss, for example. And we\'re giving excess fluids, excess blood products that could potentially tip you over the edge and throw you into your patient into a hypervolemic state, especially if the bleeding is controlled and you\'re still continuing to give products. And you kind of overshoot what was really lost. : Of course, there\'s patient factors like the heart failure, patient renal failure, patient. : Another consideration is anesthetics. : Most all of our anesthetics are going to cause vasodilation and myocardial depression. So that\'s whether you\'re doing a general anesthetic, or maybe even neuroaxial anesthesia with a high block. If it\'s enough to block : accelerator fibers that go that feed the heart, if it\'s enough to block the sympathetic nervous system. You can have, you know, effects from that. So : the caveat here really is just, you know, some people may prefer to give a really dense : regional anesthetic, or they may prefer to keep their patient very deep under anesthesia, and there could be reasons that they need to do so. : But when they go to treat the vasodilation and and the drop in blood pressure, etc. : there\'s the potential that you : give way too much fluid without really treating the underlying cause, which is that you probably need to back down on your anesthetic levels. So just kind of to keep those things in mind is that that patient may not be. : you know, hypovolemic. They could be euvolemic. But if you keep giving a lot of fluid just because you\'re trying to treat a number without kind of assessing the entire picture, you could potentially cause : a worsened state. So there are risks to fluid overload. It can affect tissue perfusion. It can affect oxygen, exchange, lead to edema, and : a big one that we\'re going to talk about is dilutional coagulopathy. So you could actually worsen a scenario of bleeding by giving too much crystalloid or blood products without replacing coagulation. Factors. : so goal directed fluid therapy. That I mentioned that before. Often we are starting to see that used with eras protocols : and it might be used in different types of surgeries with expectations of large blood loss or fluid shifts. But basically, you want to make sure that their volume status is optimal before you start vasopressors. So that\'s kind of the idea behind : using this particular strategy in the or there are mixed results : on whether or not this is better than our traditional approach of just giving the fluid that we want to give an example of what this might look like in the or is. You may have a protocol that says, Okay, you would start your case by giving 3 mls per kilo. : you know, or something like that, or some amount of fluid, and then you maintain them on a certain Ml. Per kilo per hour, and then, if they are. : if they\'re dynamic parameters, get above a certain point, then : you can give them a 250 milliliter bolus : and assess again. So that\'s kind of an example of what gtft looks like : for anesthesia. Otherwise, the rest of us you\'re going to see us hang a liter bag of Lr, you know, if that\'s not really working, and I really need a colloid, then you might see me hang a 250 ml. Bottle of 5% albumin. : Okay, mental break, little break. : You could be an animal for a day. : Which animal would you be, and is there any particular reason you would be that animal : cormorant? I don\'t even know what that is. I like. How you spell dolphin. : Wait a second. Who is the tiger grizzly? : That was a whole lot of aggressiveness in that answer. : Those are just 3 awesome and : think about it. Orcas are insanely intelligent. Tigers are lone creatures, but incredible hunters, and huge and grizzly bears are. I would have picked polar bear. But I don\'t really want to be in the arc. : Okay, fair enough. : A lot of dolphins, a lot of birds. : Yes. Okay. Okay. A loon. In particular. I do like snow leopards. : What\'s a cormorant? Or if I\'m saying that right it yeah, got it. Elizabeth Sullivan: Poor Morant! It\'s a it\'s a bird that is generally saltwater bird. It can dive really deep, swim, catch fish, and fly, and I would like to do both, and they\'re really pretty. Jennifer Kalina: One with the white beak. Elizabeth Sullivan: You might be thinking of a loon which are also very cool. Jennifer Kalina: They dive, and they disappear forever. Elizabeth Sullivan: Cormorants are a little more badass. But they\'re both pretty badass. Yeah. : Good to know. : Oh, capybaras! I love those a rich person\'s little purse dog! That\'s an interesting response. : That\'s good. : Eat, sleep, and get loved on very nice. : very nice. I would be a red panda, so I could just hang out in the tree and sleep all day. : That is my favorite animal. : What electrolyte is not found in normal solar plasma light? : Sure, there could be many. : Calcium is what we\'re looking for here. : Which isotonic crystalloid solution does not contain potassium. : Good. Your sailings and how much dextrose we already have? That question gave you a repeat. : how much sodium, chloride, potassium and calcium. : Can you find in lactated ringers? These are valley questions so like I said, you\'re going to want to know these concentrations. : Well. : yep, Nicole, you got it? 1, 31 0, 9, 4, and 3. : Max daily dose of head of starch. : which I gave you guys a range. They only had one number theirs was 20 mls per kilo. : but very good. So it depends on which of the starches what Iv fluids are typically used in patients losing large volumes of blood. Iv. Fluids. This is kind of a weirdly : raised question, in my opinion, but their answer is isotonic, crystalloid or colloid. : We still have a lot to do. Take a break. Let\'s come back at 1055, 55, : and we\'ll try to get through as much as we can. : Okay, let\'s get started again. Jennifer. I think I missed your comment about the chart from Slide 72. So I will do that and remind me if I don\'t do it. If I forget. Jennifer Kalina: 2 people posted a copy that worked so I was able to save up. : Oh, you got it. Okay. Jennifer Kalina: Yeah, thank, you. : Okay. : let\'s see. So moving on to blood physiology and transfusion, you guys all know that our cells and in particular red blood cells making up your hematocrit is about 45% plasma being 55% of blood composition. And then within that plasma. : water, protein, nutrients, etc, are present. : our blood is going to participate in maintaining homeostasis, defense. : transport of nutrients, heat exchange, especially from the core to the extremities. : sources. Our primary source for blood cells is going to be our bone marrow, particularly : in the breast. The pelvis and the spine femur and tibia are kind of like secondary sources in adults, but they are also a primary source in pediatrics. : liver and spleen. Excuse me. : help participate in regulating production of blood cells, destroying blood cells, and our stem cells can differentiate into the different types, erythrocytes, lymphocytes, etc. : On the white blood cell side. We have leukocytes like granulocytes agranulocytes and then they do participate in defense : infection, immune response, inflammation. : and the bone marrow is kind of the primary source. But we also have lymphatic organs, like the lymph nodes and the thymus : producing lymphocytes, red blood cells. They have a nice flexible shape, hemoglobins, or, O 2 binding protein. : erythropoietin and the bone marrow will help stimulate red blood cell formation, and then they are destroyed after a few months by Kupfer cells in the liver, as macrophages that will break down that red blood cell. : break down, heme into iron and bilirubin, and then we can either excrete or reuse : those products. So that is seen in this process. Here bone marrow making stimulated to make the red blood cells. They are broken down by liver macrophages, and then that hemoglobin can be broken down. Heme can be broken down, and we may reuse some of those byproducts. : Now in anemia we either have a reduction in our red blood cell count or reduction in hemoglobin from a variety of factors : it could be from hemorrhage. It could be from bone, marrow failure, dietary, deficiencies, kidney disease and sickle cell, which you do have hemolysis and destruction of your red blood cells in sickle cell : iron is absorbed in the diet, especially if you are matching that absorption with administration of vitamin C, so if you\'re taking in vitamin C, when you take an iron that helps our small intestine to absorb that a little bit better, it is bound to transferrin, which is just a glycoprotein. : It helps deliver that iron to receptors on the cell membranes. : 80% will enter into your bone marrow and can be used to make new erythrocytes. It can also be taken up by reticulo endothelial cells in the liver and spleen : hemoglobin synthesis can mobilize the release of iron stores. So if the body kind of is triggered to increase hemoglobin production that will help also trigger the release of more iron. : it is essential for enzymes essential in enzymes for energy transfer and a plasma concentration is about 50 to 1 50 : iron deficiency. I think this is probably a condition that goes undiagnosed a lot of times. It can have a very high incidence in menstruating females, but also because of inadequate dietary intake : losses in blood or changes in pregnancy. Interference with gi absorption. So, for example, patients who have bariatric surgery can wind up with iron deficiency because they cannot : absorb a lot of nutrients in the same way. : So this could potentially lead to iron deficiency anemia : because of the necessary role of iron in our erythrocyte production. : So : you can supplement iron a variety of ways, whether it\'s Pill or Iv, but it can take days to weeks : to help correct that deficiency : we can transfuse. So we\'re going to kind of move into blood products as far as transfusion. I don\'t go into this a ton, because it\'s you know, you guys all know about agglutination and the fact that : our cells have antigens and the ability to form antibodies to other types of antigens. And those things can react and possibly cause an agglutination reaction. So that is a risk of transfusion. : And additionally, we have the Rh factor, which is : that inherited protein that sits on the surface of your red blood cells. So of course, if you\'re a blood type, you have the a Antigen. If you\'re O blood type, you have neither Antigen antigen : and of course, you are a universal donor. And this is just, of course, showing when those : Agglutins and Antigens can potentially interact and cause an agglutination reaction. And so what happens is, you kind of have this clumping of cells. They can lodge themselves in the microvasculature, and it will actually trigger hemolysis as well : red blood cells. So when we : store red blood cells for transfusion, they are going to, of course, age. The longer they are stored. There are going to be a lot of different biochemical changes. As those red blood cells sit in storage, you will have a depletion of atp, a depletion of 2 3 dpg. : so if you remember 2, 3 dpg. Diphosphoglycerate, there\'s also : you may also see it termed biphosphoglycerate. So Bpg, same thing, but that is used to help stabilize : the T state of hemoglobin, and that would allow it to offload. O 2 to the tissues. So if you are depleted in that : your hemoglobin is, gonna have a hard time offloading O 2 to the tissues, which is : the point a lot of times of giving red blood cells. So you\'re going to have this deoxygenated hemoglobin that\'s accumulating in older packed cells that are sitting in storage. : Or if you are familiar with your O 2 hemoglobin dissociation, curve you\'re gonna have a left shift. : The shape of the cells can change that can affect their ability to flow through microcirculation in particular. So when you get to those very narrow capillaries. If the shape is a little bit different and it impairs flow, you can have some potential transfusion. Reactions : from that Homolysis and and occlusion, and things like that : inflammatory response will increase in older red blood cells that has been associated with trolley or acute lung. Injury decreases in O 2 delivery and Hemolysis : as those red blood cells age greater than 2 to 3 weeks because of those shape changes. Eventually you might have cells that kind of break apart. You have red blood cell fragments, those fragments, in addition to the cells that have kind of changed in their shape already. : that is going to increase the likelihood that you start getting those little aggregated clumps of cells. So that\'s a problem. Obviously, you have impaired nitric oxide scavenging : which can affect the function of your endothelial cells. It can cause free radicals to develop : reduced nitric oxide synthase as well because of those dysfunctioning endothelial cells : atpase failure because we said, of course, that it affects or it depletes your atp. It\'s also going to affect the function of different mechanisms that use atp like sodium potassium pump so you could have potassium leak that promotes a potential increase in potassium when you transfuse older red blood cells. : And there is some mixed evidence about kind of all of these changes when they really occur, and the degree to which they occur and can cause : issues in the patient receiving a transfusion. : Now when do we decide to transfuse? So we said, in the beginning, we\'re going to start with replacing blood loss : with crystalloid. : and we may do that in about a 1 and a half to one ratio, or we may decide to use a little bit of colloid to replace blood loss. So how do we know when we need to transfuse our patients when they\'re acutely anemic in the perioperative period they may have some ability to compensate, so we may see some increases in cardiac output and oxygen transport. : Unfortunately, some of those compensatory mechanisms are going to be affected by the anesthetics themselves, and maybe by surgical trauma and whatever other disease processes are going on. So we do have a lot of patients that may not be able to compensate like normal, to be able to account for this drop in hemoglobin. : So for anesthetic patients, and it\'s probably very similar in medicine. So for surgical patient. : our threshold usually around 7 to 8 hemoglobin of 7 to 8 : as an acute anemia. That is our threshold for transfusion of red blood cells. : If it\'s a cardiac patient, that threshold is gonna go up so because they need that. O 2 : supply, your threshold might be 9 or 10. So if you have a : heart failure, patient or mi patient, or something like that. You may not want them to get below a hemoglobin of 9, you know, before you decide to transfuse and help replace that very valuable red blood cell. : If it\'s a young, healthy, patient the Asa, the, you know American society for Anesthesiologists : has a task force that actually promotes waiting till you get to about 6. : So younger patients very healthy, your transfusion threshold may actually go down a little bit more, just because they have a better ability to compensate, especially after surgery and anesthesia. They should be able to kind of turn over their bone. Marrow will kind of get into gear and replace what\'s necessary without major adverse effects. So : there\'s not one specific number that we use, but there are numbers that you tend to see : in anesthesia, very patient, dependent. And it\'s usually going to mirror somewhat what you\'ve probably seen in the Icu. So we do consider intravascular volume. Do we need the blood products to help with that. So if you\'re constantly hemorrhaging : they maybe have not been able to get the bleeding under control. Maybe you are noticing that your patient has : signs and symptoms of ischemia or reduced oxygen delivery, you\'re likely going to want to initiate transfusion sooner than sitting there and trying to give a lot of crystalloid and colloid. So you\'re basically weighing : risks and benefits to both. : Approximately, one unit of packed red blood cells is going to increase your H and H. By how much? : Hemoglobin by one? What about hematocrit? : About 3% perfect. : So if you have to transfuse red blood cells. Obviously, you\'re going to make sure you have great Iv access. : We really do not care for central lines in the or yes, you will probably have a patient with a central line here and there, but by far large bore. Iv. Is kind of like the best : access for us in the or so. If you can get a 14 or 16 gauge, even an 18 in a patient that you expect to transfuse a lot of blood products. Perfect. : I shouldn\'t probably say this, but I\'m gonna say it. So in anesthesia we do, because I gave you guys that extra lecture on med safety. : there are going to be a lot of times where you do not necessarily follow : the same system checks that you might have followed in an Icu. So you may have had to have a double check when you gave insulin or heparin, or something like that that we don\'t necessarily follow in anesthesia doesn\'t mean you can\'t. You obviously should check these things with : your anesthesia team or nurse in the or, you know, if you want to have that extra layer of safety, I definitely recommend it. But : blood products, checking those and transfusing those. That\'s usually kind of the one area that you will see. : Anesthesia follows the necessary : checks and balances that are in place to help avoid transfusion errors. So we don\'t usually get around that one. So making sure that you follow whatever protocol. : Your facility has in place : filters typically used to help remove aggregates, clots and to perform some Leuko reduction which is just removing white blood cells. : Keep your blood products cold, please, until you decide to transfuse them. If you are doing a surgery where you sit, where you have blood, what we call on call to the or meaning. You\'re not sure if you\'re going to give it. But you\'ve ordered it because there\'s a high likelihood. : you know, if it\'s not a I absolutely need it right now. Kind of a thing. : Leave that blood in a refrigerator, or leave it with Blood Bank, or whatever you know, is kind of best to make sure that it stays at the proper temperatures. If you know that transfusion is imminent. : Then, you know, or if there\'s other factors at play like, maybe you don\'t have a lot of staff around to help get blood products to the or something like that, you know if you need it in the or that\'s totally fine. Just make sure it stays on ice until you\'re ready. : To get it, or with whatever you know, system. Your hospital has set up to keep it cold. : If it was a previously thought product, it should be warmed. So, using a blood warmer, if possible, just to help reduce hypothermia, risk coagulopathy risks. : And if you return that blood product to the blood bank. : you need to document or tell them if it had been kept out of refrigeration for some period of time. So in General Blood Bank is not going to send that product to another patient. If it\'s been out of refrigeration for at least 30 to 60 min. That\'s a very short time period, so it\'s very important to keep it cold and only grab it kind of when you need it. : Normal saline is recommended for dilution. You can administer red blood cells with saline, albumin plasma. At the same time you can use other isotonic crystalloids if you don\'t have normal saline. They have shown that normal salt plasma light, lr, have been used without problems, even though they have that calcium in them. : Avoid using a dexterous containing solution or a hypotonic solution. They have found breakdown of red blood cells and avoid administering red blood cells with other blood products in the same tubing, at the same time meaning platelets and cryo : if you can. You know you\'re going to want to try to flush that tubing as much as possible between those particular types of units. : plasma and ffp. : So here we have removed the red blood cells, the platelets, the coagulation factors, etc. And so what we have left is the plasma as a blood product, so it can be frozen within 8 to 24 h of collection. So if it\'s if you see, like fp, 24, that just means it\'s been frozen within 24 h. : You can obtain cryo from Ffp : and Ffp can be used interchangeably with God. Plasma, : All of the plasmas should be transfused within 24 h, once thought, and as you continue to store plasma over time, you are going to lose factors 5 and 8 considerably. So over time, you\'re going to decrease factors 5 and 8, : we typically treat plasma to help kill viruses, remove debris, etc. Lipid contaminants which could potentially cause issues. We use it to replace volume and to replace coagulation factors, especially in massive transfusion. If you give, let\'s say, 2 units of packed red blood cells for some moderate. : you know, blood loss in the or you\'re not always going to be giving plasma as well. We kind of reserve it for the patient who has been given a lot of volume, and is, therefore now diluting out coagulation factors, or they\'ve lost a lot of volume. : And then they have a depletion from that. So we\'re usually giving plasma in response to abnormal prolongation of the ability to clot : and to help treat and prevent hemorrhaging. : Plasma can be used to reverse warfarin. We\'ll talk a little bit more about that next week. : and it can be used to help : treat coagulation factor abnormalities. Sometimes when we encounter a lot of bleeding, it\'s not always the coagulation factors. It could be a problem with your platelets. So sometimes it\'s hard to know what you\'re dealing with, and so you may end up getting plasma and platelets : in that situation : to dose out plasma. You can actually calculate 10 to 15 mls per kilo. You may give a little bit lower dose, for if you\'re like reversing warfarin : anticoagulation, you wouldn\'t quite need the same dose. But if you give a dose of 10 to 15 mls per kilo, it should increase your plasma factor concentrations by about 30%. : Again, keeping it refrigerated and cold until you decide to transfuse : and then use a blood warmer because it is a thawed product. : Cryo cryo is kind of that protein fraction that they will remove from the top of thawing out frozen plasma : so : it can be stored for a long period of time. They will take that residual and refreeze it. It\'s rich in 1 8, 13 : so it\'s very concentrated in those particular factors. It does contain other factors, but we really want the 1, 8, 13 out of cryo. : The indications for cryo is to increase our fibrinogen fibrinogen is necessary to form that nice stable : fibrin clot. : And so, if you have a hemorrhaging patient or coagulopathy, and they\'re struggling to kind of maneuver through that coagulation cascade and get to an appropriate clot. Restoring fibrinogen can help also used to help treat hemophilia a and factor. 13 deficiencies : cryo should be transfused within 4 h. So this is one of those blood products that if you request cryo from Blood Bank, you need to give it, so it\'s not a like I don\'t know if we\'ll give it. I\'ll just have them send it to the or you know. Cryo, you really kind of should only request it if you\'re going to transfuse it it has to be transfused within 4 h. : It cannot be refrigerated again. Once it\'s been thought out. : The dose for cryo is one unit per 10 kilo weight. That dose can increase your fibrinogen about 50 to 100, and we usually want over 100 at least for hemostasis, but much higher than that : to get to normal. : and then blood warmer is not truly necessary for cryo, but it is preferable, because these patients that require a lot of blood products also tend to be hypothermic, and if you\'re giving platelets they should be administered separate from a cryo transfusion : moving on to platelets. Average lifespan is 8 to 12 days. 33% are sequestered in the spleen. You guys know your normal platelet count 150 to 400, and they are very active in hemostasis which we\'ll talk about next week. : So platelet transfusion. There\'s a couple different types, either. It\'s going to be whole blood pooled. So let\'s say you have. In this case you might have 10 different donors that they have pooled the platelets from all of those donors into one preparation, or you can have single donor apheresis where they will take, excuse me, the equivalent : of pooling from 4 to 6 different donors, but they\'ll take it from just one person and pool that : platelets are usually leuko reduced, so we remove the white blood cells. It helps reduce any potential immune reactions that could be associated with that preparation having white blood cells in it. So if you transfuse that preparation to : a recipient. The white blood cells in there may not recognize the recipients tissues, obviously. And it\'s trigger reactions. : And then, of course, the recipient may also trigger reactions to : You know the foreign cells that are being transfused. : administering platelets, each dose. So here we\'re talking about a single single donor apheresis apheresis : pack. So usually it\'s kind of like a 6 pack of platelets. : That dose would increase your platelet. Count about 30 to 50,000 : and then they\'re usually stored at 22°C to : which could unfortunately increase the risk of bacterial growth. : And that\'s a little bit warmer than room temperature. : There is a risk of graft versus host disease. So the graft immune cells recognize the host as foreign and it can attack the cells of the recipient : so they : there\'s a potential risk, mostly in the immunocompromised or the younger patients pediatric patients. And this is a potential issue that they\'ve seen after like bone, marrow and stem cell transplant. : So if platelet transfusions are used in a patient at a high risk for this, they will actually gamma irradiate : the platelets. To try to : you know, help minimize any potential effects that that could potentially have in that population. : Transfusion thresholds for platelet count. So : again, it\'s there\'s no specific number that we follow. That says their platelets that are at a certain level. We have to transfuse surgical patients. We typically see : a threshold of around 50 to 100. Now, that\'s going to vary depending on the patient. So let\'s say you have a neurosurgery patient. That\'s having a craniotomy, you know. You\'re working in this, the very rigid : small space of the skull and the brain. There\'s not a lot of room for error there. So if you were to have a bleed in that area, it could be very detrimental. So a neurosurgical patient. : their threshold for a platelet transfusion might be on the higher end of this range versus someone who\'s maybe having an orthopedic surgery on a lower extremity. : And this is might differ from medical patients. So medical patient. You may not see platelets given until their numbers drop to like 10,000. : So it\'s just going to kind of depend on the situation, and the patient. : Unfortunately, a certain platelet count does not give you information on the quality and function of the platelets. So just because you have a : adequate platelet count doesn\'t mean they\'re going to work well enough in that coagulation cascade : to affect, you know. : if you had a patient that ended up with hemorrhage to affect their coagulation. So if you are struggling with : coagulation in the setting of an a normal platelet, count think about the effect that : there could be some potential platelet dysfunction. : There is an unknown threshold for prophylactic and therapeutic transfusion. So again, this is just. : you know, kind of a risk benefit analysis as well as tailoring your plan specifically to your patient and situation. : But if they do have : coagulopathy, high risk of hemorrhage, then we would consider : prophylactically giving platelets. So platelets is usually just one of those blood products that\'s kind of given later in the overall sequence of different blood products to give. You would probably give plasma first, st : and then platelets. : plasma and cryo, maybe even before platelets. But platelets do have a role, especially at massive transfusion : a note for pediatrics which I got this from University of : California, San Francisco, and their guidelines. So you can see it\'s a little bit different just because of the weight basing for peds. : doses for Prbcs Ffp platelets. : cryo. I don\'t remember what was under here, but I changed it for you, because it was a little bit different than what mo most sources said. So cryo really should be about one to 2 units per 10 kilos : and some sources will say a unit per 6, but that\'s about the same as 2 per 2 per 10 : But those are just some kind of ideas for how to transfuse in the pediatric population. You don\'t have to memorize these, but you should be familiar with them, and you\'ll hopefully learn more about it when you get to pediatric anesthesia. : Let\'s see, transfusion. Adverse effects. Obviously inflammatory response can be initiated. : If you\'re giving allogeneic blood blood from another individual. : It\'s going to have bioactive substance that can cause issues in the recipient a totally different individual. So we can actually have more than just a kind of triggering a reaction. You can actually affect : their ability to mount an immune response, so transfusions can cause immunomodulatory or immunosuppressive effects. : Obviously we do assess for febrile reaction. : They could be a release of inflammatory mediators, activate neutrophils. But I have on here. Twice I have to cross that off. And then there are risks, potential risks for post-operative infection : infections from blood products. This has gotten a lot safer over time, just because, you know, science has improved over years in the way we treat blood products to help inactivate a lot of viruses. But it\'s still a potential risk. : Taco versus trolley. You guys probably know these 2 more than I do. I\'m not sure there\'s it\'s something you will always see interop in that acute period. But it\'s definitely a risk. : So taco volume overload. It\'s cardiogenic. So it\'s related to poor cardiovascular status. If they were awake you might see acute dyspnea, but you might have some hypertension tachycardia and heart failure, exacerbation in this particular patient. : Now, if you compare that, or contrast that to trolley acute lung injury, it\'s non-cardiogenic pulmonary edema. So if they develop acute lung injury within 6 h of transfusion : they may have trolley, so we find neutrophil, endothelial activation, vascular injury, and edema so acute onset hypoxemia is something that is usually assessed for pulmonary infiltrates, but no evidence of heart failure : now with trolley. Usually there\'s some sort of kind of initiating event. So I mentioned once before about the lipids and stored blood : those could potentially trigger this inflammatory event, so could a virus, or even a patient just being under cardiopulmonary bypass is enough to trigger : this pulmonary edema, and then if they get another transfusion, so maybe you know, you didn\'t really appreciate full on trolley the 1st time they got a blood product. But then you give another blood product that could further trigger things that could be enough to kind of tip them over into this particular adverse event. : There are other factors like antibody specificity, the patient\'s underlying condition that determines whether or not they are going to have this type of pulmonary edema. If you did assess that a patient had trolley, or you suspected : really you should close the loop on something like this and alert Blood bank which you know most health systems probably already have some sort of protocol in place where that does trigger, that this is associated with transfusion. But the blood bank may not accept further blood products from that donor if they know that it was associated with : acute lung injury. : Let\'s see below what approximate hemoglobin level is transfusion typically indicated. So think of the healthy adult : good. You guys are right in the range. 6 to 8. But it\'s patient specific. : What electrolyte is present in lactated ringers, minimizing its usefulness during transfusion. : You guys all know this. : Yes, that is in there. But why transfusion? Yes, calcium was what I was looking for. : What is the function of citrate in stored blood, which I did not talk about this : but if you know or don\'t know, citrate is an anticoagulant. : and they combined calcium, which is one of our clotting factors. : Good job which blood product contains the greatest concentration of fibrinogen. : It\'s the one you wait to use at the very end? Cryo, very good! Oh. : what is the threshold for fibrinogen replacement? I did not talk about this in particular, but once you start to get below 80 to 100. That\'s a good trigger for giving : cryo. And then, which factors are reduced from the storage of : plasma which I mentioned this. I think I mentioned this. Yeah, which factors : coagulation factors go down as you continue to store. F. 15, yes, 5 and 8, : 5 and 8 go down : alright our last section on massive transfusion. This does kind of start to get you guys a little more into : advanced anesthesia topics. But we\'ll kind of look at it here just a little bit So : we oftentimes will have patients come in with, just. : you know, a huge traumatic event and hemorrhaging at the same time. We can also, of course, cause a lot of surgical trauma depending on the procedure where you might end up with life, threatening or uncontrolled bleeding. : I can\'t remember trying to think of like, you know, the things that I\'ve seen or heard in the or I think there was a case : once at my last hospital that it was an interventional pulmonology case. : and they nicked somehow or pierced the pulmonary artery. : That was a day. You know I\'ve been in personally plenty of traumas with gunshot wounds or something like that, and they\'re rolling them straight into the or and there\'s a : er nurse, or a paramedic, or somebody on top of the stretcher, like, you know, rolling in blood straight from the bag into the patient. So you will, you know, depending on where you are. : What facilities you\'re at. You may have these cases and and see these things where you just have this kind of massive trauma. : massive hemorrhage. And then there\'s going to be a lot of pathophysiologic sequelae that go with that. Meanwhile you\'re trying to help manage things. From a volume standpoint, a coagulation, standpoint, etc. So how do we kind of balance all of that? And it takes a lot of. It\'s a team effort, because it\'s going to take some : guidance and direction between surgery and anesthesia. So it\'s not like you\'re doing it all alone. But : You know, these are very big cases to kind of process through. So with massive hemorrhage usually comes massive transfusion, and that can push a patient into a coagulopathy very quickly. : with extensive injury to vascular structures and tissues. They can have kind of like widespread damage that ends up, resulting from that. So one thing we see, for example, is endothelialopathy. : So if we have enough vascular structures that are damaged from like a penetrating injury or from surgical trauma, it can cause this kind of wider spread problem in those endothelial cells that are responsible for coagulation and all kinds of things, maintaining the structure and integrity of our vessels. : So you can lose a lot of : our basic, you know, homeostatic responses just because of the damage that\'s involved. So we tend to see coagulopathy, inflammation, vascular permeability, edema, multi-organ, dysfunction, and endothelialopathy. : Now, once upon a time. : it used to be that you would have that emergency trauma patient, come to the or and we would flood them with crystalloid, because it\'s already kind of hanging up, usually ready to go. And we\'re just going to give them a lot of iv fluid. You may even see that. : you know. Response. Teams have given a lot of Iv fluid. But you know we\'ve kind of been shifting more. So to. : you know, we need to prioritize blood products. : More so over flooding them with too much crystalloid. So if you think about like giving plasma. For example, one of the benefits to that is that it can help restore those tight junctions between the endothelial cells : and the proteins in that can help restore that osmotic influence, or the oncotic pressures, or whatever so, and it has anti-inflammatory effects. So there are going to be benefits to giving blood products in addition to, you know, supplying O 2, and giving coagulation factors, etc, that are going to be preferable over flooding them with a lot of crystalloids which just have salt in them. : Associated with some of these pathologic effects. With the coagulopathy we have an effect on our clotting factors, platelets, accelerated clot breakdown, which is not good. So you lose your balance between anticoagulation and procoagulation. Unfortunately. And then, when a patient comes in, they\'re hypothermic. They\'re acidotic. It really just worsens that whole process. It\'s just kind of this never ending loop : of issues, dilutional coagulopathy. When we give high volume resuscitation without replacing factors or platelets which can unfortunately : just worsen blood loss. We\'re consuming : factors by trying to clot, or we have a dysfunction of factors. We have depletion of factors. : and then, if we give a lot of volume on top of that, we\'re just really, you know, affecting the few factors that we do have and their ability to form a clot. : We can have excessive fibrinolysis, which is clot breakdown. That increases bleeding hypofibrinogenemia. If I\'m saying that right which is an excess reduction we said, our threshold is to kind of definitely get them over 80 to 100 in Fibrinogen. : but the state of having too little would prolong your Pt. Ptt, and if it\'s worse, if it\'s bad enough, we really need to give them cryo, which is rich in 1, 8 and 13, one being : or 1, 8 and 13, which is going to include your fibrinogen, or you can give them fibrinogen concentrate, which is going to be more expensive, probably a little bit harder to get your hands on. So that\'s why we tend to use cryo : hypocalcemia can occur from citrate toxicity. Hyperkalemia, because we\'re giving a lot of red blood cells. : There\'s a risk of arrhythmias related to that hypothermia. If we\'re giving a lot of cold blood products, especially if you\'re giving them fast enough that you may be giving products without a blood warmer, or before you have access to a blood warmer. So there\'s some other risks associated with those things. These are pathologic processes that we\'re potentially contributing to even during the process of resuscitation. : This image is just to kind of show you : all of the different things that kind of go into this trauma induced coagulopathy. You know, this is different than the idea of like a Dic : which is a disseminated process, meaning it\'s a little more widespread. It\'s going to probably occur throughout your blood vessels where you have this abnormal clotting and blockage of the vessels whereas trauma induced coagulopathy. It can occur at different little sites where you\'ve disrupted the endothelium : and you know it can happen inside the vessel. It can happen outside the vessel. And it\'s just kind of this : system that just kind of spreads based on very small little. You know, areas where the trauma is actually occurring. And you\'re going to have a lot of bleeding and issues with coagulation : in trauma-induced coagulopathy : labs. We will monitor labs when we can interrupt in cases like this. So coagulation profiles. : you know, if we have a loss of factors, if we have hemodilution, you may want to draw. Pt, ptt, obviously those can take a while to get back to get that : kind of evidence back, or that picture back to show you what\'s going on with those parameters. Tag and 10 of obviously is much better, especially if you\'re trying to do goal directed management. It\'s going to tell you more information about how class are forming, how firm they are, etc. : I am not testing you on a tag or a 10. You\'re definitely going to learn all about these later. I\'m not going to ask you about Alpha Angles, or any of that. This is just to kind of give you an idea of what : we may monitor during the process of massive transfusion. : So if you\'re giving greater than 10 units in 24 h, that\'s the usual definition : for massive transfusion, it is usually associated with a higher mortality indicative of the severity of the injury. Your facility will have some sort of protocol for massive transfusion, so you would want to learn what that is. It\'s going to tell you kind of what products are given when to initiate it. What\'s the process for starting a massive transfusion protocol. And then : the ideal transfusion ratio. There\'s been a lot of studies out here about what ratio products should you tr