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Okay, so let's care screen. Hello, everybody. Um I mean, you see what I can do. What's going on here? Share a screen? Yeah. Oops. Uh, let me just do that again. Uh, that's okay. How about Okay? Can everybody see this? Can you see that? Okay, good. Okay. So, um, good afternoon. I'm Doctor John Bogle. I'm a recently retired consultant, UK UK based consultant in the intensive care medicine and anaesthetics. And so, um, we talked last few route lectures on the importance of fluids in establishing and optimizing hemodynamics. This is probably gonna be the commonest thing you're going to do when you're trying to improve someone's oxygen delivery, which we always said was the most important thing you can do. Delivering oxygen to the cells. So today we're going to talk about how to optimize chemo dynamics with fluids and how to decide. And this is a really important decision if you're gonna give fluid or not. So this is a typical clinical case. Um, that, um So I'm just trying to get something go. There you go. Typical clinical case. See this all the time. Typical story. 82 year old lady admitted to the accident, emergency department or in the ward, her past medical history he's got. He's got a skeptic, heart disease, cardiac failure and diabetes. She's breathless, and he if you listen to her chest with a stethoscope, you can hear crackles and crepitation XYZ. And she has a dry mouth. Her blood picture is a bit low. Her heart. Her temperature is a little bit high, quite high. Actually, He's found to be an acute renal failure with a poor urine output in a raised creatinine urea. You're wondering if you're overloaded or two you under filled, and this is something you see very frequently and the number of times I've had Patient's referred to the intensive care unit where I was, uh, a consultant, uh, by the junior doctors with this sort of scenario. And I asked them, You know, why did you or why did you not get fluid? And basically they couldn't really tell. They just sort of said, Well, you know, I thought I heard crackles. I'm like, Okay, but that doesn't mean she's in pulmonary Dhiman, necessarily, I'd say Give a call from the crackles disappeared. So So it's really, really hard to know. And so do you get fluid in this case or not? And it's a really basic and almost banal question, but it's really important. And most of the time we guess so what we gonna What are we going to talk about today? We're gonna talk about Why is it important to assess fluids? The status of fluids? What is the goal of optimizing? How do you predict to if we can? Are we gonna be able to improve cardiac output by giving fluid or not? That's the goal, really, What works and what doesn't. How do you get fluid and so right? The first question is, why is it important to assess a person's fluid status? Well, it's important because you all know the starling curve so you have on the X axis but filling the pre load of the of the ventricle and the Y axis. Here it's cardiac out, but but it's also lung water because the starling curve curve, which you all know about, um, has got another curve that's related to it that a lot of people don't know about. And that's called the Extravascular lung water curve. And it's the mirror image of the starling curve So what does that mean? So if somebody has got what you feel is a low cardiac output for their needs and you want to fill them, so as you fill them, they increase their cardiac output on the starling curve, with minimal increasing pressure on the on the X axis minimal. And the lung water curve, as you can see, is flat, so there's very little extra long wear added when you're filling in this scenario. But as you keep filling again, you're still getting an increase in cardiac output. But you're not getting, um, much people feeling, uh, addition of lung water to the to the person's lung, so so far you're safe. But if you get to the top of your starting curve and you keep feeling now, see, that's where you get a big cardiac output increase. Very little lung water. Here you get a very small increase in cardiac output, but a big increase in lung water if you're on the flat part of your starling curve. So those two curves are worth remembering because that will determine why. Um, it's important not to go too far to the right on your starting curve and and get to the flat part where you're not increasing Kartik out, but because you will be increasing lung water. And if you are on the safe part of your starting curve, your lungs would look like this. There'll up fluffy and they're pink. Looks like a sponge innersoles. If you get to the lung water curve, that's on the dangerous side. So you're getting a lot of water going into the lung. Your lungs will look like this, a dermatitis lungs. And I would say that is not healthy. So just to recap, um uh, one of the first lectures I gave the dangers of either giving too little or too much fluid. That's why you got to get the balance just right. And they're both associated with increased mortality. So you want to get this balance of fluids, right? Not too much, not too little. And this was just a recap of the previous one of the previous lectures on the consequences of, uh of fluid imbalance. And so if you give too little, you can get gut ischemia. Now, this example here is gross necrosis. But the lecture that I gave was very subtle and that you can get trans location of bacteria from the gut into the lymphatics and release of side icons that will not be causing ischemia, but will make you sick with the PLO proinflammatory state. So that's very subtle. Signs of organ is Kenya. On the other hand, if you give too much fluid, you can get the venous congestion side of things. You can get kidney failure and liver failure. Um, and, uh and, uh, the various, uh, and gut failure. Of course, you get again translocation of bacteria. So too little and too much both will, uh, impact the guts ability to keep bacteria in the gut and not seeking out there seeking out into the lymphatics into the bloodstream, causing pro inflammatory states. And also this We talked about the glycolax that important, um, the devil that covers the interior of all the blood vessels and keeps, uh, it keeps everything intact. It's a very important organ if you like, So you want to be in the middle, the optimal fluid status, and that's what's so difficult to find. So, yes, to also, um, if you have a severely ill patient, whether he's in the ward, the accident emergency department or the intensive care unit. You'd want to know what percentage of people, if I gave a bolus of flu to, will respond by increasing our cardiac output. And what percentage will not hence will be damaged by the extra fluid. That's not going to increase cardiac output. As you saw earlier, it will flow into the lungs, and in fact, the answer is many, many, many studies 50%. So when you get someone who's severely ill and you feel this person needs an increased cardiac output because they're obtunded, their blood pressure's low. They're not passing urine. If you just guess which is what most people seem to do and just give fluid, you'll be right half the time and you be wrong half the time. So you might as well just take a coin out of your pocket and flip it heads or tails. But that's really not the best way to do medicine. So next question is, what is the goal of optimizing? Well, we just said if you look at the starling curve we want to do is stay on a steep part of the starling curve and don't forget what I've said. Several times in the past. Anybody listening to this lecture, who's healthy is on the steep part of their starting crew, which means that if you gave me a leader of fluid into a vein, I wouldn't and you measure my cardiac output, I would increase it. Do I need an increased cardiac output? No, I'm feeling healthy. I'm talking about someone who's ill, and you feel that they would improve if they had an improved cardiac output. So first you want to fill and optimize them, so you want to go too far, too far to the top of the starting care, just in the steep part, and then you assess again. And if the cardiac output still not adequate, then you have to alter the cardiac output. So the first bit steep part of the car of the starting curve is where the person has an increase. A large increase in cardiac output, a small increase in filling pressure like the CBP, for example. And they are fluid, responsive. If they're on the flat part, they're not fluid responsive. And if that's the case and you still feel they need more cardiac output, then you have to do something different, and that could be like using Inotropes. So what are we trying to achieve by improving the cardiac output? Well, we want to increase their cardiac output. That is an effective cardiac output. It's adequate. What does that mean? Well, if I'm on a I'm sitting here with five liters of cardiac output a minute, which is more or less the normal value, and I'm sitting here, I'm feeling fine. If I were to get on my bicycle or go for a run immediately, my cardiac output should increase. If it stays at five liters a minute, that's not enough for me. So even though my number may be normal, it's not an adequate, effective cardiac output from my metabolic needs. You want an adequate BP. You have to have that for flow, and this is really important. You may achieve an adequate macro circulation, but you also need to improve your micro circulation. The to have to be improved together, and they often do, but not always. So how do we know if the cardiac output is adequate? Well, there's clinical signs that are very soft. They're not they're not great. So you want a normal BP normal sensorium. So someone is talking to you, making jokes, saying they're hungry, but you know, they're probably okay. Warm toes, Good urine output again. Not a guarantee. But that's, uh, that's a pretty good sign. I put in red capillary refill. That's a really important one, because that's something you can do at the bedside. Doesn't need any fancy material. Doesn't need anything particularly sophisticated. All you do is you have to use a standardized way of looking at capillary refill and measure it continuously in the same patient, and you can you'll see in a second. That's quite a good technique. Biochemistry. Things called the central venous sent central venous oxygen saturation. We take a sample from the superior vena cava. It could come back around 70 72% if it comes back at 50%. You know they're sucking up more oxygen because these cells aren't getting enough. And so the blood between back to the right heart that you're sampling in the superior vena cava, for example, is low. That means that the cells aren't getting enough function. They're just basically sucking up everything they can. So that's a sign that's important. PCO to derived indices. Now. I haven't got time to go into those today, but they're becoming more and more popular, and maybe some other time we can talk about them lactate. That's a very common one we use to see if someone has, uh, it's a sign of a poor Um, well, it's it's a it's a little bit more complicated than people originally thought. But essentially, if you have a high lactate, that's a bad sign based deficits or an acidosis metabolic acidosis as, uh, reflected in a base deficit and advanced technologies like something called Sidestream Dark field spectroscopy. And I'll show you example of that. But that's probably it's probably unlikely you'll have that to hand. So what are the problems with assessing blood going? We're not very good at assessing blood volume, so if someone says, Oh, he's hypovolemic, that's That's not easy to assess. Really. We want to really know is not are you? What's your not what your blood volume is? You wanna know? Is your cardiac out but adequate? And if it's not adequate, what we want to know, will it improve with fluids? If it won't, then there's no point in getting fluids you have to think of something else to do. You don't want to know the patient's volume status. You want to know. Are they fluid? Responsive? That's the question. Are they fluid responsive? Now? How do we know we're not good at assessing volume? Well, this was an interesting study conducted in 2020 in an intensive care unit where they used radioactive labeled albumin to accurately assess someone's blood volume. And they took six patient's different times of after I t. Admission. By the way, these I've seen several studies that have done in different circumstances, and they all say the same thing. And so what they looked at was the actual ideal blood volume, and they did the clinical estimate. So these were six senior doctors estimating, Is this patient normal hypo or hyper Vellini? And this is what the doctor said hypovolemic hyper. You euvolemic so normal Valentic, hyper, hyper and hyper. And what did the measurements say? So, in fact, only one out of six was accurate. Correct. So this is again just an illustration showing that we're not very good at assessing someone's blood volume, just looking at them clinically and remember, you have to have a good macro circulation, so you have to resuscitate somebody. So the BP becomes normal and their heart rate becomes normal and the respiratory rate becomes normal. That is a prerequisite. It doesn't mean you're well. It just means that's the first step. It's not necessarily enough because you also have to think of the micro circulation. So this was a very interesting study, done in 2020 and what they did was they measured skin blood flow. Using a laser Doppler doesn't really matter the technique. It's just looking at peripheral profusion. So the micro circulation and they looked at them hours after being attempted resuscitation. So this is what this is what a healthy volunteers skin blood flow would be. And here were two groups, survivors and those that didn't survive when they came into the hospital with circulatory shock and they were resuscitated. So this is the survivors, and as you can see over time, they're micro circulation as monitored by skin. Blood flow improved, and those that didn't improve didn't survive. But what was really amazing about this study was this that all of them had those results despite achieving normal systemic hemodynamics. So the blood pressure's became the same. They went up. The heart rates came down to normal values. The everything that we would look at in the ward that the nurses would look at were normalized after resuscitation. But one group improve their micro circulation, and they survived and one group didn't. So how would you tell The difference between the two and one of the ways you can do that is using the capillary refill time. And so we know lactate is very strongly associated with with mortality, and in this study they looked at mortality based on lactate, but also on capillary refill time. And what they found was there was no difference. In fact, it was slightly better when you looked at peripheral profusion using capillary refill time and capillary refill. Time is very simple to do, but you have to standardize it so you can't have you're doing it one way and then a nurse coming and doing it another way, because your results may be different so standard up. You can do it many ways to standardize it, and once you do that, then you can use that to follow someone and look at their micro circulation, and then you resuscitate them to the point where they're completely refill. Time becomes normal, and once it's normal, you know you've resuscitated adequately, and here's us to show you what the more sophisticated visual techniques look like. So this is a a video of the micro circulation that's a normal one. You can see big boulevards and small side streets, and you can see the cells rolling through. That's normal. This is what someone who is in septic shock looks like and you can see it's absolutely awful. There's well, you can see yourself. There's very, very sparse, uh, capillaries, and they're very sluggish, and that's pretty terrible. So now the question is, How do you predict if someone will improve their cardiac output by getting fluid, what works and what doesn't so fluid or not, either? Well, in the real world, what we often do is we just give a bolus and we watch the response. So we give a small bolus of a leader or two of fluid and see if the BP comes up. If the patient suddenly feels better, if they start passing urine, that sort of thing, it's probably safe to do with smallish volumes. I wouldn't give 10 leaders. I give, you know, a couple of leaders at the most and see how they get on. And that is assuming that they don't have a an impending risk of pulmonary edema. If you think they're going into pulmonary edema, I wouldn't do that. But if if it's a sort of typical case, you could give a small small bullous and see how they get on. That's in the real world. But the other thing you can do if you're not really sure if they're very, um except, you know, they're very dangerously unwell if they think you think they may go into pulmonary edema and then then try and predict how they respond now I'm gonna have to quickly give you a very quick recap what we talked about last week on venous return physiology because the following techniques that will help you predict are based on this. Okay, so venous return. Um, let's get rid of this so venous return quickly. You had, as I said to you last time to get any flow in any hydraulic system. Any flow requires a gradient between the upstream pressure In the case of the upstream pressure in venous return. It's the distention of the capillaries and the venue ALS and the downstream pressure. So the gradient is what's upstream versus what's downstream, and the downstream pressure is your CBP, and that's really important. That's the filling pressure of your right heart. And the bigger the gradient, the greater the flow, the smaller the gradient, the slower the flow. And if there's no gradient, so if the two upstream and downstream pressures are equal, there's no flow. That's what happens when you're dead. And so you can see here that the up stream pressure is not the right heart. It's not the systolic pressure. It's way down. So that's where the vineyards and the capillaries are. And the downstream pressure is there, where the blood returns to the right heart. So the gradient is really small. It's about eight millimeters of mercury, so just very quickly what upstream pressure? Just to remind you, it was what we call this unstressed volume. So your air mattress is totally collapsed. You have to fill it, and as you fill it, it obtains a certain shape. But there's still no tension. There's no bounciness to the air mattress, as we said last time, so the pressure inside it is still zero, so you can't sleep on it. And then, as you feel it some more, it doesn't distend anymore. It doesn't get bigger, but it gets bouncier and now you can't sleep on it. And that's called the stress falling. So that's the upstream picture. But what I want to focus on for the tools do you have to understand this? To understand the tools that we use to predict is the downstream pressure. And we said that in your thorax, normally when you're breathing, your heart, which is in your thorax, is surrounded by your inter thoracic pressure, which is of the order of zero when you expire. Two minus three minus four minus five. So all your life, when you've been breathing spontaneously when I assume you have been your your heart is surrounded by the pressure is generated in your thorax, and it's the order of zero to minus three. Let's say something like that if your cough maybe goes up to plus 10, but it's it's really low, very low pressures. If you blow hard on a trumpet or you do what they call a valsalva maneuver, you can increase. Your pressure's up to about 100 and 50 centimeters of water. That's a lot, and your heart's not used to being squeezed like that. So what happens if you squeeze your heart? Well, as I said before in the last lecture, if you squeeze a syringe full of air, you can compress it. It will compress. If you fill that syringe full of water and you cap it, you cannot compress it. The pressure goes up, but the volume doesn't change. So when you think about your heart, if you bear down on your heart by blowing on a trumpet, you will squeeze your heart, which is full of fluid, and so it won't compress. But it will increase the pressure. So if you were to do a valsalva maneuver, say, for example, you stand in front of a mirror and blow as hard as you can on your thumb, you'll see your neck veins will stick out. That's because you're squeezing your heart and you're raising your C V P. You're raising your central venous pressure, uh, the pressure in your right heart. So what happens is If you do that, your CDP goes up and let's say your mean systemic feeling pressure stays the same. Your gradient gets smaller, and so your venous return is reduced and it gets so reduced that it could even make you faint because you're not getting enough blood coming back to your right heart. So squeezing your heart with ventilation, for example, will, um, will you give a pulse of gas into someone's thorax by ventilating them, you'll squeeze the heart and temporarily you'll raise the CBP by raising the CBP. You reduce the venous return, and so you'll see fluctuations in cardiac output if you're on the steep part of your starting curve. So how do you predict fluid responsiveness? How do you predict it? Well, people have tried using static measures. They measure the CBP. The CBP is five. It's 10. It's 15. Um, we were. We were taught that for decades we were taught that that was the way we determine somebody's fluid status. Look at the CDP. Other people look at the echo. How big is your heart? There's another way that we use, and you probably haven't come across. It's called the Global and Diastolic index. It's a It's an indirect measure, uh, calculation rather of the size of your heart. These are all static measures saying, How big or how how big is your heart in volume, or how high is the pressure of your heart and they're static. They don't work. They do not predict fluid responsiveness. Now, I'm not saying they're not important, but if you're asking a specific question, is this patient's fluid responsive? They will not tell you that answer, using them as static measures. There are other ways of using them, but not a static measures what you want to do, our dynamic measures using heart lung interactions or, when I say heart lung interactions. That's exactly what I just said to you a second ago about seeing how you when you bear down, you raise a CBP temporarily. When you put pressure on, uh, in the in a ventilator, for example, and you'll see how the heart reacts to that, those are the reactions we're going to be used. Why is CDP illogical, by the way? So imagine you have a person who will respond to fluid okay, and you were able to measure the gradient between the mean systemic feeling, pressure and the c D. P. So what that means is that when I give you volume, I'm going to be increasing your stress volume. I'll be raising your mean systemic feeling pressure, which is the upstream volume. Okay, that's the upper volume of the upper pressure and the gradient and the C D P may raise. It may rise a bit, but it could rise less than the means is taking 200 pictures. The gradient gets bigger. It's the gradient that counts. And if you look at the patient's that have respond to fluid and it's not easy measuring this, this is experimental battery. It's not. It's easy to measure CDP. It's not easy measuring systemic feeling pressure If, before infusion, that was the gradient. After infusion, the gradient went up. And so they responded by pumping out more blood. So they responded to fluid and increase their cardiac output in those patients' that we're on the flat part of the starling curve. And so, by giving Oh, sorry. This make sure was a cartoon here, So those were on the flat part of starting curve, so they weren't going to respond to, uh, fluid by increasing the cardiac output, they would increase the mean, systemic feeling pressure. But they also increase the CBP equally so the gradient, the difference between the two, it's the difference that counts doesn't change. And so here, you see before the infusion, that's what the gradient looked like. And after infusion, it stayed the same. The gradient. So even though the CBP might have gone up, it would have gone up to the same proportion as the mean systemic feeling pressure. So they both go up equally, so there's no increase in gradient, and so there's no improvement in cardiac output. So the CBP and both of those examples went up. But in fact they had different gradients. And so the CDP itself wasn't able to tell you if a patient was flu responsive. How about dynamic measures? Well, heart, lung interactions. What do we do? We divide them up into two types. Spontaneous inflation. So someone's breathing on their own. They're not ventilated. In that case, you can look for a drop in CBP. Now it sounds like I'm contradicting myself. I didn't say the CBP was not useful. I said it wasn't useful as an absolute number you can't say, Oh, it's 12. Therefore, he's going to respond to fluid, or it's too he's not. He's not gonna respond to fluid or vice versa. The number itself doesn't matter. It's the movement of the CBP, or you have ventilated patient's, in which case, with ventilation, you can look for cardiovascular variations with inspiration, so you push a bolus of gas into someone's thorax. You increase the pressure of your thorax, and that's something that your heart's not used to because you normally your breathing you're sucking gas in with negative pressure. When I'm ventilating you, I'm putting positive pressure into your thorax and squeezing your heart so you want to do is measure the cardiovascular variation. As I pump gas in, raise the pressures pumpkin. Let gas out, lower the pressure and so you can look at pulse pressure. Variation. Stroke volume Variation. If you're measuring cardiac output. Systolic pressure variation. So you're looking at the top of the BP curve and, maybe quite importantly, pulse oximeter variation. So here's a clinical case, and this I'll never forget this case. This was a 68 year old man. His past medical history was that he had multiple sclerosis. He lived alone. He appeared neglected. He was a very, uh, independently minded gentleman. He wanted to live like on his own terms. He was neglected. He smelled awful. And but it didn't matter. He wanted to live his own life. He was found down by a neighbor because he hadn't been making noise for a couple of days and he was taken to the hospital and they found he had rhabdomyolysis. So basically his muscle tissue was dying and he was releasing, creating canes myoglobin. His creatinine was going up because you do get renal failure as your myoglobin blocks off your tubules. His urine output was very poor. He's at very high risk of developing chronic acute and then eventually chronic renal failure. He was taken to the hospital and our intensive care unit was full. So he took him to the wards and we went out. There's something called outreach because some of the doctors and nurses who are from the intensive care unit to go out to see patients in the wards and they advised, given that we didn't have the space in the intensive care unit to give this person enough fluid to improve his cardiac out. Sorry is urine output by 100 to 200 miles an hour. The point there is you're trying to flush out the kidneys and flush out the myoglobin that's damaging the kidney tubules that hopefully may save your kidneys. But after three or four hours, we went up to see him again. And the nurses, for some reason, didn't give him much fluid at all. And so he said, Okay, we now had a bed. We'll take him tie to you. And we were a bit bit frustrated by the fact that the nurses didn't give him the fluid that we asked him to. We gave him three liters of fluid immediately. It had no effect. So we decided we're going to have to dialyze it because his kidneys aren't gonna work. So three leaders was a reasonable amount of fluid, had no effect on it. While the younger doctor was putting in the central venous catheter of the CBC to be able to dialyze the patient, he was using ultrasound and he said to me, Have a look at this and the internal jugular vein while this man who was breathing spontaneously, quietly breathing spontaneously. Quietly, you vein was just collapsing every time he took a breath in. And it was extent distending when he breathed out collapsing and distending. So that's something that was saying to us. He's really very, uh, you know, it's very remarkable how that vein was opening and closing, opening, closing when he was breathing. So what would you do? Well, that was a sign to us that he was extremely fluid, responsive. It was like the same as having a central venous pressure dropping. So we gave him another three liters of fluid. I must confess I would have been reluctant to do if I hadn't seen that sign. And guess what? He starts passing urine. And so the thing about this case that was amazing was this man, if we hadn't given him that fluid, if he'd lost his kidneys a he would have been he would have lost his independence because he would've been reliant on us taking him to dialysis three times a week because his kidneys would have been dead and secondly, for the community would have cost a fortune. So we lose and we lose in this case because we found out that he could still respond to fluid. We basically saved his independence, saved his kidneys, saved his independence and he didn't have to go to dialysis. That was a really great save purely because we were using a technique that showed or the younger doctor did showed that that he was going to respond to fluid, so we gave him a lot more than we would have Normally, that was a really good good technique technique. So this is just to show you in one study if you look at a drop in CBP, you can see those people who respond. And if you don't get the drop in CVP, um, you don't get the responders. So basically it's like looking at it with ultrasound, you can also use ultrasound. It might be better using ultrasound because if you don't see that that movement, then you're probably not gonna respond to fluid. If you do see a large movement, you will. And if you you know that's that's a reasonable technique. What about dynamic pressures? How do you respond to someone who's being positively pressure ventilated? That's usually in I t. U or in the operating room so you can see on the bottom. Here you have these green bars. That's every time you give a pulse of gas. So it's inspiration. Gas goes in, pressure in the thorax goes up, which is something that your heart's not used to because you're breathing normally. You're sucking gas into your pressure goes down, not up. And what happens when you look at the BP You can see it goes up and down, up and down there to pressures you can see here. There's baseline, your systolic pressure goes up and then your systolic pressure goes down. So when you give a pulse of gas, you squeeze the heart. You raise the CBP because you're squeezing that heart. It's full of fluid. By raising the CBP, you're reducing the gradient that determines venous return. And then when you let the and so the so the blood doesn't come back to the right heart, the right heart can't pump blood to the left heart, and the left heart can't pump blood to create that BP. When you let the gas out, then the CBP drops, and when the CDP drops, blood can come back because you re establish your venous return gradient and now it gets that infusion of blood and then it pumps to the left side. And then the left side pumps out and see your BP goes up so it goes up and down, up and down. But you also may notice that not only does this historic pressure go up and down, but if you measure the difference between the systolic pressure and the diastolic pressure, just look at the size of those waves. They're going bigger and smaller, bigger and smalling. That's the pulse pressure, and we often use pulse pressure variation. And you can use pulse pressure variation to determine if someone is going to be responsive or not if they're ventilated. But you have to be ventilate and in science with. So what are we really saying? You put this on a graph. This is your again your starting curve. We want to know, Are we on the steep or flat part of our starting curve? Do we respond to food or not? And if we get any of those measurements are varying. That's why the V in their post pressure variation systolic pressure variation stroke volume. If you're measuring the stroke volume variation you can see if they're waving back and forth. And so that means you're on the steep part of your starling curve. If you're on the flat part of your starting curve, you don't get variations. So one hand your fluid responsive. So that's if you see those variations, your fluid responsive. If you don't see them, you're not fluid responsive. And the thing that's really interesting is you can even use the plethysmograph, so your pulse oximetry you put your clip on your finger. Now, if you look at these two way forms, one of them is arterial pressure, and one is the waveform you get, Which is the flow away form, not a pressure wave form from your plethysmograph. That's your pulse oximetry. Can you tell which is which, Which is the arterial curve, which is the plethysmograph curve? And don't forget. The plethysmograph curve is non invasive, so you can do that anywhere in the world or wherever. Well, there's your pulse. There's your arterial pulse pressure. Remember we said the old prospector, going up and down, getting bigger and smaller when you ventilated somebody but your pulse oximeter plethysmograph. We call that P, O, P or pop, you can see that maximum minimum as well. Those are the pulse pressure very interesting, so you can even use a noninvasive tool. And that's really interesting. And some of the new manufacturers are going to be putting in, um, dedicated software that will tell you what the maximum minimum, what the variations are, and they both give similar information both of those carbs. This is really important, I felt, because this may sound a bit theoretical, and maybe you'll be thinking yourself. I don't know what how that's interesting, but I don't know how I could actually apply this. Well, you can. During the first wave of covid I was working and the the guidelines and I have to say that nobody knew this was a new illness to us, The guidelines said. These people probably have sick lungs. Sick lungs are best kept dry. You don't want to create pulmonary edema and therefore keep these patient's dry and give them not only don't give them fluids, but give them diuretics and dry them out even more. And the problem with that was, I think there were a lot of mistakes made, but what was really interesting was in our unit. We use a lot of these techniques that you just heard about. And we were very attuned to these this physiology, this these principles. And we noticed on this monitor we didn't have time to put in a lot of fancy hemodynamic monitoring because there were so many patient's And there were a lot of young doctors who were very young and they didn't know how to use these tools. So we just had oximetry. And sometimes we had arterial catheters. But in both of these arterial catheters or just oximetry, we noticed that the waves were way they were swinging up and down, up and down. And we were thinking to ourselves, Boy, these people really are very fluid, responsive. So we decided not not to, uh, to restrict fluid and not to give them diuretics. So we did the opposite to what everybody told us to do. And that was I was almost daring in our part. Well, it turns out we were using the physiology that we saw in front of our eyes as opposed just guessing and what happened. Well, after the first wave of covid, a group of experts got together around a table, and they came to a conclusion that the first wave was not well done. Why? Because they now realized that a lot of the patient's were So let me just do this again. A lot of the patient's were hypothalamic, and because they restricted fluid, they had a high incidence of renal injury. And so, in fact, they might have benefited from fluid, which is exactly what we did. And we had a lot, much lower incidence of renal failure. And bear in mind that if your kidneys fail in this sort of illness, your chances of dying go up about six times. So I'm pretty sure that a lot of people died didn't have to die because we're giving. We weren't using the physiology that was in front of our eyes. We were not trying to say we were better than everybody else, but we were using this this, this knowledge to help us determine whether we give fluid or not. And we did the opposite to everybody else. And they said we weren't paying enough attention to individual monitoring. Well, we were, and after this lecture, hopefully you will be, too. How do you fluid? Well you ought to give fluid. If you're going to test somebody for fluid responsiveness, you want to give a small volume, and quickly you don't want to give it over half an hour or an hour. You want to give. You don't want to give two leaders. You want to give something like two or 300 mils and give it really, really quickly over about. I don't know, a couple of minutes, three minutes or four minutes or five minutes, let's say but not half an hour because often what the nurses will do, they'll have a pump and they'll they'll put it up to you know they'll they'll put up 300 mills and they'll give it over half an hour. That's not gonna work. You got to give a bolus that stresses the system quickly. So how do you do it? How do we do it? Well, you do require cardiovascular monitoring to be able to do this. So what we do in the intensive care unit is we measure your stroke volume and stroke volume is just a cardiac output per beat of your heart we give you. It would make her the stroke volume. We give a bolus of fluid so say two or 300 mils quickly. We then re measure the stroke volume. If it's gone up by more than 10% that means you're responding and we do it again. It's gone up by more than 10%. You're responding, then we do it again. You stopped responding because you've got up less than 10% and we stop. So it's a very controlled way of filling somebody without actually causing harm. We're not just pouring fluid in, but this is actually quite important. The next thing you could do if you want to give fluid, but you don't want to overload somebody, you're not sure what to do. You can raise the legs, so that's really important, because raising the legs is the equivalent of giving a transfusion of about 300 mL of blood. The beauty of this, though, is if you do it, you're basically giving the patient 300 mils of blood. If they respond and I'll show you how, what I mean by responding in a second, then great, Then you can carry on giving fluid. If they don't respond, you just put the legs down and they haven't been overloaded with fluid, so it's a way of giving fluid without giving fluid. It's a very, very safe way. It's reliable. There been lots of studies that have looked at all different techniques. It's a very reliable way of giving fluid to somebody to test if they're responsive or not. The beauty of this is, um oh, yeah, you And too, when we say respond, you got to be very careful what you mean by respond. Responding means either measuring stroke volume or the pulse pressure, but not the BP per se. The BP is not a good monitor of, uh, stroke of stroke volume. Pulse pressure is so you can look at the different scenes systolic and diastolic, how they change, but not just looking at the BP, saying, Oh, it's gone up. And the beauty of this technique is you can even use it in spontaneously breathing. Patient's not just ventilated patient's, so both spontaneously or ventilated patient's. Why is BP not a good surrogate for cardiac output? There have been several studies. This is one of the most recent studies that looked at How does the BP compared to cardiac output. It's all over the place. You can have a low BP in a very high cardiac output. You can have a normal BP and a low cardiac output, so it's really very difficult to marry the two together. So if you're going to lift someone's legs and do a passive leg raising, pl are, they call it passive leg raising. Uh, you have to measure something that is a so either is cardiac output and stroke volume or a surrogate. So pulse pressure variation, for example, or the P. O. P. The plethysmograph would do as well. Um, just is just to remind you of another. This is a true story that I was involved in. This was a gentleman who was having an upper GI bleed. He had a massive blood loss from his up from his stomach. He was taken to endoscopy and they were trying to clip, uh, I think it was an ulcer he had, and he was pouring blood during the procedure and to the point where he had a cardiac arrest and they called us to come down to the cardiac arrest. And then when we got there, they were misogyny his heart, and they were pouring fluid in because it was blood lost. But the cardiac, uh, massage appeared ineffective. Um, Why? I say that is because the entitle CO2, which is a very good monitor of how effective your cardiac output is when you're massaging the heart was very low. So it wasn't working. Why would that be? Well, the reason would be is because you cannot massage an empty heart. If your heart is an empty, you can pump it all day. Nothing's going to go out of it. So what do we do? We lifted his legs. We did a passive leg raising. Not to see if he was going to be fluid. Responsive was to give him a rapid infusion of fluid because the problem there is that if you're giving fluid through a vein, it's too slow. You've got to fill it very quickly. And one of the really quickest ways of doing that is just lift the legs. So don't forget that it's just a really good clinical tool to remember. So we're gonna just recap on this. So how do you deal with someone who's, um who's you feel that cardiac outputs too low and you want to personalize their fluid management. Is it too low? We'll do you want to get fluid or not? If it's really obvious that they have a fluid loss, they're pouring blood on the floor. Well, there's no point in doing tests. You just give fluid. If it's not obvious, like the woman who had crepitations that would have poor urine output. You're not sure where you are with their pulmonary edema or or low or low fluids. Then you want to start using dynamic in disease to say, Are you well, you can give a bolus and see how it goes, but you can. You can, um, usually use dynamic in disease, and you want to know, Are they breathing spontaneously or ventilated? So that would be a fluid challenge. Give a bolus and small bullets and see if they get on or passive leg raising. That's a very good one. If they're breathing spontaneously, look for a drop in the central venous pressure or you have ultrasound. Look at the neck veins and see if they if they if they get massively dilated and then collapse, as in the patient with multiple sclerosis and who had wrapped in dialysis. That was a great That was a great example. And if they're being ventilated, then you can use any of the various surrogates or actual direct measurements of stroke volume. So either post pressure variation so the difference between systolic and diastolic and see how they get increase and decrease as you ventilate. Stroke volume, systolic pressure variation or plethysmograph. UH, P O P. Uh, autism. A graph thinking whether it's p o. P anyway. So it's, uh, if the answer is negative, you don't get fluid. You might have to give inotropes. If it's positive, we'll then you give flute. So to recap what we talked about. If you under overfill somebody, you have harmful consequences. Remember that of the patient's that are severely ill and you think, Do I need fluid or not? Well, half of them will respond, and half of them will. So either you flip a coin, which is not the best way to do medicine, or you try and approach this intelligently. Using these principles, the starling curve will help you determine whether someone is going to respond to fluid by increasing their cardiac output, or they won't. And if they won't and you give fluid, you're more likely to cause harm by, uh, giving fluid into the lungs or causing a lot of back pressure or damage from glycolax, as we talked about earlier. Don't forget that these techniques rely on your understanding of what determines venous return and especially the increase in central venous pressure. The downstream picture. As you ventilate somebody, we want to make sure that we resuscitate the micro circulation, and one of the ways to follow that is using completely refill time. That's a good technique and one of the best techniques to either resuscitate somebody urgently like in the case of that cardiac arrest that was hypovolemic, or someone from trauma, for example, raise the legs that will immediately give you 300 bills while you're giving fluid as well. But it's to determine if someone is going to respond to fluid. You can lift the legs and and see how they respond, whether they prove their their stroke volume or a surrogate. The stroke volume Not BP, but pulse pressure or P. O. P. And remember, you want the question you're asking is, Are you fluid, responsive or not not. Are you hypovolemic? Are you fluid? Responsive or not? And you don't want to flip a coin you want to use? Use the principles that we talked about today and use your brain. That's what happened during the covid outbreak. We used our brains and our understood our principles, and I think we saved a few lives. Okay, so that's really all I have to say today. If you have any questions, I'm happy. I'll be happy to try and answer that for you. Any questions? Um, there are no questions in the chance, but if anyone wants to a mute themselves or put something in now, um, otherwise you could do the feedback, Please. It will take you two minutes. Do the feedback form that I've post in the chat and then, at the end, up with the certificate. Uh, thank you very much, Doctor Vogel. Okay, Um, I don't know if anyone wants to ask anything now, but otherwise I think you've got a lecture again next week. Yeah, Every week. Yeah. So, um, if anyone's got questions, they can maybe save it for next time because they don't have them now. Thank you very much. Okay. We'll see you next week, then. I see you next week. Thank you.