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Summary

This online teaching session is for medical professionals looking for an overview of shock. Through this overview, attendees will learn the basics of shock, how to recognize shock in patients, and the five categories of shock that medical professionals need to be aware of. Lecture slides will provide a framework to use when thinking about shock, with specific information on arrhythmias, cardiogenic shock, hypovolemia, obstructive shock, and distributive shock. Attendees will also have the opportunity to ask questions, get their answers clarified, and get a summary of the session at the end.
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Learning objectives

Learning Objectives for Shock for Medical Audience: 1. Understand the definition and features of shock as a systemic hypoperfusion syndrome. 2. List the various end organs affected by shock, including the cardiovascular system, kidney output, skin, and brain. 3. Describe the blood flow components (cardiac output, systemic vascular resistance, stroke volume) that impact blood pressure and perfusion. 4. Identify the five major categories of shock (arrhythmic, cardiogenic, hypovolemic, obstructive, distributive/vasodilator) and their associated signs and symptoms. 5. Recognize potential treatments for arrhythmic, cardiogenic, and other shock types.
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the working. I do work with the, uh, the whales air ambulance, and so come across unwell people of all sorts of like bringing the emergency department and the intensive care unit to to the people where they need it by the roadside or or at their home or where ever they may be. Um, so I can't see the chapter you because I'm doing this on an iPad. And obviously that's turned my video office well for you. So you were here, so But a day end of this where you will stop talking, 10 slides off, and then you better see me and and hopefully we'll see you guys and we'll have a chat about anything that has come up in the session. And but feel free to put your questions in the chat in the meantime, and then we'll go through a summary of them at the end. And so this is an overview of shock. Um, the, uh that that the each part of this every slide that I've got here is it's unfortunate talk, so I'll try and keep it fairly brief on Been simple on if I bring up anything that you're unsure about, then we can talk about that at the end, and hopefully you'll have a good overview of whatever framework of how to think about shock. So eh, so what is shock? I mean, the word means different things to different people, but particularly the English language. It's it's Ah, you see on the TV or when patients say someone was shocked or they are in shark, or that it might mean that they've had a a bit of an emotional time of it. And they're and they're good cup, cup of tea with some sugars in it. But medically, we're talking about the the impact off many different conditions that come together. That that looks similar and so really shocked is more like a syndrome. Uh, so it's a systemic hypoperfusion syndrome. So what we're really looking for is is the impact of of the poor flow of blood through around the body and the impact that will have. So we'll be looking at how to have to recognize that what it looks like on day and then what to do about it. So, first off, how do you recognize that shock? So if the body is being poorly perfused then, really, the way to find that out is to look at all the different end organs and and look at the effect that that four profusion is having on them. So there's a list of common features on the right here, so you might be spotting things that with the cardiovascular system itself. So, for example, tachycardia bradycardia, often with hypertension. But then they're looking at the other end organs that you can easily access. So they're so looking at your own output. So how well the kidneys are being refused and there's a oliguria rather than an area, particularly. So you have a low urine, something less than about half a mil a kilo per hour. It would be a sign that the kidneys have been pulled in perfused on then the skin being on the outside really easy to be to to access and then assess. So you were looking at both temperature on modeling. So if you, uh, know a bit about about shocking hypertension already, then you'll know that when the body struggling it will start to base. It constricts on day, the peripheries will be less well perfused under the core, and that will affect capillary refill time peripherally, but also will allow cooling of the extremities on so you can if you're assessing and it was running your your back, your hand up, up someone's arm. You can potentially even feel a a temperature differential level on the the worst that the shock state is. Then the higher up the arm, the that you'll you'll you'll get warm. That's an easy thing to check. Modeling. Uh, you can look online and see that there's there are lots of in stages of modeling that really even a little bit. It could be a sign that this is a significant amount of of shock. Oh, a poor profusion going on. Another end organ to look for is the brain that very rapidly if he's affected by poor profusion on day. So the first stages of that low perfusion will be starting to look confusion, delirium and then, eventually, a decreased conscious level. Potentially their seizures on DCU oma before death in shoes. Um, when you're trying to differentiate between types of shocks, then other things just just quickly to look out for ah, things like rashes. I'll come come Teo talk about that a little bit more later on when we're talking about different types of shock on then the doing a blood test, looking for the serum lactate, which could be done as a laboratory sample or ast part of ah point. We can test by the bedside as a blood gas on. And if that's raised, then there is can be a sign off global hyperfusion. But that's not the only reason why lactate goes up s so you have to be looking holistically at the patient. Not none of these Ah, um, indicated by themselves on. And if you you may have we have one or two of the speech is initially presenting to you, so you have to have a high index of suspicion. So the big graphic there is that to start, you thinking about the first principles of blood flow around the body on and the components off BP. So the components of BP made a halls the cardiac output. I say that that's the amount of blood that's being pumped out of the heart in liters per minute and the systemic vascular resistance or essentially, how, how, how much tone there is in the blood vessels you know how much resistance to flow the rest. So normally the blood vessels have got a little bit of squeezing them, holding them just tight enough that the BP will be maintained. If they are based, dilate dilated, then that will reduce the BP. Um, and if they are too tight, then the BP will go up. But if they're really sites, then that will actually, conversely, reduce the cardiac output because it's too difficult for the heart to squeeze and pump them around the around the body. The cardiac output is a function off the stroke volume. So how much blood comes out of the heart and everybody eat, multiplied by the number of times it BPM. So the heart rate times a stroke volume and that will be determined by at the amount of pressure of the blood that's coming back in from the others from from the venous side. And so that that will be something we call pre load. And then the, um, the stroke volume will be determined again by the amount amount that the blood that was filling into the ventricle and how contract I'll the part ventricle is, and so how how hard it's pumping and how it will empty. And then I'll talk a little bit about other things that can go wrong with the heart in a minute. So if you would like to have a framework of have to think about shock, then you would potentially divide them up into about five different categories, and I'll go through each one of these in turn. But briefly, there's a rhythmic problems or electrical heart problems cardiogenic the things that wrong with the heart themselves. Um, Hypovolemia. So where the feeling is is impaired because there just isn't fluid in the in the vascular system. Obstructive. So where the flow is impaired on distributive or vasodilator Ishaq, where the you've lost the the systemic vascular resistance and the the blood is just pulling in the vascular tree rather getting back to the heart So arrhythmic problems boiled down. Teo, it's basic level, really. The if the heart isn't, um pumping. Well, then, um so I mean, it's a delivery of the front door, definitely. So just get distracted. And so yes, everything is ah, I'm caused by that the heart not following a little more so Excuse me. Yes, I don't talk. Okay. Already talk about timing and right. So everything is so normally the electrical activity in the heart as well coordinated. And it helps the Atria and the ventricles to contract in a coordinated fashion. And everything is like, Ah, BF where there's no court know it's activity. Obviously we'll keep your Codec a arrest. But then there are other problems as well. Say those things, like intricate tachycardia or Sinus tachycardia, or even or if the heart, This is a heart block where the ventricular race has become too low. So they so, uh, if if there was a tachycardia and you can get a drop in cardiac output because the heart's beating so fast that it would just can't relax isn't enough time in diastole for its fill up. So the stroke volume decreases s. So even though the heart rate of time, the actual amount of blood being pumped out, the heart is low, bradycardia the other way around, so the heart can be quite full or in violated. But the heart rate is is so low that the cardiac output goes down a so both of those will generate a low cardio capital state at the ah. Treatment of arrhythmias is pretty well described on, but you can read about them in the recess council guidelines. They produce some nice flow charts for for to show exactly what you should be thinking about what to do for each of those, um, to say this is a bit simplistic that and there are lots of other things to talk about with good terms of electrical problems, of the heart. But, um, I'll move on. I am. So it is, Ah, heart muscle problem. Or there are problems with other individual parts of hearts. It's the bowels. Then you can get cardiogenic. Ah, shock. So this is an echo showing a poorly functioning hearts. The left ventricle. This is the on the I shaved this point around. So that's the left ventricle. The normally it looks nice and muscular and tighten, and when will be contracting well all the way around it. But what you can see here is that the the walls off the left ventricle are just shimmering. Really, they're not contracting the particularly powerful E, and so a lot of the volume that's in the heart is pooling. There so the so. There's a very low stroke volume, a low ejection fraction. And that's because of decreased contractility and dilatation off the left ventricle. The think things that you might might cause that Or cardiac ischemia. Um, so particularly if you've had a myocardial infarction, um, or just the accumulation of drugs so excessive Peter blockers, calcium channel blockers and and so on can affect contractility on back early, uh, in the setting of polypharmacy, potentially to decrease renal confusion. Then drugs can accumulate on Do the heart broken, be affected by accumulation of drugs in terms of the other things as well, so there can be out for help flow obstruction to the heart. So particularly in critical aortic stenosis. Or, if there's a left ventricular outflow tract obstructions that have caused by potentially hypertropic cardiomyopathy or something similar. Then there's a There's a fixed obstruction, and it's like trying to pour as fluid through a sin straw. But you can only do that at a maximum rate. Eso the uh, again with a with a fixed amount that you can fit through that obstruction. It means that you can only have a fixed cardiac output, and it can't go any higher than that affect things there. Ah, the future profusion is worth it through through that straw's. If you were to actually do give us a drug that would decrease the heart rate or or lower contractility during that time or worse, they'll drop the SPR then then the the BP can be critically affected with very small amounts of change. So the those patients are really on a knife edge. And the other thing that could happen is that a the valves themselves can be regurgitating. So that means that they're not functioning properly and causing a one way system for the blood to go through the heart on the S. Because of that, the heart will have a lot of wasted energy, and that flow that is generating will be going in two different directions. Eso the cardiac output will fall because of that. So moving on to a hypovolemia s. So this is one I deal with quite often with withdraw medications because of blood loss. And if there's no blood coming back to the heart through the venous system Oh, not much. Then the feeling of those ventricles will be will be lowered were dropping the stroke volume on so causing low BP on low perfusion that can account for, uh, there were two ways of thinking about hypovolemia and it really it's that What? What is it that's been lost? So if it if it's blood that's been lost, then the bonuses on treating the replacing, the Bloods that's been lost with blood. And so in the UK on DA around the world, we have a major hemorrhage paps, which are standing by in hospital, ready to be given when we also have some of that on on our aircraft in the prehospital environment. And so we would give and the equivalent of whole blood eso. That's a breakdown of 1 to 1 to one ratios off red cells, fresh frozen plasma on platelets to any quickly and equal doses. Um, which, when recombination is about a close to it's a whole blood is we can get without actually giving whole blood, um, and that will allow us to keep hemoglobin levels up. It works is an excellent colloid on DPA avoids clotting factors, including fibrinog, and if you if you give a cryoprecipitates or any if they concentrated factors um that will help to maintain clotting as well as as keeping the fluids in the right place. If you give crystalloids to those patients and that can drop their body temperature if it's not warmed enough and I leave those crossing practice on dilute the oxygen carrying capacity with the with the red cells. Um, it worst in acidosis strips the vascular ah, like a k licks and cause interstitial fluid loss into the into the tissues on so fluid will leak out so well. With happen magic shot, you really need to be trying to replace blood with blood and other fluid losses. So so you can lose fluid in lots of different ways. Potentially from the GI tract. Now, say vomiting, diarrhea, um, dumping of fluids, actually just into the bowel and from endo toxins from food poisoning and so on. Um, the renally so that will be covered in other lectures. But excessive renal losses, um, dehydration from being too hot, say, from having a temperature from being septic. So lots of sweating. Oh, just just heat stroke from being out in the heat. So all of those things will will be losing fluid or water um, with the without salts on and but you don't lose the cellular component. So So they become the more concentrated and so replacing fluid that's been lost with more fluids and crystalloids is what you would want to do there. Okay, so a quick talk about flow for fluid challenges and this is an important point to get your head around early is that when you're trying to give a fluid challenge for somebody in shock, you want that to go in at a reasonable speed so that you could then see the effect that that fluid challenge has has. And this is the standard colors in the UK for cannula caliber. There, on the left hand side, you've got an orange, which is a 14 gauge cannula, and it works. It's way smaller and smaller, down to the little near flown type, which is the yellow ones for us, which is 24 gauge as an aside, and the the gauge number gets bigger as that can really get smaller because that's based on the British wire gauge s so it sounds seems a bit counterintuitive, but you could fit many more little wires inside a big conduit then you could do with a big one. Um, so that's the reason why the grass there is just a representation of the left inside the Y axis Is that mills for minutes of your flow rate that you can get through the different cannulas so you can see how it changes, sort of significantly. And and it's actually, uh, um in the square law for the for the diameter of the these devices. So a big, short Angela will will allow you to a much higher flow rate than a a long, small thin. One of the things that you can do to increase the flow rate will be to add pressure to the bag. That's a fluid that you're giving so that you put it in a pressure bag or all, run it through a pump. Somehow, um, what you don't want in the way are lots of things that will restrict flow, such as the little by a nectar devices that go on the end of January, vote for infection control purposes or three way taps, and things does that that will will just slow things down and excessively long giving sets a swell, well reduced flow I am the HDLs port us to to memorize, uh, these features of shock. Um, and they may well turn up into into exams because these things are still in the book, but they they don't really show up. Um, you're exactly as as described, so the classes of hemorrhagic shock will go through from 1 to 4. And this table would suggest that you could tell how much blood someone's lost by looking at whether their blood pressure's normal or decreased, what they're they're false. Pressure is normal, decreased, looking at their pulse rate, their spiritually eight, where they're confused or or lethargic or so and and to an extent, that's true. But the it doesn't correlate with the amount of blood loss that they've lost. So people can have a huge variation in their presentation. And but I put it in there just for completeness, boroughs it. So that's the way you should look at case you want some numbers and figures. Um, the other part, the table on the bottom is also from 80 or less, which suggests that all right, there is a certain BP, which you would lose each of these pulses. So if the systolic BP less than 80. Then you would lose your radio. Less than 70. Is your femoral less than 60. You lose your karate. Um and that's also been shown not to be exactly true. On there is intubation variability between the pressures that will be these. These pulses are lost, Okay, but they do go in that order. So if you were resuscitated a blunt trauma patient, you could potentially try to get them to a point where they got a radio pulse where you're heading to say it's okay to try and stop the bleeding. And if you got a penetrating drama than you might be happy with carotid only, but it gives you some idea sickly without having to formally go through and try and get a BP. But if you got what got some of those policies, then you've got a rough idea that there is some BP. It's all and live some profusion on going. And if the radio is gone, then you know that they're hypotensive. Okay, so moving on to the next type of shock and let's talk about obstructive shock next. So that's where there's some sort of obstruction either inside or outside of the cardiovascular system, which is impeding flow through the vascular tree. So the x ray there is of a large left sided tension pneumothorax. You can see that the longest compressed on the left side is there alone. Know lung markings outside of the chest wall of the little, um feels there on the left side. You can see the lung collapsed against the against the heart. It is a tricky with deviation, which is a late sign. Intention. Pneumothorax is excess. But this is just a all the classical features on this, just extra eso the mediastinum shifted over to that side on dispersant will be having decreased flow because of the compression on the mediastinum itself. Good stopping venous return from coming back into the chest from the abdomen, legs, arms and head. And the treatment for that course will be an emergency decompression of the left side of the chest. I'm I'll also tell show you cardiac tempered ours, but which is where the fluid is on the outside of their heart. But on the inside of the pericardial sac, um, which presses down on the heart. Massive pulmonary embolism is where there is a huge clot sitting in the pulmonary vasculature, which is just stopping blood from being able to get through there. Um, abdominal compartment syndrome is similar to when you've got an obstructive cause in the chest. But that's where the high pressures within the abdominal compartment usually from interstitial bowel swelling, um, from excessive crystalloid infusion, but for lots of other reasons as well. And and that can cause compression on the I. D. C and decreased venous return and then high mean interested pressure just from Bensel a shin. So if the patient very stiff lung fully compliant, lands on a ventilator and they're having to have high, freshest for for re oxygenation, then that will also impede flow and venous return. So I got some pictures to show you a couple of videos and this is a cardiac temporalis. Um, I'll get up certain, eat home him all connect, Right. Okay. So, yeah, so this is the heart in a forest and long axis of you. Um, this is the fluid in the pericardial sac all the way around the outside. The fluid is black. Um, and you can see how it's pressing down on the outside walls of the heart. The heart is floating around in this fluid on it. The ventricles here on here. Ah, funny, very difficult to toe. Actually fill because there's no room for the hearts to two refills been squished from the outside and being strangled that you said, if you like, um, the treatment for that is to decompress the pericardium on, Be in. If that's blood that's causing the card it temple. Not then then then it will require a big open procedure to get the clot out. But if it's fluid, then that could be done with a pericardiocentesis line drain in pulmonary embolism. The the reason. The reduced flow from the it broke through the vascular tree in the London's causes the back pressure off and of off blood into the right side of the heart. So there are a few things that say that you can see here again another parasternal on excessive you. So this is that the heart with under filled left ventricle on this side, um, is a 44 different parts, I think. But, um, so the left ventricle was under filled because the fluids just not with the Bloods not being able to get there from the from the pulmonary tree on this one on the top, right. This is a the right side of the right ventricle, which is pressing down on the on the left side of the heart. Normally, the left side is much more well filled, is nice and muscular. And you get a circular if you this is a Paris stone or short axis. You. So you're looking at 90 based on the first picture, and you should get a circle of ventricular muscle there. But there's this been flattened by the excessive pressure on the on the right side. So you gotta decide there and then this is a form of a pickle. Four chamber of you. So this is the apex of the heart, and you're looking up through it and you get the right ventricle in this which you can see is very large, dilated, and then the right atrium, which is dilated as well, because of that back pressures always coming all the way through on the right side. Um, I went by the body with McConnell. Sign on that. You can see that the tricuspid regurgitation, which is there's a colored doctor placed across the Tricuspid valve here on there. There is a jet of blood going the wrong way because of that back pressure pushing all the way back, Um, distributive causes s. So that's where the flu is gone in the wrong place that you've got surveys a dietician, which gives you a low systemic vascular resistance, which then, of course, drops the BP. Um, that's could be caused globally. So all of the vasculature is is basically elated on, but it's most common that you would see that s so that could be caused by widespread sepsis. Or is this systemic inflammatory response? Um, And if Alexis um, adrenal crisis So an Addisonion crisis, for example, and or the collection of drugs that we talked about talked about before where you might have Ah, they're nitrates in isosorbide or a or casting channel blockers or, um, gtm, that sort of thing where you get widespread basis allocation. From that, um has also the case and a lot of the general anesthetic medications that they all cause the global based agitation on diaper attention. It might just be localized to say the the bottom part of the body in a spinal shock. So, for example, if you've got a spinal cord injury, then that will cause sympathetic chain disruption distal to the to the injury and will cause widespread body base of validation. And we see that with the with regional anesthesia where we've done a There's a breakpoint block, a spinal block on that will also course hypertension for the same reason. So when it comes to diagnosis and there are two schools of thought how you can diagnose things, UM, one is the history examination. Special investigations and treatments on Dad is useful when you got the time to think about it, and you want to find out exactly what's going on. But in the first instance, you need to work out with any resuscitation, require it on, so go through a C A B C D approach. See for catastrophic hemorrhage. In the beginning, that air we breathe in circulation, disability and exposure, and so I'll talk a little bit about the results in a minute. But so but some specific things that you might want to look for when you've got a patient with shock. Um, starting with with history and so potentially. If the patient's already got a cardiac history before then it will put you on a track that you're looking maybe a cardiogenic or arrhythmic problem. Um, in case they've already got a history of adrenal disease, then you'll give you a clue that they might be having them to save your crisis. Previous clots or family history of clots would raise your index of suspicion for for a pump for Marie ambulance. And if they've immunosuppressive or have got long dwelling in basic devices such a hitman line or the central lines or the vascular access Well, maybe just strain that's been put in recently or a long standing indwelling urinary catheter. That sort of things, then that that increases the infective risk. And so I would suggest, possibly subsist. Ah, if they had a recent surgical procedure or just had a trauma, then they're more likely to be bleeding, and particularly if they're already on, um, anticoagulants. And then they would be more like to believe for a given injury. I am so that takes you into the current medications. So and in addition to anticoagulant, so you'd be looking for things that be that might affect like pressure. Maybe accumulate. Or maybe even if they just had a recent change in their medication that they that that might be the cause. Thinking, of course, that that certain medications interact with others on vertically the metabolism of others and so giving something my course in accumulation of something else. Um, the special investigations that you would consider doing is a baseline, somebody who is showing shock states and the liver tests. You're going to look for sepsis. You're gonna check the clotting on book for the weird and wonderful things like that, like hypothyroidism and and adrenal crisis. And as I said to you before taking the lactate, And if you got access to a blood gas machine actually at the point point of care, then that's a very quick thing that you could do. And it doesn't tell you what type of shock they've got necessarily. But if it's normal, it can false. You reassure you can, but if it's raised, then it look. If you have some confirmation that this person this is needs further investigation and a C G will clearly show electrical problems and potentially show you signs of Micardis Kenya on then there's the imaging to do So So, looking at plain films, um, it's a pretty dramatic, left sided chest X ray, which which is the same person he's got the CT scan on there, which is showing a a massive hemothorax, which is the white up the left side of the chest when they're supine on. Then if you look at the CT, you can see that this is collecting all behind the lung, which is why you get that whole right out on there. Um, bedside ultrasound is pretty useful if you got access to it. So you can very quickly rule out pneumothorax. You conduce bedside echo on look for signs of temper nard and it looks sounds of Micardis gave me over looking at the muscular motions and check the valves. Um, you can do a fast can look potentially looking for free fluid in the belly for for bleeding on. Then, of course, that you can do a CT, which will be give you better a resolution on a lot of these potential causes. Um, there is another bedside test, which was mentioned in one of the questions when I I loved into a trauma recess talk that you guys were getting and they mentioned Strawberry last Agassi. Now, this is quite advanced testing. All hospitals have got this. Um, but it gives you a bedside check off clotting. You take a small sample, put it into the machine, and then over a period of time, depending on whether you got access to a rapid test or the normal chart slopes lower ones. Then you can take up to 20 to 30 minutes or even an hour to get the absolute values right. The end of the test. But it's and what it does is it It watches the clock form on. We'll give you an indication of clot strength over time, say, and the the picture. The graphic we've got here and get my point again is yes. So there's a period of time where there's no clots in. That's all that's There are time, and that's where the enzymes are sort of get starting to get into gear, and then the clot formation, which takes you up to a maximum clock strength, which is called the maximum amplitude the M A. And then once that's happened, then the clot will start to get weaker and start to break down on the period of fiber and license. Now all of that's normal and should be happening. But looking at the different numbers that rate the shape of the curves could give you an idea as to which bit of the clotting cascade isn't working in a bleeding patient. And so you can, uh, replaced clotting factors. Or you can give a fibrinogen and platelets to to make the most maximum for tude stronger on if you've got excessive fibrinolysin. So this is coming down far too much in the 1st 30 minutes, then suggestion that you need to give some more antifibrinolysin. It's such a strong person Casodex on, and that's a useful test. I have not the job done and know that this is in existence. And so what are you gonna do about your shop patients then? So it is likely that you're going to need to start doing some sort of resuscitation before you're absolutely sure of the diagnosis. And if you got a patient on the ward, for example, and you come to them your first unseen, then and then you're gonna have limited information on, you're going to need to do some things to start with to start resuscitate in this patient because hypoperfusion for a long time will have adverse effects and that it will get worse and worse and potentially a course infarctions or or death. So, um, so you need to have in your mind a few things that you're going to try first off. So when it comes to fluid resuscitation, you need to decide whether you're going to be giving crystalloids or blood products on. Going to be giving bolus is of fluid, and it may be 500 miles or so in a well patient. And, you know normally well, somebody with existing cardiac disease all over frailty. You might reduce that down to, say, 250 miles Teo, because that the risk of them already being fluid overloaded it is higher. Um, there are other treatments, a swell, which are slightly more advanced, things that are only generally available in theaters or in the emergency department intensive care. And those are the medicines that will affect the vascular tone or actually get the increased cardiac contractility or the heart rate themselves. So a vase a process are things that increase vascular tone and cause days a constriction. So there are medicines that commonly in you such a snore adrenaline, which could usually can only be given centrally metaraminol, which is a perfectly available vasal constrictor, and medicines like fancy and I left friend. And so one will also do that. Um, adrenaline is the go to and catchall medication because it activates the adrenal receptors all around the body of all types, and it causes increased contractility. That's what only tropic means on. We'll also increase heart rate. So it's also krona trophic and has some days oppressor activity as well. And so if that's all you've got, then that's a that's pretty pretty useful to treat all of those things, but it's often you be useful to be a bit more subtle on day to control the vascular system a bit more nuanced. The other thing about adrenaline, though, is that it stabilizes mast cells s O in another, and that's why we give it in an F L access is to reduce the inflammation in the cascade of of information caused by neti granulation of Mars cells and anaphylaxis. Yes, that is useful for that. And then, of course, you need to think about your cause on by the longer term medication might be required to stabilize this patient. So so in an infection, then they need antibiotics. And if they've got on dream all crisis, they couldn't get steroids. If it is a critical, then they get some thyroxin. So and so, Yeah, Once you've drilled down, you know the reason. Then there will be other treatments available as well. I wanted to just mention about fluid responsiveness. So this is the concept that the vascular tree can cope with a certain amount of fluid on, but it will improve. It's good the cardiac output if you give some mobile, but only up until a point and then. But after that point, giving some more doesn't help so on, Potentially can can make things worse by overdistended, they have the ventricles. So how do you know whether your patient will tolerate more fluid or no? So you can just give him some more fluid and that you could give him a fluid challenge and see whether it makes a difference? But the downside of that is that once you've given it, you can take it back out and So if that did, it turned out to be too much, you know, one but one bolus too much, then then then then you potentially make things worse. So there are things that you can do to try to work out whether the patient will respond before you get the fluids. The most simple thing, excluding former patients with their potential fell back injury leg injury except except, and you can just lift the patient's legs up. Well, there's well, there's supine on. Do see whether that improves their BP brings the heart rate down. So, um, because that will auto transfuse the blood that was pulling in the legs back into the trunk on will essentially gives the trunk of fluid challenge when you like the legs down again. Then it all goes back to the way it was before, and you're not lost anything. The middle picture is demonstrating something called pulse pressure variation, and if you got an arterial line in situ, then you can see how the BP changes with respiration. This works best if you got a ventilated patient where every breath is the same size and the pressure in the chest is changing the same amount each time so you can compare breaths. But it does work with spontaneously breathing patients as well. To some extent, the arterial line timeframe trace on that picture has been reduced, so you'll see that the C G and the pulse trace don't match up with the same number of heart beats is on the arterial line, but you can see how there's a swing between the maximum systolic pressure between inspiration on expiration on. That suggests that that increase in thoracic pressure during inspiration has decreased venous return and has dropped the BP, which then gets better during expiration when beings return is improved them. Eso that that first with that swing on, probably it's fluid. Responsive. Um, the ultrasounds video on the left hand side is off the liver on the ivc, so I'll get my little pointer again and show you that the this is the inferior vena cable as it comes through through that route. First, the liver was dying from into the right atrium. Over here on. Do you concede that with with breathing inspiration that the obviously is collapsing and that the walls of kissing each other and and that's not normal. So that that's that patient is under filled on good do with an increase in their venous pressure to go. And there's like that is that that's going to increase their selling if you give them a for fluid bolus. I'm There are clever ways of monitoring cardiac output itself. Um, there you can use a primary artery catheter, which will use them a dilution as a technique. They're do other devices that avoid a pulmonary artery catheter. Those those devices are pretty risky, Um, such as PICO and let go. Now What they do is you have a central line in I one that's close to the heart. So ideally, um, internal jugular or subclavian, a central line on a known quantity off cold fluid with with the Peko on day or lithium containing medication on a little copay and then a detector is placed in the arterial line, often in the femoral artery, which will then detect that either arrival of cold fluid or the lithium concentration over time. Now the grass on this on this side here, it will show you that detection of the change in temperature is that this is for PICO um, you can say that very quickly. The temperature drops is colder, it is higher on the Y axis, and then it goes warmer again. There's another hum because that's the blood has gone round again, and that you get another hit from that cold fluid because that the mixing is in perfect. But the idea is that that the area under the curve, um, it can be used to calculate what the flow is that what they went through the heart to arrive at that destination? Um, the esophageal Doppler. And this is a picture of an office Provigil, Doppler trace. And what that is, is a is ah, ultrasound probe that gets put plugged, place down the esophagus and then is angled at the descending aorta, which is right next to the esophagus on. Then the flow through that through the aorta is calculated by looking at the velocity of the red cells. So this is velocity on the Y axis and time on the X axis, Um, and you can see that there is increase in flow during systole. The problem with the esophageal Doppler is that it's It uses a lot of assumptions on needs to be focused perfectly as well. Um, the assumptions are that it guess is the cross sectional area of the aorta, um, about based on the patient's sex, height and weight, Eh? So there was a lot of guesswork involved in there, but you could can be used for for looking at trends over time. Once the ah PICO and lip code devices have been calibrated, then they can be used to They can use pulse pressure variation to then given idea of what the cardiac output is. And so they live locally on also that the actual shape of the arterial I'm Tracy, the pulse Contour analysis and that that could be used over a period of time. Teo, try and monitor cardiac output and less invasively. But there's some drift on that. And so every survey to 8 to 12 hours and you need to do the the actual cold dilution or lithium dilution again to recap rate the device. So that's the sort of the cutting edge high tech end. Um, so we went from clinical assessment all the way through to, and it's a high tech Um, the summary is that the clinical assessment is going to tell you the vast majority information need to know. Um, you should consider first principles of how how the hell perfusion works and that will give you a framework of how to it. Start assessing and thinking about shock. You probably will need to start research before you get the diagnosis. Scans will help you differentiate between lots of different types of shock. And I'm happy to get some questions. I'm sorry that it did. Just talking about you a lot, but I'll go back to them back into Zine. Thank you so much, Doctor. Um um River gossip questions. Yes. There is a couple of questions in the chat. Now, pull is asking the CV pee monitoring. Have much utility in shock. Right? So CVP has been shown not to be particularly useful. Um, the if you think about what you're what you're asking the test to do. You're asking whether looking a pressure on the right side of the of the heart is giving you an idea of what the volume on flow is coming out of the left side of the heart s. So that's a big ask. And there are a lot of things in the way. So that is the right side of the heart. The pulmonary vasculature on the lungs and then the left side of the heart. And so there's a lot that can get in the way of there. Um, it's been shown that that CVP as an individual measurements ah, off left ventricular estimate and end-diastolic ceiling is is there's a poor correlation between the two. Um, that said the, um if that's all you've got, then looking at the trend of CVP over time, it may be more useful, so but as a static measurement, it's not particularly useful. Super. Thank you so much, Doctor Daryl, if I'm going to meet you, so if you can ask your question, please. We can't hear you. Tariff. If he can hear us, we still can. You Can you hear me? Okay. Yes, we can hear you now. Fantastic. So earlier on Mikey, you showed a nice echo. I think it was because you look in the LV was particularly large. It wasn't contracting that well. It had a poor ejection fracture. But you could also see the septum really kind of migrated over to the right ventricle. I wanted to know what your thoughts regarding the significance of the right side of the heart on because it literally is very heavy on L. The LV, the left side of the heart. But I wanted to know if she's going to You felt the right side part. Thanks. Thank you very much. Guaranteed question. You know that obviously, the right side of the heart is important. Um, it's ah, it's contributing to the carpet capital all the way through the ah, through through through the lungs. And it's a lower pressure system. But right sided heart failure is is particularly difficult to treat. Um, so really involvement with cardiologists? Uh, it is absolutely mandatory particular to get a decent quality echo, um, the when it's caused by a primary embolus, Of course. Then then, then then the treatments are pretty clear, and things up, such as from from the License for Massive Pee, is shown to be useful or even a clock retrieval. But but right, right sided heart failure is the presenting complaint for somebody who's who's got a spear scheme of heart disease, and they completed their infarct, for example. It's very difficult to get on top of that on, but It's got a high, more mortality, I think. Thanks. Thank you so much, Doctor Mary. It's also asking in the chart What is the role of serum Lactate in shock? Yes, so so as a center before left is they got a lot of reasons why it might go up, but in a shocked state, then it is either because there is a scheme you're going on somewhere. And so it's a sign of the anaerobic metabolism. Um, that might be just be localized. So for it might well be, you know, for example, ischemic bowel or something, Um, or critical ischemic limb. But in a in a global shot state, it's Z often a sign that there is excessive activation of the sympathetic system s so you'll see that somebody who's on adrenaline infusion well, they're locked. It will go up just just because eh, so So it's a sign that said that this there's a lot of stress on the system. So if it's raised, so above the level of four will be a warning sign for you that there's something bad going on. I understand using it as a marker of your resuscitation to see that it's coming down is a reasonable strategy, and but it is important to recognize that that's not not the only thing that makes, like, take it up into summer stopped. The mic Pahlevi is asking is cardiac tamponade also for happened Really Next shock? Um, they can go inside, so you for particularly with a trauma pension. Who's got a cardiac tamponade? He's got other injuries, then they might well believe a swell. But actually, the temple not only requires a very small amount of fluid to have escaped from from inside the heart into the pericardium, so particularly be an individual stab wound, for example, and you only need a little is 50 mills to go into the pericardial sac to toe course hypertension, um, and and complete cardiovascular collapse. Really so And so you don't have to be hyper believe it to have a temper. Nard on divisive ESA And so once, Once the fluid has been released and the heart's free to fill again, then you can have ah, astonishingly quick return circulation. Um, so it's It's in all of our and s O PS that if you do a clam shells or Khatemi for a patient with and clear out the clot, then you the in traumatic cardiac arrest. And you you better have some sedatives ready, Teo to be able to sedate the patient once they certainly perfused their brain again after finger Summer Since, um, like, um, record of the question by Mary and she's asking, what is the optimal BP to achieve? Happened Really Limit shock. Yeah, so that's a huge debate. It in bleeding patients. Then we just I think we're moving who we must be talking about, um, particularly yes. In in in trauma or or post surgery, for example. Then there's a There are lots of schools of thought. One is that the BP should be kept really low. S so, for example, a systolic of, say, 80 because you don't want to be blowing the clot off. Which is is that the theory is what would happen if you push the BP too high. Um, there's there's some evidence that that makes that that's been that's the case has been overstated, but but it's not been completely disproven yet. Um, and other people think that the brain profusion is particularly the most important thing. Uh, and so would advocate above BP more of over 100 million, 110 to make sure that the cerebral perfusion pressure is maintained. Um, so. But so that's That's particularly important in patients who've also sustained a traumatic brain injury because secondary brain prevention protectionist is a crucial during those times I am. And so I think the answer lies somewhere in between the two of those, um, there was ah ah, a move now to to do what's called damage control resuscitation on Do that is where, rather than not give fluids and only titrate a radio pulse that you couldn't continuously give fluids. Um, look to that sort of BP. So maybe 80 to 90 systolic, but then also give the patient very small doses of medications such as analgesia. It's such a Xopenex and things which will gradually reduce the sympathetic tone to make room for more blood to give so so that you can actually have more flow. But without pressure, eh? So you can keep the patient more hypotensive, improved cardiac out for improved peripheral profusion on deuce the acidosis that the patients who it is developing on prove preserve their quite well obviously. That way. Super. Thank you so much, Doctor. Mike, I've got follow up. Question. Mary's asking kind of patient have more than one type of shock. Yes, yes, absolutely. Yes. All of these things can can come inside with each other. Um, you might have, ah, patient with come back on the list. Um, you would be a common example who then developed an arrhythmia, Uh, because of their ischemia. Um, the, uh if you want. We said before about trauma patients, you might have a tension pneumothorax on behind a Valium. It from from bleeding into somewhere us. So So, yes, they can all come inside on behind. It's a suspicion off the others. Once you found one should remain traffic. And I think she's asking, how is it different in management, off trauma in hospital and pre hospital system. Okay, so what we like to do, really is is bring almost all of the things that you would would do to resuscitate a a patient who sustained critical trauma to the roadside. So we've got and honest anesthesia, surgical skills, blood product resuscitation, Um, but a tiny portable gas machine on on blood clotting on an assistant on so one that we can bring with us, but the away through the pathway for a trauma patient, the important thing is to continue to move towards definitive hemostasis. So the the the most important treatment for bleeding is to stop the bleeding to it. So you you need to be moving along the time that whilst resuscitated a Z, your first priority is to get that patient to a team that will be able to stop the bleeding and that that might be on a trip through ah hospital through a CT scanner down to with the radio, the theater or an interventional radiologist. You can then actually stopped the bleeding for you because the patients never going to get better if you with what you're pouring in through the cannula, it's pouring out through through an artery. Everything December symptomatic. Um, Mary's asking. How do you usually decide crystalloid on blood in fluid resuscitation? Yes, So you the ah yes, they're thinking about the actual cause of the loss is important. There is some evidence that even giving a small amount of crystalloid in massive hemorrhage will disrupt the endothelial glycolax and will cause fluid loss and so so given treating blood loss with blood products is a key feature, but then and so patients have lost water or or salty water from them. For whatever reason, you would try to replace that with with similar fluid. That crystal light. I think. Thank you so much, Doctor Mike. Is there any other question that anyone wants to ask? Then feel free to meet yourself, or you can also simply just write in the chart box below. I think there's no further questions. Oh, we do actually have one more question. Sorry. How long do you need to raise the legs, right? Yes, So it's not for long. So you'll normally see a A change in the pulse volume that you can feel free for feeling the pulse so you can see on the arterial line. You'll see that change within 30 seconds to a minute on. Then you can hold it there for maybe a minute more teeth, and then you can put put them back down again and you're on very quickly again. Within sort of 30 seconds. You'll see that they that goes back to the way it was before. Perfect. Thank you so much. Doctor Mike, you for coming over and spending your morning Friday reverse. I'm really did enjoy this session today. I'm especially in terms of knowing how to decipher between the all different types of shocks. What I'll do is I'll keep the channel open for a couple more minutes in case, um, she didn't still haven't received their feedback link. Um, next session will be out two o'clock with Dr Rachel Clark on. She'll be going over palliative care on managing end of life symptoms in general hospital wards. So thank you so much, Doctor Maria, for coming over and under accession. Take everybody. Yeah. Thank you, doctor.