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Join us for an on-demand session with Zack Moyer, an F1 based in London, who recently passed the notoriously difficult MRC S Part A. Despite being fresh from a challenging general surgical rotation, Zach has the knowledge and experience to teach the applied physiology part of MRC S. Not only does he bring real-life experience to the table, but he is also extremely passionate about teaching. Utilizing a patient, engaging approach, Zack delves into complex concepts such as shock, mean arterial pressure, cardiac output, stroke volume, and systemic vascular resistance. This session is perfect for those preparing for their MRCS exams, as well as medical professionals looking to refresh and enhance their knowledge. For Zack, it's all about fostering excellence in the medical field and he provides plenty of opportunities for interaction and questions. If you're serious about furthering your medical understanding, this session is not to be missed.
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Learning objectives

1. Understand and explain the concept and different types of shock in physiological terms. 2. Correctly define and calculate mean arterial pressure (MAP) using given systolic and diastolic blood pressure values. 3. Understand the components of cardiac output and stroke volume, and how they influence each other. 4. Learn to calculate systemic vascular resistance and explain its significance in a clinical setting. 5. Apply knowledge of shock, MAP, cardiac output, and systemic vascular resistance to clinical cases and scenarios, improving problem-solving and clinical decision-making skills.
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Computer generated transcript

The following transcript was generated automatically from the content and has not been checked or corrected manually.

Today to the London Foundation trainee Surgical Society teaching session today. And we've got Zack with us who is an F one who's teaching us, er, taking us through the applied physiology part of the MRC S. So, er, all of it that everybody finds tricky so well done. Zack, thank you for taking us through that. I'll hand it over to you, take it away. Yeah, absolutely. You have to forgive me. I'm not the most clued up on a medical. How do I share my screen? So there is a little button at the bottom, it says present. Now there are some tips as well that will probably have popped up in the chart for you about um, different ways of coming, how to share and make sure you're sharing the right thing. Yes. Yes. Yes, I can see. All right. I just need to um. Mm. Ok. That's a little bit annoying I think. Is that working or is that really weird? It's giving us a kind of infinite view we can see going on for? Ok. I'll try again. Sorry about that. It could, well, just be that it's that sort of screen with metal on it rather than if you're kind of switching it to something else that might just be. How about this? Oh, yeah, that's perfect. All right. Ok. Uh, happy crack on. Yeah. Yeah. Ok. Ok, cool. So welcome everyone. My name is Zack Moyer. I'm an F one and working in London, in the southwest London region. Um, I've, uh, in terms of what, what little experience I have, um, I've just come off a, a really nice general surgery rotation uh at my uh hospital. And uh in that time I sat the MRC S pass a exam uh in January, which was uh notoriously difficult and I think the lowest passmark ever recorded. Um Thankfully I passed that though, I felt like I didn't. Um I'm very grateful and I'll be sitting my part pee uh in the next uh few weeks, uh which is ambitious. I've been told. And, uh again, I don't think I'm gonna pass that but um uh I'll keep you guys posted. But yeah, in terms of te teaching experience, um I've taught, I lots of medical students, um thousands, I think in, in my years um throughout medical school and uh even as F one, so I'm really passionate about teaching and uh I'll try my best there. Um Especially teaching my fellow doctor colleagues. Um II intend no arrogance or, you know, trying to be, you know, uh aloof in my status. I'm not, I'm, I'm just, I'm just like the rest of you, um, if anything lower. So let's just get started before I, ever, before I ever like start sessions and I teach, uh, I like to set the mindset as, as the correct intention. Um, so that, you know, um, we can, we can evaluate what we're learning here. Um, uh, I think we're all doing really, really, you know, noble and amazing thing. We, we're coming out of our own hours, our own time to sit down. Um, th this evening after a long day of work, you probably come off some on calls and whatnot. It's not easy. Um, as doctors and, uh, we're still here trying to, to learn to study, um, while employed, er, to try and get those qualifications and become better doctors and surgeons, hopefully. Um, so it's a really noble, honorable thing. Um, so we really do need to hold ourselves to that account. Um, again, not speaking out of arrogance or anything like that. I'm, I'm really trying to humble myself if anything and remind myself first. So again, our mindset, our intention is correct and with that, it is, this is a principle that I always start every session with and I've always had good outcomes with that. Um, with that, um, we can start, like, is there anything better, um, is there any reward for excellence except excellence? We're trying to achieve excellence here? Let's crack on with it. Um, so, yeah, why don't we get started with a question in terms of today's session. Uh, it's a lot of physiology. I appreciate. Some of you might have part a coming up in the next sitting, um, er, which is, er, in a few weeks, a few days actually. But, uh, for those of you that are sitting in the sitting after, uh, this will be really good for you. Cos we're coming in a lot of key physiology with a few questions. This isn't that question focused. So let's have a crack at this. Um And this one at the end, so let's get the chat open over here. Um If you, if you don't wanna put messages in the chat, that's fine. I don't mind. I usually ask for people to, you know, um get as involved as possible. Uh However, if you don't feel confident that's fine, no worries. Um But you will benefit the most otherwise I'll just be talking to myself the whole time. Uh And I'm, I'm very good at doing that, believe me. So, um yeah, a patient with tachycardia hypertension is to receive uh vasopressor, which which of the following conditions is likely to be treated when they're given vasopressor. What kind of shock here? And we're gonna go into details today about shock like in, in extreme detail and I'm gonna cover it in a, in a way that I feel like was never taught to us before. Um So yeah, so that's really, really good. Uh good job guys. So, um, septic shock would be, would be a, a, uh, a, a good one. definitely. So we're gonna talk a lot about vasopressor in a minute and, um, just be patient with me, but this is just setting the scene of what we're looking at. Ok. And this is a very typical question that would come up in part a fine. So let's crack on with it. So, um, how many of us are there? I mean, there's only a few of us that's fine. We, we can be really intimate and, and I, and I like that. I like, I much prefer that actually. So can anyone define shock in, in a good definition? A good healthy definition? One that would be all encompassing and quite nice. No worries. No worries, Dr Don't worry, that's fine. But yeah, so shock, I'll, I'll just crack on with it cos just um, absolutely. Yeah. Well done. Exactly. So, uh it's inadequate perfusion. It's a, it's an inability to get those, the tissues, those vital nutrients and um metabolic requirements um to support the cellular mitochondrial respiration. That's all it is very, very broad definition. And as you can imagine, there's lots of different, you know, er, types of shock. So let's crack on with that. So, while we're here, I wanna crack some really important definitions through, they're important, they'll come later. But can anyone define what map is, what is map mean? Arterial pressure, you can define it with a formula. I'm happy with that. And that's even easier. Does anyone know how to calculate map or what, what would the, what we're working with here? And these, these are key physiological principles that we have to have locked out um before part part a really? So I'll, I'll put like a, I'll do f at most 30 seconds per question because II know we got, we got things to do. Uh got a crack on so map. Um I'll help you guys out is another word for BP. It's not the same map is a better way to assess BP. OK. So that's good. That's good guys. Well done. Exactly. That's a good start. So it's something to do with diastolic, something to do with systolic. There's quite a few ways, um, to, uh calculate it. I like to calculate it like this. I feel like the ways that were mentioned in the chat somewhat confuse me a little bit. Um, so the way I do it personally is, um, er, two times the diastolic. So let's work it out together. So let's say someone's um, 1 20/80. Uh, so 80 is a diastolic. So we do 80 times two, so two times diastolic plus the systolic, which was 120. So we're gonna add 120 to that, all of that divided by three, none of this, one third or 0.33 even though it's the same maths and there is a three. I find it easier divided by three. There you go. They're mapping 9093. So, um it's important though, to correlate what, what we accept for maps. I mean, in um BP, you know, 90/50 90/60 is when we get worried in map, anything less than 65 we're not happy with. So we've got a formula for map. What's the actual definition of a map is this, it is the cardiac output times by the systemic vascular resistance. All failure essentially has to do with this essentially broadly speaking, we're gonna get into it in, in a lot more detail. But if you can appreciate that, it's either problems, you know, with the amount of things coming out of the heart and the ability for the, the the that that outcome to be adequately pressured to get to the places it needs to go to simply put. So let's crack on. So if we've got map, what's cardiac output, I'll help you guys out really quickly. Just for the sake of time, cardiac output is the stroke volume times by the heart rate. Got it output how much the heart is pushing out. And we can define that by the physical volume of blood in a minute of how many heartbeats are being contracted. So for example, the cardiac output per minute would be uh how many heartbeats push out 30 40 100 and 20 mils of blood. That's all. It is really simple. Ok, fine how to define stroke volume really easy. It is the amount of blood at the start before the heart contracts. So once it's fully full and then minus that from the, the amount of blood that, that little bit of blood that's left in the heart at the end of contraction. Minus those two, the blood can only go through the aorta. We hope unless there's a problem. Um And that's, that's your stroke problem. So if we want to increase the cardiac output, we need to increase either the heart rates or the stroke volume. Basically. So we can increase that, we can increase the stroke volume. How by reducing the amount of blood at the end or increase the amount of blood at the start in the heart? Ok. Cool. I'm happy with that. Let's keep it moving. Now, what is systemic vascular resistance? This is a really hard formula to learn. Um It's come up in question. So just just be aware of it. So systemic vascular resistance is, is a bit of a complex one. It is let's break it down. It's the mean arterial pressure minus the central venous pressure. So it's the difference in the pressures between the arterial and venous systems divided by the cardiac output. And you times order that by 80 as you can tell, it's a very academic answer. If it comes up, you know how to answer it. Now, I think it holds very little value in the actual conceptual understanding of systemic vascular resistance. The point is how well can the pipes of the body maintain adequate pressure to carry the cardiac output? That's all it is. Ok. Fine shock is unbelievably easy to understand. Um I've had a very poor understanding throughout medical school and until recently in my surgical placement, um I spent like an afternoon with anesthetist and I kindly basically said to them, um, I'm usually trying to spend time on the other end of the table operating. And I never really appreciate you guys. I wanna appreciate you guys a lot. Please teach me what, you know, so they gave me amazing resources. They spent like, you know, unnecessary amounts of time talking to me or when they could have just, you know, scrolled on their phone or something like that. Um And they just told me that essentially it's, it's, it's one of three things f uh shock is one of three things. It's either the pump that is because remember what a shock it is is it is the inability to perfuse with nutrients, systemic body and the tissues. Ok. So it's either that the pump that's pushing that nutrient that, that, that, that, that content is failing. So it's a pump failure fine. It's either than if it's not the pump, the pipes coming, the plumbing coming from the pump is not, you know, tight enough or is very leaky or doesn't pro provide enough, you know, adequate back pressure to allow that pump to carry, er, pressure. Basically, it's like a hose, right. Um, if you have a very wide hose and a very poor poor tap, it's not gonna go anywhere. Is it that, that water is gonna stay where it is? But if you have AAA nice, uh, tight Luminal, um, hose with a, with a good pump with a good tap, it will shoot water up. So that's one thing. So pump failure, pipe failure. And the last thing is what happens if there's not, not enough content for those pumps and for those pipes, um an issue of the tank, an issue of volume. So that's where you got hypervolemia. So broadly speaking, pump failure, reduced cardiac output. That's what it means. This is predominantly called cardiogenic shock or there's a subtype called obstructive shock, which often gets mixed with cardiogenic shock. But it's referring to not that the heart isn't pumping correctly, it can pump, the muscle is fine. It's the fact that there is something blocking immediately outside of the heart, things like tamponade pneumothoraces, massive P ES these things. Ok, an issue with the pipes. This is by far the most common type of failure. By far the most common type of failure where there is a reduced systemic vascular resistance. This is known as distributive shock and can be sub broken down into septic shock, neurogenic shock, anaphylactic shock. All of those are grossly inflammatory processes minus neurogenic um where you lose the ability, you have increased permeability of those. Um uh you know, the, the the systemic vascular system er allowing for um the contents to not adequately be able to be pressured enough to push itself across. Ok. In neurogenic shock, it's not the fact that there is an inflammatory response. It's that the central nervous system isn't providing that sympathetic tone to squeeze fine. The last bit is the tank, is there not enough volume to even even with a good pump or a good set of pipes? If you, if there's not enough volume, you're not gonna move anything anywhere. It's a dry system. So either, so this is called reduced preload. Either there's not enough volume in the blood or not enough volume in the plasma really or you've lost all your blood. So we call this hypervolemic and the subcategory is hemorrhagic shock is one of them as well. So let's go into all of these at in detail. Ok. Um Let's go through a quick case. So a 30 year old lady has fallen off a motorbike, er, at speed. Um, you know, admitted under trauma, blood pressure's 100/50. Um let's work out while we're here. Why don't we work out the map? So just for fun. So 100 so 50 times two plus 100 divided by three, they're just on the edge there. They're just on the edge of er, what is acceptable map. So 65 we said it was acceptable. They're at 67 despite not not responding to fluid challenges. That's scary. That's real, real scary, man. So we've gotta be careful with that. Ok. Um So how would we assess this patient? Does anyone have an idea in the chat? Uh There's just one answer really to this. How do we assess this patient? And I'm looking for a very specific answer. Yeah. So let's put both of your answers together and we've got a beautiful answer there. So the answer is, um we would assess them in an at e fashion following the ATL S guidelines. Absolutely. Right. Um So that's perfect. So, um no, at this point, they could have any type of shock. We have not differentiated anything un very unlikely to be septic, almost impossible to be anaphylactic. Um very potentially neurogenic if they've had head trauma, fine. Um But it's likely despite fluid challenges, um their, their blood pressure's not coming up. This is probably AAA kind of um you know, hypervolemic hemorrhage, they're probably bleeding. The question is they don't have any obvious external hemorrhage. So, a good principle and trauma that we're taught is there's five places where blood can go. It's either blood is on the floor or four more. That's it. So, what are these four, the four other places blood can be if it's not on the floor around the patient will be intrathoracic intraperitoneal, retroperitoneal or pelvic slash the thigh. They're that kind of the same, uh, set of viscera almost. So, if you can understand that, that's good. So, I want someone in the charts, um, to now answer the next question. Uh, I want you to appreciate this, this, this teaching is relatively holistic. Um, it's quite hard, um, to do a lecture purely on, on shock, um, when it's a really deep anesthetic topic and we're not doing anesthetics right now. Um But I try to make it holistic in the sense of what might come up. So let's have a look at this. So can someone please try and interpret these films of this patient? It's a, it's a bit difficult. I mean, I don't know if you want to unmute or do it. You're more than welcome to. Um I'm, I'm quite relaxed. Uh I don't mind people speaking but it's a small session. So I'm happy if you're happy. If not, I'll just crack on with it and, and do my best. Oh, it's not, it's not easy. Yeah, pain is a good start. We've got an obvious set of fracture here. Obvious fracture, which is good. Any more details on that? If not, I'll, I'll help you guys out. No worries. I'm sorry if someone is still frantically typing their answer and trying to press enter, but I'm gonna crack on, feel free to, to write the answer in the meantime. Ok. So I'll have a crack at it. The answer is gonna come up, I'll have a, have a crack at it. So, um whenever we interpret films, we're always gonna say the patient details, which we don't have here, then we're gonna say this is um a radiograph or of um with ap and lateral films of um a patient's er, right femur and lower hip joint which shows a very obvious, obliquely um oblique complete fracture with full displacement at the mid er midfemoral shaft. Um And there's also something else but it's not so obvious and I think it's something to do with the other leg. So what does it say? Ap lateral radiograph? Right femur. Um I hope I said FFI if I said humoral, forgive me, I think I said humoral. No worries, no worries, no worries, Jack. If I said humoral, forgive me, I meant the femur. Um There's also what appears so in the other leg, I don't know if you can see there was a um an intra medullary nail here suggest they've had trauma in the past, but that's not relevant. OK. So why am I mentioning this? We're talking about shock. Why am I mentioning this? The reason is so does anyone know why I mention this? If they've had major trauma, their blood pressure's not adequate. They've got a massive femoral fracture. What's likely happened here, guys breathe in the thigh? The next question I need to ask you guys, how much blood can you lose in the thigh. How much blood? Yeah, Julie. Yeah, thank you, London FT S. That's very good. Exactly. About a liter per leg. So, if you've had polytrauma, that's 2 L gone. And that's automatically put you into a, a very high grade of shock of hemorrhagic of a class of hemorrhagic shock. So, how much blood can be lost? So, we said 1 to 2 L uh for femoral fractures, about half a liter for tibial fractures. And then up to 3 L if they've had major pelvic trauma, which is why you need to stabilize the pelvis with a a pelvic um uh stabilizing device. Um really good eh uh good job, good job. OK. So what's next? Now? Um this is very obviously hemorrhagic shock, hypovolemic shock. I think we're all happy with that. The question is, can someone define what hypovolemic shock it is, please. Yes, we define what shock is generally, but each type of shock is different. So here we're having a tank problem, an issue of preload, an issue of getting volume to be sent across the body. So how are we gonna divide, define that kind of shock? So there's always gonna be an inability to perfuse the tissues but secondary to what as a direct consequence of again, feel free to type the answer. I'm just gonna crack on ina inadequate information due to a direct loss of circulating blood volume that could be from hypovolemia. Generally speaking, a reduction in blood plasma volume, a reduction er leaky blood vessels as well could cause this. I know that counts as distribution, but that's still gonna cause hypervolemic shock and obviously bleeding as well. So let's crack on with that. So loss of blood loss of plasma. So major burns is a huge problem here. You lose that skin barrier. So you will lose a huge amount of blood. I need to ask you guys. Now, what is the name of the resuscitation protocol for fluids in major burns in major burns? What is the name of the resusci, the, the in the, the IV fluid resuscitation protocol that we use in, in major burns. It's something that we have to know it in part A and you should be able to calculate it as well. So it is called the modified part formula. Uh I hope someone just did that uh almost, almost part and part in formula. So, absolutely. Right. So in an adult, if they've had major, more than 15% of total body surface area burns, we should resuscitate them with um four times by the total body surface area times by their body weight. So for example, if someone has had 20% burns across their body, we'll do four times by 20. And if they're standard like 75 kg male like me, they should get 6 L of fluids. The question is, how are we gonna administer that fluid? And the fluid should be a good crystalloid fluid. So, something like Harman's is really good. Um So we should give, we're gonna divide that fluid in half. So, 3 L and 3 L, the 1st 3 L needs to be given in the first eight hours of, of trauma of the burn, of the burn, not admission of the burn. And then the next 83 L needs to be given over the next 16 hours. So, um that's fine. Ok. And it's also a reason that we don't give colloids in the 1st 24 hours. Colloids have oncotic capabilities. So, if you're giving someone a albumin and they're losing it through their plas, losing it through their skin, they could cause third spacing where you're losing that fluid from the intravascular compartment into the burns compartment, which is not good. So we try to give crystalloids cos they have low oncotic pressures. Ok. Cool er loss of body sodium and water. So that's gonna be renal issues, aldosterone issues. Um uh What, what else could it be? Um inadequate oral intake as well? So, essentially a concept called third spacing, please understand that third spacing though. It's distributive, this can cause hypervolemia as well. So I hope I hope you can appreciate that fine. Uh diarrhea, vomiting all these things fine. So here's the kicker at the bottom of the page and I'm gonna have this with every type of shock. You need to be aware of what will happen to the central venous pressure, the pulmonary artery wedge pressure, the cardiac output and the systemic vascular resistance. So we'll start at the end. This patient is not having enough circulating volume. The body recognizes this with the baroreceptors, it will squeeze. So you'll have a high systemic vascular resistance. You will also detect that there's low BP. So the cardiac output will be increased and they'll try and increase the heart rate that's fine. Despite this, the central venous pressure is still going to be low because there's not enough fluid there in the to begin with. And it's the same with the arterial side as well. That's all BP will be low. However, they respond well to um fluid boluses. Um What would you initiate in a, in this patient there? Um If they're, if they're, if they're having, you know, major blood loss, what are we gonna start a very common concept? Typical part, a question. We're gonna start the major hemorrhage. Yeah. Good job guys. Yeah, cool. Replace blood with blood uh as best as we can and we'll cross match 6 to 10 units. Um We'll do a fast scan, which is an ultrasound scan, er, where we look for focal signs of bleeding as well. Fine, good job well done guys. Now, this is a very important slide that I want you all to be comfortable with. It takes time to learn and you might have to write it out a few times, but you should be able to learn it. There are different classes of hemorrhagic shock that you need to be able to identify and they use a variety of parameters. It i it's not something that I can, you know, say, ok, blood loss up to here and here is this one and then blood volume percentage is up to here and here. And this one I can't give you that. I can't spoon feed you this. but I can tell you some quick tricks, BP is normal in the first two shocks levels. So if you see a normal BP, that's a kicker. That's a, that's a key thing that you need to know that your, if it's normal BP, the shock is here somewhere. The, the shock is gonna be here somewhere. If it's decreased BP, you know, you're somewhere here. Fine. Heart rate is a good way to classify it because they're absolutely different. So if the heart rate is between 100 and 120 that's always 2120 to 143 and, and so forth and the same thing with urine output as well. Ok. If you can, I do that, that's p that's actually very, very good. Uh The respiratory rate, I've seen conflicting answers for that. So I'd I'd just be careful with the respiratory rate with that being said. What class of shock does this patient have of hemorrhagic or hyperemic shock? Yeah. 000, so we have some mixed answers. I believe the answer is indeed class two because of the heart rate being, let's look, just check the heart rate. Yeah, it's within that. Uh the reduced pu pulse pressure, but the normal BP, reduced pulse pressure, but normal BP. Good job and the urine output of 25 mils. Let's see that. Yeah. So there we go. We're, we're firmly in class two though. So don't worry, guys. Good job. Very typical part. A question. They're gonna get this all the time. You need to be able to identify your different classes of shot guys. Ok. Uh Again, I wish I could just give it to you in your hands, but I really can't. All right. All right. Next thing. Ok, let's move on to cardiogenic shock. So, um, in terms in terms of like hypervolemic shock, um, there's quite a few things that we can, we, we can do there, but I'm gonna cover what agents and what kind of med medications that we can give in, in a lot of detail. It will be, um, mind numbing, I guarantee you. Um It's a good question. Uh London FT SS as far as I'm aware. Um, it's, it's difficult. It's ad let's, let's go back to that, then let's have a look at it. My inclination is, for example, if someone objectively lost 1700 L of blood in an operation, but they're still like having class two symptoms. I would put them in class three. But that's, that's anecdotal. Er, you should probably check, we should probably check some guidelines for that. Um, I, I've not really read into it if I'm honest. So I don't want, I don't wanna, I don't wanna talk too much where my expertise does not lie. Ok. Fine, cardiogenic shock. What did we say? This was? We said so. Ok, guys, we, we've left the tank, the tank has been left with, we, we've, we've fluid repeated them. We've put, we've, we've replenished their fluids, we've given them lots of IVF, we've given them cross matched o negative blood. Um, er, we've replaced their volume, which is really good. Good. Ok. Now we have a different issue, a different patient. There's an issue with the pump. Can anyone define what cardiogenic shock is? I need a good, healthy definition of cardiogenic shock. Yes, it's gonna start with an inability to adequately perfuse the tissues. Why? What's it secondary to? I've kind of given away the answer a little bit but, you know, make me happy. Let's see. Let's see. Something. If not, I'll just crack on. Yeah, I mean, fine. Exactly. Um, but it's specifically left ventricular dysfunction. Er, so yeah, again, inability um to deliver oxygen and nutrients to the organs. Yep, direct result of myocardial dysfunction, heart muscle, not pumping properly. Fine. Ok, cool. Let's go over some courses. There's quite a few but I'm gonna help you out with it. Um And always good to categorize things in terms of, you know, the heart rhythm rate. Um, you know, any ischemic episodes, valvular problems, um, uh direct toxins medications that have slowed the heart down these things. Ok. So let's cover it. Brain and rhythm. Very simply, are they bradycardic or are they, uh, is the heart going so fast? They cannot get an eye like a sensible cardiac output is not, is not achievable even with a high heart rate. Fine. Um right and left failures, left failure specifically would be a myocardial infarction. This is the most important one here. Ok. Fine, valvular problems are the valves obstructing or not allowing blood to get out of the aorta direct toxic in, in involvement. So what do we say? Medication toxicity, calcium channel blockers, especially the non dihydropyridines. So your dilTIAZem and verapamil directly slow the AVN down beta blockers have again, beta one adrenergic antagonistic effects, they slow the heart rate down brash syndrome. Um is a, is AAA multitude of things, but it's secondary to a V node. Uh dysfunction. OK. That's really good, good job guys. Um And of course, if you've had thoracic trauma, um your heart will and it's been like bruised, it won't contract properly and it could actually develop er toxic symptoms. Unfortunately, now, there's one thing here, you might say, wait, Zack, you've missed out things like tamponade pneumothorax. I want you to appreciate that. That's not inherently a problem of the myocardium. It's a problem of something compressing the fixed compartment of the fibrous me peri pericardium. So that's what a tampon does. A massive pe blocks the pulmonary um arteries. Um A tension pneumothorax would cause mediastinal compression and uh a huge obstructive pressure. So, yes, it's a form of pump failure perhaps, but it's not myocardial dysfunction per se. Um I hope you can appreciate that. Fine. Let's crack on. Um again, the same concepts that I'm gonna keep crying on at the bottom. You need to understand them cos they'll come up. Let's look at the, the end of it first, in cardiogenic shock, the obvious problem is the fact that there is a reduced cardiac output. So the cardiac output will be reduced. The body tries to fight this with baro baroreceptor responses with a increased systemic vascular resistance to try and help the heart get some preload back into the heart, some afterload and preload fine. The central venous pressures and the pulmonary artery wedge pressures will also be high because again, it's trying to fight that, that really crappy pumping of the heart. There's no hyperemia, there's no hypotension. So it's ok. I mean there is hypertension but there's no um how do I say hemorrhage is what I was trying to say, sorry, there's no loss of, you know, um plasma or, or blood content fine, cool. This is just a little bit about er obstructive shock. Um again, very similar to cardiogenic, the same parameters at the bottom. Just I want you to understand that they are um you know, though there are pump failure, perhaps it's not a direct myocardial problem. Fine, cool cardiac shock. Awesome. Fine. Let's go over a case. There's a 50 or eight year old gent uh admitted to ITU following AAA normal total hip replacement. Ok. They've been requiring metaraminol in recovery and their BP is still yet to normalize. The pre op hemoglobin was 12.5 and a heme Q done in itu heme Q if you don't know is a uh a quick itu tool where you can get a quick blood sample like a V VG like that at that level of speed and you can find out so many things you can find out again. Um er again the hemoglobin, er there's also a tag which, which will tell you like if they're having any clotting disorders as well. This is all itu kind of stuff which is quite nice, fine. Um The, the operation was OK. Uh There was, there was less than 500 mL of intraoperative blood loss, which is um you know, very normal and in the operation they always give a lot of fluids as well. Um And there wasn't a massive drop in um in hemoglobin, not, not a huge huge drop. So the question is what kind of shock is going on here and we're gonna do it the same as before atl sat E approach. At this point, this could be any kind of shock. Again, they could have hemorrhaged even though it doesn't look like it, there could be in sepsis even though it's way too soon. Uh They could have neurogenic shock secondary to the anesthetics, especially if they had a spinal or an epidural, it could have gone really high and caused a, you know, a, a neurogenic problem. Uh There's a lot that could be happening right now. Ok. So at this point, we need to rule all of them out. If this was a cardiogenic shock, what uh what, what do we want our intervention to ultimately do? It's a good question. So the, what I'm trying to ask here is guys, I'm gonna tell you this was cardiogenic shock. Let's just assume this was cardiogenic shock. If we were to intervene with medication and therapy, what would we want that medication and therapy to achieve to do? It needs to increase certain things. What would it want? What would we want it to increase ultimately? Do we have any ideas? Thoughts concerns? Oh, lots of messages. Oh my God. Increase the inotropia of the heart of the myocardium. Exactly cardiac output and and systemic vascular resistance. We wanna keep that up as well. So how do we increase the cardiac output? We have to increase the heart rate. That's one thing and the stroke volume somehow. So that's really good. So we'll give medications again. Just go back to your form. Me, don't forget your form. Ok. So we wanna increase the, er, somehow we wanna increase the stroke volume and the heart rate ultimately. Right. I'm happy with that. Fine. Now, we need to learn some terms. So there are some drugs that we're gonna learn about that. We need to be aware, you're gonna see them in the questions and if you don't know what they are, that's a bad start to that question in your part, a exam. So we need to know what these questions are. Er these er drugs are, how they work and when do we use them? We know that and we're gonna be in a very good place. So there's a, there's a term called a symt sympathomimetic. Um It's really simple, they mimic the sympathetic er activation of the adrenergic receptors. Um So the one that they was mentioned in the question was metaraminol. Metaraminol is a really, really common drug used in the ITU setting. And er the anesthetic setting's a powerful alpha one agonist, really powerful. So it, it helps with systemic vascular resistance. That's why they were giving it to try and fight that sys that, that low BP by increasing the systemic afterload o of the so that the heart has something to push against. So we get some kind of pressure, some something that allows the heart to, you know, get it, it's output adequately done. Ok. Next I hope we can all identify what inotrope is. I'm just gonna, it's way too basic. I hope you all know what it is. Something that increases cardiac contractility. A pharmacological agent that increases the contraction of the heart. Very good. Typically be to one good a chrono is something that increases the heart rate, which is also very good and both of these things. So if there's something that is positive inotropic and post positively chronotropic, that suggests a positively cardiac output kind of drug, which is really good. Um There's fancier drugs out there that increase loose trop so the ability to relax, which is also very important, but that doesn't concern us right now. Fine. So let's look at this. These are the drugs that you need to be aware of. Um and we're gonna go into detail with some of them. So you've got your adrenergic agonists, that's your adrenaline NORAD as well. Um You've got dopaminergic agents. So dopamine, fine, they work on D 1 D2 receptors and beta one receptors. Dobutamine, one of the most common, one of the most common um dopamine er drugs that we use. Ok, you've got more advanced drugs like phosphodiesterase inhibitors um that we will not touch today and again, vasodilators, we won't touch them today. Fine. Next thing you guys tell me which receptor does nor noradrenaline mainly bind to typical part a question. You either know it or you don't, don't play games, London FT SS Jack our in house sho says alpha one. What do our other colleagues say? Is he right? Judy Duques says beater 10 my God, this is spicy. We've got, we've got some action here. Oh my God. Who's gonna win? Oh, hello. You see a good deal for us. Uh, no, we've left Julie and our dust. Julie come back to us. It is alpha one. Unfortunately. No worries guys. Good job. I'm just trying to be, I'm just being silly. Don't worry. Good job. Exactly. So alpha one, so noradrenaline, really important drug. Um, we're gonna talk about what it does. Ok. It's something, it's a class of drug called vasopressor. Something that causes peripheral vasoconstriction, really important that we're gonna use it and use it in the it. Second, a lot, a lot of no ad is used in ICU. So it's, it works with alpha one, alpha two, agonism, but it's more potently alpha one than alpha two. Ok. Always remember if it's a vasopressor, it doesn't really affect beta one, beta one is predominantly left ventricular contraction. Alpha one is your smooth muscle cells. Uh, a lot of the time, er, it also will, of course have alpha one will have some um uh cardiogenic um uh inotropic effects as well and um chronotropic effects, but it is a very potent vaso constrictor. So we use noradrenaline, um, uh neurogenic distributive septic shock, the inability to maintain, er, the pipes basically. Ok. I just wanna go back one second. Uh fine. OK. So let's go back to this case. So thank you for that little question. We talked about noradrenaline. Here's a summary table. We've all seen this table. It's very famous, it's on E MRC S. Um So you should all be aware of it, aware of it. Adrenaline activates most things NORAD typically alpha one, dobutamine beta one dopamine. Uh yes, it does do dopamine receptors, of course, but it also has some alpha beta. Ok. So in this patient that we just saw the one who had a total hip replacement and is having metaraminol and whatnot. Um an echocardiogram uh shows left in dysfunction. What inotropic agent is the best thing to give in cardiogenic shock. What do we give want to be given cardiogenic shock? Part? A question comes up left ventricular dysfunction shock. What did we give Julie? You've left us all in the dust. We, we are the losers. You're the winner. Wow, we didn't, I didn't even have a chance to even catch my breath and you already won. Yeah. What, what a come back, come back of the century. Congrats er top 10 moments of London FT Ss Julie's come back. All done. Fine. So absolutely. Is dobutamine good. So it's the first choice agent always. Ok. And it's also used just as a quick fact. We use it a lot in um in um when assessing uh cardiac function, we can do something called debut stress test testing. Um er because it increases the heart rate, it's positively contro positively inotropic. Er, it's a beta one agonist at heart even though it's derived from dopamine. Ok. So b1 b2 agonist with some vasodilation, some vasodilation, this is caveat. I'll tell you why. Ok. Um positively atropic, positively chron chronotropic increases contractility and heart rate. If someone's heart is not pumping properly in terms of heart like acute pulmonary failure, um heart failure gives something that will squeeze the heart better and increase the heart rate. Those are the most important things for cardiac output. I'm happy with that fine. Uh These are just the mechanisms of action of like what, what actually happens. Um But that's a bit, we don't need to talk about that right now. Let's just crack on. I'm just worried of the time. I don't wanna spend more than an hour on today only because I know I know we have quite a few things to crack on with. Um Yeah. OK. Fine. Uh Now we have another question. So a 23 year old woman is admitted with severe pyonephritis and um perinephric abscess or not good er during the er attempted percutaneous drainage, she developed hypertension and tachycardia of the physiological changes described below. What, which is not typically associated with such an event. What do we think is the answer a bit more challenging this question but not impossible. Eh The damn damn damn London FT Ss. Wow, they put us all to shame Jack. Leave some for the rest of us, man. What are you doing? What are you doing? Absolutely. Right. So good. So this woman during the procedure has developed, you know, shock. Um There's another principle I'd like to say, well, yes, we used a lot of key nice anesthetic words to define shock, but I hope you can all appreciate that shock ultimately is kind of low BP with high heart rate, really grossly speaking. So this patient, when you see hypertension and tachycardia, this is shock, right? This is not good. Um So they severe pyonephritis. So they have a severe infection with localized abscess. So they're, they're gonna be very, very, very septic, very septic. They're gonna have a cytokine storm inflammatory markers all over the place. Every blood vessel is contracting and um uh and dilating. There's gonna be gross inflammatory um dysfunction here. This is without a doubt sepsis. So let's look, go through each one which one is least likely to happen. So you do get tachycardia and sepsis, you do get systemic inflammatory responses. Your kidneys do shut down in sepsis, increased systemic vascular. Your body would try to do that at the start, but it would fail and it would lose. So you'd have decreased systemic vascular resistance, well done and you will have increased body output. Absolutely. You would cos your, your heart rate, your BP, you're trying to maintain something there. Good job. Hold on. And here we're going up to one of the final parts of shock, distributive shocks. We've covered hypervolemic, we've covered cardiogenic. Let's cover the last little bit of distributive shock. Er, and, er, then afterwards you have permission to pass part A and hopefully a, ok. So again, this is an issue of the pipes. Um, no, no, Julie Julie. Ah, it's been so good having you, man. Um, The pleasure and honor has truly been mine any time. Um Hope to see you at more sessions that these guys organize. Um Yeah, feedback is I love a bit of you know, feedback. I don't need food. I don't need water. I've seen feedback forms. That's all I need. Give me those and, and I'm good. Er so let's just finish off today and we'll be done really quickly. So pipe failure is distributed for shock. Your heart can pump as hard as it once you can have 20 L of blood in, in your body. But if the pipes are not tight, you're not getting that blood anywhere, are you? So it's a pipe failure. So the definition of pipe failure or a distributive shock is a relative state of hypovolemia without hemorrhage or loss resulting from a incorrect distribution of the intravascular volume around the body. It's a poor placement of the of the fluid. You might have enough fluid in there, but you're not placing it in the right places. That's all it is. And as I said, it is by and large, the most common form of shock because sepsis is more common than major trauma. Ok. For the si, for the simple answer is that more people develop sep sepsis than they do major hemorrhage protocols and stuff like that. Ok. Cool. So, in terms of that, um two principles really, it's either centrally. They're not, they've not, they've not got enough tone, they've not got enough vascular tone to keep the pipes tight or the pipes are so loose and leaky that they third space. They, it's not in the space of where it should be. If that makes sense, it, they, it gets lost to the um peripheries, er, that fluid. So it's a shift of the intra vascular volume to the interstitial fluid, which is not good. All right, let's crack on and finish this off. E so the causes, here's where we get everything it all comes out here. So, sepsis, very, very common, the most common. And that, and that causes a, a systemic upset and inflammatory response. Loads of cytokines, lots of interleukins, lots of vascular smooth muscle cells that go to sleep and relax. That's the problem. Anaphylaxis is a very similar thing. It's a gross inflammatory response. Any inflammatory disease, pancreatitis, embolisms, fine neurogenic is the other one. So, if you're gonna take something from today, sepsis and neurogenic are both very, very, uh important distributive shocks. Um So let's just finish that off a sec. Yeah. So uh remember you have very important set of tones in the body. You've got a vagal tone and sympathetic tone, vagal tone. Those are your parasympathetics and sympathetic with sympathetics. If you have a spinal cord injury or a um uh like anesthesia, that an epidural or a spinal anesthesia that puts the spine to sleep essentially or inhibits it, you will have a loss of sympathetic tone and the parasympathetic tone will, will um how do I say take precedent? The reason being the parasympathetic tone comes from higher up in the, in the central nervous system, it comes from the brainstem, er, and the, the, the central er, the more the, the core cerebrum. But sympt tone is predominantly pushed by the um the sympathetic trunk and whatnot. Er, that being said, if you do sympathetic tone, your blood vessels dilate your heart rate goes down and your vagal tone takes over, which inherently has a bradycardic effect and a vasodilatory effect. That's the problem. So, sepsis does. And here's the key thing in sepsis. I hope I hope you can appreciate this. They will have warm peripheries and will respond to intravenous fluids in neurogenic shock. They will not respond to intravenous fluids very well. They won't appreciate that the fluid has entered their vascular space and they won't increase the systemic vascular resistance after that because the, the vagal tone is so strong, the overpowering vagal tone is so strong if that makes sense. Ok, let's crack on some important definitions of sepsis. You need to know off by heart sss systemic inflammatory response syndrome is as follows. It is in the name and you have two of the following. You need to know these two and it follows, you know, the QOF um what's it called criteria? Just be, be aware of that and make sure that you are fully clued up on Q sofa, um especially for sepsis. So, one of the two of the four following you need to have them to have, sir. Um I mean it's relatively easy if I'm honest, um either have a temperature, be tachycardic um and have white cells, it's not too hard. So then what is sepsis, sepsis is SARS specifically from infection. Then severe sepsis is when you're starting to get hypotensive and hyperperfusion as well as end organ damage. Fine. Then septic shock, I'll define it for you is severe sepsis that does not respond to fluid resuscitation where the map is below 65 and the lactate is more than 2 to 4. That's, that's what septic shock by definition is. Again, QOF is your, is your, is your best friend here? Ok. So let's crack on with another question here. 52 year old man developed septic shock following a Hartman's er resection er for a perf perforated diverticular disease. Good, good, good. Uh He has started on an adrenaline infusion in which of the following is least likely to occur. Adrenaline infusion. Yeah. What do we think? Any, any clues, any ideas, if not, I've got you guys, don't worry. I always got you guys. Let's talk about adrenaline then. So we know we give adrenaline in things like anaphylaxis um in cardiac arrest because it has some really good effects. Um it, it's very, very, it's an adrenergic agonist. So we, we know what that will do. So we know it will increase the heart rate, it will cause peripheral vaso constriction. These two are very part a they always like to mention these side things about glucose and you know insulin sensitivity and stuff like that. So just some key things about adrenaline, it inhibits insulin. It promotes glycogenolysis and gluco neogenesis and lipolysis. Thus all increasing serum glucose. Why? Because you need serum glucose in the acute fight to fight response. It does not, it does cause by the way, peripheral vasoconstriction very much. So, but centrally on the coronary arteries, it does not cause vasoconstriction. So that's the answer. B that's the least likely one to occur. There's a quick thing about adrenaline, very positively, inotropic vasopressive and chronotropic beta two effects. Ultimately, and alpha effects, we we saw this before it affects alpha one, alpha two, beta, one beta two. all to increase the systemic vascular resistance and the heart rate. Ok. Uh Just as a side thing, it does increase glucose, just be aware of that OK. I'm happy with that if you are last little bit. Now, guys, all almost there. So, neurogenic shock. So we covered septic shock as a as a form of distributive shock. We know anaphylactic shock inside out uh a neurogenic shock. Ok. This is a type of distributive shock again, hypertension. However, there is bradycardia. The reason there's bradycardia is because there's loss of synthetic tone and unopposed vagal stimulation of the of the um S AM. Ok. Thus, the autonomic pathways are disrupted and you're not able to adequately get a cardiac output out. This is a pipe failure, ok. Loss of sympathetic tone and unopposed vagal activity and it will cause these three things, as we just said, fine. Now, this last slide on the whole thing, how can we help treat patients with, you know, um neurogenic shock? Ultimately, they're bradycardic fine. So we need to increase the cardiac output somehow. Hopefully, with an inotrope that would increase contractility fine and they just this decreased systemic vascular resistance. We need to increase um the systemic vascular resistance. So, dopamine in, in neuro in like uh neurosurgery itu and whatnot is one of the most common drugs. Ok. It's really good at vasoconstriction um when in com combination with inotropes, um we can give some inotropes uh such as um adrenaline's one of them. Um but we can also increase the heart rate with atropine. Er remember in bradycardia, we give atropine because it is a um Muscarinic antagonist. Um So that's fine. I think um in terms of that, I think that would be me almost done. That's a quick overview of all of the shocks that we have and trying to apply them to questions in part and physiological principles that will put you in a good stead for the exam, hopefully. Um But yeah, part A is an awful exam guys. So the fact that, you know, you are um studying for it while working, er, is a good sign and uh just keep it up, uh go get through your questions. Um It does get easier. The exam will feel horrible. Um But you'll be surprised at your result, I'm sure put in the hours, put in the work, do the questions and you'll, you will be fine. And does anyone have any questions uh for me? Uh that's me done. Er, any questions, any concerns, anything that you want me to try and address if I can, uh if you're on linkedin, drop me a connect and email me if there's any issues or anything you want to clarify. And again, I cannot thank LFT Ss our good friend Jack. So kind for them to let me teach. So kind. No, thank you so much for coming along. Zack. Really our pleasure to have you um uncover that really fantastically in detail. I hope we don't have any anesthetic consultants listening in or they'll poach you away from the surgical life because you, no doubt, be excellent in there as well. Um So yeah, I, if there are any questions, feel free to throw them into the chat, anyone, um, you'll get a feedback link as well, which I'll um pop into the chat. Now, it will also get emailed out to you. Um, if you put that in, then you'll be able to get a certificate for attending it. Also, all the feedback goes to Zac, which of course helps him with his portfolio, his development as an educator. Um And um yeah, it's really helpful for us as well as a society in terms of organizing these events and knowing what we can do and what we can do better. Um But yeah, if there are no other questions going into the chat hall, I left then is just thank you, Zach for coming along. Good luck with part B. I'm sure you'll absolutely. Um based on the way you talk about, um, I really enjoyed that. I got out of the session. Thank you, Jack. Thank you so much. Thanks guys. All right, bye bye. Thanks everyone for coming. Our next one is next week 22nd. Um And I think we have colorectal surgery, so we'll see you all for that.